{"id":"ec489e46-a5dd-506f-89d3-068aff87e6ab","stable_key":"a9dd23c6-978a-5755-8bd8-f29bd1fe0cda:nia-clin-dp1-human-flush","predicate":"reduces_nicotinic_acid_induced","statement":"In healthy men and women, the DP1 antagonist MK-0524 reduced nicotinic-acid-induced flushing symptoms and the rise in skin perfusion.","claim_class":"observational","status":"source_derived_draft","evidence_grade":"ungraded","direction":"negative","is_public":true,"mechanism_event_id":"6a1a4256-ca98-55a9-9a00-b0d3cc3849e5","mechanism_event_label":"Blocking a prostaglandin receptor reduced the flush in people; that result alone says nothing about long-term cardiovascular outcomes.","subject":{"id":"9ebcef37-189c-5599-b463-108eff6c929a","slug":"laropiprant","display_name":"Laropiprant / MK-0524","entity_type_key":"small_molecule"},"object":{"id":"29e3af6f-14d3-567d-b15a-fb09c23534ad","slug":"cutaneous-perfusion","display_name":"Cutaneous perfusion","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"6a1a4256-ca98-55a9-9a00-b0d3cc3849e5","stable_key":"a9dd23c6-978a-5755-8bd8-f29bd1fe0cda:nia-clin-dp1-human-flush-event","event_type":"observed_intervention","label":"Blocking a prostaglandin receptor reduced the flush in people; that result alone says nothing about long-term cardiovascular outcomes.","description":"In healthy men and women, the DP1 antagonist MK-0524 reduced nicotinic-acid-induced flushing symptoms and the rise in skin perfusion.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"687b5c92-c9e6-5d8f-b517-1d5f2903567d","slug":"ptgdr","display_name":"Human prostaglandin D2 receptor 1 / PTGDR","entity_type_key":"protein"},"role":"antagonized_receptor","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"51dae53e-ef81-5060-98e8-b1a519819cb6","slug":"prostaglandin-d2","display_name":"Prostaglandin D2","entity_type_key":"small_molecule"},"role":"receptor_ligand","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"9751fdb6-9b30-586f-b07a-79b8e2cd62dd","slug":"nicotinic-acid","display_name":"Nicotinic acid","entity_type_key":"small_molecule"},"role":"trigger","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""},{"entity":{"id":"9ebcef37-189c-5599-b463-108eff6c929a","slug":"laropiprant","display_name":"Laropiprant / MK-0524","entity_type_key":"small_molecule"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":3,"notes":""},{"entity":{"id":"29e3af6f-14d3-567d-b15a-fb09c23534ad","slug":"cutaneous-perfusion","display_name":"Cutaneous perfusion","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":4,"notes":""}]},"contexts":[{"dimension":"cross_nutrient","value_text":"Human prostaglandin D2 receptor 1 / PTGDR (antagonized_receptor); Prostaglandin D2 (receptor_ligand); Nicotinic acid (trigger)","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"evidence_span","value_text":"{\"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\"}","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Mouse receptor pharmacology with separate healthy-human flushing study","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"Nicotinic acid with or without the DP1 antagonist MK-0524","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"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.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Niacin research collection; topical membership is not evidence of a direct dietary effect.","comparator":null,"unit":null,"notes":"","entity":{"slug":"niacin","display_name":"Niacin (vitamin B3)","entity_type_key":"nutrient_element"}},{"dimension":"organism","value_text":"Homo sapiens","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"Blocking a prostaglandin receptor reduced the flush in people; that result alone says nothing about long-term cardiovascular outcomes.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[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","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Skin perfusion","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"1626f782-358e-55d7-8d20-9f52c0b34723","evidence_kind":"source_excerpt","locator":"Lines 1361-1373","start_line":1361,"end_line":1373,"excerpt":"### nia-clin-dp1-human-flush\nIn healthy men and women, the DP1 antagonist MK-0524 reduced nicotinic-acid-induced flushing symptoms and the rise in skin perfusion.\nCondition category: normal\nnutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: Blocking a prostaglandin receptor reduced the flush in people; that result alone says nothing about long-term cardiovascular outcomes.\norganism: Homo sapiens\ntissue_or_cell_type: Skin perfusion\nexperimental_model: Mouse receptor pharmacology with separate healthy-human flushing study\nlimitations: 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.\nexposure: Nicotinic acid with or without the DP1 antagonist MK-0524\ncross_nutrient: Human prostaglandin D2 receptor 1 / PTGDR (antagonized_receptor); Prostaglandin D2 (receptor_ligand); Nicotinic acid (trigger)\nevidence_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\"}\n[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","model_system":"Mouse receptor pharmacology with separate healthy-human flushing study","directness":"author_interpretation","verification_status":"source_derived_draft","notes":"Exact curation-document quotation, not publisher quotation. Study 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","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"a62b7b5b-786a-57e9-85e9-67c6912a5054","stable_key":"import-a9dd23c6-978a-5755-8bd8-f29bd1fe0cda","title":"Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17)","document_type":"imported_text","citation_label":"AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. 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