Schisandrol B

Schisandrol B at a Glance

Schisandrol B is a dibenzocyclooctadiene lignan of the schisandra berry (Schisandra chinensis, wuweizi), the “five-flavour berry” prized in traditional Chinese medicine as an adaptogen and liver tonic. It sits in the same structural family as the more abundant schisandrin (schisandrol A) and schisandrin A, but carries its own hydroxyl substitution pattern — and, importantly, its own second name: it is identical to gomisin A ^{1,4Reference 1Jiang Y et al. · 2016AnimalSchisandrol B protects against acetaminophen-induced acute hepatotoxicity in mice via activation of the NRF2/ARE signaling pathwayView study →Reference 4Ikeya Y et al. · 1979The constituents of Schizandra chinensis BaillView study →}.

The most developed line of research on the isolated molecule is hepatoprotection. In rodent models it defends the liver against paracetamol (acetaminophen) overdose, carbon-tetrachloride injury, endotoxin-driven fulminant failure and bile-acid (cholestatic) damage, working through the NRF2/ARE antioxidant programme, the pregnane X receptor (PXR) bile-acid pathway, and restoration of mitochondrial biogenesis ^{1,2,3,4,5,6Reference 1Jiang Y et al. · 2016AnimalSchisandrol B protects against acetaminophen-induced acute hepatotoxicity in mice via activation of the NRF2/ARE signaling pathwayView study →Reference 2Zeng H et al. · 2017Schisandrol B protects against cholestatic liver injury through pregnane X receptorsView study →Reference 3Yang X et al. · 2026AnimalSchisandrol B protects against lithocholic acid-induced cholestatic liver injury in mice through mitochondrial biogenesisView study →Reference 4Ikeya Y et al. · 1979The constituents of Schizandra chinensis BaillView study →Reference 5Hwang IS et al. · 2013Protective effects of gomisin A isolated from Schisandra chinensis against CCl₄-induced hepatic and renal injuryView study →Reference 6Kim SH et al. · 2008AnimalAnti-apoptotic and hepatoprotective effects of gomisin A on fulminant hepatic failure induced by D-galactosamine and lipopolysaccharide in miceView study →}.

The other concrete, real-world angle is not an efficacy claim but a drug interaction: schisandrol B is a mechanism-based inhibitor of CYP3A and a modulator of P-glycoprotein, reliable enough at CYP3A4 that pharmacologists have used it as a selective isoform probe ^{7,8,10Reference 7Wu JJ et al. · 2016Gomisin A is a novel isoform-specific probe for the selective sensing of human cytochrome P450 3A4 in liver microsomes and living cellsView study →Reference 8Zhai J et al. · 2017AnimalTime- and NADPH-dependent inhibition on CYP3A by gomisin A and the pharmacokinetic interactions between gomisin A and cyclophosphamide in ratsView study →Reference 10Wan CK et al. · 2006Gomisin A alters substrate interaction and reverses P-glycoprotein-mediated multidrug resistance in HepG2-DR cellsView study →}. All of the therapeutic evidence below is preclinical — cell and animal work — and it is not sold as a single-molecule supplement.

Schisandrol B and Gomisin A Are the Same Molecule

The single most important thing to settle about this compound is a naming one. Schisandrol B and gomisin A are two names for one molecule — not two related lignans.

• They share one PubChem record (CID 634470), which lists schisandrol B, gomisin A, (+)-gomisin A and wuweizi alcohol B as synonyms of the same structure ^{4Reference 4Ikeya Y et al. · 1979The constituents of Schizandra chinensis BaillView study →}.
• They share the same molecular formula (C₂₃H₂₈O₇), the same canonical structure, and the same CAS registry number (58546-54-6); chemical suppliers list the material as “Schisandrol B (Gomisin A)” ^{4Reference 4Ikeya Y et al. · 1979The constituents of Schizandra chinensis BaillView study →}.
• The two names are historical: gomisin A is the name Ikeya and colleagues gave the molecule in 1979 when they characterised the schisandra dibenzocyclooctadiene lignans; schisandrol B is the parallel schisandrol/schisandrin naming used in much of the later pharmacology literature ^{4Reference 4Ikeya Y et al. · 1979The constituents of Schizandra chinensis BaillView study →}.

This matters because the two literatures have grown up in parallel: hepatoprotection and CYP3A work is often published under “schisandrol B,” while the antihypertensive, P-glycoprotein and older acetaminophen studies are published under “gomisin A.” They describe the same compound, and both are merged here.

Not to be confused with gomisin B, C, D, J, N etc. — those are distinct lignans. Only gomisin A equals schisandrol B.

Schisandrol B vs. Schisandrol A

A second, near-inevitable confusion is with schisandrol A, which is a different molecule:

• Schisandrol A = schisandrin (unqualified “schisandrin”/“schizandrin”) — the most abundant single lignan of the berry.
• Schisandrol B (this one) = gomisin A — a distinct, less abundant lignan differing in its methylenedioxy/methoxy substitution.

The “A/B” pairing refers to the two schisandrols; it is not the same axis as the schisandrin A (deoxyschisandrin) / schisandrin B (wuweizisu B) pairing, which is a separate set of lignans again. Berry chemistry is crowded with near-homonyms, so claims should always be pinned to a CAS number or structure, not a name alone.

What It's Used For

The evidence machinery is preclinical and clusters around the liver, with a well-characterised drug-metabolism angle and thinner cardiovascular and oncology threads.

Evidence by IndicationStrength of support · Beta

Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. Every row here rests on isolated-compound preclinical work; there is no human isolate trial, so read each row’s basis.

01HepatoprotectionPromising52%Multiple rodent models (APAP, CCl₄, endotoxin, cholestasis); NRF2/PXR/mitochondrial mechanisms ^{1,2,3,4,5,6Reference 1Jiang Y et al. · 2016AnimalSchisandrol B protects against acetaminophen-induced acute hepatotoxicity in mice via activation of the NRF2/ARE signaling pathwayView study →Reference 2Zeng H et al. · 2017Schisandrol B protects against cholestatic liver injury through pregnane X receptorsView study →Reference 3Yang X et al. · 2026AnimalSchisandrol B protects against lithocholic acid-induced cholestatic liver injury in mice through mitochondrial biogenesisView study →Reference 4Ikeya Y et al. · 1979The constituents of Schizandra chinensis BaillView study →Reference 5Hwang IS et al. · 2013Protective effects of gomisin A isolated from Schisandra chinensis against CCl₄-induced hepatic and renal injuryView study →Reference 6Kim SH et al. · 2008AnimalAnti-apoptotic and hepatoprotective effects of gomisin A on fulminant hepatic failure induced by D-galactosamine and lipopolysaccharide in miceView study →}

02Drug-Metabolism Modulation (CYP3A / P-gp)Shaky40%In-vitro CYP3A4 probe + rat cyclophosphamide PK interaction; P-gp inhibition ^{7,8,10Reference 7Wu JJ et al. · 2016Gomisin A is a novel isoform-specific probe for the selective sensing of human cytochrome P450 3A4 in liver microsomes and living cellsView study →Reference 8Zhai J et al. · 2017AnimalTime- and NADPH-dependent inhibition on CYP3A by gomisin A and the pharmacokinetic interactions between gomisin A and cyclophosphamide in ratsView study →Reference 10Wan CK et al. · 2006Gomisin A alters substrate interaction and reverses P-glycoprotein-mediated multidrug resistance in HepG2-DR cellsView study →}

03Cardiovascular / AntihypertensiveShaky26%Single mouse angiotensin-II model, nitric-oxide preservation ^{9Reference 9Park JY et al. · 2012Antihypertensive effect of gomisin A from Schisandra chinensis on angiotensin II-induced hypertension via preservation of nitric oxide bioavailabilityView study →}

04Anticancer AdjuvantShaky22%In-vitro MDR reversal + mouse paclitaxel augmentation ^{10,11Reference 10Wan CK et al. · 2006Gomisin A alters substrate interaction and reverses P-glycoprotein-mediated multidrug resistance in HepG2-DR cellsView study →Reference 11Wang T et al. · 2022Gomisin A enhances the antitumor effect of paclitaxel by suppressing oxidative stress in ovarian cancerView study →}

Mechanisms

The load-bearing dual point: the same NRF2/PXR/mitochondrial machinery that makes schisandrol B hepatoprotective in rodents sits alongside a CYP3A/P-gp inhibition that makes it a drug-interaction risk — the two are the molecule’s most reproducible findings, and both are mechanistic rather than clinically proven.

Pharmacokinetics

Systematic human pharmacokinetics for isolated schisandrol B are not established; most exposure data come from whole-berry or lignan-extract dosing, where schisandrol B is a minor lignan relative to schisandrol A. As a lipophilic dibenzocyclooctadiene it is absorbed orally and metabolised principally by CYP3A4, with 8-hydroxylation the major route ^{7Reference 7Wu JJ et al. · 2016Gomisin A is a novel isoform-specific probe for the selective sensing of human cytochrome P450 3A4 in liver microsomes and living cellsView study →}. Its own metabolism by CYP3A, combined with its mechanism-based inhibition of that enzyme, is why it perturbs the pharmacokinetics of co-administered CYP3A substrates such as cyclophosphamide in rats ^{8Reference 8Zhai J et al. · 2017AnimalTime- and NADPH-dependent inhibition on CYP3A by gomisin A and the pharmacokinetic interactions between gomisin A and cyclophosphamide in ratsView study →}. Quantitative human figures — oral bioavailability, half-life, active metabolites — are not characterised for the isolate and are flagged in the gaps tracker; claims resting on in-vitro potency should be read against this uncertainty.

Clinical Trials

There are no clinical trials of isolated schisandrol B / gomisin A for any indication. Human exposure occurs only within whole schisandra-berry preparations, whose (limited) clinical literature concerns the multi-lignan extract, not this single molecule.

Last checked: July 2026.

Isolate vs. Plant Studies

This molecule is unusually isolate-forward on the mechanism side and plant-only on the human side. Nearly all the pharmacology above uses the purified compound — schisandrol B or gomisin A dosed to rodents or applied to cells — which is a strength for attributing a mechanism to this molecule rather than the berry as a whole ^{1,2,7Reference 1Jiang Y et al. · 2016AnimalSchisandrol B protects against acetaminophen-induced acute hepatotoxicity in mice via activation of the NRF2/ARE signaling pathwayView study →Reference 2Zeng H et al. · 2017Schisandrol B protects against cholestatic liver injury through pregnane X receptorsView study →Reference 7Wu JJ et al. · 2016Gomisin A is a novel isoform-specific probe for the selective sensing of human cytochrome P450 3A4 in liver microsomes and living cellsView study →}. But there is no human trial of the isolate: real-world human exposure is always as one lignan inside whole schisandra berry, alongside schisandrin, schisandrin A, schisantherin A and the rest. Because those co-occurring lignans share the CYP3A/P-gp activity, the whole berry’s drug-interaction potential cannot be reduced to schisandrol B alone — and the berry’s traditional liver-tonic reputation reflects the mixture, not this single molecule.

Prevalence in Nature

Schisandrol B occurs in the fruit (berries) of Schisandra chinensis (wuweizi / five-flavour berry), the same organ that carries the rest of the schisandra lignan complex, and is also reported in the related Schisandra sphenanthera (nan-wuweizi) ^{4,5Reference 4Ikeya Y et al. · 1979The constituents of Schizandra chinensis BaillView study →Reference 5Hwang IS et al. · 2013Protective effects of gomisin A isolated from Schisandra chinensis against CCl₄-induced hepatic and renal injuryView study →}. Within the berry it is a minor lignan relative to the dominant schisandrol A (schisandrin), which alone can reach ~0.4–0.8% of the dried fruit; total lignans typically make up only a few percent of the dried berry, and the individual share of schisandrol B is not well quantified in the sources reviewed here. Lignan content — and the balance between individual lignans — varies with species, cultivation region and chemotype (northern varieties generally richer). A precise, cited schisandrol-B concentration figure is a documented gap.

Discovery & Synthesis

Schisandrol B was isolated from Schisandra chinensis fruit and named gomisin A by Ikeya, Taguchi and co-workers in 1979, in the landmark series of papers that characterised the schisandra dibenzocyclooctadiene lignans (the gomisins A, B, C, F, G and the schisandrins) and established their absolute structures ^{4Reference 4Ikeya Y et al. · 1979The constituents of Schizandra chinensis BaillView study →}. The parallel name schisandrol B comes from the schisandrin/schisandrol nomenclature adopted in much of the later Chinese pharmacology literature; both names denote CAS 58546-54-6. Manufacture today is by extraction and chromatographic isolation from schisandra berries — the material sold for research is a plant isolate rather than a synthetic product — although total syntheses of the dibenzocyclooctadiene lignan skeleton are documented in the natural-products literature. The precise first total synthesis of schisandrol B specifically is not well documented in the sources reviewed here.

Patents: not yet researched.

Toxicity & Safety

Schisandrol B carries a low intrinsic-toxicity flag. The schisandra berry has a long history of dietary and medicinal use; the isolated lignan has been dosed to rodents in hepatoprotection studies without notable toxicity, and its documented liver effects are protective in the models tested ^{1,2,3,4,5,6Reference 1Jiang Y et al. · 2016AnimalSchisandrol B protects against acetaminophen-induced acute hepatotoxicity in mice via activation of the NRF2/ARE signaling pathwayView study →Reference 2Zeng H et al. · 2017Schisandrol B protects against cholestatic liver injury through pregnane X receptorsView study →Reference 3Yang X et al. · 2026AnimalSchisandrol B protects against lithocholic acid-induced cholestatic liver injury in mice through mitochondrial biogenesisView study →Reference 4Ikeya Y et al. · 1979The constituents of Schizandra chinensis BaillView study →Reference 5Hwang IS et al. · 2013Protective effects of gomisin A isolated from Schisandra chinensis against CCl₄-induced hepatic and renal injuryView study →Reference 6Kim SH et al. · 2008AnimalAnti-apoptotic and hepatoprotective effects of gomisin A on fulminant hepatic failure induced by D-galactosamine and lipopolysaccharide in miceView study →}. The real caution is not intrinsic toxicity but a pharmacokinetic drug-interaction risk: as a mechanism-based CYP3A inhibitor and P-glycoprotein blocker, schisandrol B can raise the blood levels of co-administered drugs cleared by those pathways — a class that includes many statins, immunosuppressants (e.g. tacrolimus, cyclosporine), some chemotherapeutics (cyclophosphamide) and other CYP3A4/P-gp substrates ^{7,8,10Reference 7Wu JJ et al. · 2016Gomisin A is a novel isoform-specific probe for the selective sensing of human cytochrome P450 3A4 in liver microsomes and living cellsView study →Reference 8Zhai J et al. · 2017AnimalTime- and NADPH-dependent inhibition on CYP3A by gomisin A and the pharmacokinetic interactions between gomisin A and cyclophosphamide in ratsView study →Reference 10Wan CK et al. · 2006Gomisin A alters substrate interaction and reverses P-glycoprotein-mediated multidrug resistance in HepG2-DR cellsView study →}.

Safety at a Glance

✅ Low / no toxicity

• Low intrinsic toxicity. From a long-used food/medicinal berry; the isolated lignan is hepatoprotective, not hepatotoxic, in rodent models.
• CYP3A drug-interaction potential. Mechanism-based CYP3A inhibition can increase exposure to CYP3A-substrate medicines (statins, tacrolimus/cyclosporine, cyclophosphamide, and others).
• P-glycoprotein inhibition. May raise absorption/levels of P-gp-substrate drugs; the effect adds to that of the other schisandra lignans in whole-berry use.
• Human safety of the isolate is uncharacterised. No human trials, no repeat-dose or reproductive-toxicity dataset for the pure compound; intake decisions belong to the herb/product level.

Dosage

There is no established human dose for isolated schisandrol B. It is not sold as a single-molecule supplement; human exposure is as one lignan within whole schisandra-berry preparations, which are dosed as the berry or a standardised multi-lignan extract, not as this compound. The figures in the research above are preclinical rodent and in-vitro doses chosen for mechanistic study. These are doses studied in research and are not a personal recommendation.

References

1. Jiang Y, Fan X, Wang Y, et al. (2016). Schisandrol B protects against acetaminophen-induced acute hepatotoxicity in mice via activation of the NRF2/ARE signaling pathway. Acta Pharmacologica Sinica. https://pubmed.ncbi.nlm.nih.gov/26806302/
2. Zeng H, Jiang Y, Chen P, et al. (2017). Schisandrol B protects against cholestatic liver injury through pregnane X receptors. British Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/28128437/
3. Yang X, et al. (2026). Schisandrol B protects against lithocholic acid-induced cholestatic liver injury in mice through mitochondrial biogenesis. Chinese Medicine. https://pubmed.ncbi.nlm.nih.gov/41975487/
4. Ikeya Y, Taguchi H, Yosioka I, Kobayashi H (1979). The constituents of Schizandra chinensis Baill. I. Isolation and structure determination of five new lignans, gomisin A, B, C, F and G, and the absolute structure of schizandrin. Chemical & Pharmaceutical Bulletin. https://doi.org/10.1248/cpb.27.1383
5. Hwang IS, Kim JE, Lee YJ, et al. (2013). Protective effects of gomisin A isolated from Schisandra chinensis against CCl₄-induced hepatic and renal injury. International Journal of Molecular Medicine. https://pubmed.ncbi.nlm.nih.gov/23381504/
6. Kim SH, Kim YS, Kang SS, et al. (2008). Anti-apoptotic and hepatoprotective effects of gomisin A on fulminant hepatic failure induced by D-galactosamine and lipopolysaccharide in mice. Journal of Pharmacological Sciences. https://pubmed.ncbi.nlm.nih.gov/18270473/
7. Wu JJ, Ge GB, He YQ, et al. (2016). Gomisin A is a novel isoform-specific probe for the selective sensing of human cytochrome P450 3A4 in liver microsomes and living cells. The AAPS Journal. https://pubmed.ncbi.nlm.nih.gov/26361765/
8. Zhai J, Zhang F, Gao S, et al. (2017). Time- and NADPH-dependent inhibition on CYP3A by gomisin A and the pharmacokinetic interactions between gomisin A and cyclophosphamide in rats. Molecules. https://pubmed.ncbi.nlm.nih.gov/28786954/
9. Park JY, Yun JW, Choi YW, et al. (2012). Antihypertensive effect of gomisin A from Schisandra chinensis on angiotensin II-induced hypertension via preservation of nitric oxide bioavailability. Hypertension Research. https://pubmed.ncbi.nlm.nih.gov/22534517/
10. Wan CK, Zhu GY, Shen XL, et al. (2006). Gomisin A alters substrate interaction and reverses P-glycoprotein-mediated multidrug resistance in HepG2-DR cells. Biochemical Pharmacology. https://pubmed.ncbi.nlm.nih.gov/16889754/
11. Wang T, et al. (2022). Gomisin A enhances the antitumor effect of paclitaxel by suppressing oxidative stress in ovarian cancer. Oncology Reports. https://pubmed.ncbi.nlm.nih.gov/36169181/

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