Molecular target
Tumor Necrosis Factor-α
Pro-inflammatory cytokine central to autoimmune disease pathophysiology (RA, IBD, psoriasis, ankylosing spondylitis). Neutralized by monoclonal antibodies (adalimumab, infliximab) and a soluble receptor fusion protein (etanercept). Multiple plant compounds (curcumin, boswellia, andrographis, EGCG) modulate TNF-α expression downstream of NF-κB.
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 Tumor Necrosis Factor-α
These medications have Tumor Necrosis Factor-α 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 Tumor Necrosis Factor-α
Each plant below contains a named compound documented to act on Tumor Necrosis Factor-α. The compound and the reason for the connection are shown on every edge — a shared mechanism, not a therapeutic equivalence.
- ArctigeninLignan
Studies report arctigenin as the most potent bioactive component of A. lappa; in vitro and preclinical data indicate modulation of NF-κB signalling, suppression of TNF-α and IL-6, and inhibition of COX-2/PGE2 pathways. AMPK activation has also been reported in preclinical models.
- ArctiinLignan glycoside
Arctiin is the glycosidic precursor to arctigenin; studies report anti-inflammatory activity including inhibition of cytokine induction (IL-6, TNF-α) and downstream NF-κB signalling. In vitro data also suggest collagen-stimulating activity relevant to dermal matrix remodelling.
- BerberineIsoquinoline alkaloid (protoberberine)
Studies report berberine activates AMPK, modulates PPAR-γ and insulin receptor signalling, and suppresses NF-κB-mediated inflammatory cascades; investigated in glycaemic regulation and metabolic contexts.
- CoptisineIsoquinoline alkaloid (protoberberine)
Review literature describes coptisine as exhibiting anti-inflammatory, anti-cancer, anti-bacterial, and cardioprotective activity in preclinical models, reportedly via NF-κB, COX-2, TNF-α, and IL-6 pathway modulation.
- Rosmarinic acidPhenolic acid
Preclinical studies report inhibition of NF-κB signalling and downstream inflammatory mediators; antioxidant activity attributed in part to free-radical scavenging.
- LuteolinFlavonoid
Preclinical data suggest modulation of inflammatory cytokines; studies have investigated potential interference with thyroid hormone signalling.
- EmodinAnthraquinone
In vitro studies report competitive inhibition of casein kinase II (CKII) and suppression of cyclin B/cdc2 kinase activity; casein kinase II is not listed in the allowed target set, so mechanistic detail is described here rather than mapped to a target ID. Also investigated for NF-κB pathway modulation in preclinical models.
- Helenalinsesquiterpene lactone
Inhibits NF-κB activation, reducing downstream TNF-α and prostaglandin E2 production; the principal anti-inflammatory and (in oral exposure) toxic constituent.
- γ-Linolenic acid (GLA)omega-6 fatty acid
Converted to dihomo-γ-linolenic acid (DGLA), then to series-1 prostaglandins (PGE1) — anti-inflammatory eicosanoids. The metabolic pathway shifts the inflammation profile toward less inflammatory mediators, providing the basis for benefit in inflammatory arthritis and atopic conditions.
- MahanineCarbazole alkaloid
In vitro studies report induction of apoptosis in HL-60 leukemia cells and cytotoxic activity; proposed mechanisms include modulation of apoptotic signalling pathways.
- Echinacea alkamides
Alkamides, acting via CB2, modulate TNF-α and other cytokine production in monocytes/macrophages — a documented compound-specific immunomodulatory effect, not a generic anti-inflammatory claim.
- 1,8-Cineole (eucalyptol)monoterpenoid oxide
Mucolytic and expectorant via direct ciliary stimulation; anti-inflammatory through NF-κB pathway suppression (reduces TNF-α and prostaglandin production in respiratory epithelium); CYP3A4 induction is the underlying mechanism for several drug interactions.
- Mistletoe lectin I (ML-I)ribosome-inactivating protein
Type II ribosome-inactivating protein — induces apoptosis in tumor cell lines and triggers cytokine release (TNF-α, interleukins) when administered subcutaneously. Mechanistic basis for use in adjuvant cancer therapy in central European integrative oncology.
- Alantolactone fractionsesquiterpene lactone
Anti-inflammatory and expectorant — irritates respiratory mucosa to stimulate ciliary clearance of mucus; the same chemistry underlies historical antimycobacterial use against tuberculosis (alantolactone shows activity against M. tuberculosis in vitro).
- Lupeolpentacyclic triterpene
Anti-inflammatory and anti-lithiatic — reduces calcium oxalate stone formation in animal models. Smooth-muscle relaxant on bladder and ureter, supporting traditional use in BPH and urinary calculi.