Molecular target
5-Lipoxygenase
Also: ALOX5 · id 5-LOX
Enzyme producing leukotrienes — inflammatory mediators distinct from prostaglandins. Boswellic acids inhibit 5-LOX, offering an inflammation pathway parallel to NSAIDs.
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.
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Pharmaceutical agents
Drugs that act on 5-Lipoxygenase
These medications have 5-Lipoxygenase 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 5-Lipoxygenase
Each plant below contains a named compound documented to act on 5-Lipoxygenase. 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).
- PetasinSesquiterpene ester
Primary anti-migraine and anti-allergic constituent; calcium channel modulation + leukotriene inhibition.
- IsopetasinSesquiterpene ester
Isomer of petasin; similar pharmacology.
- BaicalinFlavonoid glycoside
Preclinical studies report inhibition of NF-κB pathway activation and downstream pro-inflammatory cytokines (TNF-α, IL-6); also reported to modulate 5-lipoxygenase activity. Ex vivo data suggest pro-apoptotic effects in leukocytes from ALL patients (Orzechowska et al., 2014).
- BaicaleinFlavonoid aglycone
Preclinical reports describe inhibition of COX-2 and 5-LOX, suppression of NF-κB, and AMPK activation relevant to metabolic signalling (Zhao et al., 2019; Wang et al., 2018).
- AKBA (Acetyl-11-keto-β-boswellic acid)Pentacyclic triterpene
Most potent boswellic acid for 5-LOX inhibition — distinct from NSAID COX inhibition, making the mechanism complementary rather than duplicative.
- Other boswellic acidsTriterpene
Secondary triterpenes with similar but lower-potency activity.
- ChamazuleneTerpenoid (sesquiterpene)
Preclinical evidence suggests inhibition of arachidonic acid cascade components; may contribute to anti-inflammatory and analgesic actions investigated topically
- Gingerols (6-, 8-, 10-gingerol)Phenolic ketone
Primary fresh-ginger constituents; broad eicosanoid modulation. 6-gingerol is the most abundant.
- CurcuminPolyphenol (curcuminoid)
Beyond its anti-inflammatory NF-kB/COX/LOX activity, curcumin has been investigated in preclinical cancer models for EGFR-pathway and PI3K–Akt–mTOR signaling inhibition and for anti-angiogenic (VEGF) effects. Research only — not a treatment claim.