Molecular target
Platelet-Activating Factor Pathway
Phospholipid mediator of inflammation, platelet aggregation, and bronchoconstriction. Ginkgolides are PAF antagonists, contributing to ginkgo's circulatory effects and bleeding-risk profile.
Educational use only. This page summarizes published research and traditional-use records for educational purposes. It does not diagnose, treat, cure, or prevent any disease. Do not start, stop, or change medications based on this information. Discuss any decisions about therapies — pharmaceutical or botanical — with a qualified clinician who knows your medical history.
No PHI / HIPAA notice: Do not share Protected Health Information (PHI) of any patient on this site — including names, dates of birth, addresses, MRNs, or any identifying information. Use abstract case framing only. Sharing PHI with non-covered entities risks HIPAA violation regardless of platform capability.
Pharmaceutical agents
Drugs that act on Platelet-Activating Factor Pathway
These medications have Platelet-Activating Factor Pathway among their molecular targets. Sharing a target is a mechanistic relationship — it does not make any plant below an alternative to, or substitute for, these drugs.
Botanical connections
Plants whose compounds act on Platelet-Activating Factor Pathway
Each plant below contains a named compound documented to act on Platelet-Activating Factor Pathway. The compound and the reason for the connection are shown on every edge — a shared mechanism, not a therapeutic equivalence.
- Procyanidins / Flavanols (epicatechin, catechin)Polyphenols
Studies report inhibition of platelet activation, modulation of eicosanoid pathways, and upregulation of nitric oxide bioavailability. Murphy et al. (2003) reported inhibition of platelet function in healthy volunteers following cocoa flavanol supplementation.
- Ginkgolides A, B, C, JDiterpene trilactone
Specific PAF antagonists — the basis of ginkgo's antiplatelet activity and the clinically important bleeding-interaction profile.
- Hydroxysafflor yellow A (HSYA)Quinochalcone C-glycoside
Preclinical studies report inhibition of platelet aggregation via TXA2 and PAF pathways, modulation of NF-κB signalling, and influences on nitric oxide production; investigated in cardiovascular and cerebrovascular contexts.