Named Bioactive Compounds · Compound
Gomisin A
Moderate Evidencelignan1 PubMed Study
Hermetica Superfood Encyclopedia
Gomisin A is a dibenzocyclooctadiene lignan derived from Schisandra chinensis berries that demonstrates hepatoprotective and antioxidant properties. This bioactive compound works primarily through Nrf2 pathway activation and cytochrome P450 enzyme modulation.
Gomisin A is a bioactive lignan (dibenzocyclooctadiene class) isolated from the fruit of Schisandra chinensis (Chinese magnoliavine), also known as Wuweizi in traditional Chinese medicine. This compound has a molecular formula of C23H28O7 and is commercially available as a ≥98% HPLC-purified extract from fruit sources.
No human clinical trials, RCTs, or meta-analyses have been conducted on Gomisin A. Current research is limited to preclinical pharmacological studies including in vitro and animal models demonstrating hepato-protective, anti-diabetic, and anti-oxidative effects.
No clinically studied dosage ranges are available as human trials have not been conducted. Gomisin A is classified as harmful if swallowed (GHS H302). Consult a healthcare provider before starting any new supplement.
Gomisin A is a dibenzocyclooctadiene lignan (molecular formula C₂₃H₂₈O₇, MW ~416.47 g/mol) isolated primarily from the fruit of Schisandra chinensis (five-flavor berry). It is not a macronutrient source and has no meaningful caloric, protein, fiber, or carbohydrate contribution. Key biochemical and bioactive profile: • **Chemical class:** Dibenzocyclooctadiene lignan (also classified as a schisandrin-type lignan). • **Typical concentration in source plant:** Schisandra chinensis dried fruit contains approximately 0.01–0.1% w/w Gomisin A, varying with cultivar, harvest time, and geographic origin. It co-occurs with other lignans including schisandrin (schizandrin), schisandrin B, schisandrol A, schisandrol B, gomisin B, gomisin C, gomisin G, gomisin J, and gomisin N. • **Key functional groups:** Contains multiple methoxy groups (–OCH₃), a methylenedioxy bridge, and hydroxyl functionality, which contribute to its lipophilicity and redox-active antioxidant behavior. • **Bioactive mechanisms (preclinical):** Acts as a phase I and phase II hepatic enzyme modulator; shown to influence cytochrome P450 activity (particularly CYP3A4 inhibition in vitro, IC₅₀ values reported in the low micromolar range ~1–10 µM); upregulates glutathione (GSH) and superoxide dismutase (SOD) in hepatocyte models; activates Nrf2/ARE antioxidant response pathway; may modulate PPARγ and AMPK signaling related to glucose and lipid metabolism. • **Lipophilicity:** Estimated LogP ~3.5–4.2, indicating high lipophilicity; absorption is expected to be enhanced with dietary fat co-ingestion. • **Bioavailability notes:** Oral bioavailability in animal models (rat) is estimated to be low-to-moderate (~10–30%), limited by significant first-pass hepatic metabolism and Phase I oxidation by CYP enzymes. Enterohepatic recycling of lignan metabolites may prolong effective exposure. No human pharmacokinetic data are published. Absorption may be improved by lipid-based delivery systems or co-administration with other Schisandra lignans (potential synergistic inhibition of CYP-mediated clearance). • **Vitamins/minerals:** Gomisin A as an isolated compound provides no vitamins or minerals. When consumed as part of whole Schisandra chinensis fruit or extract, the matrix provides small amounts of vitamin C (~30–60 mg/100 g dried fruit), vitamin E, organic acids (citric, malic, tartaric, quinic acid contributing to the characteristic sour taste), trace minerals (potassium, magnesium, iron, zinc in minor amounts), and additional polyphenolic antioxidants. • **Standardized extract context:** Commercial Schisandra extracts are often standardized to total schisandrins (2–9% total lignans); Gomisin A typically represents a minor fraction (~0.5–2% of total lignans in standardized extracts), roughly 0.01–0.18 mg per typical 500 mg extract capsule, though this varies considerably by manufacturer and standardization target. • **Safety/interaction note (preclinical):** Due to CYP3A4 inhibitory potential, Gomisin A may theoretically alter pharmacokinetics of co-administered drugs metabolized by this enzyme; no human drug interaction studies are available.
Gomisin A activates the Nrf2-ARE (antioxidant response element) signaling pathway, enhancing cellular antioxidant enzyme production including glutathione S-transferase and superoxide dismutase. The compound modulates cytochrome P450 enzymes, particularly CYP2E1, reducing oxidative stress in hepatocytes. Additionally, Gomisin A inhibits NF-κB activation, suppressing inflammatory cytokine production and protecting liver cells from damage.
Current evidence for Gomisin A comes exclusively from animal studies and in vitro research, with no human clinical trials published to date. Rodent studies using doses of 10-50 mg/kg body weight showed significant hepatoprotective effects against carbon tetrachloride-induced liver damage, with 40-60% reductions in ALT and AST levels. Laboratory studies demonstrated antioxidant activity with IC50 values of 15-25 μM against various free radicals. The preliminary nature of this evidence limits definitive conclusions about human efficacy and optimal dosing.
Safety data for Gomisin A in humans is limited due to lack of clinical studies, though traditional use of Schisandra suggests general tolerability. Animal studies report no acute toxicity at doses up to 200 mg/kg, but chronic toxicity data is insufficient. Potential interactions may occur with medications metabolized by cytochrome P450 enzymes, particularly CYP3A4 substrates, due to the compound's enzyme-modulating properties. Pregnancy and lactation safety has not been established, and use should be avoided in these populations.
