Amentoflavone: A Comprehensive Reference
1. Identity and Chemical Characterization
Names and Classification
Amentoflavone (also abbreviated AMF or AME) belongs to the class of biflavonoids and polyflavonoids. It abundantly exists in Selaginella tamariscina (Selaginellaceae family), possesses the molecular formula C30H18O10, and has a molecular weight of 538.46 g/mol. Its IUPAC name is 8-(5-(5,7-dihydroxy-4-oxo-4H-chromen-2-yl)-2-hydroxyphenyl)-5,7-dihydroxy-2-(4-hydroxyphenyl)-4H-chromen-4-one. The Chemical Abstracts Service (CAS) registry number is 1617-53-4.
Amentoflavone is a common biflavonoid that naturally occurs in many plants and is also considered an apigenin dimer linked by a C3′–C8″ covalent bond. It is therefore also referred to by the synonym 3′,8″-biapigenin and as didemethyl-ginkgetin. Its PubChem CID is 5281600.
Amentoflavone possesses a dimer of two apigenin units with six hydroxyl groups located at the C5, C7, C4′, C5″, C7″, and C4‴ positions. It is considered a flavonoid lipid molecule and is a very hydrophobic compound, practically insoluble in water (0.0072 g/L at 25 °C), but readily soluble in alcohol and DMSO.
Biosynthesis in Plants
CYP90J orthologs have been identified as the key enzymes in biflavonoid biosynthesis; gymnosperm-specific CYP90Js catalyze intermolecular C–C bond formation in the biosynthesis of these biaryl natural products. Phylogenetic analysis reveals that the CYP90J subfamily evolved from CYP90E of lycophytes and is found exclusively in gymnosperms. Molecular dynamics simulations show that regioselective dimerization of apigenin to amentoflavone is driven by spatial constraints and π–π stacking interactions.
2. Botanical Sources
Amentoflavone is a flavonoid compound found in over 120 plants. Over 120 plants have been found to contain this bioactive component, belonging to families including Selaginellaceae, Cupressaceae, Euphorbiaceae, Podocarpaceae, and Calophyllaceae.
The Selaginella genus, comprising 21 species, is the most prevalent source of amentoflavone. Other significant botanical families containing this compound include Cupressaceae, Euphorbiaceae, and Clusiaceae. Named plant sources include Ginkgo biloba, Chamaecyparis obtusa (hinoki), Biophytum sensitivum, Selaginella tamariscina, Hypericum perforatum (St. John's Wort), and Xerophyta plicata.
Additional documented plant sources include Celaenodendron mexicanum, Cupressus funebris, Garcinia multiflora, Rhus succedanea, and Cupressocyparis leylandii. Typically, amentoflavone is extracted from the leaves, aerial parts, and whole plants.
Extraction and Preparation
The principal methods for extracting amentoflavone include ultrasonic-assisted extraction, microwave-assisted extraction, organic solvent extraction, and semi-bionic extraction. Amentoflavone is even listed as the chemical marker of Selaginellae Herba ("Juanbai" in Chinese, representing the whole plants of Selaginella tamariscina or Selaginella pulvinata) for quality evaluation in the Chinese Pharmacopoeia.
To overcome water insolubility and low bioavailability, researchers have developed drug delivery carriers such as N-vinyl pyrrolidone-maleate-guerbet alcohol monoester polymer micelles, amorphous solid dispersions with polyvinylpyrrolidone K-30 (PVP K-30), and amentoflavone-loaded vitamin E polyethylene glycol succinate (TPGS)/soluplus mixed micelles. These carriers have effectively improved the solubility and bioavailability of amentoflavone. TPGS/soluplus mixed nanomicelles have been successfully prepared with a particle size of 67.33 ± 2.01 nm and Zeta potential of −0.84 ± 0.04 mV, achieving encapsulation efficiency of 99.18 ± 0.76% and drug loading of 2.47 ± 0.01%.
3. Traditional and Historical Use
Traditional Chinese Medicine
Amentoflavone, as a natural biflavonoid compound, is widely used in traditional Chinese medicine. In China, the parent plant Selaginella tamariscina (known as "Juan bai") is listed in the Pharmacopoeia. In South Korea, the use of this plant ("Kwon Baek") is mentioned in the book Dongui-Bogam (Heo Jun, 1613), at the origin of Hyungsang medicine.
The therapeutic potency of Selaginella tamariscina extracts is linked to the presence of biflavonoids, chiefly amentoflavone, and selaginellin-type phenolic compounds. Standard alcoholic extracts of native S. tamariscina are adapted to treating inflammatory diseases and cancers, whereas extracts of the carbonized plant (S. tamariscina carbonisatus) are adapted to treating bleedings.
Traditional Indian, African, and American Systems
Amentoflavone has been isolated from nearly 120 plants used in traditional medicine by the Chinese, Indians, Africans, and Americans. Plants containing amentoflavone have been used as folk phytomedicines for a very long time, including Calophyllum inophyllum and Selaginella bryopteris in traditional Indian medicine, Byrsonima intermedia in traditional American medicine, and Cnestis ferruginea and Drypetes gerrardii in traditional African medicines.
Historical Isolation
Amentoflavone is an active phenolic compound that has been isolated from Selaginella tamariscina for over 40 years. It was initially isolated from the leaves of Selaginella tamariscina, Selaginella rupestris, and Ginkgo biloba by Okigawa et al. (1971), Chakravarthy et al. (1981), and Lobstein-Guth et al. (1988), respectively.
4. Key Active Constituents and Mechanisms of Action
Structural Basis for Activity
Biflavonoids, including amentoflavone, represent a unique subclass of flavonoids with superior clinical activity compared to their monomeric counterparts, offering distinct therapeutic benefits by targeting multiple pathways. However, the exact mechanism of flavonoid dimerization in plants remains under investigation. Amentoflavone is an apigenin dimer with multiple double bonds and hydroxyl groups in its molecular structure. The C2–C3 double bond is susceptible to hydrogenation, whereas the hydroxyl groups are prone to substitution with methoxy groups.
Anti-Inflammatory Mechanisms
Amentoflavone plays a key role in the oxidant/antioxidant balance by suppressing the production of inflammatory mediators (NO, COX-2) and pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), and by inhibiting the activation of NF-κB signaling pathways in vitro and/or in vivo.
In RAW264.7 macrophages stimulated with LPS, amentoflavone dose-dependently suppressed the production of nitric oxide and prostaglandin E2. It suppressed nuclear translocation of c-Fos, a subunit of activator protein (AP)-1, and inhibited the activity of extracellular signal-regulated kinase (ERK), which mediates c-Fos translocation. It also suppressed the formation of a molecular complex including ERK and c-Fos.
Antioxidant Mechanisms
Amentoflavone, isolated from Garcinia brasiliensis, exhibited inhibitory effects on the production of superoxide anion and total reactive oxygen species in phorbol 12-myristate 13-acetate-stimulated human neutrophils. In human erythrocytes, it also inhibited oxidant hemolysis and lipid peroxidation.
Amentoflavone activates AMPK-dependent Nrf2 signaling, promoting transcription of antioxidant enzymes and protecting against Aβ-induced neurotoxicity. In transgenic Alzheimer's disease (AD) mice, where the Nrf2 pathway was compromised alongside increased brain Aβ levels, treatment with amentoflavone significantly boosted Nrf2 expression and its translocation, which in turn increased HO-1 and NQO-1 levels, thereby reducing oxidative stress in the brain.
Neuroprotective Mechanisms
Amentoflavone can enhance autophagy by binding to multiple amino acid residues of the mTOR protein, thereby inhibiting further phosphorylation of mTOR and exerting a neuroprotective effect against Alzheimer's disease.
Mechanistic studies have revealed that amentoflavone effectively inhibits the expression of pro-inflammatory factors (TNF-α, IL-1β, IL-6, iNOS, COX-2) and enhances the expression of anti-inflammatory factors (IL-4, TGF-β, Arg-1, CD206), promoting the polarization of microglia towards the M2 anti-inflammatory phenotype. It also significantly ameliorates the reduction in tyrosine hydroxylase-positive neurons and the increase in α-synuclein expression observed in LPS-induced Parkinson's disease models.
Anticancer Mechanisms
Amentoflavone suppresses tumor pathological progress and metastasis in vitro and in vivo through several molecular mechanisms, including cell cycle arrest, apoptosis and autophagy induction. It exerts anti-cancer effects also by initiating p53 and inhibiting NF-κB, PI3K-AKT, ERK, and MAPK/mTOR signal pathways.
GABA-A Receptor Modulation
Several studies have shown that amentoflavone binds to benzodiazepine receptors. Using two-electrode voltage-clamp methodology, amentoflavone has been shown to be a negative modulator of GABA at GABA(A) α1β2γ2L receptors expressed in Xenopus laevis oocytes. This action appears to be independent of the flumazenil-sensitive benzodiazepine modulatory sites on the GABA(A) receptor.
Phosphodiesterase Inhibition
Amentoflavone shows molecular mechanisms including phosphodiesterase inhibition, effects on muscular strength, acetylcholinesterase inhibition, inhibition of PTP1B, weak vasodilation, and also inhibits fatty acid synthesis.
Thrombin Inhibition
Among biflavonoids from Ginkgo biloba, luteolin, apigenin, quercetin, kaempferol, isorhamnetin, and the biflavonoids ginkgetin, isoginkgetin, bilobetin, and amentoflavone presented IC50 values between 8.05 and 82.08 μM against thrombin. Since the biflavonoids exhibited the most potent anticoagulant effect, time-dependent enzyme inhibition tests showed that ginkgetin, isoginkgetin, bilobetin, and amentoflavone exhibited mixed-type inhibition of thrombin.
5. Scientific Evidence by Area of Use
Important note on evidence levels: The overwhelming majority of evidence for amentoflavone derives from in vitro (cell culture) and in vivo animal studies. As of the time of this writing, no large-scale, controlled human clinical trials have been published for amentoflavone as an isolated compound. Owing to the poor solubility and low bioavailability of amentoflavone, it has not yet been developed as a drug for treating diseases. All findings described below should be understood in the context of the preclinical evidence base from which they are drawn.
5.1 Inflammation
In LPS-stimulated RAW264.7 macrophage cells, amentoflavone dose-dependently suppressed the production of nitric oxide and prostaglandin E2. In rat astrocytoma cell lines and related models, amentoflavone suppressed the production of NO, COX-2, and pro-inflammatory cytokines including TNF-α, IL-1β, and IL-6, and inhibited the activation of NF-κB signaling pathways. The anti-inflammatory evidence is largely in vitro and in animal models; no human interventional trials have been published for isolated amentoflavone.
Evidence from psoriasis models is notable: a 2016 study (cited in the literature) found that amentoflavone protects against psoriasis-like skin lesions through suppression of NF-κB-mediated inflammation and keratinocyte proliferation.
5.2 Neurodegenerative Diseases and Neuroprotection
The neuroprotective effect of amentoflavone is evident in its ability to act against neurodegenerative diseases, including ischemic stroke, epilepsy, Parkinson's disease, and Alzheimer's disease.
Alzheimer's disease (AD): Amentoflavone significantly raised brain antioxidant markers glutathione (GSH) and catalase (CAT) and lowered malondialdehyde (MDA) levels in experimental models. It activates AMPK-dependent Nrf2 signaling, promoting transcription of antioxidant enzymes and protecting against Aβ-induced neurotoxicity. These findings come exclusively from animal and cell studies; there are no published human clinical trials in this indication.
Parkinson's disease (PD): In LPS-induced PD models, amentoflavone inhibited the expression of pro-inflammatory factors (TNF-α, IL-1β, IL-6, iNOS, COX-2) and enhanced anti-inflammatory mediators (IL-4, TGF-β, Arg-1, CD206), promoting M2 microglial polarization. It also significantly ameliorated the reduction in tyrosine hydroxylase-positive neurons and the increase in α-synuclein expression, suggesting neuroprotective effects in this model.
Epilepsy: In hippocampal neuron studies, amentoflavone has been investigated for anti-inflammatory, antioxidative, and antiapoptotic properties relevant to status epilepticus, with NF-κB p65 immunoreactivity in the hippocampus examined as a biomarker. All evidence remains at the preclinical level.
Overall, amentoflavone exerts neuroprotective effects through coordinated modulation of oxidative stress, inflammatory signaling, and ferroptosis pathways. However, the evidence strength for all neurodegenerative disease applications is currently preliminary and limited to preclinical models.
5.3 Cardiovascular System
Amentoflavone is capable of acting on cardiocerebrovascular diseases through a variety of mechanisms, though there is currently no published literature regarding its use in the treatment of atherosclerosis as a clinically tested intervention. Preclinical data suggest relevant mechanisms including lipid modulation and vascular protection. A 2004 study published in Planta Medica investigated vasorelaxation by amentoflavone isolated from Selaginella tamariscina, reporting effects on vascular smooth muscle. All cardiovascular evidence is preclinical.
5.4 Anticancer Activity
Numerous studies on amentoflavone have revealed its cytotoxic potential against different cancers, including hepatocellular carcinoma (HCC), breast cancer, osteosarcoma, bladder cancer, and ovarian cancer. The antitumor potential of amentoflavone has been extensively investigated, revealing therapeutic promise across a spectrum of cancers including breast, lung, prostate, and colorectal malignancies.
In pancreatic cancer research, through network pharmacology and molecular docking, the putative core targets and signaling pathways underlying the antineoplastic potential of amentoflavone were elucidated. Therapeutic efficacy and mechanisms were corroborated in both in vitro pancreatic cancer cell models and in vivo animal models. Key targets identified included SRC, AKT1, PI3KR1, VEGFA, ESR1, EGFR, and AR.
All anticancer evidence for isolated amentoflavone is preclinical (cell lines and animal xenograft models). No human clinical trials have been reported for amentoflavone as a standalone agent in oncology.
5.5 Antiviral Activity
Amentoflavone has broad-spectrum antiviral activity in addition to its anti-inflammatory and antioxidant effects, and is a naturally occurring human thrombin inhibitor.
Herpes Simplex Virus (HSV-1): In vitro studies demonstrated the antiviral activity of amentoflavone toward HSV-1 (F strain), as well as several acyclovir (ACV)-resistant strains including HSV-1/106, HSV-1/153, and HSV-1/Blue at high concentrations. Time-of-drug-addition assays revealed that amentoflavone mainly impaired HSV-1 early infection. It affected cofilin-mediated F-actin reorganization and reduced the intracellular transportation of HSV-1 from the cell membrane to the nucleus.
HIV, HBV, Influenza: Amentoflavone showed antiviral effects against several viruses including HIV, herpes simplex virus type 1, and hepatitis B and C virus. Amentoflavone suppresses hepatitis B virus (HBV) infection through the inhibition of HBV attachment.
SARS-CoV-2: Amentoflavone has been proposed to exert anti-SARS-CoV-2 effects via binding towards the main protease (Mpro/3CLpro), spike protein receptor binding domain (RBD), and RNA-dependent RNA polymerase (RdRp) of SARS-CoV-2. Clinical studies with Hypericum and Ginkgo extracts (both of which contain amentoflavone) as additional or alternative supplements are registered, but these evaluate whole-plant extracts, not isolated amentoflavone. All SARS-CoV-2 evidence for isolated amentoflavone is currently limited to molecular docking and in vitro data.
5.6 Metabolic and Antidiabetic Effects
Amentoflavone acts as an antidiabetic agent through the inhibition of α-glucosidase and α-amylase enzymes. Potent inhibitors of protein tyrosine phosphatase 1B (PTP1B) and phosphodiesterase-4 (PDE4), as well as repressors of pro-inflammatory cytokine expression, have been identified in Selaginella tamariscina extracts where amentoflavone is the primary compound.
Amentoflavone, the primary compound in Selaginella rupestris extracts, reduced intestinal lipid absorption by inhibiting fatty acid transport in high-fat-diet (HFD)-fed mice. AMF-enriched extracts effectively protected against HFD-induced metabolic changes. These findings are limited to animal models. There are robust experimental data, based on in vitro and in vivo models, documenting the use of Selaginella tamariscina extracts to treat type 2 diabetes, several inflammatory diseases, and some cancers (in combination with standard chemotherapy), though this evidence relates to the whole plant extract rather than isolated amentoflavone.
5.7 Antidepressant and Anxiolytic Effects
Amentoflavone has been reported to have anxiolytic and antidepressant pharmacological effects, primarily in animal behavioral models. The mechanism most studied relates to its activity at the GABA(A) receptor. Amentoflavone mainly shows antagonist activity at the κ-opioid receptor and at the allosteric benzodiazepine site of the GABA(A) receptor as a negative allosteric modulator. Evidence for antidepressant effects in humans is entirely lacking; all data are preclinical.
5.8 Antimicrobial Activity
Like other biflavonoids, amentoflavone has been reported to possess antibacterial activity, in addition to antioxidant, anticancer, antiviral, anti-inflammatory, and UV-blocking effects. Specific studies have documented its inhibitory effects against various bacterial strains and fungi in vitro. The evidence remains at the laboratory stage with no human clinical data.
5.9 Musculoskeletal Protection
The current literature comprehensively discusses amentoflavone's diverse biological activities, including musculoskeletal protection. Preclinical studies have examined its effects in models of bone loss, cartilage damage, and muscle injury, but these findings have not been confirmed in human trials.
6. Pharmacokinetics and Bioavailability
Oral Absorption
Physicochemical properties of amentoflavone have been evaluated using in vitro assays including water solubility, stability in both simulated gastric and intestinal fluids, logD, pKa, and permeability studies in a monolayer Caco-2 model. Results suggest that amentoflavone is a compound with moderate intestinal absorption, and that poor solubility is the key rate-limiting step for oral absorption.
Studies on pharmacokinetics and biliary excretion showed that the percentage of amentoflavone conjugates in bile was determined to be up to 96.73%, and no amentoflavone conjugates were detected in rat plasma under standard conditions. This finding indicates extensive first-pass and pre-systemic metabolism, contributing to its poor systemic bioavailability.
Metabolism
Thirty-four kinds of metabolites of amentoflavone have been identified in rats in studies examining nanomicelle formulations. The extensive biotransformation via phase I and phase II reactions (glucuronidation and sulfation in particular) substantially limits the intact compound's plasma exposure after oral administration.
Formulation Strategies
To improve solubility and bioavailability, nanomicelles have been prepared using TPGS and soluplus as carriers. Particle size, zeta potential, encapsulation efficiency, drug loading, stability, cytotoxicity, cellular uptake, and metabolites in rats were studied and compared with free amentoflavone. The physical and chemical properties of these mixed micelles were stable within 60 days, and the cytotoxicity of the mixed micelles was substantially greater than that of amentoflavone monomers.
7. Dosage Forms and Dosages Reported in Studies
There is no established or clinically validated dosage for amentoflavone as an isolated supplement in humans. The following information reflects dosages and forms appearing in peer-reviewed preclinical research only and cannot be applied to human supplementation guidance.
- In cytochrome P450 enzyme inhibition studies, amentoflavone (AMF) is a highly potent inhibitor of CYP2C9 with an IC50 value of 0.035 μM, and also inhibits CYP2C19, CYP2D6, and CYP3A with IC50 values of 23.6, 24.3, and 4.8 μM, respectively.
- In gut bacterial β-glucuronidase (GUS) inhibition assays, the IC50 values of amentoflavone against GUS-mediated DDAOG and SN-38G hydrolysis were 0.62 μM and 0.49 μM, respectively.
- In animal pharmacokinetic studies, amentoflavone has been administered via oral gavage in rodent models, typically at doses in the range of milligrams per kilogram of body weight, with specific doses varying by study. No universal dose has been validated for clinical use.
- In thrombin inhibition experiments using fluorometric probes, biflavonoids including amentoflavone presented IC50 values between 8.05 and 82.08 μM.
Amentoflavone appears commercially as a standardized extract powder, often derived from Selaginella tamariscina or Hypericum perforatum. The supplement industry typically offers capsule or powder forms. However, no peer-reviewed human clinical trial has established an efficacious or safe human oral dose for isolated amentoflavone.
8. Body Systems and Health Areas Associated with Amentoflavone
Peer-reviewed literature reports pharmacological effects including anti-inflammatory, anti-microorganism, anti-oxidant, anti-angiogenic, neuroprotective, musculoskeletal protective, radioprotective, metabolism-regulating, anxiolytic/antidepressant, and anti-cancer activities. The following body systems have been investigated, predominantly at the preclinical level:
- Central Nervous System: Neuroprotection against Alzheimer's disease, Parkinson's disease, ischemic stroke, and epilepsy; GABA(A) receptor modulation; antidepressant/anxiolytic effects.
- Cardiovascular System: Thrombin inhibition, vasorelaxation, anti-atherosclerotic mechanisms, anti-angiogenic activity.
- Immune System: Suppression of pro-inflammatory cytokine production; modulation of macrophage and microglial polarization.
- Metabolic System: Inhibition of α-glucosidase, α-amylase, PTP1B, and fatty acid synthase; potential relevance to type 2 diabetes and obesity.
- Oncology: Cytotoxic activity across multiple cancer cell lines through apoptosis induction, cell cycle arrest, and inhibition of angiogenesis.
- Antiviral Defense: Activity against HSV-1, HIV, HBV, influenza, and putative SARS-CoV-2 protease binding.
- Musculoskeletal System: Investigated in bone and cartilage models.
- Skin: Anti-psoriatic effects; included as an ingredient in patented cosmetic preparations.
9. Safety Considerations and Drug Interactions
CYP Enzyme Inhibition — Drug Interaction Risk
The most thoroughly documented and clinically relevant safety concern for amentoflavone is its potent inhibition of cytochrome P450 enzymes. Amentoflavone can interact with many medications by being a potent inhibitor of CYP3A4 and CYP2C9, which are enzymes responsible for the metabolism of some drugs in the body.
Several studies have reported that the interaction of amentoflavone with drugs inhibits the catalytic activities of CYP enzymes. It is a highly potent inhibitor of CYP2C9 with an IC50 value of 0.035 μM, and also inhibits CYP2C19, CYP2D6, and CYP3A with IC50 values of 23.6, 24.3, and 4.8 μM, respectively.
Biflavone components including amentoflavone were identified as the main CYP3A4 inhibitory components in Ginkgo biloba and Selaginella tamariscina, which display very strong inhibitory effects toward CYP3A4. These results suggest the potential for pharmacokinetic interactions between the identified biflavones and clinical drugs undergoing CYP3A4-mediated biotransformation. This information is important for guiding the rational use of herbal medicine in combination with synthetic pharmaceuticals.
CYP3A4 is mainly expressed in the liver and intestines of adult humans and has a wide substrate spectrum. It participates in the metabolic clearance of more than 50% of commonly used clinical drugs, including tyrosine kinase inhibitors, dihydropyridine calcium antagonists, benzodiazepines, sedative-hypnotics, and statins.
UGT Inhibition
Compared with herbal extracts, which induce cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) activity (producing a negative herb–drug interaction), amentoflavone is a potent inhibitor of CYP3A4, CYP2C9, and UGT. UGT inhibition may further increase plasma concentrations of co-administered drugs that depend on glucuronidation for elimination.
Anticoagulant Interactions
Administration of amentoflavone should also be calibrated against antithrombotic drugs like warfarin, rivaroxaban, or betrixaban to avoid bleeding. Given amentoflavone's dual roles as a thrombin inhibitor and CYP2C9 inhibitor (an enzyme critical to warfarin metabolism), coadministration with anticoagulant medications carries a theoretically elevated risk of bleeding complications.
Blood–Brain Barrier Penetration
Several researchers have noted that amentoflavone's large molecular size (538.46 g/mol) and hydrophilicity profile significantly constrain its ability to cross the blood–brain barrier after systemic oral administration. This is particularly relevant when considering its in vitro CNS mechanisms, which may not fully translate to in vivo settings at physiologically achievable brain concentrations from standard oral dosing.
Genotoxicity Signal
One study reported the mutagenic activity of amentoflavone in the Salmonella typhimurium (Ames) assay. This preliminary genotoxicity signal has not been confirmed or refuted in more comprehensive genotoxicity or carcinogenicity testing programs. The clinical significance of this finding is unclear.
Prooxidant Activity
While amentoflavone generally demonstrates antioxidant properties, one study revealed that amentoflavone also exhibits prooxidative activity through Nrf2 activation induced by ROS-mediated activation of the p38-AKT pathway in HaCaT cells. This context-dependent antioxidant/prooxidant duality is common among polyphenols and may have implications in specific cell types or disease settings.
Overall Evidence Assessment
This polyphenolic compound has been discovered to have some important bioactivities, including anti-inflammation, anti-oxidation, anti-diabetes, and anti-senescence effects on many important reactions in the cardiovascular and central nervous system. However, owing to the poor solubility and low bioavailability of amentoflavone, it has not been developed as a drug for treating these diseases. The currently available scientific evidence is predominantly preclinical. Amentoflavone is therefore considered to be a promising therapeutic agent warranting clinical research, rather than one with established human clinical efficacy.
References
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