Component
Ivermectin concentration in brain
Central nervous system exposure to ivermectin across the blood-brain barrier.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Ivermectin accumulated thirty-six to sixty fold in the brain of mdr1a,b knockout mice compared with wild type, while selamectin accumulated only five to ten fold.
Experimental context and source evidence
- duration
- Not stated here
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- mdr1a,b double knockout mice and bcrp knockout mice, against wild type
- exposure
- Ivermectin 0.2 mg/kg and selamectin 12 mg/kg, intravenous, oral and dermal spot-on
- limitations
- Breast cancer resistance protein knockouts showed no difference, so this margin is specific to P-glycoprotein and not to efflux transport in general.
- organism
- mdr1a,b double knockout mice and bcrp knockout mice, against wild type
- plain_language
- Ivermectin accumulated thirty-six to sixty fold in the brain of mdr1a,b knockout mice compared with wild type, while selamectin accumulated only five to ten fold.
- primary_references
- Brain penetration of ivermectin and selamectin in mdr1a,b P-glycoprotein- and bcrp- deficient knockout mice. (2009). https://pubmed.ncbi.nlm.nih.gov/19161460/ DOI: 10.1111/j.1365-2885.2008.01007.x
- route
- In vivo
- tissue
- Brain penetration, organ distribution and plasma kinetics
Ivermectin: mechanism of action across parasite, host barrier and mammalian targets (2026-09-22) · lines 68–77
Original AI-assisted curation of sixteen primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Study-specific citations, concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft
## ivermectin-brain-accumulation-without-pgp Ivermectin accumulated thirty-six to sixty fold in the brain of mdr1a,b knockout mice compared with wild type, while selamectin accumulated only five to ten fold. Model/species: mdr1a,b double knockout mice and bcrp knockout mice, against wild type Tissue/system: Brain penetration, organ distribution and plasma kinetics Exposure: Ivermectin 0.2 mg/kg and selamectin 12 mg/kg, intravenous, oral and dermal spot-on Route: In vivo Duration: Not stated here Limits: Breast cancer resistance protein knockouts showed no difference, so this margin is specific to P-glycoprotein and not to efflux transport in general. Primary reference: Brain penetration of ivermectin and selamectin in mdr1a,b P-glycoprotein- and bcrp- deficient knockout mice. (2009). https://pubmed.ncbi.nlm.nih.gov/19161460/ DOI: 10.1111/j.1365-2885.2008.01007.x Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
Complete structured claim and evidenceMice lacking the mdr1a P-glycoprotein gene showed about one hundred fold increased sensitivity to ivermectin, and mdr1a P-glycoprotein was the major P-glycoprotein of the blood-brain barrier.
Experimental context and source evidence
- duration
- Not stated here
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- mdr1a homozygous knockout mice compared with wild type
- exposure
- Ivermectin, described in this report as a centrally neurotoxic pesticide
- limitations
- The comparison is a complete gene disruption, which is a stronger manipulation than partial pharmacological inhibition of P-glycoprotein.
- organism
- mdr1a homozygous knockout mice compared with wild type
- plain_language
- Mice lacking the mdr1a P-glycoprotein gene showed about one hundred fold increased sensitivity to ivermectin, and mdr1a P-glycoprotein was the major P-glycoprotein of the blood-brain barrier.
- primary_references
- Disruption of the mouse mdr1a P-glycoprotein gene leads to a deficiency in the blood-brain barrier and to increased sensitivity to drugs. (1994). https://pubmed.ncbi.nlm.nih.gov/7910522/ DOI: 10.1016/0092-8674(94)90212-7
- route
- In vivo
- tissue
- Blood-brain barrier and tissue drug distribution
Ivermectin: mechanism of action across parasite, host barrier and mammalian targets (2026-09-22) · lines 57–66
Original AI-assisted curation of sixteen primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Study-specific citations, concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft
## pgp-restricts-ivermectin-brain-entry Mice lacking the mdr1a P-glycoprotein gene showed about one hundred fold increased sensitivity to ivermectin, and mdr1a P-glycoprotein was the major P-glycoprotein of the blood-brain barrier. Model/species: mdr1a homozygous knockout mice compared with wild type Tissue/system: Blood-brain barrier and tissue drug distribution Exposure: Ivermectin, described in this report as a centrally neurotoxic pesticide Route: In vivo Duration: Not stated here Limits: The comparison is a complete gene disruption, which is a stronger manipulation than partial pharmacological inhibition of P-glycoprotein. Primary reference: Disruption of the mouse mdr1a P-glycoprotein gene leads to a deficiency in the blood-brain barrier and to increased sensitivity to drugs. (1994). https://pubmed.ncbi.nlm.nih.gov/7910522/ DOI: 10.1016/0092-8674(94)90212-7 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.