Component

Shikimic acid

A nonaromatic plant and microbial metabolite connecting chorismate biosynthesis, cofactor requirements, microbial vitamin precursors and context-specific mammalian experimental responses.

64 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

Human evidence only

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

Shikimate is the carboxylate conjugate base of shikimic acid, with the same stereochemical scaffold.
Shikimic acid → Shikimate anion source_derived_draftungraded
Experimental context and source evidence
evidence_access
Authoritative chemical identity/property records, PUG REST properties retrieved; not a biological experiment. Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_model
Chemical identity records; acid-base relation rather than a therapeutic effect.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
Shikimate is the carboxylate conjugate base of shikimic acid, with the same stereochemical scaffold.
primary_references
PubChem shikimic acid CID 8742 and shikimate CID 7057976 | 2026 | https://pubchem.ncbi.nlm.nih.gov/compound/8742 | https://pubchem.ncbi.nlm.nih.gov/compound/7057976
primary_references
The metabolism of shikimate in the rat. | 1978 | DOI 10.1042/bj1700257 | PMID 637841 | https://pubmed.ncbi.nlm.nih.gov/637841/ | https://doi.org/10.1042/bj1700257 | https://pmc.ncbi.nlm.nih.gov/articles/PMC1183892/
source_locator
Reviewed reference lines 5-5; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 5–5
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Chemical identity records; acid-base relation rather than a therapeutic effect. · source_derived_draft · unverified_draft
**One chemical scaffold, two protonation states.** Shikimic acid is (3R,4S,5R)-3,4,5-trihydroxycyclohex-1-ene-1-carboxylic acid, C7H10O5, molecular mass 174.15 g/mol. Its ring is not aromatic, so calling it a phenolic compound is chemically misleading even when a paper does so. Shikimate is its carboxylate conjugate base (C7H9O5−); charge is meaningful, but these must remain connected identities. Neither is oseltamivir, anisatin, triacetylshikimic acid or 3,4-O-isopropylidene shikimic acid. Plants and many microorganisms use the biosynthetic pathway; humans have no complete endogenous shikimate pathway. Absence of that pathway does not mean an ingested molecule cannot be absorbed or metabolized by the host–microbiome system. [PubChem shikimic acid CID 8742 and shikimate CID 7057976](https://pubchem.ncbi.nlm.nih.gov/compound/8742) [The metabolism of shikimate in the rat.](https://pubmed.ncbi.nlm.nih.gov/637841/)
Complete structured claim and evidence
Antibiotic treatment suppressed characteristic shikimate-derived metabolic products in rats.
Shikimic acid → Rat gut-dependent shikimate biotransformation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_contrast
{"intervention": "Shikimic acid after antibiotic treatment", "comparator": "Shikimic acid without antibiotic treatment", "endpoint": "Antibiotic treatment suppressed characteristic shikimate-derived metabolic products in rats.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Rat oral tracer study with antibiotic perturbation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Broad microbial perturbation, not selective EPSPS inhibition or lack of host metabolism.
plain_language
Antibiotic treatment suppressed characteristic shikimate-derived metabolic products in rats.
primary_references
The metabolism of shikimate in the rat. | 1978 | DOI 10.1042/bj1700257 | PMID 637841 | https://pubmed.ncbi.nlm.nih.gov/637841/ | https://doi.org/10.1042/bj1700257 | https://pmc.ncbi.nlm.nih.gov/articles/PMC1183892/
source_locator
Reviewed reference lines 85-85; exact primary location described in quoted passage where extracted.
trigger_kind
machinery_impairment Imported condition classification; unverified.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 85–85
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat oral tracer study with antibiotic perturbation. · source_derived_draft · unverified_draft
**Gut metabolism and host conjugation must be distinguished.** The 1978 rat study traced oral shikimic acid into urinary hippurate, hexahydrohippurate, tetrahydrohippurate, two dihydroxycyclohexanecarboxylate isomers, catechol conjugates and expired CO2. Antibiotic treatment suppressed the characteristic conversion, implicating initial gut-microbial transformations. Host metabolism of microbial products still occurs. Hippurate contains a glycine conjugate, but product detection does not establish clinically significant glycine depletion or an identical human quantitative pathway. No assertion that parent shikimic acid is directly converted to every final product in one reaction is made. [The metabolism of shikimate in the rat.](https://pubmed.ncbi.nlm.nih.gov/637841/)
Complete structured claim and evidence
Shikimic acid reduced the LPS-associated protein readout for mouse-il6 in BV2 cells.
Shikimic acid → Mouse interleukin-6 / Il6 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
LPS without SA added · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS without SA stimulus · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "SA plus LPS", "comparator": "LPS without SA", "endpoint": "Shikimic acid reduced the LPS-associated protein readout for mouse-il6 in BV2 cells.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "shikimic-acid", "state": "added"}, {"entity_slug": "lipopolysaccharide", "state": "stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Expression or secretion endpoint; not direct enzyme catalytic inhibition, binding or a human response.
plain_language
Shikimic acid reduced the LPS-associated protein readout for mouse-il6 in BV2 cells.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 63-63; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 63–63
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h. · source_derived_draft · unverified_draft
**Inflammatory expression and phosphorylation are distinct endpoints.** In the same BV2/LPS model, shikimic acid reduced Il6, Tnf, Nos2 and Ptgs2 transcripts at 12 h; protein/secretion measurements at 24 h also decreased. At 1 h, p65 and IκB phosphorylation decreased and IκB degradation was reduced. These changes do not establish direct inhibition of COX-2 catalysis or direct binding to every signaling protein. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
Shikimic acid reduced the LPS-associated transcript readout for mouse-il6 in BV2 cells.
Shikimic acid → Mouse interleukin-6 / Il6 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
LPS without SA added · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS without SA stimulus · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "SA plus LPS", "comparator": "LPS without SA", "endpoint": "Shikimic acid reduced the LPS-associated transcript readout for mouse-il6 in BV2 cells.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "shikimic-acid", "state": "added"}, {"entity_slug": "lipopolysaccharide", "state": "stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Expression or secretion endpoint; not direct enzyme catalytic inhibition, binding or a human response.
plain_language
Shikimic acid reduced the LPS-associated transcript readout for mouse-il6 in BV2 cells.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 63-63; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 63–63
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h. · source_derived_draft · unverified_draft
**Inflammatory expression and phosphorylation are distinct endpoints.** In the same BV2/LPS model, shikimic acid reduced Il6, Tnf, Nos2 and Ptgs2 transcripts at 12 h; protein/secretion measurements at 24 h also decreased. At 1 h, p65 and IκB phosphorylation decreased and IκB degradation was reduced. These changes do not establish direct inhibition of COX-2 catalysis or direct binding to every signaling protein. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
Shikimic acid reduced the LPS-associated protein readout for mouse-nos2 in BV2 cells.
Shikimic acid → Mouse inducible nitric oxide synthase / Nos2 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
LPS without SA added · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS without SA stimulus · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "SA plus LPS", "comparator": "LPS without SA", "endpoint": "Shikimic acid reduced the LPS-associated protein readout for mouse-nos2 in BV2 cells.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "shikimic-acid", "state": "added"}, {"entity_slug": "lipopolysaccharide", "state": "stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Expression or secretion endpoint; not direct enzyme catalytic inhibition, binding or a human response.
plain_language
Shikimic acid reduced the LPS-associated protein readout for mouse-nos2 in BV2 cells.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 63-63; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 63–63
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h. · source_derived_draft · unverified_draft
**Inflammatory expression and phosphorylation are distinct endpoints.** In the same BV2/LPS model, shikimic acid reduced Il6, Tnf, Nos2 and Ptgs2 transcripts at 12 h; protein/secretion measurements at 24 h also decreased. At 1 h, p65 and IκB phosphorylation decreased and IκB degradation was reduced. These changes do not establish direct inhibition of COX-2 catalysis or direct binding to every signaling protein. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
Shikimic acid reduced the LPS-associated transcript readout for mouse-nos2 in BV2 cells.
Shikimic acid → Mouse inducible nitric oxide synthase / Nos2 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
LPS without SA added · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS without SA stimulus · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "SA plus LPS", "comparator": "LPS without SA", "endpoint": "Shikimic acid reduced the LPS-associated transcript readout for mouse-nos2 in BV2 cells.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "shikimic-acid", "state": "added"}, {"entity_slug": "lipopolysaccharide", "state": "stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Expression or secretion endpoint; not direct enzyme catalytic inhibition, binding or a human response.
plain_language
Shikimic acid reduced the LPS-associated transcript readout for mouse-nos2 in BV2 cells.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 63-63; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 63–63
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h. · source_derived_draft · unverified_draft
**Inflammatory expression and phosphorylation are distinct endpoints.** In the same BV2/LPS model, shikimic acid reduced Il6, Tnf, Nos2 and Ptgs2 transcripts at 12 h; protein/secretion measurements at 24 h also decreased. At 1 h, p65 and IκB phosphorylation decreased and IκB degradation was reduced. These changes do not establish direct inhibition of COX-2 catalysis or direct binding to every signaling protein. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
Shikimic acid reduced the LPS-associated protein readout for mouse-ptgs2 in BV2 cells.
Shikimic acid → Mouse cyclooxygenase-2 / Ptgs2 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
LPS without SA added · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS without SA stimulus · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "SA plus LPS", "comparator": "LPS without SA", "endpoint": "Shikimic acid reduced the LPS-associated protein readout for mouse-ptgs2 in BV2 cells.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "shikimic-acid", "state": "added"}, {"entity_slug": "lipopolysaccharide", "state": "stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Expression or secretion endpoint; not direct enzyme catalytic inhibition, binding or a human response.
plain_language
Shikimic acid reduced the LPS-associated protein readout for mouse-ptgs2 in BV2 cells.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 63-63; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 63–63
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h. · source_derived_draft · unverified_draft
**Inflammatory expression and phosphorylation are distinct endpoints.** In the same BV2/LPS model, shikimic acid reduced Il6, Tnf, Nos2 and Ptgs2 transcripts at 12 h; protein/secretion measurements at 24 h also decreased. At 1 h, p65 and IκB phosphorylation decreased and IκB degradation was reduced. These changes do not establish direct inhibition of COX-2 catalysis or direct binding to every signaling protein. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
Shikimic acid reduced the LPS-associated transcript readout for mouse-ptgs2 in BV2 cells.
Shikimic acid → Mouse cyclooxygenase-2 / Ptgs2 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
LPS without SA added · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS without SA stimulus · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "SA plus LPS", "comparator": "LPS without SA", "endpoint": "Shikimic acid reduced the LPS-associated transcript readout for mouse-ptgs2 in BV2 cells.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "shikimic-acid", "state": "added"}, {"entity_slug": "lipopolysaccharide", "state": "stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Expression or secretion endpoint; not direct enzyme catalytic inhibition, binding or a human response.
plain_language
Shikimic acid reduced the LPS-associated transcript readout for mouse-ptgs2 in BV2 cells.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 63-63; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 63–63
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h. · source_derived_draft · unverified_draft
**Inflammatory expression and phosphorylation are distinct endpoints.** In the same BV2/LPS model, shikimic acid reduced Il6, Tnf, Nos2 and Ptgs2 transcripts at 12 h; protein/secretion measurements at 24 h also decreased. At 1 h, p65 and IκB phosphorylation decreased and IκB degradation was reduced. These changes do not establish direct inhibition of COX-2 catalysis or direct binding to every signaling protein. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
Shikimic acid reduced the LPS-associated protein readout for mouse-tnf in BV2 cells.
Shikimic acid → Mouse tumor necrosis factor / Tnf source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
LPS without SA added · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS without SA stimulus · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "SA plus LPS", "comparator": "LPS without SA", "endpoint": "Shikimic acid reduced the LPS-associated protein readout for mouse-tnf in BV2 cells.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "shikimic-acid", "state": "added"}, {"entity_slug": "lipopolysaccharide", "state": "stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Expression or secretion endpoint; not direct enzyme catalytic inhibition, binding or a human response.
plain_language
Shikimic acid reduced the LPS-associated protein readout for mouse-tnf in BV2 cells.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 63-63; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 63–63
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h. · source_derived_draft · unverified_draft
**Inflammatory expression and phosphorylation are distinct endpoints.** In the same BV2/LPS model, shikimic acid reduced Il6, Tnf, Nos2 and Ptgs2 transcripts at 12 h; protein/secretion measurements at 24 h also decreased. At 1 h, p65 and IκB phosphorylation decreased and IκB degradation was reduced. These changes do not establish direct inhibition of COX-2 catalysis or direct binding to every signaling protein. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
Shikimic acid reduced the LPS-associated transcript readout for mouse-tnf in BV2 cells.
Shikimic acid → Mouse tumor necrosis factor / Tnf source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
LPS without SA added · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS without SA stimulus · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "SA plus LPS", "comparator": "LPS without SA", "endpoint": "Shikimic acid reduced the LPS-associated transcript readout for mouse-tnf in BV2 cells.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "shikimic-acid", "state": "added"}, {"entity_slug": "lipopolysaccharide", "state": "stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Expression or secretion endpoint; not direct enzyme catalytic inhibition, binding or a human response.
plain_language
Shikimic acid reduced the LPS-associated transcript readout for mouse-tnf in BV2 cells.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 63-63; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 63–63
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2: 5/10 µM SA plus LPS 1 µg/mL; transcript at 12 h, protein/secretion at 24 h. · source_derived_draft · unverified_draft
**Inflammatory expression and phosphorylation are distinct endpoints.** In the same BV2/LPS model, shikimic acid reduced Il6, Tnf, Nos2 and Ptgs2 transcripts at 12 h; protein/secretion measurements at 24 h also decreased. At 1 h, p65 and IκB phosphorylation decreased and IκB degradation was reduced. These changes do not establish direct inhibition of COX-2 catalysis or direct binding to every signaling protein. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
SA reduced p65 and IκB phosphorylation under LPS challenge.
Shikimic acid → Mouse BV2 p65/IκB phosphorylation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
LPS alone added · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS alone stimulus · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "SA plus LPS", "comparator": "LPS alone", "endpoint": "SA reduced p65 and IκB phosphorylation under LPS challenge.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "shikimic-acid", "state": "added"}, {"entity_slug": "lipopolysaccharide", "state": "stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2; 10 µM SA, LPS 1 µg/mL, 1 h.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
SA reduced p65 and IκB phosphorylation under LPS challenge.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 63-63; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 63–63
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2; 10 µM SA, LPS 1 µg/mL, 1 h. · source_derived_draft · unverified_draft
**Inflammatory expression and phosphorylation are distinct endpoints.** In the same BV2/LPS model, shikimic acid reduced Il6, Tnf, Nos2 and Ptgs2 transcripts at 12 h; protein/secretion measurements at 24 h also decreased. At 1 h, p65 and IκB phosphorylation decreased and IκB degradation was reduced. These changes do not establish direct inhibition of COX-2 catalysis or direct binding to every signaling protein. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
Shikimic acid lowered the LPS-associated nitrite readout.
Shikimic acid → Mouse BV2 nitrite release source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "Shikimic acid in the endpoint-specific assay", "comparator": "Matched assay without shikimic acid", "endpoint": "Shikimic acid lowered the LPS-associated nitrite readout.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2 cells; 5/10 µM SA, LPS 1 µg/mL, 24 h for inflammatory endpoints; separate viability test.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Assay-specific redox or viability signal; not a unique ROS identity or direct scavenging mechanism.
plain_language
Shikimic acid lowered the LPS-associated nitrite readout.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2 cells; 5/10 µM SA, LPS 1 µg/mL, 24 h for inflammatory endpoints; separate viability test. · source_derived_draft · unverified_draft
**Microglial redox responses were measured at micromolar exposure.** In mouse BV2 cells, 5 or 10 µM shikimic acid with 1 µg/mL LPS for 24 h decreased nitrite and DCFH-DA oxidation readouts; concentrations up to 10 µM did not significantly reduce the reported CCK8 viability signal. These are assays of inflammatory/redox response and metabolic viability, not measurements of a unique reactive-oxygen species or proof of direct radical scavenging. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
Shikimic acid lowered LPS-associated DCFH oxidation.
Shikimic acid → Mouse BV2 DCFH-DA oxidation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "Shikimic acid in the endpoint-specific assay", "comparator": "Matched assay without shikimic acid", "endpoint": "Shikimic acid lowered LPS-associated DCFH oxidation.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2 cells; 5/10 µM SA, LPS 1 µg/mL, 24 h for inflammatory endpoints; separate viability test.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Assay-specific redox or viability signal; not a unique ROS identity or direct scavenging mechanism.
plain_language
Shikimic acid lowered LPS-associated DCFH oxidation.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2 cells; 5/10 µM SA, LPS 1 µg/mL, 24 h for inflammatory endpoints; separate viability test. · source_derived_draft · unverified_draft
**Microglial redox responses were measured at micromolar exposure.** In mouse BV2 cells, 5 or 10 µM shikimic acid with 1 µg/mL LPS for 24 h decreased nitrite and DCFH-DA oxidation readouts; concentrations up to 10 µM did not significantly reduce the reported CCK8 viability signal. These are assays of inflammatory/redox response and metabolic viability, not measurements of a unique reactive-oxygen species or proof of direct radical scavenging. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
Shikimic acid up to 10 micromolar did not significantly reduce CCK8 signal.
Shikimic acid → Mouse BV2 CCK8 viability signal source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "Shikimic acid in the endpoint-specific assay", "comparator": "Matched assay without shikimic acid", "endpoint": "Shikimic acid up to 10 micromolar did not significantly reduce CCK8 signal.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2 cells; 5/10 µM SA, LPS 1 µg/mL, 24 h for inflammatory endpoints; separate viability test.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Assay-specific redox or viability signal; not a unique ROS identity or direct scavenging mechanism.
plain_language
Shikimic acid up to 10 micromolar did not significantly reduce CCK8 signal.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 59-59; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 59–59
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2 cells; 5/10 µM SA, LPS 1 µg/mL, 24 h for inflammatory endpoints; separate viability test. · source_derived_draft · unverified_draft
**Microglial redox responses were measured at micromolar exposure.** In mouse BV2 cells, 5 or 10 µM shikimic acid with 1 µg/mL LPS for 24 h decreased nitrite and DCFH-DA oxidation readouts; concentrations up to 10 µM did not significantly reduce the reported CCK8 viability signal. These are assays of inflammatory/redox response and metabolic viability, not measurements of a unique reactive-oxygen species or proof of direct radical scavenging. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
SA at 100–200 mg/kg showed lower scores in the EAE behavioral comparison.
Shikimic acid → Mouse EAE behavioral score source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA 100–200 mg/kg", "comparator": "EAE vehicle", "endpoint": "SA at 100–200 mg/kg showed lower scores in the EAE behavioral comparison.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse EAE model, dose-specific observation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
SA at 100–200 mg/kg showed lower scores in the EAE behavioral comparison.
primary_references
Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
source_locator
Reviewed reference lines 73-73; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 73–73
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse EAE model, dose-specific observation. · source_derived_draft · unverified_draft
**Repair and injury prevention separated in time.** In the mouse focal lysolecithin model, shikimic acid groups did not have a smaller demyelinated region at day 7, but 100–200 mg/kg groups had less demyelination and more mature-oligodendrocyte staining at day 14. The article also reported improvement in EAE scores at 100–200 mg/kg, with a 50-mg/kg behavioral null. These model/time-dependent observations do not establish treatment of human multiple sclerosis. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidence
SA at 50 mg/kg showed no significant improvement in the EAE behavioral comparison.
Shikimic acid → Mouse EAE behavioral score source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA 50 mg/kg", "comparator": "EAE vehicle", "endpoint": "SA at 50 mg/kg showed no significant improvement in the EAE behavioral comparison.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse EAE model, dose-specific observation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
SA at 50 mg/kg showed no significant improvement in the EAE behavioral comparison.
primary_references
Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
source_locator
Reviewed reference lines 73-73; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 73–73
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse EAE model, dose-specific observation. · source_derived_draft · unverified_draft
**Repair and injury prevention separated in time.** In the mouse focal lysolecithin model, shikimic acid groups did not have a smaller demyelinated region at day 7, but 100–200 mg/kg groups had less demyelination and more mature-oligodendrocyte staining at day 14. The article also reported improvement in EAE scores at 100–200 mg/kg, with a 50-mg/kg behavioral null. These model/time-dependent observations do not establish treatment of human multiple sclerosis. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidence
SA increased CREB phosphorylation in human dermal papilla cells.
Shikimic acid → Human cAMP response element-binding protein 1 / CREB1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA", "comparator": "Vehicle", "endpoint": "SA increased CREB phosphorylation in human dermal papilla cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human cells; 1 µM SA, 15 min.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Signaling readout, not demonstrated direct receptor or kinase binding.
plain_language
SA increased CREB phosphorylation in human dermal papilla cells.
primary_references
Shikimic acid, a mannose bioisostere, promotes hair growth with the induction of anagen hair cycle. | 2019 | DOI 10.1038/s41598-019-53612-5 | PMID 31740717 | https://pubmed.ncbi.nlm.nih.gov/31740717/ | https://doi.org/10.1038/s41598-019-53612-5 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6861222/
source_locator
Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human cells; 1 µM SA, 15 min. · source_derived_draft · unverified_draft
**Hair-follicle findings include human tissue, not a human treatment trial.** In isolated human hair follicles, 1 or 10 µM shikimic acid increased shaft elongation during 12-day culture. Dermal papilla cells showed higher MTT readouts, and 1 µM exposure increased MYC, HGF, KGF and VEGF transcripts at 24 h and p38/CREB phosphorylation at 15 min. Transcript increases are not proof of increased secreted growth-factor flux. Mannose-receptor staining establishes receptor presence, not that this receptor was necessary for the response. Topical 10–100 mM exposure also affected anagen-related measurements in mice; neither system establishes oral human hair regrowth. [Shikimic acid, a mannose bioisostere, promotes hair growth with the induction of anagen hair cycle.](https://pubmed.ncbi.nlm.nih.gov/31740717/)
Complete structured claim and evidence
SA increased shaft elongation in isolated human follicles.
Shikimic acid → Human isolated hair-follicle shaft elongation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA", "comparator": "Vehicle", "endpoint": "SA increased shaft elongation in isolated human follicles.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Ex-vivo human follicles; 1/10 µM SA, 12-day culture.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Isolated tissue, not clinical oral or topical human hair regrowth.
plain_language
SA increased shaft elongation in isolated human follicles.
primary_references
Shikimic acid, a mannose bioisostere, promotes hair growth with the induction of anagen hair cycle. | 2019 | DOI 10.1038/s41598-019-53612-5 | PMID 31740717 | https://pubmed.ncbi.nlm.nih.gov/31740717/ | https://doi.org/10.1038/s41598-019-53612-5 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6861222/
source_locator
Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Ex-vivo human follicles; 1/10 µM SA, 12-day culture. · source_derived_draft · unverified_draft
**Hair-follicle findings include human tissue, not a human treatment trial.** In isolated human hair follicles, 1 or 10 µM shikimic acid increased shaft elongation during 12-day culture. Dermal papilla cells showed higher MTT readouts, and 1 µM exposure increased MYC, HGF, KGF and VEGF transcripts at 24 h and p38/CREB phosphorylation at 15 min. Transcript increases are not proof of increased secreted growth-factor flux. Mannose-receptor staining establishes receptor presence, not that this receptor was necessary for the response. Topical 10–100 mM exposure also affected anagen-related measurements in mice; neither system establishes oral human hair regrowth. [Shikimic acid, a mannose bioisostere, promotes hair growth with the induction of anagen hair cycle.](https://pubmed.ncbi.nlm.nih.gov/31740717/)
Complete structured claim and evidence
SA increased p38 phosphorylation in human dermal papilla cells.
Shikimic acid → Human dermal papilla p38 phosphorylation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA", "comparator": "Vehicle", "endpoint": "SA increased p38 phosphorylation in human dermal papilla cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human cells; 1 µM SA, 15 min.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
SA increased p38 phosphorylation in human dermal papilla cells.
primary_references
Shikimic acid, a mannose bioisostere, promotes hair growth with the induction of anagen hair cycle. | 2019 | DOI 10.1038/s41598-019-53612-5 | PMID 31740717 | https://pubmed.ncbi.nlm.nih.gov/31740717/ | https://doi.org/10.1038/s41598-019-53612-5 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6861222/
source_locator
Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human cells; 1 µM SA, 15 min. · source_derived_draft · unverified_draft
**Hair-follicle findings include human tissue, not a human treatment trial.** In isolated human hair follicles, 1 or 10 µM shikimic acid increased shaft elongation during 12-day culture. Dermal papilla cells showed higher MTT readouts, and 1 µM exposure increased MYC, HGF, KGF and VEGF transcripts at 24 h and p38/CREB phosphorylation at 15 min. Transcript increases are not proof of increased secreted growth-factor flux. Mannose-receptor staining establishes receptor presence, not that this receptor was necessary for the response. Topical 10–100 mM exposure also affected anagen-related measurements in mice; neither system establishes oral human hair regrowth. [Shikimic acid, a mannose bioisostere, promotes hair growth with the induction of anagen hair cycle.](https://pubmed.ncbi.nlm.nih.gov/31740717/)
Complete structured claim and evidence
SA increased the KGF/FGF7 transcript readout in human dermal papilla cells.
Shikimic acid → Human keratinocyte growth factor / FGF7 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA", "comparator": "Vehicle", "endpoint": "SA increased the KGF/FGF7 transcript readout in human dermal papilla cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human dermal papilla cells; 1 µM SA for 24 h, qPCR.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Transcript level is not measured secretion, target binding or clinical hair growth.
plain_language
SA increased the KGF/FGF7 transcript readout in human dermal papilla cells.
primary_references
Shikimic acid, a mannose bioisostere, promotes hair growth with the induction of anagen hair cycle. | 2019 | DOI 10.1038/s41598-019-53612-5 | PMID 31740717 | https://pubmed.ncbi.nlm.nih.gov/31740717/ | https://doi.org/10.1038/s41598-019-53612-5 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6861222/
source_locator
Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human dermal papilla cells; 1 µM SA for 24 h, qPCR. · source_derived_draft · unverified_draft
**Hair-follicle findings include human tissue, not a human treatment trial.** In isolated human hair follicles, 1 or 10 µM shikimic acid increased shaft elongation during 12-day culture. Dermal papilla cells showed higher MTT readouts, and 1 µM exposure increased MYC, HGF, KGF and VEGF transcripts at 24 h and p38/CREB phosphorylation at 15 min. Transcript increases are not proof of increased secreted growth-factor flux. Mannose-receptor staining establishes receptor presence, not that this receptor was necessary for the response. Topical 10–100 mM exposure also affected anagen-related measurements in mice; neither system establishes oral human hair regrowth. [Shikimic acid, a mannose bioisostere, promotes hair growth with the induction of anagen hair cycle.](https://pubmed.ncbi.nlm.nih.gov/31740717/)
Complete structured claim and evidence
SA increased the HGF transcript readout in human dermal papilla cells.
Shikimic acid → Human hepatocyte growth factor / HGF source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA", "comparator": "Vehicle", "endpoint": "SA increased the HGF transcript readout in human dermal papilla cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human dermal papilla cells; 1 µM SA for 24 h, qPCR.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Transcript level is not measured secretion, target binding or clinical hair growth.
plain_language
SA increased the HGF transcript readout in human dermal papilla cells.
primary_references
Shikimic acid, a mannose bioisostere, promotes hair growth with the induction of anagen hair cycle. | 2019 | DOI 10.1038/s41598-019-53612-5 | PMID 31740717 | https://pubmed.ncbi.nlm.nih.gov/31740717/ | https://doi.org/10.1038/s41598-019-53612-5 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6861222/
source_locator
Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human dermal papilla cells; 1 µM SA for 24 h, qPCR. · source_derived_draft · unverified_draft
**Hair-follicle findings include human tissue, not a human treatment trial.** In isolated human hair follicles, 1 or 10 µM shikimic acid increased shaft elongation during 12-day culture. Dermal papilla cells showed higher MTT readouts, and 1 µM exposure increased MYC, HGF, KGF and VEGF transcripts at 24 h and p38/CREB phosphorylation at 15 min. Transcript increases are not proof of increased secreted growth-factor flux. Mannose-receptor staining establishes receptor presence, not that this receptor was necessary for the response. Topical 10–100 mM exposure also affected anagen-related measurements in mice; neither system establishes oral human hair regrowth. [Shikimic acid, a mannose bioisostere, promotes hair growth with the induction of anagen hair cycle.](https://pubmed.ncbi.nlm.nih.gov/31740717/)
Complete structured claim and evidence
SA increased the VEGF transcript readout in human dermal papilla cells.
Shikimic acid → Vascular endothelial growth factor A source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA", "comparator": "Vehicle", "endpoint": "SA increased the VEGF transcript readout in human dermal papilla cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human dermal papilla cells; 1 µM SA for 24 h, qPCR.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Transcript level is not measured secretion, target binding or clinical hair growth.
plain_language
SA increased the VEGF transcript readout in human dermal papilla cells.
primary_references
Shikimic acid, a mannose bioisostere, promotes hair growth with the induction of anagen hair cycle. | 2019 | DOI 10.1038/s41598-019-53612-5 | PMID 31740717 | https://pubmed.ncbi.nlm.nih.gov/31740717/ | https://doi.org/10.1038/s41598-019-53612-5 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6861222/
source_locator
Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human dermal papilla cells; 1 µM SA for 24 h, qPCR. · source_derived_draft · unverified_draft
**Hair-follicle findings include human tissue, not a human treatment trial.** In isolated human hair follicles, 1 or 10 µM shikimic acid increased shaft elongation during 12-day culture. Dermal papilla cells showed higher MTT readouts, and 1 µM exposure increased MYC, HGF, KGF and VEGF transcripts at 24 h and p38/CREB phosphorylation at 15 min. Transcript increases are not proof of increased secreted growth-factor flux. Mannose-receptor staining establishes receptor presence, not that this receptor was necessary for the response. Topical 10–100 mM exposure also affected anagen-related measurements in mice; neither system establishes oral human hair regrowth. [Shikimic acid, a mannose bioisostere, promotes hair growth with the induction of anagen hair cycle.](https://pubmed.ncbi.nlm.nih.gov/31740717/)
Complete structured claim and evidence
SA increased Human HepG2 ACC phosphorylation.
Shikimic acid → Human HepG2 ACC phosphorylation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA treatment", "comparator": "Matched untreated cells", "endpoint": "SA increased Human HepG2 ACC phosphorylation.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human HepG2 cell signaling assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Context-specific signaling; no asserted mediation of a separate in-vivo lipid effect.
plain_language
SA increased Human HepG2 ACC phosphorylation.
primary_references
Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC. | 2019 | DOI 10.3390/ijms20030582 | PMID 30700011 | https://pubmed.ncbi.nlm.nih.gov/30700011/ | https://doi.org/10.3390/ijms20030582 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6387373/
source_locator
Reviewed reference lines 77-77; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 77–77
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human HepG2 cell signaling assay. · source_derived_draft · unverified_draft
**Lipid accumulation studies identify responses, not direct inhibition.** In HepG2/Huh7 and 3T3-L1 experiments, shikimic acid was associated with lower lipid staining and altered lipogenic proteins, including lower MID1IP1, LXRα and SREBP-1c; AMPKα and ACC phosphorylation increased in the reported cell contexts. Genetic manipulation of MID1IP1 and compound-C experiments probed pathway involvement. These cultured-cell observations do not prove direct binding to MID1IP1, human fatty-liver efficacy, or that AMPK causes the triglyceride change in the separate mouse-feeding study. Individual cell-dose details remain in the original paper rather than being guessed. [Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC.](https://pubmed.ncbi.nlm.nih.gov/30700011/)
Complete structured claim and evidence
SA increased Human HepG2 AMPK phosphorylation.
Shikimic acid → Human HepG2 AMPK phosphorylation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA treatment", "comparator": "Matched untreated cells", "endpoint": "SA increased Human HepG2 AMPK phosphorylation.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human HepG2 cell signaling assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Context-specific signaling; no asserted mediation of a separate in-vivo lipid effect.
plain_language
SA increased Human HepG2 AMPK phosphorylation.
primary_references
Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC. | 2019 | DOI 10.3390/ijms20030582 | PMID 30700011 | https://pubmed.ncbi.nlm.nih.gov/30700011/ | https://doi.org/10.3390/ijms20030582 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6387373/
source_locator
Reviewed reference lines 77-77; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 77–77
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human HepG2 cell signaling assay. · source_derived_draft · unverified_draft
**Lipid accumulation studies identify responses, not direct inhibition.** In HepG2/Huh7 and 3T3-L1 experiments, shikimic acid was associated with lower lipid staining and altered lipogenic proteins, including lower MID1IP1, LXRα and SREBP-1c; AMPKα and ACC phosphorylation increased in the reported cell contexts. Genetic manipulation of MID1IP1 and compound-C experiments probed pathway involvement. These cultured-cell observations do not prove direct binding to MID1IP1, human fatty-liver efficacy, or that AMPK causes the triglyceride change in the separate mouse-feeding study. Individual cell-dose details remain in the original paper rather than being guessed. [Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC.](https://pubmed.ncbi.nlm.nih.gov/30700011/)
Complete structured claim and evidence
SA lowered MID1IP1 expression in the tested human hepatoma cells.
Shikimic acid → Human MID1 interacting protein 1 / MID1IP1 source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA treatment", "comparator": "Matched untreated cells", "endpoint": "SA lowered MID1IP1 expression in the tested human hepatoma cells.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
HepG2/Huh7 24-hour expression assays.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Expression response, not direct binding or purified-enzyme inhibition.
plain_language
SA lowered MID1IP1 expression in the tested human hepatoma cells.
primary_references
Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC. | 2019 | DOI 10.3390/ijms20030582 | PMID 30700011 | https://pubmed.ncbi.nlm.nih.gov/30700011/ | https://doi.org/10.3390/ijms20030582 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6387373/
source_locator
Reviewed reference lines 77-77; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 77–77
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · HepG2/Huh7 24-hour expression assays. · source_derived_draft · unverified_draft
**Lipid accumulation studies identify responses, not direct inhibition.** In HepG2/Huh7 and 3T3-L1 experiments, shikimic acid was associated with lower lipid staining and altered lipogenic proteins, including lower MID1IP1, LXRα and SREBP-1c; AMPKα and ACC phosphorylation increased in the reported cell contexts. Genetic manipulation of MID1IP1 and compound-C experiments probed pathway involvement. These cultured-cell observations do not prove direct binding to MID1IP1, human fatty-liver efficacy, or that AMPK causes the triglyceride change in the separate mouse-feeding study. Individual cell-dose details remain in the original paper rather than being guessed. [Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC.](https://pubmed.ncbi.nlm.nih.gov/30700011/)
Complete structured claim and evidence
SA reduced lipid staining in the tested human hepatoma cell contexts.
Shikimic acid → Human hepatoma-cell lipid staining after shikimic acid source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA treatment", "comparator": "Matched untreated cells", "endpoint": "SA reduced lipid staining in the tested human hepatoma cell contexts.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
HepG2/Huh7 cell study; full source retained, exact individual dose unextracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Cell staining is not human fatty-liver treatment efficacy.
plain_language
SA reduced lipid staining in the tested human hepatoma cell contexts.
primary_references
Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC. | 2019 | DOI 10.3390/ijms20030582 | PMID 30700011 | https://pubmed.ncbi.nlm.nih.gov/30700011/ | https://doi.org/10.3390/ijms20030582 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6387373/
source_locator
Reviewed reference lines 77-77; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 77–77
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · HepG2/Huh7 cell study; full source retained, exact individual dose unextracted. · source_derived_draft · unverified_draft
**Lipid accumulation studies identify responses, not direct inhibition.** In HepG2/Huh7 and 3T3-L1 experiments, shikimic acid was associated with lower lipid staining and altered lipogenic proteins, including lower MID1IP1, LXRα and SREBP-1c; AMPKα and ACC phosphorylation increased in the reported cell contexts. Genetic manipulation of MID1IP1 and compound-C experiments probed pathway involvement. These cultured-cell observations do not prove direct binding to MID1IP1, human fatty-liver efficacy, or that AMPK causes the triglyceride change in the separate mouse-feeding study. Individual cell-dose details remain in the original paper rather than being guessed. [Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC.](https://pubmed.ncbi.nlm.nih.gov/30700011/)
Complete structured claim and evidence
The SA-treated LPC groups showed less demyelination at day 14.
Shikimic acid → Mouse LPC-model demyelination volume source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA after LPC challenge", "comparator": "Vehicle after LPC challenge", "endpoint": "The SA-treated LPC groups showed less demyelination at day 14.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse focal LPC demyelination; 100–200 mg/kg SA groups; day-specific histology.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Repair-time distinction, not proof of protection from initial injury or human MS efficacy.
plain_language
The SA-treated LPC groups showed less demyelination at day 14.
primary_references
Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
source_locator
Reviewed reference lines 73-73; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 73–73
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse focal LPC demyelination; 100–200 mg/kg SA groups; day-specific histology. · source_derived_draft · unverified_draft
**Repair and injury prevention separated in time.** In the mouse focal lysolecithin model, shikimic acid groups did not have a smaller demyelinated region at day 7, but 100–200 mg/kg groups had less demyelination and more mature-oligodendrocyte staining at day 14. The article also reported improvement in EAE scores at 100–200 mg/kg, with a 50-mg/kg behavioral null. These model/time-dependent observations do not establish treatment of human multiple sclerosis. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidence
The SA-treated LPC groups showed no significant reduction at day 7.
Shikimic acid → Mouse LPC-model demyelination volume source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA after LPC challenge", "comparator": "Vehicle after LPC challenge", "endpoint": "The SA-treated LPC groups showed no significant reduction at day 7.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse focal LPC demyelination; 100–200 mg/kg SA groups; day-specific histology.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Repair-time distinction, not proof of protection from initial injury or human MS efficacy.
plain_language
The SA-treated LPC groups showed no significant reduction at day 7.
primary_references
Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
source_locator
Reviewed reference lines 73-73; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 73–73
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse focal LPC demyelination; 100–200 mg/kg SA groups; day-specific histology. · source_derived_draft · unverified_draft
**Repair and injury prevention separated in time.** In the mouse focal lysolecithin model, shikimic acid groups did not have a smaller demyelinated region at day 7, but 100–200 mg/kg groups had less demyelination and more mature-oligodendrocyte staining at day 14. The article also reported improvement in EAE scores at 100–200 mg/kg, with a 50-mg/kg behavioral null. These model/time-dependent observations do not establish treatment of human multiple sclerosis. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidence
Shikimic acid increased AKT phosphorylation in BV2 cells.
Shikimic acid → Mouse BV2 AKT phosphorylation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "Shikimic acid", "comparator": "Matched cells without SA", "endpoint": "Shikimic acid increased AKT phosphorylation in BV2 cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2 signaling time-course.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Pathway response is not direct ligand binding or clinical efficacy.
plain_language
Shikimic acid increased AKT phosphorylation in BV2 cells.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 61-61; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 61–61
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2 signaling time-course. · source_derived_draft · unverified_draft
**AKT and Nrf2 involvement does not identify the binding target.** BV2 experiments recorded increased AKT phosphorylation and nuclear Nrf2. MK2206 pretreatment attenuated Nrf2 activation and partially reversed redox/nitrite responses. A reagent labeled RA also attenuated the Nrf2 response; its identity and selectivity are not independently resolved here, so no vitamin-A or retinoic-acid interaction is created from that abbreviation. Pharmacological perturbation supports pathway involvement while leaving the initiating target and off-target alternatives open. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
Shikimic acid increased nuclear Nrf2 accumulation in BV2 cells.
Shikimic acid → Mouse BV2 nuclear Nrf2 accumulation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "Shikimic acid", "comparator": "Matched cells without SA", "endpoint": "Shikimic acid increased nuclear Nrf2 accumulation in BV2 cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2 signaling time-course.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Pathway response is not direct ligand binding or clinical efficacy.
plain_language
Shikimic acid increased nuclear Nrf2 accumulation in BV2 cells.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 61-61; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 61–61
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2 signaling time-course. · source_derived_draft · unverified_draft
**AKT and Nrf2 involvement does not identify the binding target.** BV2 experiments recorded increased AKT phosphorylation and nuclear Nrf2. MK2206 pretreatment attenuated Nrf2 activation and partially reversed redox/nitrite responses. A reagent labeled RA also attenuated the Nrf2 response; its identity and selectivity are not independently resolved here, so no vitamin-A or retinoic-acid interaction is created from that abbreviation. Pharmacological perturbation supports pathway involvement while leaving the initiating target and off-target alternatives open. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
Small neutrophil, eosinophil and hematocrit increases occurred in the high-dose feeding group.
Shikimic acid → Mouse hematological changes after shikimic-acid feeding source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "High dietary shikimic-acid concentration", "comparator": "Control feed", "endpoint": "Small neutrophil, eosinophil and hematocrit increases occurred in the high-dose feeding group.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
ICR mice; 28-day feeding study.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Measured shifts do not establish beneficial immunity or long-term safety.
plain_language
Small neutrophil, eosinophil and hematocrit increases occurred in the high-dose feeding group.
primary_references
Pharmacokinetic Profile and Evaluation of Acute and Subchronic Oral Toxicity of Shikimic Acid in Mice. | 2025 | DOI 10.1021/acsomega.5c03740 | PMID 40852254 | https://pubmed.ncbi.nlm.nih.gov/40852254/ | https://doi.org/10.1021/acsomega.5c03740 | https://pmc.ncbi.nlm.nih.gov/articles/PMC12368620/
source_locator
Reviewed reference lines 51-51; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 51–51
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · ICR mice; 28-day feeding study. · source_derived_draft · unverified_draft
**Mouse distribution and bounded toxicity observations.** The 2025 mouse study reported intravenous half-lives approximately 0.76–0.85 h at 4–16 mg/kg and oral bioavailability approximately 11.09–20.44% at 50–100 mg/kg. A short plasma half-life does not prove unchanged renal excretion. In a separate 28-day feeding experiment, dietary concentrations were 5.56, 16.67 and 50 g/kg FEED, not mg/kg body weight. High-dose animals had small hematological shifts and lower triglycerides; acute survival through tested doses is not evidence of lifetime human safety. No validated human monocarboxylate-transporter assignment was found in the reviewed sources. [Pharmacokinetic Profile and Evaluation of Acute and Subchronic Oral Toxicity of Shikimic Acid in Mice.](https://pubmed.ncbi.nlm.nih.gov/40852254/)
Complete structured claim and evidence
Estimated oral shikimic-acid bioavailability was approximately 11.09–20.44% in the tested mice.
Shikimic acid → Mouse oral shikimic-acid exposure source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_model
Mouse oral 50–100 mg/kg versus intravenous reference arms.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Species/route-specific pharmacokinetic estimate, not human exposure. Rat nominal-dose arithmetic caveat and complete time parameters remain in the source passage.
plain_language
Estimated oral shikimic-acid bioavailability was approximately 11.09–20.44% in the tested mice.
primary_references
Pharmacokinetic Profile and Evaluation of Acute and Subchronic Oral Toxicity of Shikimic Acid in Mice. | 2025 | DOI 10.1021/acsomega.5c03740 | PMID 40852254 | https://pubmed.ncbi.nlm.nih.gov/40852254/ | https://doi.org/10.1021/acsomega.5c03740 | https://pmc.ncbi.nlm.nih.gov/articles/PMC12368620/
source_locator
Reviewed reference lines 51-51; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 51–51
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse oral 50–100 mg/kg versus intravenous reference arms. · source_derived_draft · unverified_draft
**Mouse distribution and bounded toxicity observations.** The 2025 mouse study reported intravenous half-lives approximately 0.76–0.85 h at 4–16 mg/kg and oral bioavailability approximately 11.09–20.44% at 50–100 mg/kg. A short plasma half-life does not prove unchanged renal excretion. In a separate 28-day feeding experiment, dietary concentrations were 5.56, 16.67 and 50 g/kg FEED, not mg/kg body weight. High-dose animals had small hematological shifts and lower triglycerides; acute survival through tested doses is not evidence of lifetime human safety. No validated human monocarboxylate-transporter assignment was found in the reviewed sources. [Pharmacokinetic Profile and Evaluation of Acute and Subchronic Oral Toxicity of Shikimic Acid in Mice.](https://pubmed.ncbi.nlm.nih.gov/40852254/)
Complete structured claim and evidence
The high-dose feeding group had lower triglycerides in the 28-day mouse study.
Shikimic acid → Mouse triglycerides after shikimic-acid feeding source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "50 g/kg feed for 28 days", "comparator": "Control feed", "endpoint": "The high-dose feeding group had lower triglycerides in the 28-day mouse study.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
ICR mice; 50 g shikimic acid per kg feed at the high dietary concentration.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Feed concentration is not body-weight dose; no demonstrated AMPK mediation or human efficacy.
plain_language
The high-dose feeding group had lower triglycerides in the 28-day mouse study.
primary_references
Pharmacokinetic Profile and Evaluation of Acute and Subchronic Oral Toxicity of Shikimic Acid in Mice. | 2025 | DOI 10.1021/acsomega.5c03740 | PMID 40852254 | https://pubmed.ncbi.nlm.nih.gov/40852254/ | https://doi.org/10.1021/acsomega.5c03740 | https://pmc.ncbi.nlm.nih.gov/articles/PMC12368620/
source_locator
Reviewed reference lines 51-51; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 51–51
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · ICR mice; 50 g shikimic acid per kg feed at the high dietary concentration. · source_derived_draft · unverified_draft
**Mouse distribution and bounded toxicity observations.** The 2025 mouse study reported intravenous half-lives approximately 0.76–0.85 h at 4–16 mg/kg and oral bioavailability approximately 11.09–20.44% at 50–100 mg/kg. A short plasma half-life does not prove unchanged renal excretion. In a separate 28-day feeding experiment, dietary concentrations were 5.56, 16.67 and 50 g/kg FEED, not mg/kg body weight. High-dose animals had small hematological shifts and lower triglycerides; acute survival through tested doses is not evidence of lifetime human safety. No validated human monocarboxylate-transporter assignment was found in the reviewed sources. [Pharmacokinetic Profile and Evaluation of Acute and Subchronic Oral Toxicity of Shikimic Acid in Mice.](https://pubmed.ncbi.nlm.nih.gov/40852254/)
Complete structured claim and evidence
Injected SA preserved TH-associated measurements after intranigral LPS.
Shikimic acid → Mouse TH-associated measures after intranigral LPS source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
LPS challenge without SA injected · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS challenge without SA prior model challenge · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "SA after LPS challenge", "comparator": "LPS challenge without SA", "endpoint": "Injected SA preserved TH-associated measurements after intranigral LPS.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "shikimic-acid", "state": "injected"}, {"entity_slug": "lipopolysaccharide", "state": "prior model challenge"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse; SA 100 mg/kg intraperitoneal daily for four weeks.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Inflammatory mouse model, not human Parkinson disease treatment or measured oral brain target engagement.
plain_language
Injected SA preserved TH-associated measurements after intranigral LPS.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 65-65; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 65–65
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse; SA 100 mg/kg intraperitoneal daily for four weeks. · source_derived_draft · unverified_draft
**The neuroinflammation experiment used injected treatment.** After intranigral LPS challenge, mice receiving shikimic acid 100 mg/kg intraperitoneally daily for four weeks showed improved motor-related readouts and preservation of TH-associated measures, with lower microglial markers. This is an inflammatory mouse model; human Parkinson disease efficacy, oral brain exposure and a specific molecular target were not established. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
SA increased MBP-associated OPC differentiation after 72 hours.
Shikimic acid → Rat myelin basic protein / Mbp source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "Shikimic acid", "comparator": "Vehicle", "endpoint": "SA increased MBP-associated OPC differentiation after 72 hours.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Primary rat OPCs, 1–100 µg/mL; 100 µg/mL (about 574 µM) used for follow-up.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Differentiation marker, not all-cell proliferation or human therapeutic exposure.
plain_language
SA increased MBP-associated OPC differentiation after 72 hours.
primary_references
Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
source_locator
Reviewed reference lines 69-69; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 69–69
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Primary rat OPCs, 1–100 µg/mL; 100 µg/mL (about 574 µM) used for follow-up. · source_derived_draft · unverified_draft
**Oligodendrocyte differentiation differs from proliferation.** In primary rat oligodendrocyte precursor cultures, shikimic acid at 1–100 µg/mL increased MBP-associated differentiation after 72 h, with 100 µg/mL used for subsequent experiments. That highest concentration is calculated as about 574 µM. BrdU incorporation and TUNEL readouts did not significantly change. Increased MBP and fewer NG2-positive cells therefore support maturation in this model, not universal stimulation of cell proliferation. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidence
SA increased mTOR phosphorylation in cultured rat OPCs.
Shikimic acid → Rat OPC mTOR phosphorylation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA 100 µg/mL", "comparator": "Vehicle", "endpoint": "SA increased mTOR phosphorylation in cultured rat OPCs.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Primary rat OPC signaling assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
SA increased mTOR phosphorylation in cultured rat OPCs.
primary_references
Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
source_locator
Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Primary rat OPC signaling assay. · source_derived_draft · unverified_draft
**Perturbations expose a conditional signaling route.** In those rat precursor cultures, rapamycin blocked the shikimic-acid-associated rise in MBP, while the MEK inhibitor U0126 did not abolish it. PI3K inhibitors wortmannin and LY294002 reduced the elevated mTOR-phosphorylation readout toward control. These are joint experimental contrasts supporting pathway dependence; they do not establish that shikimic acid binds mTOR or that all MEK activity is irrelevant. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidence
Pig plasma complement/immunoglobulin changes correlated with shikimic-acid concentration.
Shikimic acid → Pig plasma complement and immunoglobulin concentration changes after shikimic acid source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_model
Single-dose healthy-pig time-course and PK–PD association.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Not proof of new antibody synthesis or infection protection; no human dose inference.
plain_language
Pig plasma complement/immunoglobulin changes correlated with shikimic-acid concentration.
primary_references
Pharmacokinetic-Pharmacodynamic Modeling of the Immune-Enhancing Effect of Shikimic Acid in Growing Pigs. | 2024 | DOI 10.1021/acs.jafc.4c09250 | PMID 39542831 | https://pubmed.ncbi.nlm.nih.gov/39542831/ | https://doi.org/10.1021/acs.jafc.4c09250 | https://pmc.ncbi.nlm.nih.gov/articles/PMC11613447/
source_locator
Reviewed reference lines 49-49; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 49–49
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Single-dose healthy-pig time-course and PK–PD association. · source_derived_draft · unverified_draft
**Pig exposure is not a human pharmacokinetic estimate.** In a six-pig crossover study, 50 mg/kg intragastric shikimic acid produced Cmax 10823.44 ng/mL (calculated 62.15 µM), Tmax 1.78 h and half-life 1.81 h. With a 2 mg/kg intravenous comparator, estimated bioavailability was 21.68%; intravenous half-life was 3.66 h. Rapid plasma C3, C4 and immunoglobulin changes correlated with drug concentration. This is not proof of new antibody synthesis or improved infection resistance. PK–PD fits to healthy pigs cannot supply an effective human dose. [Pharmacokinetic-Pharmacodynamic Modeling of the Immune-Enhancing Effect of Shikimic Acid in Growing Pigs.](https://pubmed.ncbi.nlm.nih.gov/39542831/)
Complete structured claim and evidence
Oral shikimic acid produced Cmax 10823.44 ng/mL and estimated bioavailability 21.68% in pigs.
Shikimic acid → Pig oral shikimic-acid exposure source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_model
Six growing pigs, crossover; oral 50 mg/kg versus intravenous 2 mg/kg.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Species/route-specific pharmacokinetic estimate, not human exposure. Rat nominal-dose arithmetic caveat and complete time parameters remain in the source passage.
plain_language
Oral shikimic acid produced Cmax 10823.44 ng/mL and estimated bioavailability 21.68% in pigs.
primary_references
Pharmacokinetic-Pharmacodynamic Modeling of the Immune-Enhancing Effect of Shikimic Acid in Growing Pigs. | 2024 | DOI 10.1021/acs.jafc.4c09250 | PMID 39542831 | https://pubmed.ncbi.nlm.nih.gov/39542831/ | https://doi.org/10.1021/acs.jafc.4c09250 | https://pmc.ncbi.nlm.nih.gov/articles/PMC11613447/
source_locator
Reviewed reference lines 49-49; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 49–49
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Six growing pigs, crossover; oral 50 mg/kg versus intravenous 2 mg/kg. · source_derived_draft · unverified_draft
**Pig exposure is not a human pharmacokinetic estimate.** In a six-pig crossover study, 50 mg/kg intragastric shikimic acid produced Cmax 10823.44 ng/mL (calculated 62.15 µM), Tmax 1.78 h and half-life 1.81 h. With a 2 mg/kg intravenous comparator, estimated bioavailability was 21.68%; intravenous half-life was 3.66 h. Rapid plasma C3, C4 and immunoglobulin changes correlated with drug concentration. This is not proof of new antibody synthesis or improved infection resistance. PK–PD fits to healthy pigs cannot supply an effective human dose. [Pharmacokinetic-Pharmacodynamic Modeling of the Immune-Enhancing Effect of Shikimic Acid in Growing Pigs.](https://pubmed.ncbi.nlm.nih.gov/39542831/)
Complete structured claim and evidence
Ex-vivo 2 mM shikimic acid decreased ADP-induced platelet aggregation.
Shikimic acid → Human ADP-stimulated platelet aggregation with shikimic acid source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_contrast
{"intervention": "Shikimic acid at the endpoint-specific concentration", "comparator": "Matched stimulated blood without shikimic acid", "endpoint": "Ex-vivo 2 mM shikimic acid decreased ADP-induced platelet aggregation.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Blood from 22 sedentary humans, exposed ex vivo to 0.1–2 mM shikimic acid.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No ingestion, clinical thrombosis measurement or direct receptor binding. PAC-1 is retained as an assay label, not a procaspase-targeting compound.
plain_language
Ex-vivo 2 mM shikimic acid decreased ADP-induced platelet aggregation.
primary_references
Anti-platelet and anti-thrombogenic effects of shikimic acid in sedentary population. | 2016 | DOI 10.1039/c6fo00927a | PMID 27480079 | https://pubmed.ncbi.nlm.nih.gov/27480079/ | https://doi.org/10.1039/c6fo00927a
source_locator
Reviewed reference lines 55-55; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 55–55
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Blood from 22 sedentary humans, exposed ex vivo to 0.1–2 mM shikimic acid. · source_derived_draft · unverified_draft
**Human blood was exposed outside the body.** Veach 2016 added 0.1–2 mM shikimic acid to blood from 22 sedentary participants. ADP-induced aggregation decreased at 2 mM, whereas collagen-induced aggregation did not significantly decrease. Flow cytometry recorded lower PAC-1 signal at 2 mM, CD62P at 1–2 mM, monocyte–platelet aggregates at 0.5–2 mM and CD31 at 1 mM. PAC-1 here is a platelet activation assay label; the abstract’s expansion as a procaspase-activating compound is not imported as a drug mechanism. This ex-vivo experiment is not an oral trial, direct P2Y12-binding assay or clinical thrombosis result. The millimolar exposures exceed the micromolar animal oral peaks cited above, without establishing any human equivalence. [Anti-platelet and anti-thrombogenic effects of shikimic acid in sedentary population.](https://pubmed.ncbi.nlm.nih.gov/27480079/)
Complete structured claim and evidence
Shikimic acid at 1 mM decreased CD31 signal in the ex-vivo study.
Shikimic acid → Human platelet CD31 signal with shikimic acid source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_contrast
{"intervention": "Shikimic acid at the endpoint-specific concentration", "comparator": "Matched stimulated blood without shikimic acid", "endpoint": "Shikimic acid at 1 mM decreased CD31 signal in the ex-vivo study.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Blood from 22 sedentary humans, exposed ex vivo to 0.1–2 mM shikimic acid.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No ingestion, clinical thrombosis measurement or direct receptor binding. PAC-1 is retained as an assay label, not a procaspase-targeting compound.
plain_language
Shikimic acid at 1 mM decreased CD31 signal in the ex-vivo study.
primary_references
Anti-platelet and anti-thrombogenic effects of shikimic acid in sedentary population. | 2016 | DOI 10.1039/c6fo00927a | PMID 27480079 | https://pubmed.ncbi.nlm.nih.gov/27480079/ | https://doi.org/10.1039/c6fo00927a
source_locator
Reviewed reference lines 55-55; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 55–55
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Blood from 22 sedentary humans, exposed ex vivo to 0.1–2 mM shikimic acid. · source_derived_draft · unverified_draft
**Human blood was exposed outside the body.** Veach 2016 added 0.1–2 mM shikimic acid to blood from 22 sedentary participants. ADP-induced aggregation decreased at 2 mM, whereas collagen-induced aggregation did not significantly decrease. Flow cytometry recorded lower PAC-1 signal at 2 mM, CD62P at 1–2 mM, monocyte–platelet aggregates at 0.5–2 mM and CD31 at 1 mM. PAC-1 here is a platelet activation assay label; the abstract’s expansion as a procaspase-activating compound is not imported as a drug mechanism. This ex-vivo experiment is not an oral trial, direct P2Y12-binding assay or clinical thrombosis result. The millimolar exposures exceed the micromolar animal oral peaks cited above, without establishing any human equivalence. [Anti-platelet and anti-thrombogenic effects of shikimic acid in sedentary population.](https://pubmed.ncbi.nlm.nih.gov/27480079/)
Complete structured claim and evidence
Shikimic acid at 1–2 mM decreased CD62P signal in the ex-vivo assay.
Shikimic acid → Human platelet CD62P signal with shikimic acid source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_contrast
{"intervention": "Shikimic acid at the endpoint-specific concentration", "comparator": "Matched stimulated blood without shikimic acid", "endpoint": "Shikimic acid at 1–2 mM decreased CD62P signal in the ex-vivo assay.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Blood from 22 sedentary humans, exposed ex vivo to 0.1–2 mM shikimic acid.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No ingestion, clinical thrombosis measurement or direct receptor binding. PAC-1 is retained as an assay label, not a procaspase-targeting compound.
plain_language
Shikimic acid at 1–2 mM decreased CD62P signal in the ex-vivo assay.
primary_references
Anti-platelet and anti-thrombogenic effects of shikimic acid in sedentary population. | 2016 | DOI 10.1039/c6fo00927a | PMID 27480079 | https://pubmed.ncbi.nlm.nih.gov/27480079/ | https://doi.org/10.1039/c6fo00927a
source_locator
Reviewed reference lines 55-55; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 55–55
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Blood from 22 sedentary humans, exposed ex vivo to 0.1–2 mM shikimic acid. · source_derived_draft · unverified_draft
**Human blood was exposed outside the body.** Veach 2016 added 0.1–2 mM shikimic acid to blood from 22 sedentary participants. ADP-induced aggregation decreased at 2 mM, whereas collagen-induced aggregation did not significantly decrease. Flow cytometry recorded lower PAC-1 signal at 2 mM, CD62P at 1–2 mM, monocyte–platelet aggregates at 0.5–2 mM and CD31 at 1 mM. PAC-1 here is a platelet activation assay label; the abstract’s expansion as a procaspase-activating compound is not imported as a drug mechanism. This ex-vivo experiment is not an oral trial, direct P2Y12-binding assay or clinical thrombosis result. The millimolar exposures exceed the micromolar animal oral peaks cited above, without establishing any human equivalence. [Anti-platelet and anti-thrombogenic effects of shikimic acid in sedentary population.](https://pubmed.ncbi.nlm.nih.gov/27480079/)
Complete structured claim and evidence
Shikimic acid did not significantly inhibit collagen-induced platelet aggregation in the tested human blood assay.
Shikimic acid → Human collagen-stimulated platelet aggregation with shikimic acid source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_contrast
{"intervention": "Shikimic acid at the endpoint-specific concentration", "comparator": "Matched stimulated blood without shikimic acid", "endpoint": "Shikimic acid did not significantly inhibit collagen-induced platelet aggregation in the tested human blood assay.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Blood from 22 sedentary humans, exposed ex vivo to 0.1–2 mM shikimic acid.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No ingestion, clinical thrombosis measurement or direct receptor binding. PAC-1 is retained as an assay label, not a procaspase-targeting compound.
plain_language
Shikimic acid did not significantly inhibit collagen-induced platelet aggregation in the tested human blood assay.
primary_references
Anti-platelet and anti-thrombogenic effects of shikimic acid in sedentary population. | 2016 | DOI 10.1039/c6fo00927a | PMID 27480079 | https://pubmed.ncbi.nlm.nih.gov/27480079/ | https://doi.org/10.1039/c6fo00927a
source_locator
Reviewed reference lines 55-55; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 55–55
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Blood from 22 sedentary humans, exposed ex vivo to 0.1–2 mM shikimic acid. · source_derived_draft · unverified_draft
**Human blood was exposed outside the body.** Veach 2016 added 0.1–2 mM shikimic acid to blood from 22 sedentary participants. ADP-induced aggregation decreased at 2 mM, whereas collagen-induced aggregation did not significantly decrease. Flow cytometry recorded lower PAC-1 signal at 2 mM, CD62P at 1–2 mM, monocyte–platelet aggregates at 0.5–2 mM and CD31 at 1 mM. PAC-1 here is a platelet activation assay label; the abstract’s expansion as a procaspase-activating compound is not imported as a drug mechanism. This ex-vivo experiment is not an oral trial, direct P2Y12-binding assay or clinical thrombosis result. The millimolar exposures exceed the micromolar animal oral peaks cited above, without establishing any human equivalence. [Anti-platelet and anti-thrombogenic effects of shikimic acid in sedentary population.](https://pubmed.ncbi.nlm.nih.gov/27480079/)
Complete structured claim and evidence
Shikimic acid at 0.5–2 mM decreased monocyte–platelet aggregates.
Shikimic acid → Human monocyte–platelet aggregate formation with shikimic acid source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_contrast
{"intervention": "Shikimic acid at the endpoint-specific concentration", "comparator": "Matched stimulated blood without shikimic acid", "endpoint": "Shikimic acid at 0.5–2 mM decreased monocyte–platelet aggregates.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Blood from 22 sedentary humans, exposed ex vivo to 0.1–2 mM shikimic acid.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No ingestion, clinical thrombosis measurement or direct receptor binding. PAC-1 is retained as an assay label, not a procaspase-targeting compound.
plain_language
Shikimic acid at 0.5–2 mM decreased monocyte–platelet aggregates.
primary_references
Anti-platelet and anti-thrombogenic effects of shikimic acid in sedentary population. | 2016 | DOI 10.1039/c6fo00927a | PMID 27480079 | https://pubmed.ncbi.nlm.nih.gov/27480079/ | https://doi.org/10.1039/c6fo00927a
source_locator
Reviewed reference lines 55-55; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 55–55
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Blood from 22 sedentary humans, exposed ex vivo to 0.1–2 mM shikimic acid. · source_derived_draft · unverified_draft
**Human blood was exposed outside the body.** Veach 2016 added 0.1–2 mM shikimic acid to blood from 22 sedentary participants. ADP-induced aggregation decreased at 2 mM, whereas collagen-induced aggregation did not significantly decrease. Flow cytometry recorded lower PAC-1 signal at 2 mM, CD62P at 1–2 mM, monocyte–platelet aggregates at 0.5–2 mM and CD31 at 1 mM. PAC-1 here is a platelet activation assay label; the abstract’s expansion as a procaspase-activating compound is not imported as a drug mechanism. This ex-vivo experiment is not an oral trial, direct P2Y12-binding assay or clinical thrombosis result. The millimolar exposures exceed the micromolar animal oral peaks cited above, without establishing any human equivalence. [Anti-platelet and anti-thrombogenic effects of shikimic acid in sedentary population.](https://pubmed.ncbi.nlm.nih.gov/27480079/)
Complete structured claim and evidence
Ex-vivo 2 mM shikimic acid decreased the platelet PAC-1 activation signal.
Shikimic acid → Human platelet PAC-1 flow-cytometry signal source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_contrast
{"intervention": "Shikimic acid at the endpoint-specific concentration", "comparator": "Matched stimulated blood without shikimic acid", "endpoint": "Ex-vivo 2 mM shikimic acid decreased the platelet PAC-1 activation signal.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Blood from 22 sedentary humans, exposed ex vivo to 0.1–2 mM shikimic acid.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
No ingestion, clinical thrombosis measurement or direct receptor binding. PAC-1 is retained as an assay label, not a procaspase-targeting compound.
plain_language
Ex-vivo 2 mM shikimic acid decreased the platelet PAC-1 activation signal.
primary_references
Anti-platelet and anti-thrombogenic effects of shikimic acid in sedentary population. | 2016 | DOI 10.1039/c6fo00927a | PMID 27480079 | https://pubmed.ncbi.nlm.nih.gov/27480079/ | https://doi.org/10.1039/c6fo00927a
source_locator
Reviewed reference lines 55-55; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 55–55
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Blood from 22 sedentary humans, exposed ex vivo to 0.1–2 mM shikimic acid. · source_derived_draft · unverified_draft
**Human blood was exposed outside the body.** Veach 2016 added 0.1–2 mM shikimic acid to blood from 22 sedentary participants. ADP-induced aggregation decreased at 2 mM, whereas collagen-induced aggregation did not significantly decrease. Flow cytometry recorded lower PAC-1 signal at 2 mM, CD62P at 1–2 mM, monocyte–platelet aggregates at 0.5–2 mM and CD31 at 1 mM. PAC-1 here is a platelet activation assay label; the abstract’s expansion as a procaspase-activating compound is not imported as a drug mechanism. This ex-vivo experiment is not an oral trial, direct P2Y12-binding assay or clinical thrombosis result. The millimolar exposures exceed the micromolar animal oral peaks cited above, without establishing any human equivalence. [Anti-platelet and anti-thrombogenic effects of shikimic acid in sedentary population.](https://pubmed.ncbi.nlm.nih.gov/27480079/)
Complete structured claim and evidence
The rat tracer study recovered shikimate-derived carbon in catechol-conjugates.
Shikimic acid → Catechol conjugates, unresolved individual forms source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_model
Rat oral tracer study; gut-dependent metabolism with host processing.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Multistep tracer fate, not one direct host enzyme reaction or identical quantitative human metabolism.
plain_language
The rat tracer study recovered shikimate-derived carbon in catechol-conjugates.
primary_references
The metabolism of shikimate in the rat. | 1978 | DOI 10.1042/bj1700257 | PMID 637841 | https://pubmed.ncbi.nlm.nih.gov/637841/ | https://doi.org/10.1042/bj1700257 | https://pmc.ncbi.nlm.nih.gov/articles/PMC1183892/
source_locator
Reviewed reference lines 85-85; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 85–85
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat oral tracer study; gut-dependent metabolism with host processing. · source_derived_draft · unverified_draft
**Gut metabolism and host conjugation must be distinguished.** The 1978 rat study traced oral shikimic acid into urinary hippurate, hexahydrohippurate, tetrahydrohippurate, two dihydroxycyclohexanecarboxylate isomers, catechol conjugates and expired CO2. Antibiotic treatment suppressed the characteristic conversion, implicating initial gut-microbial transformations. Host metabolism of microbial products still occurs. Hippurate contains a glycine conjugate, but product detection does not establish clinically significant glycine depletion or an identical human quantitative pathway. No assertion that parent shikimic acid is directly converted to every final product in one reaction is made. [The metabolism of shikimate in the rat.](https://pubmed.ncbi.nlm.nih.gov/637841/)
Complete structured claim and evidence
The rat tracer study recovered shikimate-derived carbon in hexahydrohippuric-acid.
Shikimic acid → Hexahydrohippuric acid source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_model
Rat oral tracer study; gut-dependent metabolism with host processing.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Multistep tracer fate, not one direct host enzyme reaction or identical quantitative human metabolism.
plain_language
The rat tracer study recovered shikimate-derived carbon in hexahydrohippuric-acid.
primary_references
The metabolism of shikimate in the rat. | 1978 | DOI 10.1042/bj1700257 | PMID 637841 | https://pubmed.ncbi.nlm.nih.gov/637841/ | https://doi.org/10.1042/bj1700257 | https://pmc.ncbi.nlm.nih.gov/articles/PMC1183892/
source_locator
Reviewed reference lines 85-85; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 85–85
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat oral tracer study; gut-dependent metabolism with host processing. · source_derived_draft · unverified_draft
**Gut metabolism and host conjugation must be distinguished.** The 1978 rat study traced oral shikimic acid into urinary hippurate, hexahydrohippurate, tetrahydrohippurate, two dihydroxycyclohexanecarboxylate isomers, catechol conjugates and expired CO2. Antibiotic treatment suppressed the characteristic conversion, implicating initial gut-microbial transformations. Host metabolism of microbial products still occurs. Hippurate contains a glycine conjugate, but product detection does not establish clinically significant glycine depletion or an identical human quantitative pathway. No assertion that parent shikimic acid is directly converted to every final product in one reaction is made. [The metabolism of shikimate in the rat.](https://pubmed.ncbi.nlm.nih.gov/637841/)
Complete structured claim and evidence
The rat tracer study recovered shikimate-derived carbon in hippuric-acid.
Shikimic acid → Hippuric acid / benzoylglycine source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_model
Rat oral tracer study; gut-dependent metabolism with host processing.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Multistep tracer fate, not one direct host enzyme reaction or identical quantitative human metabolism.
plain_language
The rat tracer study recovered shikimate-derived carbon in hippuric-acid.
primary_references
The metabolism of shikimate in the rat. | 1978 | DOI 10.1042/bj1700257 | PMID 637841 | https://pubmed.ncbi.nlm.nih.gov/637841/ | https://doi.org/10.1042/bj1700257 | https://pmc.ncbi.nlm.nih.gov/articles/PMC1183892/
source_locator
Reviewed reference lines 85-85; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 85–85
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat oral tracer study; gut-dependent metabolism with host processing. · source_derived_draft · unverified_draft
**Gut metabolism and host conjugation must be distinguished.** The 1978 rat study traced oral shikimic acid into urinary hippurate, hexahydrohippurate, tetrahydrohippurate, two dihydroxycyclohexanecarboxylate isomers, catechol conjugates and expired CO2. Antibiotic treatment suppressed the characteristic conversion, implicating initial gut-microbial transformations. Host metabolism of microbial products still occurs. Hippurate contains a glycine conjugate, but product detection does not establish clinically significant glycine depletion or an identical human quantitative pathway. No assertion that parent shikimic acid is directly converted to every final product in one reaction is made. [The metabolism of shikimate in the rat.](https://pubmed.ncbi.nlm.nih.gov/637841/)
Complete structured claim and evidence
The rat tracer study recovered shikimate-derived carbon in shikimate-derived-dihydroxycyclohexanecarboxylates.
Shikimic acid → Shikimate-derived dihydroxycyclohexanecarboxylate isomers source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_model
Rat oral tracer study; gut-dependent metabolism with host processing.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Multistep tracer fate, not one direct host enzyme reaction or identical quantitative human metabolism.
plain_language
The rat tracer study recovered shikimate-derived carbon in shikimate-derived-dihydroxycyclohexanecarboxylates.
primary_references
The metabolism of shikimate in the rat. | 1978 | DOI 10.1042/bj1700257 | PMID 637841 | https://pubmed.ncbi.nlm.nih.gov/637841/ | https://doi.org/10.1042/bj1700257 | https://pmc.ncbi.nlm.nih.gov/articles/PMC1183892/
source_locator
Reviewed reference lines 85-85; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 85–85
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat oral tracer study; gut-dependent metabolism with host processing. · source_derived_draft · unverified_draft
**Gut metabolism and host conjugation must be distinguished.** The 1978 rat study traced oral shikimic acid into urinary hippurate, hexahydrohippurate, tetrahydrohippurate, two dihydroxycyclohexanecarboxylate isomers, catechol conjugates and expired CO2. Antibiotic treatment suppressed the characteristic conversion, implicating initial gut-microbial transformations. Host metabolism of microbial products still occurs. Hippurate contains a glycine conjugate, but product detection does not establish clinically significant glycine depletion or an identical human quantitative pathway. No assertion that parent shikimic acid is directly converted to every final product in one reaction is made. [The metabolism of shikimate in the rat.](https://pubmed.ncbi.nlm.nih.gov/637841/)
Complete structured claim and evidence
The rat tracer study recovered shikimate-derived carbon in tetrahydrohippuric-acid.
Shikimic acid → 3,4,5,6-Tetrahydrohippuric acid source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_model
Rat oral tracer study; gut-dependent metabolism with host processing.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Multistep tracer fate, not one direct host enzyme reaction or identical quantitative human metabolism.
plain_language
The rat tracer study recovered shikimate-derived carbon in tetrahydrohippuric-acid.
primary_references
The metabolism of shikimate in the rat. | 1978 | DOI 10.1042/bj1700257 | PMID 637841 | https://pubmed.ncbi.nlm.nih.gov/637841/ | https://doi.org/10.1042/bj1700257 | https://pmc.ncbi.nlm.nih.gov/articles/PMC1183892/
source_locator
Reviewed reference lines 85-85; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 85–85
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Rat oral tracer study; gut-dependent metabolism with host processing. · source_derived_draft · unverified_draft
**Gut metabolism and host conjugation must be distinguished.** The 1978 rat study traced oral shikimic acid into urinary hippurate, hexahydrohippurate, tetrahydrohippurate, two dihydroxycyclohexanecarboxylate isomers, catechol conjugates and expired CO2. Antibiotic treatment suppressed the characteristic conversion, implicating initial gut-microbial transformations. Host metabolism of microbial products still occurs. Hippurate contains a glycine conjugate, but product detection does not establish clinically significant glycine depletion or an identical human quantitative pathway. No assertion that parent shikimic acid is directly converted to every final product in one reaction is made. [The metabolism of shikimate in the rat.](https://pubmed.ncbi.nlm.nih.gov/637841/)
Complete structured claim and evidence
SA did not significantly change the rat-opc-brdu readout.
Shikimic acid → Rat OPC BrdU incorporation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA 100 µg/mL", "comparator": "Vehicle", "endpoint": "SA did not significantly change the rat-opc-brdu readout.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Primary rat OPCs, 100 µg/mL SA versus vehicle.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
SA did not significantly change the rat-opc-brdu readout.
primary_references
Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
source_locator
Reviewed reference lines 69-69; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 69–69
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Primary rat OPCs, 100 µg/mL SA versus vehicle. · source_derived_draft · unverified_draft
**Oligodendrocyte differentiation differs from proliferation.** In primary rat oligodendrocyte precursor cultures, shikimic acid at 1–100 µg/mL increased MBP-associated differentiation after 72 h, with 100 µg/mL used for subsequent experiments. That highest concentration is calculated as about 574 µM. BrdU incorporation and TUNEL readouts did not significantly change. Increased MBP and fewer NG2-positive cells therefore support maturation in this model, not universal stimulation of cell proliferation. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidence
SA did not significantly change the rat-opc-tunel readout.
Shikimic acid → Rat OPC TUNEL labeling source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_contrast
{"intervention": "SA 100 µg/mL", "comparator": "Vehicle", "endpoint": "SA did not significantly change the rat-opc-tunel readout.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Primary rat OPCs, 100 µg/mL SA versus vehicle.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
SA did not significantly change the rat-opc-tunel readout.
primary_references
Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
source_locator
Reviewed reference lines 69-69; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 69–69
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Primary rat OPCs, 100 µg/mL SA versus vehicle. · source_derived_draft · unverified_draft
**Oligodendrocyte differentiation differs from proliferation.** In primary rat oligodendrocyte precursor cultures, shikimic acid at 1–100 µg/mL increased MBP-associated differentiation after 72 h, with 100 µg/mL used for subsequent experiments. That highest concentration is calculated as about 574 µM. BrdU incorporation and TUNEL readouts did not significantly change. Increased MBP and fewer NG2-positive cells therefore support maturation in this model, not universal stimulation of cell proliferation. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidence
Nominal oral shikimic acid produced Cmax 904 ng/mL and estimated bioavailability 10.4% in rats.
Shikimic acid → Rat oral shikimic-acid exposure source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_model
Male Sprague–Dawley rats, five per route; nominal oral 100 mg/kg versus intravenous 2 mg/kg.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Species/route-specific pharmacokinetic estimate, not human exposure. Rat nominal-dose arithmetic caveat and complete time parameters remain in the source passage.
plain_language
Nominal oral shikimic acid produced Cmax 904 ng/mL and estimated bioavailability 10.4% in rats.
primary_references
Pharmacokinetics of Shikimic Acid Following Intragastric and Intravenous Administrations in Rats. | 2020 | DOI 10.3390/pharmaceutics12090824 | PMID 32872397 | https://pubmed.ncbi.nlm.nih.gov/32872397/ | https://doi.org/10.3390/pharmaceutics12090824 | https://pmc.ncbi.nlm.nih.gov/articles/PMC7558350/
source_locator
Reviewed reference lines 47-47; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 47–47
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Male Sprague–Dawley rats, five per route; nominal oral 100 mg/kg versus intravenous 2 mg/kg. · source_derived_draft · unverified_draft
**Rat exposure is measurable but incomplete.** In five male Sprague–Dawley rats per route, reported oral shikimic acid 100 mg/kg produced Cmax 904 ± 48 ng/mL (calculated 5.19 µM), Tmax 2.7 ± 1.5 h and terminal half-life 1.26 ± 0.20 h. The intravenous comparator was 2 mg/kg; estimated absolute bioavailability was 10.4%. The Methods contains a dose/volume arithmetic inconsistency, so these are the nominal dose and Table 3 estimates, not an independently reconstructed administered dose. Occasional double peaks do not prove enterohepatic recycling. Neither rat transport mechanism nor human oral exposure is established by these numbers. [Pharmacokinetics of Shikimic Acid Following Intragastric and Intravenous Administrations in Rats.](https://pubmed.ncbi.nlm.nih.gov/32872397/)
Complete structured claim and evidence
SA reduced nitrite and selected cytokine responses in LPS-challenged RAW264.7 cells.
Shikimic acid → Mouse RAW264.7 LPS-induced cytokine/nitrite response source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_condition
LPS without SA added · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
LPS without SA stimulus · Lipopolysaccharide Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "SA plus LPS", "comparator": "LPS without SA", "endpoint": "SA reduced nitrite and selected cytokine responses in LPS-challenged RAW264.7 cells.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "shikimic-acid", "state": "added"}, {"entity_slug": "lipopolysaccharide", "state": "stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse RAW264.7; accessible abstract, cell dose not independently extracted.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
SA reduced nitrite and selected cytokine responses in LPS-challenged RAW264.7 cells.
primary_references
Shikimic acid inhibits LPS-induced cellular pro-inflammatory cytokines and attenuates mechanical hyperalgesia in mice. | 2016 | DOI 10.1016/j.intimp.2016.07.016 | PMID 27454847 | https://pubmed.ncbi.nlm.nih.gov/27454847/ | https://doi.org/10.1016/j.intimp.2016.07.016
source_locator
Reviewed reference lines 67-67; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 67–67
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse RAW264.7; accessible abstract, cell dose not independently extracted. · source_derived_draft · unverified_draft
**Other inflammatory models are separate evidence.** Rabelo 2016 reported lower nitrite, TNF and IL-1β responses and reduced ERK/p38 phosphorylation in LPS-exposed mouse RAW264.7 macrophages. Rodent pain outcomes were also reported at 50–200 mg/kg depending on the test. Only the indexed abstract was available for this extraction, so unverified route, cell dose and timing are not invented. Lower p38 signaling here and higher p38 phosphorylation in hair cells are different conditions, not automatically conflicting studies. [Shikimic acid inhibits LPS-induced cellular pro-inflammatory cytokines and attenuates mechanical hyperalgesia in mice.](https://pubmed.ncbi.nlm.nih.gov/27454847/)
Complete structured claim and evidence
The anisatin record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.
Shikimic acid → Anisatin source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_model
Editorial identity/scope connection, not experimental causation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation, not a human metabolic conversion or automatic ingredient attribution.
plain_language
The anisatin record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.
primary_references
Anisatin modulation of the gamma-aminobutyric acid receptor-channel in rat dorsal root ganglion neurons. | 1999 | DOI 10.1038/sj.bjp.0702700 | PMID 10455311 | https://pubmed.ncbi.nlm.nih.gov/10455311/ | https://doi.org/10.1038/sj.bjp.0702700 | https://pmc.ncbi.nlm.nih.gov/articles/PMC1566146/
primary_references
Neurotoxicities in infants seen with the consumption of star anise tea. | 2004 | DOI 10.1542/peds.2004-0058 | PMID 15492355 | https://pubmed.ncbi.nlm.nih.gov/15492355/ | https://doi.org/10.1542/peds.2004-0058
source_locator
Reviewed reference lines 89-89; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 89–89
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial identity/scope connection, not experimental causation. · source_derived_draft · unverified_draft
**Star-anise toxicity is a preparation-identity issue.** Anisatin inhibited GABA-activated currents in rat dorsal-root-ganglion neurons in a use-dependent fashion; an estimated EC50 was 1.10 µM. It is a different molecule from shikimic acid. Seven infant neurological cases associated with star-anise tea and evidence of toxic species contamination demonstrate preparation risk, not toxicity attributable specifically to purified shikimic acid. Botanical identity, plant part, contamination, extraction and measured composition cannot be inferred from the name star anise. [Anisatin modulation of the gamma-aminobutyric acid receptor-channel in rat dorsal root ganglion neurons.](https://pubmed.ncbi.nlm.nih.gov/10455311/) [Neurotoxicities in infants seen with the consumption of star anise tea.](https://pubmed.ncbi.nlm.nih.gov/15492355/)
Complete structured claim and evidence
The isopropylidene-shikimic-acid record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.
Shikimic acid → 3,4-O-Isopropylidene shikimic acid / ISA source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_model
Editorial identity/scope connection, not experimental causation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation, not a human metabolic conversion or automatic ingredient attribution.
plain_language
The isopropylidene-shikimic-acid record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.
primary_references
Anti-inflammatory, analgesic and antioxidant activities of 3,4-oxo-isopropylidene-shikimic acid. | 2016 | DOI 10.3109/13880209.2016.1153663 | PMID 27609150 | https://pubmed.ncbi.nlm.nih.gov/27609150/ | https://doi.org/10.3109/13880209.2016.1153663
primary_references
Anti-platelet and anti-thrombotic effects of triacetylshikimic acid in rats. | 2002 | DOI 10.1097/00005344-200202000-00013 | PMID 11791012 | https://pubmed.ncbi.nlm.nih.gov/11791012/ | https://doi.org/10.1097/00005344-200202000-00013
primary_references
Protective effects of 3,4-oxo-isopropylidene-shikimic acid on experimental colitis induced by trinitrobenzenesulfonic acid in rats. | 2012 | DOI 10.1007/s10620-012-2155-y | PMID 22476587 | https://pubmed.ncbi.nlm.nih.gov/22476587/ | https://doi.org/10.1007/s10620-012-2155-y
source_locator
Reviewed reference lines 57-57; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 57–57
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial identity/scope connection, not experimental causation. · source_derived_draft · unverified_draft
**Derivatives keep their own outcomes.** Triacetylshikimic acid (TSA) reduced stimulated platelet aggregation and shunt thrombosis in rat experiments; reported cAMP increased, while cGMP, thromboxane/prostacyclin metabolites and clotting-time endpoints included null results. Those results are not assigned to parent shikimic acid. The separately tested 3,4-O-isopropylidene derivative (ISA) has rodent inflammatory/pain studies and cell-free radical-scavenging assays. Structural similarity does not establish interchangeable pharmacokinetics, targets or safety. [Anti-platelet and anti-thrombotic effects of triacetylshikimic acid in rats.](https://pubmed.ncbi.nlm.nih.gov/11791012/) [Protective effects of 3,4-oxo-isopropylidene-shikimic acid on experimental colitis induced by trinitrobenzenesulfonic acid in rats.](https://pubmed.ncbi.nlm.nih.gov/22476587/) [Anti-inflammatory, analgesic and antioxidant activities of 3,4-oxo-isopropylidene-shikimic acid.](https://pubmed.ncbi.nlm.nih.gov/27609150/)
Complete structured claim and evidence
The oseltamivir record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.
Shikimic acid → Oseltamivir source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted. Bibliographic manufacturing context retained from draft; publisher full text unavailable in this review. No synthesis instructions or newly verified experimental quantities extracted. Review article, manufacturing background only; not affirmative primary experimental support.
experimental_model
Editorial identity/scope connection, not experimental causation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation, not a human metabolic conversion or automatic ingredient attribution.
plain_language
The oseltamivir record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.
primary_references
Influenza neuraminidase inhibitors possessing a novel hydrophobic interaction in the enzyme active site: design, synthesis, and structural analysis of carbocyclic sialic acid analogues with potent anti-influenza activity. | 1997 | DOI 10.1021/ja963036t | PMID 16526129 | https://pubmed.ncbi.nlm.nih.gov/16526129/ | https://doi.org/10.1021/ja963036t
primary_references
Metabolic engineering for microbial production of shikimic acid. | 2003 | DOI 10.1016/j.ymben.2003.09.001 | PMID 14642355 | https://pubmed.ncbi.nlm.nih.gov/14642355/ | https://doi.org/10.1016/j.ymben.2003.09.001
primary_references
Practical total synthesis of the anti-influenza drug GS-4104 | 1998 | DOI 10.1021/jo980330q | https://doi.org/10.1021/jo980330q
source_locator
Reviewed reference lines 43-43; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 43–43
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial identity/scope connection, not experimental causation. · source_derived_draft · unverified_draft
**A manufacturing precursor is not the finished drug.** Shikimic acid has served as a starting scaffold for chemical manufacture of oseltamivir. Adding the drug’s other functional groups requires chemical synthesis; humans do not turn ingested shikimic acid into oseltamivir. Manufacturing and fermentation routes are industrial context, not antiviral evidence for shikimic acid. The 1997 neuraminidase-inhibitor chemistry paper and the 1998 practical synthesis report concern synthesized drug structures. [Influenza neuraminidase inhibitors possessing a novel hydrophobic interaction in the enzyme active site: design, synthesis, and structural analysis of carbocyclic sialic acid analogues with potent anti-influenza activity.](https://pubmed.ncbi.nlm.nih.gov/16526129/) [Practical total synthesis of the anti-influenza drug GS-4104](https://doi.org/10.1021/jo980330q) [Metabolic engineering for microbial production of shikimic acid.](https://pubmed.ncbi.nlm.nih.gov/14642355/)
Complete structured claim and evidence
The shikimic-acid-prunus-patch-2026 record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.
Shikimic acid → 2026 mixed shikimic-acid/Prunus-mume acne patch source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full-text methods/results reviewed. Published January 2026 despite 2025 in DOI.
experimental_model
Editorial identity/scope connection, not experimental causation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation, not a human metabolic conversion or automatic ingredient attribution.
plain_language
The shikimic-acid-prunus-patch-2026 record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.
primary_references
Novel prospectives of shikimic acid and Prunus mume extract for enhancing bioactivity on 5α-reductase and stability in cosmetic patches for acne treatment | 2026 | DOI 10.3389/fntpr.2025.1737986 | https://www.frontiersin.org/journals/natural-products/articles/10.3389/fntpr.2025.1737986/full
source_locator
Reviewed reference lines 83-83; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 83–83
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial identity/scope connection, not experimental causation. · source_derived_draft · unverified_draft
**A mixed patch does not isolate shikimic acid efficacy.** The same report studied patches containing 0.5% shikimic acid and 0.5% P. mume extract plus additional formulation constituents in 15 volunteers aged 18–28. It was open-label, nonrandomized and split-body, over 48 h. Sebum decreased with both this patch and a 0.5% salicylic-acid comparator; the between-patch difference was not significant (p=0.12). No adverse skin effects were reported in this small short study. It does not establish isolated shikimic acid efficacy, long-term safety, oral antiandrogen action or synergy. [Novel prospectives of shikimic acid and Prunus mume extract for enhancing bioactivity on 5α-reductase and stability in cosmetic patches for acne treatment](https://www.frontiersin.org/journals/natural-products/articles/10.3389/fntpr.2025.1737986/full)
Complete structured claim and evidence
The triacetylshikimic-acid record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.
Shikimic acid → Triacetylshikimic acid / TSA source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary indexed abstract reviewed; full results, tables and supplements not independently extracted.
experimental_model
Editorial identity/scope connection, not experimental causation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Unsigned navigation, not a human metabolic conversion or automatic ingredient attribution.
plain_language
The triacetylshikimic-acid record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.
primary_references
Anti-inflammatory, analgesic and antioxidant activities of 3,4-oxo-isopropylidene-shikimic acid. | 2016 | DOI 10.3109/13880209.2016.1153663 | PMID 27609150 | https://pubmed.ncbi.nlm.nih.gov/27609150/ | https://doi.org/10.3109/13880209.2016.1153663
primary_references
Anti-platelet and anti-thrombotic effects of triacetylshikimic acid in rats. | 2002 | DOI 10.1097/00005344-200202000-00013 | PMID 11791012 | https://pubmed.ncbi.nlm.nih.gov/11791012/ | https://doi.org/10.1097/00005344-200202000-00013
primary_references
Protective effects of 3,4-oxo-isopropylidene-shikimic acid on experimental colitis induced by trinitrobenzenesulfonic acid in rats. | 2012 | DOI 10.1007/s10620-012-2155-y | PMID 22476587 | https://pubmed.ncbi.nlm.nih.gov/22476587/ | https://doi.org/10.1007/s10620-012-2155-y
source_locator
Reviewed reference lines 57-57; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 57–57
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Editorial identity/scope connection, not experimental causation. · source_derived_draft · unverified_draft
**Derivatives keep their own outcomes.** Triacetylshikimic acid (TSA) reduced stimulated platelet aggregation and shunt thrombosis in rat experiments; reported cAMP increased, while cGMP, thromboxane/prostacyclin metabolites and clotting-time endpoints included null results. Those results are not assigned to parent shikimic acid. The separately tested 3,4-O-isopropylidene derivative (ISA) has rodent inflammatory/pain studies and cell-free radical-scavenging assays. Structural similarity does not establish interchangeable pharmacokinetics, targets or safety. [Anti-platelet and anti-thrombotic effects of triacetylshikimic acid in rats.](https://pubmed.ncbi.nlm.nih.gov/11791012/) [Protective effects of 3,4-oxo-isopropylidene-shikimic acid on experimental colitis induced by trinitrobenzenesulfonic acid in rats.](https://pubmed.ncbi.nlm.nih.gov/22476587/) [Anti-inflammatory, analgesic and antioxidant activities of 3,4-oxo-isopropylidene-shikimic acid.](https://pubmed.ncbi.nlm.nih.gov/27609150/)
Complete structured claim and evidence

Where it participates (unsigned role)

MK2206 attenuated shikimic-acid-associated Nrf2 accumulation.
MK2206 → Mouse BV2 nuclear Nrf2 accumulation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
Shikimic acid without MK2206 present · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
Shikimic acid without MK2206 pretreatment · MK2206 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "MK2206 pretreatment with shikimic acid", "comparator": "Shikimic acid without MK2206", "endpoint": "MK2206 attenuated shikimic-acid-associated Nrf2 accumulation.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "mk2206", "state": "pretreatment"}, {"entity_slug": "shikimic-acid", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Mouse BV2; MK2206 10 µM for 4 h before pathway assay.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Pharmacological pathway perturbation; not proof of direct SA–AKT binding or perfect inhibitor specificity.
plain_language
MK2206 attenuated shikimic-acid-associated Nrf2 accumulation.
primary_references
Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model. | 2023 | DOI 10.3389/fphar.2023.1265571 | PMID 38026972 | https://pubmed.ncbi.nlm.nih.gov/38026972/ | https://doi.org/10.3389/fphar.2023.1265571 | https://pmc.ncbi.nlm.nih.gov/articles/PMC10652795/
source_locator
Reviewed reference lines 61-61; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 61–61
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Mouse BV2; MK2206 10 µM for 4 h before pathway assay. · source_derived_draft · unverified_draft
**AKT and Nrf2 involvement does not identify the binding target.** BV2 experiments recorded increased AKT phosphorylation and nuclear Nrf2. MK2206 pretreatment attenuated Nrf2 activation and partially reversed redox/nitrite responses. A reagent labeled RA also attenuated the Nrf2 response; its identity and selectivity are not independently resolved here, so no vitamin-A or retinoic-acid interaction is created from that abbreviation. Pharmacological perturbation supports pathway involvement while leaving the initiating target and off-target alternatives open. [Shikimic acid (SA) inhibits neuro-inflammation and exerts neuroprotective effects in an LPS-induced in vitro and in vivo model.](https://pubmed.ncbi.nlm.nih.gov/38026972/)
Complete structured claim and evidence
The PI3K inhibitor ly294002 reduced the SA-associated mTOR phosphorylation increase.
LY294002 → Rat OPC mTOR phosphorylation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
SA without the inhibitor present · LY294002 Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
SA without the inhibitor present · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "ly294002 plus SA", "comparator": "SA without the inhibitor", "endpoint": "The PI3K inhibitor ly294002 reduced the SA-associated mTOR phosphorylation increase.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "ly294002", "state": "present"}, {"entity_slug": "shikimic-acid", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Primary rat OPC joint pharmacological perturbation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
The PI3K inhibitor ly294002 reduced the SA-associated mTOR phosphorylation increase.
primary_references
Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
source_locator
Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Primary rat OPC joint pharmacological perturbation. · source_derived_draft · unverified_draft
**Perturbations expose a conditional signaling route.** In those rat precursor cultures, rapamycin blocked the shikimic-acid-associated rise in MBP, while the MEK inhibitor U0126 did not abolish it. PI3K inhibitors wortmannin and LY294002 reduced the elevated mTOR-phosphorylation readout toward control. These are joint experimental contrasts supporting pathway dependence; they do not establish that shikimic acid binds mTOR or that all MEK activity is irrelevant. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidence
Rapamycin blocked the SA-associated MBP increase.
Rapamycin / sirolimus → Rat myelin basic protein / Mbp source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
SA without the inhibitor present · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
SA without the inhibitor present · Rapamycin / sirolimus Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "rapamycin plus SA", "comparator": "SA without the inhibitor", "endpoint": "Rapamycin blocked the SA-associated MBP increase.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "rapamycin", "state": "present"}, {"entity_slug": "shikimic-acid", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Primary rat OPC joint exposure, 100 µg/mL SA.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Persistence with U0126 is not a blanket null for MEK activity. Inhibitors do not identify the direct SA target.
plain_language
Rapamycin blocked the SA-associated MBP increase.
primary_references
Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
source_locator
Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Primary rat OPC joint exposure, 100 µg/mL SA. · source_derived_draft · unverified_draft
**Perturbations expose a conditional signaling route.** In those rat precursor cultures, rapamycin blocked the shikimic-acid-associated rise in MBP, while the MEK inhibitor U0126 did not abolish it. PI3K inhibitors wortmannin and LY294002 reduced the elevated mTOR-phosphorylation readout toward control. These are joint experimental contrasts supporting pathway dependence; they do not establish that shikimic acid binds mTOR or that all MEK activity is irrelevant. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidence
The SA-associated MBP increase persisted in the presence of U0126.
U0126 MEK-pathway inhibitor → Rat myelin basic protein / Mbp source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
SA without the inhibitor present · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
SA without the inhibitor present · U0126 MEK-pathway inhibitor Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "u0126 plus SA", "comparator": "SA without the inhibitor", "endpoint": "The SA-associated MBP increase persisted in the presence of U0126.", "effect_direction": "not_reported", "combination": "joint", "conditions": [{"entity_slug": "u0126", "state": "present"}, {"entity_slug": "shikimic-acid", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Primary rat OPC joint exposure, 100 µg/mL SA.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Persistence with U0126 is not a blanket null for MEK activity. Inhibitors do not identify the direct SA target.
plain_language
The SA-associated MBP increase persisted in the presence of U0126.
primary_references
Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
source_locator
Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Primary rat OPC joint exposure, 100 µg/mL SA. · source_derived_draft · unverified_draft
**Perturbations expose a conditional signaling route.** In those rat precursor cultures, rapamycin blocked the shikimic-acid-associated rise in MBP, while the MEK inhibitor U0126 did not abolish it. PI3K inhibitors wortmannin and LY294002 reduced the elevated mTOR-phosphorylation readout toward control. These are joint experimental contrasts supporting pathway dependence; they do not establish that shikimic acid binds mTOR or that all MEK activity is irrelevant. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidence
The PI3K inhibitor wortmannin reduced the SA-associated mTOR phosphorylation increase.
Wortmannin → Rat OPC mTOR phosphorylation source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
experimental_condition
SA without the inhibitor present · Wortmannin Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_condition
SA without the inhibitor present · Shikimic acid Condition belongs to the full experimental contrast; do not separate a joint intervention.
experimental_contrast
{"intervention": "wortmannin plus SA", "comparator": "SA without the inhibitor", "endpoint": "The PI3K inhibitor wortmannin reduced the SA-associated mTOR phosphorylation increase.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "wortmannin", "state": "present"}, {"entity_slug": "shikimic-acid", "state": "present"}]} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Primary rat OPC joint pharmacological perturbation.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
Interpret only within the recorded preparation, exposure and comparator. The complete source passage retains qualifications; unspecified doses/timing have not been extracted here. No clinical efficacy, nutrient deficiency or unique molecular mediation is inferred.
plain_language
The PI3K inhibitor wortmannin reduced the SA-associated mTOR phosphorylation increase.
primary_references
Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice. | 2019 | DOI 10.1007/s12264-018-0322-7 | PMID 30684125 | https://pubmed.ncbi.nlm.nih.gov/30684125/ | https://doi.org/10.1007/s12264-018-0322-7 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6527532/
source_locator
Reviewed reference lines 71-71; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 71–71
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Primary rat OPC joint pharmacological perturbation. · source_derived_draft · unverified_draft
**Perturbations expose a conditional signaling route.** In those rat precursor cultures, rapamycin blocked the shikimic-acid-associated rise in MBP, while the MEK inhibitor U0126 did not abolish it. PI3K inhibitors wortmannin and LY294002 reduced the elevated mTOR-phosphorylation readout toward control. These are joint experimental contrasts supporting pathway dependence; they do not establish that shikimic acid binds mTOR or that all MEK activity is irrelevant. [Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice.](https://pubmed.ncbi.nlm.nih.gov/30684125/)
Complete structured claim and evidence
The 0.03 wt% mixture lowered the type-I 5α-reductase ELISA signal more than SA alone under testosterone challenge.
Shikimic acid and Prunus mume extract 1:1 mixture → Human sebocyte type-I 5-alpha-reductase ELISA amount source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary full-text methods/results reviewed. Published January 2026 despite 2025 in DOI.
experimental_contrast
{"intervention": "1:1 SA/P. mume mixture plus testosterone", "comparator": "SA alone plus testosterone", "endpoint": "The 0.03 wt% mixture lowered the type-I 5α-reductase ELISA signal more than SA alone under testosterone challenge.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
experimental_model
Human sebocytes; 10 nM testosterone, 72 h; three technical replicates.
interpretation_status
Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
limitations
ELISA protein amount in processed supernatant, not catalytic inhibition. No total-protein normalization or independent biological replication established.
plain_language
The 0.03 wt% mixture lowered the type-I 5α-reductase ELISA signal more than SA alone under testosterone challenge.
primary_references
Novel prospectives of shikimic acid and Prunus mume extract for enhancing bioactivity on 5α-reductase and stability in cosmetic patches for acne treatment | 2026 | DOI 10.3389/fntpr.2025.1737986 | https://www.frontiersin.org/journals/natural-products/articles/10.3389/fntpr.2025.1737986/full
source_locator
Reviewed reference lines 79-79; exact primary location described in quoted passage where extracted.
Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 79–79
Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human sebocytes; 10 nM testosterone, 72 h; three technical replicates. · source_derived_draft · unverified_draft
**A 2026 topical study measured protein amount.** Human sebocytes challenged with 10 nM testosterone were exposed for 72 h to shikimic acid or a 1:1 shikimic-acid/Prunus mume extract mixture. At 0.03 wt%, the mixture lowered the reported type-I 5α-reductase ELISA signal more than shikimic acid alone. The assay measured protein amount in processed supernatant, with three technical replicates and no total-protein normalization; it was not a testosterone-to-DHT catalytic assay. Docking is not measured affinity. Thus a direct 5α-reductase inhibition claim is not justified by this experiment. [Novel prospectives of shikimic acid and Prunus mume extract for enhancing bioactivity on 5α-reductase and stability in cosmetic patches for acne treatment](https://www.frontiersin.org/journals/natural-products/articles/10.3389/fntpr.2025.1737986/full)
Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

Shikimic acid

How nutrients influence it

Other things that act on it

How nutrients reach it in more than one step

What it does

What it acts on

Shikimate is the carboxylate conjugate base of shikimic acid, with the same stereochemical scaffold.

Antibiotic treatment suppressed characteristic shikimate-derived metabolic products in rats.

Shikimic acid reduced the LPS-associated protein readout for mouse-il6 in BV2 cells.

Shikimic acid reduced the LPS-associated transcript readout for mouse-il6 in BV2 cells.

Shikimic acid reduced the LPS-associated protein readout for mouse-nos2 in BV2 cells.

Shikimic acid reduced the LPS-associated transcript readout for mouse-nos2 in BV2 cells.

Shikimic acid reduced the LPS-associated protein readout for mouse-ptgs2 in BV2 cells.

Shikimic acid reduced the LPS-associated transcript readout for mouse-ptgs2 in BV2 cells.

Shikimic acid reduced the LPS-associated protein readout for mouse-tnf in BV2 cells.

Shikimic acid reduced the LPS-associated transcript readout for mouse-tnf in BV2 cells.

SA reduced p65 and IκB phosphorylation under LPS challenge.

Shikimic acid lowered the LPS-associated nitrite readout.

Shikimic acid lowered LPS-associated DCFH oxidation.

Shikimic acid up to 10 micromolar did not significantly reduce CCK8 signal.

SA at 100–200 mg/kg showed lower scores in the EAE behavioral comparison.

SA at 50 mg/kg showed no significant improvement in the EAE behavioral comparison.

SA increased CREB phosphorylation in human dermal papilla cells.

SA increased shaft elongation in isolated human follicles.

SA increased p38 phosphorylation in human dermal papilla cells.

SA increased the KGF/FGF7 transcript readout in human dermal papilla cells.

SA increased the HGF transcript readout in human dermal papilla cells.

SA increased the VEGF transcript readout in human dermal papilla cells.

SA increased Human HepG2 ACC phosphorylation.

SA increased Human HepG2 AMPK phosphorylation.

SA lowered MID1IP1 expression in the tested human hepatoma cells.

SA reduced lipid staining in the tested human hepatoma cell contexts.

The SA-treated LPC groups showed less demyelination at day 14.

The SA-treated LPC groups showed no significant reduction at day 7.

Shikimic acid increased AKT phosphorylation in BV2 cells.

Shikimic acid increased nuclear Nrf2 accumulation in BV2 cells.

Small neutrophil, eosinophil and hematocrit increases occurred in the high-dose feeding group.

Estimated oral shikimic-acid bioavailability was approximately 11.09–20.44% in the tested mice.

The high-dose feeding group had lower triglycerides in the 28-day mouse study.

Injected SA preserved TH-associated measurements after intranigral LPS.

SA increased MBP-associated OPC differentiation after 72 hours.

SA increased mTOR phosphorylation in cultured rat OPCs.

Pig plasma complement/immunoglobulin changes correlated with shikimic-acid concentration.

Oral shikimic acid produced Cmax 10823.44 ng/mL and estimated bioavailability 21.68% in pigs.

Ex-vivo 2 mM shikimic acid decreased ADP-induced platelet aggregation.

Shikimic acid at 1 mM decreased CD31 signal in the ex-vivo study.

Shikimic acid at 1–2 mM decreased CD62P signal in the ex-vivo assay.

Shikimic acid did not significantly inhibit collagen-induced platelet aggregation in the tested human blood assay.

Shikimic acid at 0.5–2 mM decreased monocyte–platelet aggregates.

Ex-vivo 2 mM shikimic acid decreased the platelet PAC-1 activation signal.

The rat tracer study recovered shikimate-derived carbon in catechol-conjugates.

The rat tracer study recovered shikimate-derived carbon in hexahydrohippuric-acid.

The rat tracer study recovered shikimate-derived carbon in hippuric-acid.

The rat tracer study recovered shikimate-derived carbon in shikimate-derived-dihydroxycyclohexanecarboxylates.

The rat tracer study recovered shikimate-derived carbon in tetrahydrohippuric-acid.

SA did not significantly change the rat-opc-brdu readout.

SA did not significantly change the rat-opc-tunel readout.

Nominal oral shikimic acid produced Cmax 904 ng/mL and estimated bioavailability 10.4% in rats.

SA reduced nitrite and selected cytokine responses in LPS-challenged RAW264.7 cells.

The anisatin record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.

The isopropylidene-shikimic-acid record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.

The oseltamivir record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.

The shikimic-acid-prunus-patch-2026 record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.

The triacetylshikimic-acid record is a distinct-compound or preparation comparison; its biological effects are not assigned to isolated shikimic acid.

Where it participates (unsigned role)

MK2206 attenuated shikimic-acid-associated Nrf2 accumulation.

The PI3K inhibitor ly294002 reduced the SA-associated mTOR phosphorylation increase.

Rapamycin blocked the SA-associated MBP increase.

The SA-associated MBP increase persisted in the presence of U0126.

The PI3K inhibitor wortmannin reduced the SA-associated mTOR phosphorylation increase.

The 0.03 wt% mixture lowered the type-I 5α-reductase ELISA signal more than SA alone under testosterone challenge.

The events it takes part in

Situations it appears in

In the sources

Open hypotheses