Amentoflavone

Amentoflavone at a Glance

Amentoflavone is the best-known biflavone — a molecule built from two apigenin units joined together by a single carbon–carbon bond between the 3’ position of one flavone and the 8” position of the other, giving its formal name 3’,8”-biapigenin ^{1Reference 1Xiong X et al. · 2021Insights Into Amentoflavone: A Natural Multifunctional BiflavonoidView study →}. Where most dietary flavones are single flat rings, amentoflavone is a bulky, twisted dimer, and that doubled structure underlies both its wide receptor promiscuity and its poor solubility.

It occurs across ferns, spikemosses and gymnosperms, and reaches people mainly as a minor constituent of three well-known botanicals — Ginkgo, St John’s wort and Selaginella spikemoss ^{1,2Reference 1Xiong X et al. · 2021Insights Into Amentoflavone: A Natural Multifunctional BiflavonoidView study →Reference 2Zhang H et al. · 2024Amentoflavone for treating cardiocerebrovascular diseases and neurological disordersView study →}. In the laboratory it does a great many things: anti-inflammatory, anticancer, antiviral, antioxidant and neuroprotective effects have all been reported. Almost all of this is in-vitro or rodent work on the isolated molecule; there are no efficacy trials in humans, and its very low oral bioavailability is a running caveat over every systemic claim ^{9,2Reference 9Qiu H et al. · 2021AnimalEvaluation on absorption risks of amentoflavone after oral administration in ratsView study →Reference 2Zhang H et al. · 2024Amentoflavone for treating cardiocerebrovascular diseases and neurological disordersView study →}.

The two properties that make amentoflavone genuinely distinctive are narrower and better defined. First, it binds the benzodiazepine site of the GABA-A receptor with high affinity — but acts, unusually, as a negative modulator, the opposite direction to a classical anxiolytic ^{3,4Reference 3Baureithel KH et al. · 1997In vitroInhibition of benzodiazepine binding in vitro by amentoflavone, a constituent of various species of HypericumView study →Reference 4Hanrahan JR et al. · 2003Semisynthetic preparation of amentoflavone: A negative modulator at GABA(A) receptorsView study →}. Second, and most consequential in practice, it is a potent inhibitor of several drug-metabolising enzymes (CYP2C9, CYP2C8, CYP3A4 and multiple UGTs), which is why it features in discussions of Ginkgo and St John’s wort herb-drug interactions ^{5,6,7,8Reference 5von Moltke LL et al. · 2004Inhibition of human cytochromes P450 by components of Ginkgo bilobaView study →Reference 6Park SY et al. · 2020Strong and Selective Inhibitory Effects of the Biflavonoid Selamariscina A against CYP2C8 and CYP2C9 Enzyme Activities in Human Liver MicrosomesView study →Reference 7Wang B et al. · 2022Potent Inhibition of Human Cytochrome P450 3A4 by Biflavone Components from Ginkgo Biloba and Selaginella TamariscinaView study →Reference 8Lv X et al. · 2018Amentoflavone is a potent broad-spectrum inhibitor of human UDP-glucuronosyltransferasesView study →}.

The Apigenin Dimer

The single fact that organises this whole page is structural: amentoflavone is two apigenins bolted together. Apigenin (4’,5,7-trihydroxyflavone) is one of the commonest dietary flavones; couple two of its molecules through a C3’–C8” biaryl bond and you get amentoflavone, C30H18O10, carrying six phenolic hydroxyls across the doubled scaffold ^{1Reference 1Xiong X et al. · 2021Insights Into Amentoflavone: A Natural Multifunctional BiflavonoidView study →}.

That dimerisation changes the molecule’s behaviour in three ways that recur throughout its pharmacology:

• Size and rigidity. The linked, non-coplanar two-flavone frame presents a much larger surface than a monomeric flavone, letting amentoflavone occupy the deep, roomy active sites of enzymes such as CYP3A4 and viral proteases far more snugly than apigenin does — a plausible reason a “double apigenin” is a far stronger CYP inhibitor than apigenin itself ^{7,12Reference 7Wang B et al. · 2022Potent Inhibition of Human Cytochrome P450 3A4 by Biflavone Components from Ginkgo Biloba and Selaginella TamariscinaView study →Reference 12Ryu YB et al. · 2010Biflavonoids from Torreya nucifera displaying SARS-CoV 3CL(pro) inhibitionView study →}.
• Poor solubility. The extra aromatic mass makes amentoflavone markedly less water-soluble than apigenin, and that low solubility is the rate-limiting step in its oral absorption ^{9Reference 9Qiu H et al. · 2021AnimalEvaluation on absorption risks of amentoflavone after oral administration in ratsView study →}.
• A shared family. Methylating amentoflavone’s hydroxyls gives the ginkgetin series of biflavones (ginkgetin, isoginkgetin, bilobetin) — hence amentoflavone’s synonym didemethyl-ginkgetin — while the closely related St John’s wort biflavone biapigenin is the I3’,II8-isomer. These relatives share amentoflavone’s enzyme-inhibiting profile ^{7Reference 7Wang B et al. · 2022Potent Inhibition of Human Cytochrome P450 3A4 by Biflavone Components from Ginkgo Biloba and Selaginella TamariscinaView study →}.

Because it is literally a dimer of apigenin, comparisons to the monomer are the most useful frame: amentoflavone tends to be more potent but less bioavailable, and reaches targets (GABA-A negative modulation, submicromolar CYP inhibition) that apigenin touches only weakly.

What It's Used For

Amentoflavone’s reported activities are broad, but the evidence is shallow: it is a preclinical, isolate-driven profile, largely cell-culture and rodent work, with no human efficacy data and a poor-bioavailability caveat over every systemic claim ^{2,9Reference 2Zhang H et al. · 2024Amentoflavone for treating cardiocerebrovascular diseases and neurological disordersView study →Reference 9Qiu H et al. · 2021AnimalEvaluation on absorption risks of amentoflavone after oral administration in ratsView 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. Every row here is preclinical isolate data, so all scores stay low by design.

01Anti-Inflammatory / NeuroprotectiveShaky34%Rodent + microglial isolate: TLR4/NF-κB, NLRP3 inflammasome, Nrf2/HO-1 ^{13,14Reference 13Rong S et al. · 2022Amentoflavone Exerts Anti-Neuroinflammatory Effects by Inhibiting TLR4/MyD88/NF-κB and Activating Nrf2/HO-1 Pathway in Lipopolysaccharide-Induced BV2 MicrogliaView study →Reference 14Rong S et al. · 2019Amentoflavone Affects Epileptogenesis and Exerts Neuroprotective Effects by Inhibiting NLRP3 InflammasomeView study →}

02AnticancerShaky32%Cell-line isolate: fatty-acid-synthase inhibition, HER2 suppression, apoptosis, NF-κB ^{10,11Reference 10Lee JS et al. · 2009Fatty acid synthase inhibition by amentoflavone induces apoptosis and antiproliferation in human breast cancer cellsView study →Reference 11Lee JS et al. · 2013Fatty acid synthase inhibition by amentoflavone suppresses HER2/neu (erbB2) oncogene in SKBR3 human breast cancer cellsView study →}

03AntiviralShaky26%In-vitro/in-silico protease inhibition (SARS-CoV 3CLpro IC50 8.3 µM) + broad screening ^{12,1Reference 12Ryu YB et al. · 2010Biflavonoids from Torreya nucifera displaying SARS-CoV 3CL(pro) inhibitionView study →Reference 1Xiong X et al. · 2021Insights Into Amentoflavone: A Natural Multifunctional BiflavonoidView study →}

04GABA-A / CNS ModulationShaky28%In-vitro binding: high benzodiazepine-site affinity but negative GABA-A modulation ^{3,4Reference 3Baureithel KH et al. · 1997In vitroInhibition of benzodiazepine binding in vitro by amentoflavone, a constituent of various species of HypericumView study →Reference 4Hanrahan JR et al. · 2003Semisynthetic preparation of amentoflavone: A negative modulator at GABA(A) receptorsView study →}

Mechanisms

The through-line is size: a dimer of apigenin fills large enzyme and receptor pockets that the monomer only grazes, which is why the strongest, most reproducible amentoflavone findings are potent enzyme inhibition rather than any single therapeutic effect.

Pharmacokinetics

Amentoflavone’s pharmacokinetics are the reason to treat its in-vitro potency cautiously. It is poorly water-soluble, and that low solubility — not membrane permeability — is the rate-limiting step in its oral absorption; solubilising formulations (e.g. PVP-K30 solid dispersions) roughly double its relative bioavailability, confirming dissolution as the bottleneck ^{9Reference 9Qiu H et al. · 2021AnimalEvaluation on absorption risks of amentoflavone after oral administration in ratsView study →}. What is absorbed is extensively glucuronidated by UDP-glucuronosyltransferases (notably UGT1A1/UGT1A3), so glucuronide conjugates dominate in plasma and free aglycone levels stay low ^{9Reference 9Qiu H et al. · 2021AnimalEvaluation on absorption risks of amentoflavone after oral administration in ratsView study →}. After oral dosing in rats the molecule concentrates in the gut, stomach and liver with little distribution elsewhere ^{9Reference 9Qiu H et al. · 2021AnimalEvaluation on absorption risks of amentoflavone after oral administration in ratsView study →}. The practical upshot: systemic exposure to free amentoflavone is modest, which undercuts systemic efficacy claims — but its highest concentrations are exactly at the gut wall and first-pass liver, where CYP/UGT inhibition (below) is most relevant.

Clinical Trials

There are no controlled human efficacy trials of isolated amentoflavone. Its entire evidence base is in-vitro and animal work; human exposure is incidental, via Ginkgo, St John’s wort and Selaginella preparations, where it is a minor biflavone.

Last checked: July 2026.

Enzyme Inhibition & Herb-Drug Interactions

This is amentoflavone’s most consequential, best-verified property — and the reason its toxicity flag, though low, carries an interaction caveat. As a bulky dimer it is a potent inhibitor of several drug-metabolising enzymes:

• CYP2C9 — a competitive inhibitor with IC50 ≈ 0.035 µM (as a Ginkgo flavone aglycone), i.e. submicromolar potency against the enzyme that clears warfarin, phenytoin, many NSAIDs and sulfonylureas ^{5Reference 5von Moltke LL et al. · 2004Inhibition of human cytochromes P450 by components of Ginkgo bilobaView study →}.
• CYP2C8 — noncompetitive inhibition, Ki ≈ 0.083 µM in human liver microsomes ^{6Reference 6Park SY et al. · 2020Strong and Selective Inhibitory Effects of the Biflavonoid Selamariscina A against CYP2C8 and CYP2C9 Enzyme Activities in Human Liver MicrosomesView study →}.
• CYP3A4 — among the strongest CYP3A4 inhibitors of the Ginkgo/Selaginella biflavone series (with ginkgetin, isoginkgetin, bilobetin), the enzyme responsible for metabolising a large share of all prescription drugs ^{7Reference 7Wang B et al. · 2022Potent Inhibition of Human Cytochrome P450 3A4 by Biflavone Components from Ginkgo Biloba and Selaginella TamariscinaView study →}.
• UGTs — a potent broad-spectrum inhibitor of human UDP-glucuronosyltransferases, with inhibition constants down to ~0.3 µM across multiple isoforms ^{8Reference 8Lv X et al. · 2018Amentoflavone is a potent broad-spectrum inhibitor of human UDP-glucuronosyltransferasesView study →}.

Because these enzymes sit at the gut wall and in first-pass liver metabolism — precisely where amentoflavone concentrates ^{9Reference 9Qiu H et al. · 2021AnimalEvaluation on absorption risks of amentoflavone after oral administration in ratsView study →} — this profile is a plausible mechanistic contributor to the herb-drug-interaction reputation of Ginkgo and St John’s wort, alongside the far larger, better-documented effect of St John’s wort’s hyperforin as a pregnane-X-receptor inducer of CYP3A4. The honest framing: amentoflavone’s in-vitro inhibition is potent and reproducible, but its poor systemic bioavailability tempers how much of that translates to a whole-body interaction; the caution is real but not established at the level of documented clinical events for the isolate.

Isolate vs. Plant Studies

Amentoflavone’s evidence is almost entirely the isolated molecule — cell lines and rodents dosed with purified compound, often parenterally to sidestep its poor oral uptake ^{10,13,14Reference 10Lee JS et al. · 2009Fatty acid synthase inhibition by amentoflavone induces apoptosis and antiproliferation in human breast cancer cellsView study →Reference 13Rong S et al. · 2022Amentoflavone Exerts Anti-Neuroinflammatory Effects by Inhibiting TLR4/MyD88/NF-κB and Activating Nrf2/HO-1 Pathway in Lipopolysaccharide-Induced BV2 MicrogliaView study →Reference 14Rong S et al. · 2019Amentoflavone Affects Epileptogenesis and Exerts Neuroprotective Effects by Inhibiting NLRP3 InflammasomeView study →}. That is a double-edged strength: the mechanistic work (FASN, NF-κB, NLRP3, protease and enzyme inhibition) genuinely concerns this molecule, not an undefined extract, so it is not confounded by co-constituents. But it also means the human-relevant question — what amentoflavone does as consumed inside Ginkgo, St John’s wort or Selaginella — is largely unanswered, because in those matrices it is a minor biflavone competing with far more abundant and, for St John’s wort, far more active constituents (hyperforin, hypericin, quercetin and its glycosides such as hyperoside) ^{1,2Reference 1Xiong X et al. · 2021Insights Into Amentoflavone: A Natural Multifunctional BiflavonoidView study →Reference 2Zhang H et al. · 2024Amentoflavone for treating cardiocerebrovascular diseases and neurological disordersView study →}. No whole-plant trial isolates an amentoflavone-attributable effect, and its own poor bioavailability makes such attribution unlikely.

Prevalence in Nature

Amentoflavone is taxonomically widespread but individually minor, reported from more than 120 plant species and especially characteristic of “lower” vascular plants and gymnosperms ^{1,2Reference 1Xiong X et al. · 2021Insights Into Amentoflavone: A Natural Multifunctional BiflavonoidView study →Reference 2Zhang H et al. · 2024Amentoflavone for treating cardiocerebrovascular diseases and neurological disordersView study →}. It is a signature biflavone of the spikemosses (Selaginella, e.g. S. tamariscina), a documented constituent of Ginkgo biloba leaf, and one of the biflavones of St John’s wort (Hypericum perforatum) ^{1,3Reference 1Xiong X et al. · 2021Insights Into Amentoflavone: A Natural Multifunctional BiflavonoidView study →Reference 3Baureithel KH et al. · 1997In vitroInhibition of benzodiazepine binding in vitro by amentoflavone, a constituent of various species of HypericumView study →}. It also occurs in conifers and other gymnosperms — hinoki cypress (Chamaecyparis obtusa), Japanese torreya (Torreya nucifera) and various Cupressaceae ^{12Reference 12Ryu YB et al. · 2010Biflavonoids from Torreya nucifera displaying SARS-CoV 3CL(pro) inhibitionView study →} — and scattered angiosperms.

Reliable quantitative content figures are scarce and poorly standardised across sources, so a comparative concentration chart would overstate the certainty of the numbers; Selaginella tamariscina is generally cited as among the richer sources. The occurrence of biflavones like amentoflavone in ferns, cycads and conifers but rarely in advanced flowering plants has long made them of chemotaxonomic interest.

Major Natural Sources

Source	Plant part	Notes
Spikemoss (Selaginella tamariscina)	whole plant	A signature, comparatively rich biflavone source 1Reference 1Xiong X et al. · 2021Insights Into Amentoflavone: A Natural Multifunctional BiflavonoidView study →
Ginkgo (Ginkgo biloba)	leaf	Present with methylated relatives (ginkgetin series) 7Reference 7Wang B et al. · 2022Potent Inhibition of Human Cytochrome P450 3A4 by Biflavone Components from Ginkgo Biloba and Selaginella TamariscinaView study →
St John’s Wort (Hypericum perforatum)	flowering tops	Minor biflavone alongside biapigenin 3Reference 3Baureithel KH et al. · 1997In vitroInhibition of benzodiazepine binding in vitro by amentoflavone, a constituent of various species of HypericumView study →
Hinoki cypress (Chamaecyparis obtusa)	leaf/wood	Conifer biflavone source
Japanese torreya (Torreya nucifera)	leaf	Source in the SARS-CoV protease study 12Reference 12Ryu YB et al. · 2010Biflavonoids from Torreya nucifera displaying SARS-CoV 3CL(pro) inhibitionView study →

Quantitative content is not well standardised across these sources; figures in the literature vary widely with species, part and method.

Discovery & Synthesis

Amentoflavone was isolated and structurally characterised as an apigenin biflavone around 1971 by Okigawa and colleagues, from Selaginella and related plants, resolving it as the 3’,8”-linked dimer of apigenin ^{1Reference 1Xiong X et al. · 2021Insights Into Amentoflavone: A Natural Multifunctional BiflavonoidView study →}. Its name reflects the catkin-bearing (Latin amentum, “catkin”) gymnosperms in which such biflavones are typical; the synonym didemethyl-ginkgetin records its relationship to the methylated Ginkgo biflavones (ginkgetin = a dimethyl amentoflavone) ^{7Reference 7Wang B et al. · 2022Potent Inhibition of Human Cytochrome P450 3A4 by Biflavone Components from Ginkgo Biloba and Selaginella TamariscinaView study →}. Structural revision and total-synthesis efforts on the biflavone class followed, the central challenge being the regioselective biaryl (C3’–C8”) coupling of two protected apigenin units. Today amentoflavone reaches the market almost entirely by extraction — chiefly from Selaginella tamariscina and Ginkgo biomass — rather than by total synthesis, because the natural sources are workable and the coupling chemistry is demanding; semisynthetic routes from Ginkgo biflavones have also been used to supply research material ^{4Reference 4Hanrahan JR et al. · 2003Semisynthetic preparation of amentoflavone: A negative modulator at GABA(A) receptorsView study →}.

Patents: not yet researched.

Toxicity & Safety

Amentoflavone’s intrinsic toxicity is low — it is a dietary-adjacent plant biflavone with no signal of acute organ toxicity at ordinary exposure, and it reaches people only as a minor, poorly-absorbed constituent of common botanicals. The flag worth carrying is not poisoning but enzyme-mediated drug interactions.

Safety at a Glance

✅ Low / no toxicity

• Low intrinsic toxicity. A widespread plant biflavone with no acute-toxicity signal at realistic dietary/herbal exposure, and poor oral absorption that limits systemic levels ^{9Reference 9Qiu H et al. · 2021AnimalEvaluation on absorption risks of amentoflavone after oral administration in ratsView study →}.
• Potent CYP inhibition in vitro. Submicromolar inhibition of CYP2C9 (IC50 ≈ 0.035 µM), plus CYP2C8 and CYP3A4 — enzymes that clear a large share of prescription drugs ^{5,6,7Reference 5von Moltke LL et al. · 2004Inhibition of human cytochromes P450 by components of Ginkgo bilobaView study →Reference 6Park SY et al. · 2020Strong and Selective Inhibitory Effects of the Biflavonoid Selamariscina A against CYP2C8 and CYP2C9 Enzyme Activities in Human Liver MicrosomesView study →Reference 7Wang B et al. · 2022Potent Inhibition of Human Cytochrome P450 3A4 by Biflavone Components from Ginkgo Biloba and Selaginella TamariscinaView study →}.
• Broad UGT inhibition. A potent, broad-spectrum inhibitor of glucuronidation enzymes, adding a second interaction route ^{8Reference 8Lv X et al. · 2018Amentoflavone is a potent broad-spectrum inhibitor of human UDP-glucuronosyltransferasesView study →}.
• Contributes to Ginkgo / St John’s wort interaction concern. A plausible mechanistic contributor to those herbs’ documented interaction reputation, though its poor bioavailability tempers the systemic relevance and no isolate-specific clinical events are established ^{2,9Reference 2Zhang H et al. · 2024Amentoflavone for treating cardiocerebrovascular diseases and neurological disordersView study →Reference 9Qiu H et al. · 2021AnimalEvaluation on absorption risks of amentoflavone after oral administration in ratsView study →}.
• Concentrated Selaginella / biflavone extracts are a different exposure from a whole-herb dose — the interaction caution scales with the amount actually delivered.

Reproductive and developmental toxicity have not been characterised for the isolated molecule; pregnancy and lactation decisions belong to the specific herb or product where intake is decided, not to this molecule page.

Dosage

There is no established or recommended human dose for isolated amentoflavone. The figures in the literature are in-vitro concentrations (e.g. FASN-inhibiting/apoptotic effects at tens of micromolar; protease IC50 8.3 µM) or rodent research doses, and they are not convertible to human self-dosing — especially given the molecule’s poor oral bioavailability, which means an oral dose delivers far less free compound to the bloodstream than the numbers imply ^{9,10,12Reference 9Qiu H et al. · 2021AnimalEvaluation on absorption risks of amentoflavone after oral administration in ratsView study →Reference 10Lee JS et al. · 2009Fatty acid synthase inhibition by amentoflavone induces apoptosis and antiproliferation in human breast cancer cellsView study →Reference 12Ryu YB et al. · 2010Biflavonoids from Torreya nucifera displaying SARS-CoV 3CL(pro) inhibitionView study →}.

Human exposure is indirect, as a minor biflavone within standardised Ginkgo, St John’s wort and Selaginella preparations, where the dose is set by the whole product, not by amentoflavone. These are research figures, not a personal recommendation.

References

1. Xiong X, et al. (2021). Insights Into Amentoflavone: A Natural Multifunctional Biflavonoid. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/35002708/
2. Zhang H, et al. (2024). Amentoflavone for treating cardiocerebrovascular diseases and neurological disorders. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/39624841/
3. Baureithel KH, et al. (1997). Inhibition of benzodiazepine binding in vitro by amentoflavone, a constituent of various species of Hypericum. Pharmaceutica Acta Helvetiae. https://pubmed.ncbi.nlm.nih.gov/9204773/
4. Hanrahan JR, et al. (2003). Semisynthetic preparation of amentoflavone: A negative modulator at GABA(A) receptors. Bioorganic & Medicinal Chemistry Letters. https://pubmed.ncbi.nlm.nih.gov/12824018/
5. von Moltke LL, et al. (2004). Inhibition of human cytochromes P450 by components of Ginkgo biloba. Journal of Pharmacy and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/15285849/
6. Park SY, et al. (2020). Strong and Selective Inhibitory Effects of the Biflavonoid Selamariscina A against CYP2C8 and CYP2C9 Enzyme Activities in Human Liver Microsomes. Pharmaceutics. https://pubmed.ncbi.nlm.nih.gov/32290339/
7. Wang B, et al. (2022). Potent Inhibition of Human Cytochrome P450 3A4 by Biflavone Components from Ginkgo Biloba and Selaginella Tamariscina. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/35295338/
8. Lv X, et al. (2018). Amentoflavone is a potent broad-spectrum inhibitor of human UDP-glucuronosyltransferases. Chemico-Biological Interactions. https://pubmed.ncbi.nlm.nih.gov/29470958/
9. Qiu H, et al. (2021). Evaluation on absorption risks of amentoflavone after oral administration in rats. Biopharmaceutics & Drug Disposition. https://pubmed.ncbi.nlm.nih.gov/34655436/
10. Lee JS, et al. (2009). Fatty acid synthase inhibition by amentoflavone induces apoptosis and antiproliferation in human breast cancer cells. Biological & Pharmaceutical Bulletin. https://pubmed.ncbi.nlm.nih.gov/19652385/
11. Lee JS, et al. (2013). Fatty acid synthase inhibition by amentoflavone suppresses HER2/neu (erbB2) oncogene in SKBR3 human breast cancer cells. Phytotherapy Research. https://pubmed.ncbi.nlm.nih.gov/22767439/
12. Ryu YB, et al. (2010). Biflavonoids from Torreya nucifera displaying SARS-CoV 3CL(pro) inhibition. Bioorganic & Medicinal Chemistry. https://pubmed.ncbi.nlm.nih.gov/20934345/
13. Rong S, et al. (2022). Amentoflavone Exerts Anti-Neuroinflammatory Effects by Inhibiting TLR4/MyD88/NF-κB and Activating Nrf2/HO-1 Pathway in Lipopolysaccharide-Induced BV2 Microglia. Mediators of Inflammation. https://pubmed.ncbi.nlm.nih.gov/36523959/
14. Rong S, et al. (2019). Amentoflavone Affects Epileptogenesis and Exerts Neuroprotective Effects by Inhibiting NLRP3 Inflammasome. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/31417409/

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