Butein (Chalcone · Anti-inflammatory · Antiproliferative · Antifibrotic)
Compiled from published pharmacological and botanical literature. Not independently verified by Herbuno. Spotted an error or have a correction? Flag it below →
| Compound | Butein (3,4,2′,4′-Tetrahydroxychalcone; 2′,3,4,4′-Tetrahydroxychalcone; Butin chalcone) |
| Chemical class | Polyphenol — Chalcone (catechol B-ring + resorcinol A-ring chalcone; structurally related to isoliquiritigenin with additional 3-OH) |
| CAS | 487-52-5 |
| Primary source | Butea monosperma (Flame of the Forest / Palash), Semecarpus anacardium, Rhus vernicifera (lacquer tree) |
| Key applications | Anti-inflammatory; antiproliferative; antifibrotic (TGF-β suppression); SIRT1 activation; antioxidant |
| Claim strength | Moderate |
| Typical form | Not commercially available as standardised extract; research-grade chalcone isolate; Butea monosperma preparations |
| Buy from Herbuno | Availability on request — request bulk pricing → |
Name origin: Butein is named after Butea monosperma (Palash, Flame of the Forest) — an Indian tree with striking orange-red flowers, sacred in Hindu tradition and used extensively in Ayurvedic medicine. It is a tetrahydroxychalcone — the catechol B-ring (3,4-dihydroxy) and resorcinol A-ring (2′,4′-dihydroxy) together providing four hydroxyl groups on the chalcone scaffold. Traditional use: Butea monosperma (Palash) is described in Charaka Samhita and Sushruta Samhita for wound healing, skin diseases, worm infestations, and anti-inflammatory applications. The flowers and bark are used in various regional Ayurvedic preparations. In Thai traditional medicine, Butea preparations are used for liver disorders and as anti-inflammatory agents. Research trajectory: Butein has attracted research interest for three distinct pharmacological properties: (1) TGF-β/Smad antifibrotic activity — suppressing hepatic stellate cell and renal fibrosis signalling; (2) SIRT1 (sirtuin-1) activation — a longevity-associated deacetylase pathway modulation; (3) broad antiproliferative activity in cancer cell lines via STAT3 and NF-κB inhibition. The structural catechol B-ring provides high antioxidant and iron chelation capacity. Commercial source: Butein is not currently available as a standardised commercial extract in the Herbuno catalogue; availability on request.
Evidence for Butein Applications
Anti-inflammatory: Butein inhibits COX-2, iNOS, and NF-κB at micromolar concentrations in macrophage activation models. TNF-α, IL-6, and IL-1β production are dose-dependently suppressed. The catechol B-ring's Michael acceptor capacity (at the chalcone enone) contributes to Keap1 cysteine modification and Nrf2 activation — providing both direct and indirect antioxidant/anti-inflammatory activity. Claim strength: Moderate.
Antifibrotic (TGF-β/Smad suppression): Butein inhibits TGF-β1-induced Smad2/3 phosphorylation in hepatic stellate cells (HSCs) — directly targeting the primary fibrogenic signal transduction pathway. In CCl₄-induced liver fibrosis and diabetic nephropathy rodent models, butein reduces collagen deposition and fibrosis marker expression (α-SMA, fibronectin) comparably to reference antifibrotic compounds. This TGF-β/Smad antifibrotic mechanism is shared with silybin, making butein a complementary candidate for liver fibrosis formulas. Claim strength: Moderate (preclinical).
SIRT1 activation and longevity pathways: Butein activates SIRT1 (sirtuin-1) in neuronal and hepatic models — promoting NAD⁺-dependent deacetylation of FOXO1, PGC-1α, and p53, with downstream effects on mitochondrial biogenesis, oxidative stress resistance, and cellular longevity pathways. This SIRT1 activation mechanism is analogous to resveratrol's primary mode of action and positions butein in the emerging longevity supplement ingredient category. Claim strength: Emerging.
Antiproliferative: Butein demonstrates activity against breast, lung, gastric, prostate, and multiple myeloma cell lines at 10–50 μM via STAT3 inhibition (suppressing Bcl-2, cyclin D1, VEGF), NF-κB suppression, and apoptosis induction. Research is preclinical. Claim strength: Emerging.
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Dosage & Formulator Specification
No human supplement dosing data exist for butein. Animal antifibrotic studies used 5–50 mg/kg doses — translating to estimated human equivalent doses of 50–500 mg/day butein isolate. No commercial botanical extract standardised to butein content is currently available. Butea monosperma bark and flower preparations in traditional Ayurvedic use are not standardised to butein.
Butein is available as a research-grade isolate (≥98% HPLC) from specialty phytochemical suppliers (Sigma-Aldrich, ChemFaces, Cayman Chemical) for research and development purposes. For supplement product development targeting butein's antifibrotic or SIRT1-activation profile, the current practical challenge is the absence of a commercially standardised botanical extract delivering reliable butein concentrations. Development of standardised Butea monosperma or Rhus vernicifera (lacquer tree sap — a rich source) extract standardised to butein content represents an emerging ingredient development opportunity.
Stability of butein follows chalcone class patterns — the alpha,beta-unsaturated ketone is susceptible to cyclisation (to butin, the corresponding flavanone) under acidic conditions or prolonged storage. Neutral to slightly alkaline pH (6–8) and cold storage best preserve butein in solution; solid forms are more stable. The catechol B-ring is susceptible to oxidation — nitrogen packaging and antioxidant protection are required for dry formulations.
No drug interactions are documented for butein. SIRT1 activation and NF-κB inhibition are theoretically relevant to anti-inflammatory drug interactions, but no clinical evidence at supplement doses exists.
Frequently Asked Questions — Butein
What is Butea monosperma (Palash) and why is it significant in Ayurveda?
Butea monosperma (Palash, Flame of the Forest, Dhak) is a medium-sized deciduous tree native to the Indian subcontinent, notable for its striking orange-red flowers that bloom before the leaves appear. It is sacred in Hinduism (associated with the fire god Agni) and extensively described in classical Ayurvedic texts — the bark, seeds, flowers, and gum (Palash gum or Butea gum) each having distinct therapeutic applications. Traditional uses include wound healing, anti-inflammatory, anthelmintic, and aphrodisiac applications. Butein is the characteristic polyphenol of Butea flowers; the seeds contain butin (butein's flavanone cyclisation product) and palasonin (a piperidine alkaloid with anthelminthic activity).
How does butein compare to fisetin, which has a similar structure?
Fisetin (3,7,3′,4′-tetrahydroxyflavone) and butein (3,4,2′,4′-tetrahydroxychalcone) are structurally related — fisetin can be conceptualised as the cyclised flavone form of a chalcone precursor with the same hydroxylation pattern. Both have catechol B-rings, SIRT1-activating properties, and antiproliferative activity against similar cancer cell lines. Key differences: fisetin has been studied in human clinical trials (senolytic studies at 500–1000 mg/day); butein has no human clinical data. Fisetin is the more commercially developed longevity ingredient; butein occupies a research-stage position in the same pharmacological space.
Is butein found in rhus lacquer and is this a commercial source?
Yes — Rhus vernicifera (Japanese lacquer tree sap, urushi) and related Rhus species contain butein alongside fisetin, sulfuretin, and other chalcones/flavones. However, Rhus lacquer preparations are traditionally used as a coating material, not an internal supplement, due to the presence of urushiol (a highly allergenic phenol). Commercial butein from Rhus sources requires careful separation from urushiol and other potentially sensitising compounds. Butea monosperma (without allergenic constituents at typical extract concentrations) is pharmacologically preferable as a butein supplement source.
Can butein be combined with silybin for liver fibrosis formulas?
Yes — butein and silybin target complementary antifibrotic mechanisms: butein directly inhibits TGF-β1/Smad2/3 phosphorylation (upstream fibrogenic signal); silybin inhibits hepatic stellate cell activation via Nrf2 antioxidant induction and membrane stabilisation, and also modulates TGF-β signalling. The combination rationale — upstream TGF-β inhibition by butein + antioxidant/membrane protection by silybin — is mechanistically sound. In the absence of a commercial butein source, this combination currently requires research-grade butein or awaits the development of a standardised botanical extract.
Related compounds: Isoliquiritigenin, Phloretin, Xanthohumol, Fisetin
Claim-strength scale – High = multiple human RCTs; Moderate = limited trials or strong preclinical convergence; Emerging = early-stage lab or animal data.
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