Schisandrin B

Schisandrin B at a Glance

Schisandrin B is a dibenzocyclooctadiene lignan and the most extensively studied bioactive of schisandra berry (Schisandra chinensis), the “five-flavour fruit” of traditional Chinese medicine. It is the workhorse of the schisandra lignan family: where schisandrin (schisandrol A) is the most abundant single lignan, schisandrin B carries the largest research literature — decades of rodent and cell work on liver protection, anti-inflammatory and neuroprotective activity, cardioprotection, and reversal of cancer drug-resistance.

The molecule is chemically the same across its several names — γ-schisandrin, wuweizisu B and gomisin N are all synonyms for schisandrin B — a naming tangle inherited from parallel Chinese (wuweizisu) and Japanese (gomisin/schizandrin) phytochemistry.

Two honest caveats frame everything below. First, essentially all of the therapeutic evidence is preclinical — isolated-molecule studies in rodents and cell lines, with no controlled human efficacy trials of the isolate. Second, and most consequential for real-world safety, schisandrin B is a potent modulator of drug metabolism: it both inhibits and (with repeated dosing) induces the CYP3A enzymes that clear a large share of prescription drugs, and it inhibits the P-glycoprotein efflux transporter. That pharmacokinetic reach — not toxicity of the molecule itself — is the reason this lignan matters clinically ^{7,16Reference 7Jackson JP et al. · 2017Prediction of clinically relevant herb-drug clearance interactions using sandwich-cultured human hepatocytes: Schisandra spp. case studyView study →Reference 16Wang Z et al. · 2018AnimalInvestigation of pharmacokinetics, tissue distribution and excretion of schisandrin B in rats by HPLC-MS/MSView study →}.

The CYP3A & P-Glycoprotein Interaction Story

This is the single most clinically important thing about schisandrin B, and it cuts both ways — which is exactly why it is easy to get wrong.

Acute inhibition. Given as a single or short-course dose, schisandrin B is a potent inhibitor of CYP3A — the enzyme subfamily that metabolises a large fraction of oral drugs. In a rodent study, schisandrin B dose-dependently inhibited hepatic CYP3A activity and markedly raised the oral bioavailability of the CYP3A probe midazolam ^{5Reference 5Li WL et al. · 2013AnimalIn vivo effect of schisandrin B on cytochrome P450 enzyme activityView study →}. In human liver microsomes and hepatocyte models, schisandra lignans (schisandrin B among them, with the related gomisin C acting as a mechanism-based inactivator) are strong CYP3A4 inhibitors, and sandwich-cultured human-hepatocyte modelling predicts a clinically relevant reduction in midazolam clearance from schisandra exposure ^{6,7Reference 6Iwata H et al. · 2004Identification and characterization of potent CYP3A4 inhibitors in Schisandra fruit extractView study →Reference 7Jackson JP et al. · 2017Prediction of clinically relevant herb-drug clearance interactions using sandwich-cultured human hepatocytes: Schisandra spp. case studyView study →}. Acutely, then, schisandrin B raises co-administered CYP3A-substrate levels — the mechanism behind the well-documented clinical use of schisandra-containing Wuzhi preparations to deliberately boost tacrolimus blood levels in transplant patients.

Repeated-dose induction. With ongoing exposure the picture inverts. Schisandrin B is a pregnane-X-receptor (PXR) agonist: it binds PXR and up-regulates CYP3A4/CYP3A11, UGT1A1 and MRP efflux transporters, enhancing bile-acid clearance and detoxification ^{4Reference 4Zhang Y et al. · 2026Schisandrin B targets PXR to enhance bile acid metabolism and alleviate ANIT-induced cholestatic liver injury via dual pathwaysView study →}. Sustained PXR-driven induction increases CYP3A capacity, which over time can lower the levels of CYP3A-cleared drugs — the opposite of the acute effect.

P-glycoprotein. Independently of CYP, schisandrin B is a direct P-glycoprotein (P-gp) inhibitor — one of the first dibenzocyclooctadiene lignans shown to block this efflux pump ^{10,12Reference 10Pan Q et al. · 2005Schisandrin B — a novel inhibitor of P-glycoproteinView study →Reference 12Pan Q et al. · 2006Dibenzocyclooctadiene lignans: a class of novel inhibitors of P-glycoproteinView study →}. Inhibiting P-gp raises the intracellular accumulation and oral absorption of P-gp substrates, the basis of its anticancer-chemosensitisation work (below) but also another route to herb-drug interactions.

The practical takeaway: schisandrin B (and any schisandra product) should be treated as a genuine perpetrator of pharmacokinetic drug interactions with CYP3A and P-gp substrates — narrow-therapeutic-index drugs such as tacrolimus, ciclosporin, and many others — with the direction of the effect depending on timing and duration of exposure ^{4,5,6,7Reference 4Zhang Y et al. · 2026Schisandrin B targets PXR to enhance bile acid metabolism and alleviate ANIT-induced cholestatic liver injury via dual pathwaysView study →Reference 5Li WL et al. · 2013AnimalIn vivo effect of schisandrin B on cytochrome P450 enzyme activityView study →Reference 6Iwata H et al. · 2004Identification and characterization of potent CYP3A4 inhibitors in Schisandra fruit extractView study →Reference 7Jackson JP et al. · 2017Prediction of clinically relevant herb-drug clearance interactions using sandwich-cultured human hepatocytes: Schisandra spp. case studyView study →}.

What It's Used For

Schisandrin B’s preclinical profile is broad and mechanistically coherent — a recurring theme of antioxidant, mitochondrial-protective and anti-inflammatory action across organs ^{1Reference 1Nasser MI et al. · 2020ReviewA comprehensive review on schisandrin B and its biological propertiesView study →}. The load-bearing caveat is the compound-page discipline: this is isolated-molecule evidence in rodents and cells, and the human data belong to whole schisandra berry/extract, not the isolate.

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. All rows here are isolate preclinical evidence (rodent/cell); no human isolate trials exist, so scores stay modest by design.

01HepatoprotectionPromising52%Decades of rodent isolate work: mitochondrial GSH + HSP induction; PXR/bile-acid ^{1,2,3,4Reference 1Nasser MI et al. · 2020ReviewA comprehensive review on schisandrin B and its biological propertiesView study →Reference 2Ip SP et al. · 1996AnimalSchisandrin B protects against carbon tetrachloride toxicity by enhancing the mitochondrial glutathione redox status in mouse liverView study →Reference 3Chiu PY et al. · 2003Hepatoprotective mechanism of schisandrin B: role of mitochondrial glutathione antioxidant status and heat shock proteinsView study →Reference 4Zhang Y et al. · 2026Schisandrin B targets PXR to enhance bile acid metabolism and alleviate ANIT-induced cholestatic liver injury via dual pathwaysView study →}

02Anti-inflammatoryShaky40%Rodent isolate; MyD88/NF-κB in LPS lung injury ^{8Reference 8Zhu W et al. · 2023Schisandrin B protects against LPS-induced inflammatory lung injury by targeting MyD88View study →}

03NeuroprotectionShaky36%Rodent/cell isolate; ferroptosis via GSK3β/Nrf2/GPX4 in AD models ^{9Reference 9Ding T et al. · 2025Schisandrin B ameliorates Alzheimer’s disease by suppressing neuronal ferroptosis and ensuing microglia M1 polarizationView study →}

04Anticancer / ChemosensitisationShaky34%In-vitro/in-vivo isolate; P-gp reversal + anti-EMT/metastasis ^{10,11,12,13Reference 10Pan Q et al. · 2005Schisandrin B — a novel inhibitor of P-glycoproteinView study →Reference 11Wang S et al. · 2017Schisandrin B reverses doxorubicin resistance through inhibiting P-glycoprotein and promoting proteasome-mediated degradation of survivinView study →Reference 12Pan Q et al. · 2006Dibenzocyclooctadiene lignans: a class of novel inhibitors of P-glycoproteinView study →Reference 13Liu Z et al. · 2012Schisandrin B attenuates cancer invasion and metastasis via inhibiting epithelial-mesenchymal transitionView study →}

05CardioprotectionShaky32%Rodent isolate; doxorubicin cardiotoxicity via glutathione redox cycling ^{14,15Reference 14Li L et al. · 2007Schisandrin B prevents doxorubicin-induced cardiotoxicity via enhancing glutathione redox cyclingView study →Reference 15Xu Y et al. · 2011AnimalSchisandrin B prevents doxorubicin-induced chronic cardiotoxicity and enhances its anticancer activity in vivoView study →}

Mechanisms

The two CYP3A rows are the crux: schisandrin B inhibits CYP3A acutely but induces it (via PXR) with repeated dosing — so the net effect on a co-administered drug depends on dose and duration.

Pharmacokinetics

Schisandrin B is a highly lipophilic lignan, which shapes both its absorption and its long tissue residence. A rat HPLC-MS/MS study reported marked sex-dependent oral bioavailability — roughly 55% in females versus ~19% in males — with a double-peak plasma profile suggesting enterohepatic recirculation, and extensive distribution into fatty and reproductive tissue ^{16Reference 16Wang Z et al. · 2018AnimalInvestigation of pharmacokinetics, tissue distribution and excretion of schisandrin B in rats by HPLC-MS/MSView study →}. Metabolism is hepatic and CYP3A-mediated, which is precisely why the molecule is entangled with the enzyme it is metabolised by — it is simultaneously a CYP3A substrate, an acute inhibitor, and a repeated-dose inducer of that pathway ^{5,6Reference 5Li WL et al. · 2013AnimalIn vivo effect of schisandrin B on cytochrome P450 enzyme activityView study →Reference 6Iwata H et al. · 2004Identification and characterization of potent CYP3A4 inhibitors in Schisandra fruit extractView study →}. Robust human ADME parameters for the isolate — Cmax, half-life, absolute oral bioavailability — are not well established; the available PK is animal, and human exposure is as one lignan within a schisandra extract ^{1,16Reference 1Nasser MI et al. · 2020ReviewA comprehensive review on schisandrin B and its biological propertiesView study →Reference 16Wang Z et al. · 2018AnimalInvestigation of pharmacokinetics, tissue distribution and excretion of schisandrin B in rats by HPLC-MS/MSView study →}.

Clinical Trials

There are no controlled efficacy trials of isolated schisandrin B. Human clinical experience is with whole schisandra berry and multi-lignan schisandra extracts (and, pharmacokinetically, with Wuzhi-type preparations used to modulate tacrolimus levels), within which schisandrin B is only one constituent.

Last checked: July 2026.

Isolate vs. Plant Studies

The evidence base here is unusually isolate-heavy on mechanism but plant-only on humans. Almost every therapeutic claim above was generated with purified schisandrin B in rodents or cell lines — the Ip/Chiu hepatoprotection series ^{2,3Reference 2Ip SP et al. · 1996AnimalSchisandrin B protects against carbon tetrachloride toxicity by enhancing the mitochondrial glutathione redox status in mouse liverView study →Reference 3Chiu PY et al. · 2003Hepatoprotective mechanism of schisandrin B: role of mitochondrial glutathione antioxidant status and heat shock proteinsView study →}, the ferroptosis/AD work ^{9Reference 9Ding T et al. · 2025Schisandrin B ameliorates Alzheimer’s disease by suppressing neuronal ferroptosis and ensuing microglia M1 polarizationView study →}, the P-gp and cardioprotection studies ^{10,11,14,15Reference 10Pan Q et al. · 2005Schisandrin B — a novel inhibitor of P-glycoproteinView study →Reference 11Wang S et al. · 2017Schisandrin B reverses doxorubicin resistance through inhibiting P-glycoprotein and promoting proteasome-mediated degradation of survivinView study →Reference 14Li L et al. · 2007Schisandrin B prevents doxorubicin-induced cardiotoxicity via enhancing glutathione redox cyclingView study →Reference 15Xu Y et al. · 2011AnimalSchisandrin B prevents doxorubicin-induced chronic cardiotoxicity and enhances its anticancer activity in vivoView study →}. As a preclinical mechanism base for the isolate, that is a genuine strength: the effects are attributed to this specific molecule, not a mixture.

The human side is the mirror image. Schisandra’s clinical use — as an adaptogen ^{17Reference 17Such S et al. · 2026ReviewSystem-level, molecular and cellular mechanisms of selected plant adaptogens — a reviewView study →}, hepatoprotective tonic, and (via Wuzhi) a deliberate CYP3A modulator — rests on whole berry and standardised multi-lignan extracts, where schisandrin B co-occurs with schisandrin (schisandrol A), schisantherin A and others ^{1Reference 1Nasser MI et al. · 2020ReviewA comprehensive review on schisandrin B and its biological propertiesView study →}. Two consequences follow: the whole-plant clinical effects cannot be assigned to schisandrin B alone, and — because these lignans share and compete for the same CYP3A/P-gp machinery — the interaction behaviour of the extract is not simply the sum of the isolate’s. A further species caveat: some schisandra pharmacokinetic and antiviral findings come from southern schisandra (S. sphenanthera), not S. chinensis, and the two should not be silently merged.

Its Role in Plants

Schisandrin B is a dibenzocyclooctadiene lignan — two phenylpropanoid units oxidatively coupled and bridged into the characteristic eight-membered carbocyclic ring that defines this schisandra-specific lignan class. Biosynthetically these lignans derive from the general phenylpropanoid pathway, arising from oxidative dimerisation of monolignol precursors followed by extensive methylenedioxy/methoxy substitution.

In the plant, lignans of this type act largely as defensive and antioxidant metabolites, concentrated in the fruit (and seed) where the plant’s investment in reproduction is protected. The dense oxygenation that makes schisandrin B a good radical scavenger in animal tissue is the same chemistry the berry uses to guard its lipids against oxidation. This is plant biology, not human pharmacology, and should not be read as evidence of a medicinal effect.

Prevalence in Nature

Schisandrin B is one of the principal lignans of schisandra berry (Schisandra chinensis), the dried “five-flavour fruit” (wu wei zi). It is less abundant than the signature lignan schisandrin (schisandrol A), which typically runs around 0.4–0.8% of the dried fruit; total schisandra lignans are generally only a few percent of the dried berry, and schisandrin B is one fraction within that pool ^{18Reference 18Kim YG et al. · 2022The growth characteristics and lignan contents of Schisandra chinensis fruits from different cultivation regionsView study →}. Reported content varies substantially with variety (the northern bei-wuweizi chemotype is generally richer than the southern) and cultivation region, so a single “typical” figure is misleading ^{18Reference 18Kim YG et al. · 2022The growth characteristics and lignan contents of Schisandra chinensis fruits from different cultivation regionsView study →}. Pharmacopoeial standards reflect this by specifying a minimum total for several named lignans together (schisandrin, schisandrol B, deoxyschisandrin and γ-schisandrin) rather than for schisandrin B alone.

Beyond S. chinensis, schisandrin B and its relatives occur in southern schisandra (S. sphenanthera) and other Schisandra/Kadsura species; the fruit is the richest and the pharmacopoeially recognised source.

Discovery & Synthesis

Schisandrin B belongs to the family of dibenzocyclooctadiene lignans isolated from schisandra fruit and structurally characterised during the 1960s–70s, when Chinese and Japanese phytochemists worked out the constituents of wu wei zi. The parallel effort left the molecule with several synonymous names — wuweizisu B (Chinese naming, wu-wei-zi-su = “schisandra element”), γ-schisandrin and gomisin N (Japanese naming) — all denoting the same compound, CAS 61281-37-6, molecular formula C23H28O6 (MW 400.5). Deduplicating these names is essential when reading the literature, since the same molecule appears under different labels across papers.

Manufacture today is by extraction and chromatographic purification from schisandra fruit, the practical source of research- and reference-grade material; total synthesis of the dibenzocyclooctadiene skeleton has been achieved in methodological work but is not the commercial route.

Patents: not yet researched.

Toxicity & Safety

Schisandrin B carries a low toxicity flag. Schisandra berry has a long history of dietary and medicinal use, and the isolated lignan shows low acute toxicity in the animal studies that dose it at pharmacological levels ^{1Reference 1Nasser MI et al. · 2020ReviewA comprehensive review on schisandrin B and its biological propertiesView study →}. The real caution is not the molecule’s own toxicity — it is what it does to the metabolism of other drugs.

Safety at a Glance

✅ Low / no toxicity

• Low intrinsic toxicity. Derived from a long-used food/medicinal berry; low acute toxicity in animal studies at research doses ^{1,2Reference 1Nasser MI et al. · 2020ReviewA comprehensive review on schisandrin B and its biological propertiesView study →Reference 2Ip SP et al. · 1996AnimalSchisandrin B protects against carbon tetrachloride toxicity by enhancing the mitochondrial glutathione redox status in mouse liverView study →}.
• Two-way CYP3A drug interactions. Schisandrin B acutely inhibits CYP3A (raising levels of co-administered CYP3A substrates) but induces it via PXR with repeated dosing (lowering them) — a real, direction-dependent interaction risk with drugs like tacrolimus and ciclosporin ^{4,5,6,7Reference 4Zhang Y et al. · 2026Schisandrin B targets PXR to enhance bile acid metabolism and alleviate ANIT-induced cholestatic liver injury via dual pathwaysView study →Reference 5Li WL et al. · 2013AnimalIn vivo effect of schisandrin B on cytochrome P450 enzyme activityView study →Reference 6Iwata H et al. · 2004Identification and characterization of potent CYP3A4 inhibitors in Schisandra fruit extractView study →Reference 7Jackson JP et al. · 2017Prediction of clinically relevant herb-drug clearance interactions using sandwich-cultured human hepatocytes: Schisandra spp. case studyView study →}.
• P-glycoprotein inhibition. By blocking P-gp efflux it can raise the absorption/accumulation of P-gp-substrate drugs — a second, independent interaction route ^{10,12Reference 10Pan Q et al. · 2005Schisandrin B — a novel inhibitor of P-glycoproteinView study →Reference 12Pan Q et al. · 2006Dibenzocyclooctadiene lignans: a class of novel inhibitors of P-glycoproteinView study →}.
• Species and product variability. Effects and lignan content differ between S. chinensis and S. sphenanthera and between varieties; extract behaviour is not the isolate’s behaviour ^{1,18Reference 1Nasser MI et al. · 2020ReviewA comprehensive review on schisandrin B and its biological propertiesView study →Reference 18Kim YG et al. · 2022The growth characteristics and lignan contents of Schisandra chinensis fruits from different cultivation regionsView study →}.

Human reproductive/developmental data for isolated schisandrin B are not established; the isolate distributes into reproductive/adipose tissue in animals ^{16Reference 16Wang Z et al. · 2018AnimalInvestigation of pharmacokinetics, tissue distribution and excretion of schisandrin B in rats by HPLC-MS/MSView study →}. Pregnancy and lactation are decided at the herb or product level, where intake is chosen, and are not adjudicated on this molecule page.

Dosage

There is no established or recommended human dose for isolated schisandrin B. The figures in the literature are preclinical rodent research doses (for example the hepatoprotective and cardioprotective mouse studies dosed in the mmol/kg or tens-of-mg/kg range) and are not convertible to human self-dosing ^{2,3,14Reference 2Ip SP et al. · 1996AnimalSchisandrin B protects against carbon tetrachloride toxicity by enhancing the mitochondrial glutathione redox status in mouse liverView study →Reference 3Chiu PY et al. · 2003Hepatoprotective mechanism of schisandrin B: role of mitochondrial glutathione antioxidant status and heat shock proteinsView study →Reference 14Li L et al. · 2007Schisandrin B prevents doxorubicin-induced cardiotoxicity via enhancing glutathione redox cyclingView study →}.

Human exposure comes from schisandra berry and standardised schisandra extracts, in which schisandrin B is one of several lignans and is not dosed in isolation. Because the same lignans drive the CYP3A/P-gp interactions above, any schisandra product taken alongside prescription medication should be treated as a potential interactant, not a neutral supplement. These are doses studied in research and are not a personal recommendation.

References

1. Nasser MI, et al. (2020). A comprehensive review on schisandrin B and its biological properties. Oxidative Medicine and Cellular Longevity. https://pubmed.ncbi.nlm.nih.gov/32256947/
2. Ip SP, et al. (1996). Schisandrin B protects against carbon tetrachloride toxicity by enhancing the mitochondrial glutathione redox status in mouse liver. Free Radical Biology & Medicine. https://pubmed.ncbi.nlm.nih.gov/8891674/
3. Chiu PY, et al. (2003). Hepatoprotective mechanism of schisandrin B: role of mitochondrial glutathione antioxidant status and heat shock proteins. Free Radical Biology & Medicine. https://pubmed.ncbi.nlm.nih.gov/12899939/
4. Zhang Y, et al. (2026). Schisandrin B targets PXR to enhance bile acid metabolism and alleviate ANIT-induced cholestatic liver injury via dual pathways. International Journal of Biological Sciences. https://pubmed.ncbi.nlm.nih.gov/41362731/
5. Li WL, et al. (2013). In vivo effect of schisandrin B on cytochrome P450 enzyme activity. Phytomedicine. https://pubmed.ncbi.nlm.nih.gov/23523258/
6. Iwata H, et al. (2004). Identification and characterization of potent CYP3A4 inhibitors in Schisandra fruit extract. Drug Metabolism and Disposition. https://pubmed.ncbi.nlm.nih.gov/15342469/
7. Jackson JP, et al. (2017). Prediction of clinically relevant herb-drug clearance interactions using sandwich-cultured human hepatocytes: Schisandra spp. case study. Drug Metabolism and Disposition. https://pubmed.ncbi.nlm.nih.gov/28698304/
8. Zhu W, et al. (2023). Schisandrin B protects against LPS-induced inflammatory lung injury by targeting MyD88. Phytomedicine. https://pubmed.ncbi.nlm.nih.gov/36270224/
9. Ding T, et al. (2025). Schisandrin B ameliorates Alzheimer’s disease by suppressing neuronal ferroptosis and ensuing microglia M1 polarization. Phytomedicine. https://pubmed.ncbi.nlm.nih.gov/40382817/
10. Pan Q, et al. (2005). Schisandrin B — a novel inhibitor of P-glycoprotein. Biochemical and Biophysical Research Communications. https://pubmed.ncbi.nlm.nih.gov/16084496/
11. Wang S, et al. (2017). Schisandrin B reverses doxorubicin resistance through inhibiting P-glycoprotein and promoting proteasome-mediated degradation of survivin. Scientific Reports. https://pubmed.ncbi.nlm.nih.gov/28827665/
12. Pan Q, et al. (2006). Dibenzocyclooctadiene lignans: a class of novel inhibitors of P-glycoprotein. Cancer Chemotherapy and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/16231181/
13. Liu Z, et al. (2012). Schisandrin B attenuates cancer invasion and metastasis via inhibiting epithelial-mesenchymal transition. PLoS One. https://pubmed.ncbi.nlm.nih.gov/22848381/
14. Li L, et al. (2007). Schisandrin B prevents doxorubicin-induced cardiotoxicity via enhancing glutathione redox cycling. Clinical Cancer Research. https://pubmed.ncbi.nlm.nih.gov/18006777/
15. Xu Y, et al. (2011). Schisandrin B prevents doxorubicin-induced chronic cardiotoxicity and enhances its anticancer activity in vivo. PLoS One. https://pubmed.ncbi.nlm.nih.gov/22164272/
16. Wang Z, et al. (2018). Investigation of pharmacokinetics, tissue distribution and excretion of schisandrin B in rats by HPLC-MS/MS. Biomedical Chromatography. https://pubmed.ncbi.nlm.nih.gov/28833320/
17. Such S, et al. (2026). System-level, molecular and cellular mechanisms of selected plant adaptogens — a review. Nutrients. https://pubmed.ncbi.nlm.nih.gov/41901106/
18. Kim YG, et al. (2022). The growth characteristics and lignan contents of Schisandra chinensis fruits from different cultivation regions. Applied Biological Chemistry. https://doi.org/10.1186/s13765-022-00746-2

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