Component

Laropiprant / MK-0524

Laropiprant / MK-0524. The model and exposure of each linked claim define its scope.

3 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.

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

  1. In healthy men and women, the DP1 antagonist MK-0524 reduced nicotinic-acid-induced flushing symptoms and the rise in skin perfusion.

    Laropiprant / MK-0524 → Cutaneous perfusion source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Human prostaglandin D2 receptor 1 / PTGDR (antagonized_receptor); Prostaglandin D2 (receptor_ligand); Nicotinic acid (trigger)
    evidence_span
    {"source_cache": "artifacts/niacin-clinical-sources/cheng2006.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24", "start_char": 0, "end_char": 1708, "text_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24"}
    experimental_model
    Mouse receptor pharmacology with separate healthy-human flushing study
    exposure
    Nicotinic acid with or without the DP1 antagonist MK-0524
    limitations
    Human reduction in flushing is separate from lipid outcomes. Dose details not present in indexed abstract. Antagonism did not prove all flushing depends on one prostaglandin receptor; male knockout mice retained an aspirin-sensitive component.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    Blocking a prostaglandin receptor reduced the flush in people; that result alone says nothing about long-term cardiovascular outcomes.
    primary_references
    [nia-clin-cheng2006] Antagonism of the prostaglandin D2 receptor 1 suppresses nicotinic acid-induced vasodilation in mice and humans. (2006). https://pubmed.ncbi.nlm.nih.gov/16617107/ DOI: 10.1073/pnas.0601574103
    tissue_or_cell_type
    Skin perfusion

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1361–1373

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse receptor pharmacology with separate healthy-human flushing study · source_derived_draft · unverified_draft

    ### nia-clin-dp1-human-flush In healthy men and women, the DP1 antagonist MK-0524 reduced nicotinic-acid-induced flushing symptoms and the rise in skin perfusion. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking a prostaglandin receptor reduced the flush in people; that result alone says nothing about long-term cardiovascular outcomes. organism: Homo sapiens tissue_or_cell_type: Skin perfusion experimental_model: Mouse receptor pharmacology with separate healthy-human flushing study limitations: Human reduction in flushing is separate from lipid outcomes. Dose details not present in indexed abstract. Antagonism did not prove all flushing depends on one prostaglandin receptor; male knockout mice retained an aspirin-sensitive component. exposure: Nicotinic acid with or without the DP1 antagonist MK-0524 cross_nutrient: Human prostaglandin D2 receptor 1 / PTGDR (antagonized_receptor); Prostaglandin D2 (receptor_ligand); Nicotinic acid (trigger) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/cheng2006.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24", "start_char": 0, "end_char": 1708, "text_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24"} [nia-clin-cheng2006] Antagonism of the prostaglandin D2 receptor 1 suppresses nicotinic acid-induced vasodilation in mice and humans. (2006). https://pubmed.ncbi.nlm.nih.gov/16617107/ DOI: 10.1073/pnas.0601574103
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Niacin–laropiprant produced major vascular-event rates of 13.2% versus 13.7% with placebo: rate ratio 0.96, 95% CI 0.90–1.03, without a significant benefit.

    Nicotinic acid → Major cardiovascular event incidence source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Laropiprant / MK-0524 (coadministered_drug)
    evidence_span
    {"source_cache": "artifacts/niacin-clinical-sources/hps2014.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05", "start_char": 0, "end_char": 2717, "text_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05"}
    experimental_model
    HPS2-THRIVE randomized trial; 25,673 adults with vascular disease on statin-based therapy
    exposure
    Extended-release nicotinic acid 2 g plus laropiprant 40 mg daily; median 3.9 years
    limitations
    Combination regimen; observed harm cannot all be assigned to nicotinic acid alone. Run-in selected participants able to tolerate initial therapy. Outcomes do not address deficiency replacement.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    This large trial also found no clear event benefit when the combination was added to statin treatment.
    primary_references
    [nia-clin-hps2014] Effects of extended-release niacin with laropiprant in high-risk patients. (2014). https://pubmed.ncbi.nlm.nih.gov/25014686/ DOI: 10.1056/nejmoa1300955
    tissue_or_cell_type
    Major vascular events and adverse events

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1403–1415

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HPS2-THRIVE randomized trial; 25,673 adults with vascular disease on statin-based therapy · source_derived_draft · unverified_draft

    ### nia-clin-hps-events Niacin–laropiprant produced major vascular-event rates of 13.2% versus 13.7% with placebo: rate ratio 0.96, 95% CI 0.90–1.03, without a significant benefit. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This large trial also found no clear event benefit when the combination was added to statin treatment. organism: Homo sapiens tissue_or_cell_type: Major vascular events and adverse events experimental_model: HPS2-THRIVE randomized trial; 25,673 adults with vascular disease on statin-based therapy limitations: Combination regimen; observed harm cannot all be assigned to nicotinic acid alone. Run-in selected participants able to tolerate initial therapy. Outcomes do not address deficiency replacement. exposure: Extended-release nicotinic acid 2 g plus laropiprant 40 mg daily; median 3.9 years cross_nutrient: Laropiprant / MK-0524 (coadministered_drug) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/hps2014.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05", "start_char": 0, "end_char": 2717, "text_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05"} [nia-clin-hps2014] Effects of extended-release niacin with laropiprant in high-risk patients. (2014). https://pubmed.ncbi.nlm.nih.gov/25014686/ DOI: 10.1056/nejmoa1300955
    Complete structured claim and evidence

  2. Niacin–laropiprant increased serious diabetes-control disturbances by 3.7 percentage points and new diabetes diagnoses by 1.3 points; gastrointestinal, musculoskeletal, skin, infection and bleeding serious adverse events also increased.

    Nicotinic acid → Serious glycemic adverse-event incidence source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Laropiprant / MK-0524 (coadministered_drug)
    evidence_span
    {"source_cache": "artifacts/niacin-clinical-sources/hps2014.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05", "start_char": 0, "end_char": 2717, "text_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05"}
    experimental_model
    HPS2-THRIVE randomized trial; 25,673 adults with vascular disease on statin-based therapy
    exposure
    Extended-release nicotinic acid 2 g plus laropiprant 40 mg daily; median 3.9 years
    limitations
    Combination regimen; observed harm cannot all be assigned to nicotinic acid alone. Run-in selected participants able to tolerate initial therapy. Outcomes do not address deficiency replacement.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    The combination had measurable harms as well as lipid effects.
    primary_references
    [nia-clin-hps2014] Effects of extended-release niacin with laropiprant in high-risk patients. (2014). https://pubmed.ncbi.nlm.nih.gov/25014686/ DOI: 10.1056/nejmoa1300955
    tissue_or_cell_type
    Major vascular events and adverse events

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1417–1429

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HPS2-THRIVE randomized trial; 25,673 adults with vascular disease on statin-based therapy · source_derived_draft · unverified_draft

    ### nia-clin-hps-glycemic-harm Niacin–laropiprant increased serious diabetes-control disturbances by 3.7 percentage points and new diabetes diagnoses by 1.3 points; gastrointestinal, musculoskeletal, skin, infection and bleeding serious adverse events also increased. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The combination had measurable harms as well as lipid effects. organism: Homo sapiens tissue_or_cell_type: Major vascular events and adverse events experimental_model: HPS2-THRIVE randomized trial; 25,673 adults with vascular disease on statin-based therapy limitations: Combination regimen; observed harm cannot all be assigned to nicotinic acid alone. Run-in selected participants able to tolerate initial therapy. Outcomes do not address deficiency replacement. exposure: Extended-release nicotinic acid 2 g plus laropiprant 40 mg daily; median 3.9 years cross_nutrient: Laropiprant / MK-0524 (coadministered_drug) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/hps2014.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05", "start_char": 0, "end_char": 2717, "text_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05"} [nia-clin-hps2014] Effects of extended-release niacin with laropiprant in high-risk patients. (2014). https://pubmed.ncbi.nlm.nih.gov/25014686/ DOI: 10.1056/nejmoa1300955
    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.

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