Molecular target
Cyclooxygenase-1
Also: PTGS1 · id COX-1
Constitutive isoform that produces prostaglandins maintaining gastric mucosa, platelet function, and renal blood flow. Non-selective NSAID inhibition drives GI and bleeding risk.
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Pharmaceutical agents
Drugs that act on Cyclooxygenase-1
These medications have Cyclooxygenase-1 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 Cyclooxygenase-1
Each plant below contains a named compound documented to act on Cyclooxygenase-1. The compound and the reason for the connection are shown on every edge — a shared mechanism, not a therapeutic equivalence.
- Phenethyl ferulatePhenolic acid ester
Identified in vitro as a principal active constituent responsible for cyclooxygenase and 5-lipoxygenase inhibitory activity in n-hexane extracts; content correlated with inhibitory potency across commercial samples (Zschocke et al., 1997).
- FalcarindiolPolyacetylene (polyyne)
Reported in vitro to inhibit 5-lipoxygenase and cyclooxygenase (Zschocke et al., 1997); additionally reported to activate Nrf2/ARE pathway, inducing antioxidant and phase-2 drug-metabolizing enzymes in cultured hepatic cells (Ohnuma et al., 2009); also demonstrated partial PPARγ agonism in reporter assays (Atanasov et al., 2013).
- (-)-Bornyl ferulatePhenolic acid ester
Identified as a minor active constituent contributing to cyclooxygenase and 5-lipoxygenase inhibition in vitro (Zschocke et al., 1997).
- 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.
- Apigenin / LuteolinFlavonoids
Preclinical studies suggest inhibition of cyclooxygenase isoforms and NF-κB-mediated inflammatory signalling; clinical translation not yet established from provided citations.
- EugenolPhenylpropanoid
Preclinical studies report eugenol inhibits COX-1/COX-2 and NF-κB signalling, suppresses PGE2 synthesis, and modulates TRPV1 and voltage-gated sodium channels; proposed as the primary driver of observed analgesic and anti-inflammatory signals.
- RutaecarpineIndoloquinazolinone alkaloid
Chiou et al. (1996) reported nitric oxide-dependent vasodilatation (full, 100% endothelium-dependent) in isolated rat aorta. Sheu et al. (2000) reported antithrombotic activity in a murine model, with prolongation of platelet plug occlusion time compared with aspirin on a molar basis.
- Methyl salicylateSalicylate ester
Methyl salicylate shares cyclooxygenase-inhibiting mechanism with salicylate class compounds; relevance at concentrations achieved from plant use is unclear.
- SalicinPhenolic glycoside
Hepatically metabolized to salicylic acid — chemically the active metabolite of aspirin. The mechanism overlap with NSAIDs is therefore direct rather than analogous.
- Salicylate fractionsalicylate (aspirin precursor)
The genus name Spiraea (older botanical name) gave aspirin its name — Bayer's 1899 acetylsalicylic acid was developed from spiraein extracted from this plant. Salicylate-induced COX inhibition produces analgesic, anti-inflammatory, and antipyretic effects, weaker but mechanistically identical to aspirin.
- Salicylic acidPhenolic acid
Salicylic acid is a recognized COX pathway modulator; direct attribution of this activity to Iris versicolor preparations has not been established in verified clinical literature.