Flavokawain C

Flavokawain C at a Glance

Flavokawain C is the minor, third member of kava’s (Piper methysticum) flavokawain chalcone triad — the group of three related chalcones, flavokawains A, B and C, that sit alongside the far more abundant kavalactones. Of the three it is the least abundant and the least studied ^{5,6Reference 5Abu N et al. · 2013ReviewThe flavokawains: uprising medicinal chalcones [review]View study →Reference 6Wang Y et al. · 2021ReviewBiological activity, hepatotoxicity, and structure-activity relationship of kavalactones and flavokavins, the two main bioactive components in kava (Piper methysticum) [review]View study →}.

Where the kavalactones drive kava’s traditional anxiolytic and sedative effects, the flavokawains are a small, chemically separate story: a cluster of chalcones whose interest is almost entirely preclinical anticancer activity. Flavokawain C has been tested against a handful of cancer cell lines — chiefly colorectal, with one mouse xenograft, and more recently liver — where the isolated molecule induces apoptosis and arrests the cell cycle ^{1,2,3,4Reference 1Phang CW et al. · 2016In vitroFlavokawain C inhibits cell cycle and promotes apoptosis, associated with endoplasmic reticulum stress and regulation of MAPKs and Akt signaling pathways in HCT 116 human colon carcinoma cells [in vitro]View study →Reference 2Phang CW et al. · 2017In vitroInduction of apoptosis and cell cycle arrest by flavokawain C on HT-29 human colon adenocarcinoma via enhancement of reactive oxygen species generation, upregulation of p21, p27, and GADD153, and inactivation of inhibitor of apoptosis proteins [in vitro]View study →Reference 3Phang CW et al. · 2021AnimalFlavokawain C exhibits anti-tumor effects on in vivo HCT 116 xenograft and identification of its apoptosis-linked serum biomarkers via proteomic analysis [animal]View study →Reference 4Wang R et al. · 2024In vitroFlavokawain C inhibits proliferation and migration of liver cancer cells through the FAK/PI3K/AKT signaling pathway [in vitro]View study →}.

The honest posture is that this is thin, early-stage, isolate-only data. There are no human studies, no pharmacokinetics, and no toxicology for flavokawain C itself. Its main role here is to complete the flavokawain triad and round out the kava chalcone story — not to stand as an established active in its own right.

Completing the Flavokawain Triad

The point is that flavokawain C is the last and smallest piece of a set of three. Understanding it means placing it against its better-known siblings.

The three kava chalcones share a chalcone backbone and differ only in their hydroxyl/methoxy substitution:

Chalcone	Structure	Relative role in kava
Flavokawain A	2′-hydroxy-4,4′,6′-trimethoxychalcone	Most abundant flavokawain (~0.46% of extract); best-studied anticancer chalcone ^{5Reference 5Abu N et al. · 2013ReviewThe flavokawains: uprising medicinal chalcones [review]View study →}
Flavokawain B	2′-hydroxy-4′,6′-dimethoxychalcone	Most cytotoxic of the three in vitro; a leading candidate in kava’s hepatotoxicity story ^{6,7,8Reference 6Wang Y et al. · 2021ReviewBiological activity, hepatotoxicity, and structure-activity relationship of kavalactones and flavokavins, the two main bioactive components in kava (Piper methysticum) [review]View study →Reference 7Narayanapillai SC et al. · 2014AnimalFlavokawains A and B in kava, not dihydromethysticin, potentiate acetaminophen-induced hepatotoxicity in C57BL/6 mice [animal]View study →Reference 8Teschke R et al. · 2011ReviewHerbal hepatotoxicity by kava: update on pipermethystine, flavokavain B, and mould hepatotoxins as primarily assumed culprits [review]View study →}
Flavokawain C	2′,4-dihydroxy-4′,6′-dimethoxychalcone	Least abundant, least studied; the extra B-ring hydroxyl distinguishes it from A ^{5Reference 5Abu N et al. · 2013ReviewThe flavokawains: uprising medicinal chalcones [review]View study →}

Two framings matter. First, flavokawain C is structurally the “in-between” chalcone — it carries the same dimethoxy pattern as flavokawain B plus an additional hydroxyl on the B-ring, so it is neither the trimethoxy A nor the plainer B. Second, in the flavokawain literature it is consistently the third-ranked and thinnest of the three: a 2013 review of the triad concluded flavokawain B was the most effective against cancer cell lines, with A and C behind it ^{5Reference 5Abu N et al. · 2013ReviewThe flavokawains: uprising medicinal chalcones [review]View study →}.

More broadly, the flavokawains complete kava’s chalcone axis, which runs separately from — and is dwarfed by — the kavalactone axis that carries the plant’s actual pharmacology and traditional use. Flavokawain C is the minor member of a minor group.

What It's Used For

Flavokawain C’s evidence is entirely preclinical and entirely on the isolated molecule. It has been studied almost exclusively as a candidate anticancer chalcone, in cell culture and one mouse xenograft, and the mechanism reported is a fairly conventional pro-apoptotic / cell-cycle-arrest profile.

A pro-apoptotic chalcone in colorectal cancer cells — the strongest thread.In HCT 116 and HT-29 human colon-cancer lines, isolated flavokawain C triggers apoptosis and cell-cycle arrest, with mitochondrial disruption, reactive-oxygen-species generation, endoplasmic-reticulum stress, and down-regulation of inhibitor-of-apoptosis proteins; a single mouse xenograft study showed reduced HCT 116 tumour growth ^{1,2,3Reference 1Phang CW et al. · 2016In vitroFlavokawain C inhibits cell cycle and promotes apoptosis, associated with endoplasmic reticulum stress and regulation of MAPKs and Akt signaling pathways in HCT 116 human colon carcinoma cells [in vitro]View study →Reference 2Phang CW et al. · 2017In vitroInduction of apoptosis and cell cycle arrest by flavokawain C on HT-29 human colon adenocarcinoma via enhancement of reactive oxygen species generation, upregulation of p21, p27, and GADD153, and inactivation of inhibitor of apoptosis proteins [in vitro]View study →Reference 3Phang CW et al. · 2021AnimalFlavokawain C exhibits anti-tumor effects on in vivo HCT 116 xenograft and identification of its apoptosis-linked serum biomarkers via proteomic analysis [animal]View study →}.

An emerging liver-cancer signal, in vitro only.In hepatocellular-carcinoma lines, flavokawain C inhibited proliferation and migration and induced DNA damage, attributed to suppression of the FAK/PI3K/AKT survival pathway ^{4Reference 4Wang R et al. · 2024In vitroFlavokawain C inhibits proliferation and migration of liver cancer cells through the FAK/PI3K/AKT signaling pathway [in vitro]View study →}.

The honest headline:every result is the isolated compound in the lab, at micromolar concentrations, with no human data, no pharmacokinetics, and no toxicology of its own. It is a trace kava constituent, and this preclinical anticancer activity says nothing about kava as consumed ^{5,6Reference 5Abu N et al. · 2013ReviewThe flavokawains: uprising medicinal chalcones [review]View study →Reference 6Wang Y et al. · 2021ReviewBiological activity, hepatotoxicity, and structure-activity relationship of kavalactones and flavokavins, the two main bioactive components in kava (Piper methysticum) [review]View study →}.

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. Both rows are preclinical, isolate-only, so the scores are deliberately low; read the per-row basis.

The best-developed application, and the only one with any in-vivo data. In HCT 116 colon-carcinoma cells the isolated molecule induced apoptosis — cell shrinkage, chromatin condensation, DNA fragmentation and phosphatidylserine externalisation — with loss of mitochondrial membrane potential, release of cytochrome c / Smac/DIABLO / AIF, endoplasmic-reticulum stress, S-phase arrest, raised ERK1/2 and lowered Akt signalling ^{1Reference 1Phang CW et al. · 2016In vitroFlavokawain C inhibits cell cycle and promotes apoptosis, associated with endoplasmic reticulum stress and regulation of MAPKs and Akt signaling pathways in HCT 116 human colon carcinoma cells [in vitro]View study →}.

In HT-29 colon cells it raised reactive oxygen species, up-regulated the cell-cycle inhibitors p21 and p27 (p53-independently) and the stress marker GADD153, and inactivated the inhibitor-of-apoptosis proteins XIAP, c-IAP1 and c-IAP2 ^{2Reference 2Phang CW et al. · 2017In vitroInduction of apoptosis and cell cycle arrest by flavokawain C on HT-29 human colon adenocarcinoma via enhancement of reactive oxygen species generation, upregulation of p21, p27, and GADD153, and inactivation of inhibitor of apoptosis proteins [in vitro]View study →}.

A mouse xenograft study then showed flavokawain C slowed HCT 116 tumour growth without visible organ toxicity or weight loss, with raised cleaved caspase-3 and reduced Ki67 in tumour tissue ^{3Reference 3Phang CW et al. · 2021AnimalFlavokawain C exhibits anti-tumor effects on in vivo HCT 116 xenograft and identification of its apoptosis-linked serum biomarkers via proteomic analysis [animal]View study →}.

Gap: all three studies use the isolated chalcone, and only one is in vivo (a single xenograft model); there are no human data, no confirmation in other colorectal models from independent groups, and no link to kava as consumed ^{1,2,3Reference 1Phang CW et al. · 2016In vitroFlavokawain C inhibits cell cycle and promotes apoptosis, associated with endoplasmic reticulum stress and regulation of MAPKs and Akt signaling pathways in HCT 116 human colon carcinoma cells [in vitro]View study →Reference 2Phang CW et al. · 2017In vitroInduction of apoptosis and cell cycle arrest by flavokawain C on HT-29 human colon adenocarcinoma via enhancement of reactive oxygen species generation, upregulation of p21, p27, and GADD153, and inactivation of inhibitor of apoptosis proteins [in vitro]View study →Reference 3Phang CW et al. · 2021AnimalFlavokawain C exhibits anti-tumor effects on in vivo HCT 116 xenograft and identification of its apoptosis-linked serum biomarkers via proteomic analysis [animal]View study →}.

Mechanisms

Target / pathway	Effect	Relevant to
Mitochondrial membrane potential	disruption → cytochrome c, Smac/DIABLO, AIF release (intrinsic apoptosis)	anticancer (colorectal)
Reactive oxygen species	increased ROS; reduced SOD activity	anticancer (colorectal)
Inhibitor-of-apoptosis proteins (XIAP, c-IAP1/2, survivin)	down-regulation → caspase-3/-8/-9 activation	anticancer (colorectal)
p21 / p27 / GADD153	up-regulation → G1 and G2/M (and S-phase) cell-cycle arrest, p53-independent	anticancer (colorectal)
Endoplasmic-reticulum stress; ERK1/2 ↑ / Akt ↓	pro-apoptotic signalling shift	anticancer (colorectal)
FAK / PI3K / AKT	inhibition of phosphorylation (proposed ATP-site binding) → reduced proliferation/migration, DNA damage	anticancer (liver)

Every mechanism here comes from cell-culture (and one xenograft) work on the isolated compound. This is a conventional pro-apoptotic chalcone profile, not a validated human drug mechanism.

Pharmacokinetics

None characterised. There are no absorption, bioavailability, metabolism, or half-life data for flavokawain C in humans or animals — the in-vivo work reports tumour-growth outcomes, not pharmacokinetics ^{3,4Reference 3Phang CW et al. · 2021AnimalFlavokawain C exhibits anti-tumor effects on in vivo HCT 116 xenograft and identification of its apoptosis-linked serum biomarkers via proteomic analysis [animal]View study →Reference 4Wang R et al. · 2024In vitroFlavokawain C inhibits proliferation and migration of liver cancer cells through the FAK/PI3K/AKT signaling pathway [in vitro]View study →}. As a lipophilic chalcone present only in trace amounts in kava, meaningful systemic exposure from normal kava use is implausible, but this has not been measured. The absence of any ADME data is itself a major limit on interpreting the in-vitro potencies.

Clinical Trials

There are no clinical trials of flavokawain C — none completed, planned, or terminated. All evidence is preclinical.

Completed	Planned	Terminated	Preclinical
—	—	—	Anticancer(colorectal in vitro + one mouse xenograft; liver in vitro) ^{1,2,3,4Reference 1Phang CW et al. · 2016In vitroFlavokawain C inhibits cell cycle and promotes apoptosis, associated with endoplasmic reticulum stress and regulation of MAPKs and Akt signaling pathways in HCT 116 human colon carcinoma cells [in vitro]View study →Reference 2Phang CW et al. · 2017In vitroInduction of apoptosis and cell cycle arrest by flavokawain C on HT-29 human colon adenocarcinoma via enhancement of reactive oxygen species generation, upregulation of p21, p27, and GADD153, and inactivation of inhibitor of apoptosis proteins [in vitro]View study →Reference 3Phang CW et al. · 2021AnimalFlavokawain C exhibits anti-tumor effects on in vivo HCT 116 xenograft and identification of its apoptosis-linked serum biomarkers via proteomic analysis [animal]View study →Reference 4Wang R et al. · 2024In vitroFlavokawain C inhibits proliferation and migration of liver cancer cells through the FAK/PI3K/AKT signaling pathway [in vitro]View study →}

Last checked: July 2026.

Isolate vs. Plant Studies

This molecule sits firmly at the isolate end of the spectrum, and that is the central caveat. Every finding above used purified flavokawain C — synthesised or isolated to homogeneity — applied directly to cancer cells or dosed into tumour-bearing mice ^{1,2,3,4Reference 1Phang CW et al. · 2016In vitroFlavokawain C inhibits cell cycle and promotes apoptosis, associated with endoplasmic reticulum stress and regulation of MAPKs and Akt signaling pathways in HCT 116 human colon carcinoma cells [in vitro]View study →Reference 2Phang CW et al. · 2017In vitroInduction of apoptosis and cell cycle arrest by flavokawain C on HT-29 human colon adenocarcinoma via enhancement of reactive oxygen species generation, upregulation of p21, p27, and GADD153, and inactivation of inhibitor of apoptosis proteins [in vitro]View study →Reference 3Phang CW et al. · 2021AnimalFlavokawain C exhibits anti-tumor effects on in vivo HCT 116 xenograft and identification of its apoptosis-linked serum biomarkers via proteomic analysis [animal]View study →Reference 4Wang R et al. · 2024In vitroFlavokawain C inhibits proliferation and migration of liver cancer cells through the FAK/PI3K/AKT signaling pathway [in vitro]View study →}. No study tested flavokawain C as delivered by kava, and none should be read as evidence about kava the beverage or extract.

The gap is especially wide here because flavokawain C is a trace constituent: at roughly 0.012% of kava extract it is present at a small fraction of even the other flavokawains, and orders of magnitude below the kavalactones ^{5Reference 5Abu N et al. · 2013ReviewThe flavokawains: uprising medicinal chalcones [review]View study →}. The micromolar concentrations that kill cells in culture are not concentrations a kava drinker would plausibly reach. So the honest reading is that flavokawain C is an interesting isolated chalcone scaffold, not a demonstrated reason to attribute anticancer properties to kava.

Prevalence in Nature

Flavokawain C occurs in kava (Piper methysticum) as the minor third member of the flavokawain chalcone group ^{5,6Reference 5Abu N et al. · 2013ReviewThe flavokawains: uprising medicinal chalcones [review]View study →Reference 6Wang Y et al. · 2021ReviewBiological activity, hepatotoxicity, and structure-activity relationship of kavalactones and flavokavins, the two main bioactive components in kava (Piper methysticum) [review]View study →}. Among the three it is consistently the least abundant, reported at roughly 0.012% of kava extract, against about 0.46% for flavokawain A — with flavokawain B intermediate ^{5Reference 5Abu N et al. · 2013ReviewThe flavokawains: uprising medicinal chalcones [review]View study →}. All three are minor components dwarfed by the kavalactones, which make up the bulk of kava’s active resin.

Within the plant the flavokawains are associated with kava’s chalcone chemistry rather than the kavapyrone (kavalactone) fraction, and cultivar/chemotype and plant part (root versus aerial tissue) shift the whole flavokawain profile — the same provenance sensitivity that governs kava’s kavalactone ratios and its safety profile ^{6Reference 6Wang Y et al. · 2021ReviewBiological activity, hepatotoxicity, and structure-activity relationship of kavalactones and flavokavins, the two main bioactive components in kava (Piper methysticum) [review]View study →}. Flavokawain-type chalcones are reported sparsely in a handful of other plants, but kava is the reference source for flavokawain C.

Discovery & Synthesis

Flavokawain C entered the literature as the third named member of the kava flavokawain series (flavokawains A–C), the chalcone fraction isolated from Piper methysticum; a precise first-isolation date for C specifically is not clearly documented in the accessible sources, which treat it as the minor companion to the better-characterised A and B ^{5,6Reference 5Abu N et al. · 2013ReviewThe flavokawains: uprising medicinal chalcones [review]View study →Reference 6Wang Y et al. · 2021ReviewBiological activity, hepatotoxicity, and structure-activity relationship of kavalactones and flavokavins, the two main bioactive components in kava (Piper methysticum) [review]View study →}. Chemically it is 2′,4-dihydroxy-4′,6′-dimethoxychalcone (C17H16O5; CAS 37308-75-1) — distinguished from flavokawain A by an extra B-ring hydroxyl in place of a methoxy group.

Because the natural abundance is so low, essentially all of the material used in the anticancer studies is isolated in small quantities or prepared synthetically rather than sourced at scale from the plant; chalcones of this type are readily accessible by base-catalysed (Claisen–Schmidt) aldol condensation of the corresponding acetophenone and benzaldehyde, though the specific synthetic route is not the focus of the biological reports ^{1,4Reference 1Phang CW et al. · 2016In vitroFlavokawain C inhibits cell cycle and promotes apoptosis, associated with endoplasmic reticulum stress and regulation of MAPKs and Akt signaling pathways in HCT 116 human colon carcinoma cells [in vitro]View study →Reference 4Wang R et al. · 2024In vitroFlavokawain C inhibits proliferation and migration of liver cancer cells through the FAK/PI3K/AKT signaling pathway [in vitro]View study →}. There is no commercial production of flavokawain C beyond research-scale reference material.

Patents: not yet researched.

Toxicity & Safety

Flavokawain C carries a low flag, but that badge reflects an absence of data rather than demonstrated safety: no dedicated toxicology, genotoxicity, or reproductive-toxicity study exists for the isolated compound, and human exposure is limited to the trace amount in kava. The one relevant signal is class context — its sibling chalcones sit inside kava’s hepatotoxicity debate.

Importantly, the flavokawains implicated in that debate are A and B, not C. In a mouse model, flavokawains A and B (not the kavalactone dihydromethysticin) potentiated acetaminophen-induced liver injury — flavokawain C was not among the tested or implicated compounds ^{7Reference 7Narayanapillai SC et al. · 2014AnimalFlavokawains A and B in kava, not dihydromethysticin, potentiate acetaminophen-induced hepatotoxicity in C57BL/6 mice [animal]View study →}. A kava-hepatotoxicity review likewise names pipermethystine and flavokavain B (plus possible mould contamination) as the assumed culprits, while noting the in-vivo evidence even for those remains limited and the amounts present may be too low to explain clinical liver injury ^{8Reference 8Teschke R et al. · 2011ReviewHerbal hepatotoxicity by kava: update on pipermethystine, flavokavain B, and mould hepatotoxins as primarily assumed culprits [review]View study →}. Flavokawain C has simply not been evaluated for hepatotoxicity either way.

Safety at a Glance

Low / no toxicity

No isolate-specific toxicity signal reported. No adverse-effect, genotoxicity, or organ-toxicity finding has been published for pure flavokawain C; the one mouse xenograft study reported no visible organ toxicity or weight loss at the doses used ^{3Reference 3Phang CW et al. · 2021AnimalFlavokawain C exhibits anti-tumor effects on in vivo HCT 116 xenograft and identification of its apoptosis-linked serum biomarkers via proteomic analysis [animal]View study →}.
Kava-class context. Flavokawain C belongs to the flavokawain chalcones, of which A and B are implicated in kava’s hepatotoxicity story; C itself is untested, so its liver-safety profile is genuinely unknown, not established as safe ^{7,8Reference 7Narayanapillai SC et al. · 2014AnimalFlavokawains A and B in kava, not dihydromethysticin, potentiate acetaminophen-induced hepatotoxicity in C57BL/6 mice [animal]View study →Reference 8Teschke R et al. · 2011ReviewHerbal hepatotoxicity by kava: update on pipermethystine, flavokavain B, and mould hepatotoxins as primarily assumed culprits [review]View study →}.
No human, ADME, or repeat-dose data. There is no pharmacokinetic, chronic-toxicity, or reproductive-toxicity dataset for the isolated compound; safety cannot be inferred from silence.
Pregnancy/lactation and interactions belong to the kava page. Any intake decision is about kava the herb, not this trace molecule — see the kava monograph.

Dosage

There is no human dose for flavokawain C, and none is implied. It has never been administered to people as an isolated compound. The figures that appear in the literature are research parameters, not intakes: micromolar concentrations in cell culture and milligram-per-kilogram doses in tumour-bearing mice ^{1,2,3,4Reference 1Phang CW et al. · 2016In vitroFlavokawain C inhibits cell cycle and promotes apoptosis, associated with endoplasmic reticulum stress and regulation of MAPKs and Akt signaling pathways in HCT 116 human colon carcinoma cells [in vitro]View study →Reference 2Phang CW et al. · 2017In vitroInduction of apoptosis and cell cycle arrest by flavokawain C on HT-29 human colon adenocarcinoma via enhancement of reactive oxygen species generation, upregulation of p21, p27, and GADD153, and inactivation of inhibitor of apoptosis proteins [in vitro]View study →Reference 3Phang CW et al. · 2021AnimalFlavokawain C exhibits anti-tumor effects on in vivo HCT 116 xenograft and identification of its apoptosis-linked serum biomarkers via proteomic analysis [animal]View study →Reference 4Wang R et al. · 2024In vitroFlavokawain C inhibits proliferation and migration of liver cancer cells through the FAK/PI3K/AKT signaling pathway [in vitro]View study →}. Real-world human exposure is confined to the trace quantity naturally present in kava root preparations, which are dosed and standardised to kavalactones, not to flavokawains ^{5,6Reference 5Abu N et al. · 2013ReviewThe flavokawains: uprising medicinal chalcones [review]View study →Reference 6Wang Y et al. · 2021ReviewBiological activity, hepatotoxicity, and structure-activity relationship of kavalactones and flavokavins, the two main bioactive components in kava (Piper methysticum) [review]View study →}. These are experimental values and are not a personal recommendation.

References

Phang CW, Karsani SA, Sethi G, Abd Malek SN (2016). Flavokawain C inhibits cell cycle and promotes apoptosis, associated with endoplasmic reticulum stress and regulation of MAPKs and Akt signaling pathways in HCT 116 human colon carcinoma cells [in vitro]. PLoS One. https://pubmed.ncbi.nlm.nih.gov/26859847/
Phang CW, Karsani SA, Abd Malek SN (2017). Induction of apoptosis and cell cycle arrest by flavokawain C on HT-29 human colon adenocarcinoma via enhancement of reactive oxygen species generation, upregulation of p21, p27, and GADD153, and inactivation of inhibitor of apoptosis proteins [in vitro]. Pharmacognosy Magazine. https://pubmed.ncbi.nlm.nih.gov/28808400/
Phang CW, Abd Malek SN, Karsani SA (2021). Flavokawain C exhibits anti-tumor effects on in vivo HCT 116 xenograft and identification of its apoptosis-linked serum biomarkers via proteomic analysis [animal]. Biomedicine & Pharmacotherapy. https://pubmed.ncbi.nlm.nih.gov/33761587/
Wang R, Li R, Yang H, Chen X, Wu L, Zheng X, Jin Y (2024). Flavokawain C inhibits proliferation and migration of liver cancer cells through the FAK/PI3K/AKT signaling pathway [in vitro]. Journal of Cancer Research and Clinical Oncology. https://pubmed.ncbi.nlm.nih.gov/38460052/
Abu N, Ho WY, Yeap SK, Akhtar MN, Abdullah MP, Omar AR, Alitheen NB (2013). The flavokawains: uprising medicinal chalcones [review]. Cancer Cell International. https://pubmed.ncbi.nlm.nih.gov/24148263/
Wang Y, Su C, Zhang B, Niu Y, Ren R, Zhao X, Yang L, Zhang W, Ma X (2021). Biological activity, hepatotoxicity, and structure-activity relationship of kavalactones and flavokavins, the two main bioactive components in kava (Piper methysticum) [review]. Evidence-Based Complementary and Alternative Medicine. https://pubmed.ncbi.nlm.nih.gov/34471418/
Narayanapillai SC, Leitzman P, O’Sullivan MG, Xing C (2014). Flavokawains A and B in kava, not dihydromethysticin, potentiate acetaminophen-induced hepatotoxicity in C57BL/6 mice [animal]. Chemical Research in Toxicology. https://pubmed.ncbi.nlm.nih.gov/25185080/
Teschke R, Qiu SX, Lebot V (2011). Herbal hepatotoxicity by kava: update on pipermethystine, flavokavain B, and mould hepatotoxins as primarily assumed culprits [review]. Digestive and Liver Disease. https://pubmed.ncbi.nlm.nih.gov/21377431/