IngredientsThe term flavoglycosides — also rendered as ginkgo flavone glycosides, ginkgoflavonglycosides, ginkgo flavonol glycosides, or flavonoid glycosides — refers to a class of polyphenolic compounds in which a flavonoid aglycone (the bioactive core) is covalently bound to one or more sugar (saccharide) moieties. Flavonoid glycosides are a class of naturally occurring compounds found abundantly in fruits, vegetables, and various medicinal plants; they are essentially flavonoids bound to sugar molecules, a configuration that enhances their solubility and bioavailability. In the specific context of dietary supplementation, the term "flavoglycosides" is most closely associated with the standardized dry leaf extract of Ginkgo biloba L. (family Ginkgoaceae), in which the content of these compounds is quantified and guaranteed to a precise percentage as a primary marker of quality and potency.
Flavonoid glycosides are compounds in which flavonoid aglycones are bound with various saccharide moieties; they can be divided into categories based on the bond connecting the flavonoid and saccharide subunits. The two principal bond types are: flavonoid O-glycosides, C-glycosides, and mixed O,C-glycosides. In Ginkgo biloba, the relevant flavoglycosides are predominantly O-glycosides of the flavonols quercetin, kaempferol, and isorhamnetin. According to aglycone patterns, the most numerous subclass of flavonoid glycosides overall are the O-glycosides of flavones and flavonols; kaempferol O-glycosides and quercetin O-glycosides are the top two in number.
The carbon-linked subtype (C-glycosides) also occurs widely in nature. Flavonoid C-glycosides are linked by the anomeric carbon of the sugar and the flavonoid skeleton through a C–C bond; natural C-glycosides have been detected on flavones, flavonols, isoflavones, and chalcones, with flavone C-glycosides being the most important subclass. The most widely distributed aglycones of flavonoid C-glycosides are apigenin and luteolin; the sugar moieties, similar to those of O-glycosides, include glucose, rhamnose, galactose, xylose, and arabinose, with flavonoid C-glucosides being the most abundant type.
Structurally, flavonoids consist of two aromatic rings (A and B rings) linked by a 3-carbon chain that forms an oxygenated heterocyclic ring (C ring); they are classified as flavan-3-ols, flavanones, flavonols, anthocyanidins, flavones, and isoflavones based on differences in the generic structure of the C ring, functional groups on the rings, and the position at which the B ring is attached.
In the specific context of Ginkgo biloba supplements, the term is frequently rendered as ginkgoflavonglycosides in the European Pharmacopoeia and regulatory literature, or simply as ginkgo flavone glycosides or ginkgo flavonol glycosides in the United States Pharmacopeia (USP) and Chinese Pharmacopoeia (ChP). The EMA and Commission E monographs use the term "ginkgoflavonglycosides" when specifying the standardized extract.
Ginkgo biloba L. of the family Ginkgoaceae is a deciduous tree 20–40 metres in height, native to eastern China, and is considered a "living fossil" since it probably originated 200 million years ago. The part of the plant used commercially for flavoglycoside production is the dried leaf. All preparations with marketing authorisation to date are from dry extract of Ginkgo biloba leaves.
Although flavoglycosides occur broadly across the plant kingdom — including fruits, vegetables, tea, citrus, and bee pollen — the main active constituents of Ginkgo extracts are flavone glycosides such as kaempferol, quercetin, and isorhamnetin, alongside terpene lactones, alkylphenols, proanthocyanidins, and organic acids. The Ginkgo leaf extract is unique in that its flavoglycosides are co-present with a chemically distinct class of bioactive compounds, the terpene trilactones (ginkgolides A, B, C, and bilobalide), which are not found in other common dietary sources of flavonoid glycosides.
The European Pharmacopoeia requires that dried G. biloba leaf is to be extracted with 60% acetone (m/m) as primary extraction solvent, and the final product is adjusted to 22.0%–27.0% ginkgo flavonoids calculated as ginkgo flavone glycosides and 5.4%–6.6% terpene lactones, with less than 5 ppm ginkgolic acids. The US Pharmacopeia specification for flavonol glycosides and ginkgolic acids is the same as the European; however, the specification for terpene trilactones can be 5.4%–12.0%. The Chinese Pharmacopoeia specifies only lower limits of at least 6% terpene trilactones and at least 24% flavonol glycosides with no upper limits.
The dry extract (DER 35–67:1) from Ginkgo biloba leaf is refined and quantified to 22–27% ginkgoflavonglycosides, represented by quercetin, kaempferol, and isorhamnetin, and 5–7% terpene lactones, with ginkgolic acid content less than 5 ppm. The most clinically studied preparation is the proprietary extract EGb 761®. The EGb 761® extract contains 24% flavone-glycosides, along with ginkgolides and bilobalide.
Ginkgo biloba extract is available in the market in the form of tablets, capsules, tinctures, liquid extract, gel, sublingual spray, and tea. However, because of potential allergic reactions to ginkgolic acids (specified to be less than 5 parts per million in assured extracts), the use of normal tinctures or fluid extracts is not recommended without assurance on this front; most commercial ginkgo products other than EGb761 have been shown to contain seriously high levels of these allergens.
Almost all clinical research evidence relates to the patented 50:1 extract EGb761 — containing 24% flavone glycosides and 6% terpenoids — at a daily dose typically corresponding to 4 to 16 g of leaf; there is a considerable body of this evidence, with over 400 clinical trials published in the scientific literature.
Quality control of commercial extracts has been complicated by the problem of adulteration. Because of widespread adulteration of commercial ginkgo extracts with rutin (so as to generate the required high flavonoid levels), a specific quality control method for standardised ginkgo extracts is now a requirement of the United States Pharmacopoeia National Formulary as well as for product registration with the Australian Therapeutic Goods Administration.
Ginkgo biloba was first recorded as a medicinal plant in the Chinese Materia Medica Shen Nong Ben Cao Jing approximately 2,000 years ago, and only the seeds were reported to be used as medicine. Much later, the leaves of G. biloba were cited for the treatment of heart and lung diseases in Traditional Chinese Medicine (TCM). A 16th-century Chinese text, the Ben Cao Gang Mu by Li Shi-Zhen, documented the prescription of Ginkgo seeds for skin infections, representing one of the earliest written descriptions of topical antimicrobial use. Ginkgo kernels have been used as medicine or eaten as a nut in traditional medicinal science.
In traditional Chinese medicine, ginkgo leaf extracts have mainly been used to treat circulatory or brain disorders and respiratory diseases. It is important to note that the classical TCM applications were directed chiefly at the seeds and their astringent, lung-tonifying properties, while the modern therapeutic focus on leaf-derived flavoglycosides emerged much later and was principally driven by 20th-century European phytopharmacological research.
In 1964, an extract of Ginkgo leaves (EGb 761) was introduced into Western medical practice, and since that time these standardized extracts (commercially available as Tanakan®, Tebonin®, Rokan®) have been used worldwide for the treatment of mild to moderate age-associated conditions. Phytopharmaceutical extracts from the leaves of Ginkgo biloba have been applied to treat cerebrovascular and peripheral vascular diseases in many countries such as Germany, France, Japan, and Korea since the 1960s.
In Germany and France, ginkgo leaf extract rapidly became one of the most commercially significant phytomedicines. Today, G. biloba is one of the most commonly used herbal medicinal products in Europe and in the United States. In Europe, G. biloba extract is primarily regulated as a herbal medicine, but in the US as a dietary supplement sold with health claims.
The European concept of "cerebral insufficiency" was central to early Western therapeutic use. The original therapeutic focus was improving peripheral circulation to the brain, fitting with the German concept of "cerebral insufficiency," a symptom complex including difficulties in concentration and memory, absentmindedness, confusion, tiredness, decreased physical performance, depressive mood, anxiety, dizziness, tinnitus, and headaches — symptoms also associated with the early stages of dementia.
For all EMA-approved products, the indication was established as: traditional herbal medicinal product for the treatment of long-standing symptoms in elderly people such as difficulties of memory and concentration, vertigo, tinnitus, and fatigue; the indications are based solely on experience and use during a long period of time.
Flavonoids present in Ginkgo biloba extract include quercetin, kaempferol, isorhamnetins, as well as proanthocyanidins. In the standardized extract, the flavoglycosides are primarily O-glycosides of three flavonol aglycones: quercetin-3-O-rutinoside (rutin), kaempferol-3-O-glucoside (astragalin), kaempferol-3-O-rutinoside, and multiple isorhamnetin glycosides. Commercially, a 40 mg extract contains the standard 24% flavonoids (quercetin, isorhamnetin glycosides, and kaempferol) and 6% terpenes (ginkgolides and bilobalides).
The principal effective component in Ginkgo biloba leaves is flavonoids, comprising at least 14 different compounds such as flavonols, flavones, flavanols, and biflavonoids. Other constituents include glucose, rhamnose, hydroxykynurenic, kynurenic, protocatechuic, vanillic, and shikimic acids, d-glucaric acid, ginkgolic acid, and related alkylphenols.
The full pharmacological profile of standardized Ginkgo biloba extract depends on the combined action of its flavoglycosides and its terpene lactone fraction. Most clinical studies have been performed with the special extract EGb 761®, which is analytically controlled to contain 24% flavone glycosides and 6% terpene lactones; the terpene lactone fraction consists of bilobalide and the ginkgolides A, B, C, and J. It is therefore important when reviewing the scientific evidence to understand that the biological activity attributed to the extract as a whole reflects the synergistic contributions of both fractions.
The fruits and leaves of the tree contain another category of constituents — ginkgolic acids and related alkyl phenols — which are linked to adverse reactions such as allergies and toxic effects; according to the monographs of the German Commission E and the WHO, the maximum safe concentration of ginkgolic acid is 5 µg/g.
The therapeutic mechanisms of action of the Ginkgo leaf extract are suggested to be through its antioxidant, antiplatelet, antihypoxic, antiedemic, hemorrheologic, and microcirculatory actions, where the flavonoid and terpenoid constituents may act in a complementary manner. Flavonoids have the ability to control the accumulation of reactive oxygen species (ROS) via scavenger activity. The flavoglycosides contribute primarily to the antioxidant arm of this mechanism. Flavonoids inhibit lipid peroxidation through at least scavenging superoxide anions, restoring superoxide dismutase (SOD) activity, and suppressing xanthine oxidase (XOD) activity.
The neuroprotective properties of Ginkgo biloba, including antioxidant, anti-apoptotic, anti-inflammatory, and vasoregulatory mechanisms, are attributed to its extract components; the synergistic activity of these chemicals activates various molecular pathways including neuronal survival, cerebral perfusion, and synaptic plasticity. EGb 761 reduces oxidative stress, limits lipid peroxidation, and preserves mitochondrial function.
Among the best-established pharmacological activities of ginkgolides is their PAF receptor antagonistic activity. While PAF antagonism is attributed primarily to the terpene fraction (especially ginkgolide B), the flavoglycosides contribute to the overall platelet-inhibitory effect of the extract. Other principles of action include PAF antagonism, modulation of the peripheral benzodiazepine receptor, and endothelium-relaxing factor, which improves the circulatory properties of blood.
In vitro, PAF promotes various biological responses such as platelet secretion and activation, neutrophil stimulation, increase of vascular permeability, and contraction of smooth muscle cells; systemic actions of PAF comprise bronchoconstriction, hypotension, thrombocytopenia, cardiac dysfunction, and recruitment of leukocytes in inflamed tissues. By antagonizing the PAF receptor, ginkgolide B in particular reduces these effects. Ginkgolide B acts as a natural product antagonist of the platelet-activating factor receptor (PAF-R), exerting a strong inhibitory effect on inflammation and platelet activation by inhibiting the elevation of PAF levels and reducing the interaction/binding of PAF with PAF-R.
Ginkgo induces the production of vascular endothelial growth factor and up-regulates the expression of its receptors; it also increases endothelial nitric oxide synthase (eNOS) promoter activity and eNOS expression, increasing endothelial nitric oxide production. Ginkgo biloba contains various pharmacologically active components, including terpene lactones and flavonoids, that could cause drug interactions through multiple mechanisms, including effects on cytochrome isozymes and P-glycoprotein (P-gp).
The suggested mechanisms of the Ginkgo leaf extract also include inhibition of beta-amyloid peptide (Aβ) aggregation, which is relevant to Alzheimer's disease pathology. This has been demonstrated in laboratory studies. Ginkgolide B, one of the major active ingredients in EGb, can inhibit the neurotoxicity induced by β-amyloid. The flavoglycoside fraction's contribution to this effect, independent of the terpene fraction, remains an active area of laboratory investigation.
Uridine diphosphate glucuronosyltransferases (UGTs) in the endoplasmic reticulum widely mediate the absorption and metabolism of endogenous and exogenous compounds by catalyzing the covalent addition of glucuronic acid and various lipophilic chemicals. Research published in 2023 demonstrated that rutin, a typical flavone O-glycoside, has a stronger UGT2B7 binding effect than its metabolites; typical dietary flavone O-glycosides generally have high binding affinities towards UGT2B7 protein. These interactions have implications for the systemic availability and potential drug interactions of flavoglycosides, as UGT enzymes are central to Phase II hepatic metabolism.
Although flavonoid compounds have various pharmacological applications, they generally exhibit low oral bioavailability due to their poor aqueous solubility. Glycosylation improves the chemical stability of flavonoids and increases the aqueous solubility of the aglycone backbone, thereby improving their bioavailability. The gut microbiota plays a further role: some phytochemicals in ginkgo leaf extracts are known to be metabolized by gut microbial enzymes. In antibacterial-treated mice, the maximum plasma concentration and area under the curve of isorhamnetin were significantly increased when compared with the control group, suggesting gut bacteria normally reduce isorhamnetin absorption.
Research indicated that Ginkgo flavonols quercetin, kaempferol, and isorhamnetin are substrates of P-glycoprotein (P-gp), and the P-gp type efflux pump might limit the bioavailability of Ginkgo flavonols. Further investigation revealed that kaempferol, quercetin, and isorhamnetin have strong mutual inhibition on efflux mediated by P-glycoprotein transporters. Formulation approaches such as phospholipid complexation have been investigated: a group prepared phospholipid complex (GBP) and solid dispersion (GBS) of G. biloba extract and demonstrated that the bioavailability of quercetin, kaempferol, and isorhamnetin in the GBP and GBS groups increased significantly in comparison with the standard G. biloba extract group.
Clinical studies on the treatment of Alzheimer's disease (AD) with Ginkgo biloba leaf extract (EGb) have been reported since the 1980s, and many clinical studies have been carried out during the following 30 years; however, the benefits of EGb on the treatment of AD remain controversial.
A 2015 systematic review and meta-analysis of 21 randomized controlled trials (RCTs) involving 2,608 patients found that Ginkgo biloba is potentially beneficial for the improvement of cognitive function, activities of daily living, and global clinical assessment in patients with mild cognitive impairment or Alzheimer's disease; however, due to limited sample size, inconsistent findings, and methodological quality of included trials, more research is warranted.
A comprehensive updated review of RCTs (published 2020, Frontiers in Pharmacology) concluded that EGb may be able to improve the cognitive function in patients who suffered from mild dementia during long-term administration (more than 24 weeks) and appropriate dosage (240 mg per day). Although a few available large-scale clinical trials suggest that EGb is relatively efficacious in delaying the progress of dementia, several other trials showed negative results.
The largest single trial — the Ginkgo Evaluation of Memory (GEM) Study — was a randomized, double-blind, placebo-controlled RCT. The GEM study enrolled 3,069 community-dwelling participants aged 72 to 96 years at 6 academic medical centres in the United States between 2000 and 2008, with a median follow-up of 6.1 years. The intervention was a twice-daily dose of 120 mg extract of G. biloba (n = 1,545) or identical-appearing placebo (n = 1,524); the conclusion was that compared with placebo, the use of G. biloba 120 mg twice daily did not result in less cognitive decline in older adults with normal cognition or with mild cognitive impairment.
Earlier clinical evidence, reviewed in earlier positive meta-analyses, was based on studies using standardized extract at doses of 120–240 mg/day. Those studies used standardized ginkgo extract (24% or 25% ginkgo-flavone glycosides and 6% terpenoids given by any route of administration), including EGb 761 120 mg/day or 240 mg/day, or Tanakan 120 mg/day. The use of ginkgo extract in dementias of the Alzheimer or multi-infarct type is based mainly on positive results from good-quality placebo-controlled studies that enrolled approximately 1,200 patients; the effect on cognitive symptoms was within the range of a 25% reduction. Memory, concentration, and alertness were the first symptoms to be relieved, with tinnitus and dizziness improving somewhat later; a minimum of 4 to 6 weeks were needed before a pronounced effect could be expected.
An umbrella review of systematic reviews published in 2025 (ScienceDirect) found that for neurocognitive disorders, most systematic reviews were in favour of EGb 761® regarding cognition and behavioural and/or psychological symptoms; EGb 761® might have positive effects on tinnitus, macular degeneration, or schizophrenia, but more evidence is needed; in general, EGb 761® appears to be safe; however, methodological quality was poor in all systematic reviews.
Evidence strength: The evidence for cognitive benefit in established mild-to-moderate dementia is mixed. Several well-conducted RCTs (including GEM) found no statistically significant benefit in preventing cognitive decline in cognitively normal older adults. Positive signals are observed primarily in patients with pre-existing mild dementia in trials of 24 weeks or longer at 240 mg/day, but methodological limitations — including heterogeneity of populations, outcome measures, and study quality — prevent a firm consensus.
Because tinnitus development is associated with vascular access, dietary flavonoids such as those present in G. biloba extract have antioxidant and vasodilatory effects and may play a role in alleviating tinnitus symptoms.
A randomized, double-blind clinical trial published in 2018 compared EGb 761® with pentoxifylline in 197 patients with sub-chronic or chronic tinnitus. Patients were randomized to receive 120 mg EGb 761® or 600 mg pentoxifylline, each twice a day, over a 12-week period. For both treatment groups, significant improvements were observed in the tinnitus questionnaire, loudness and annoyance scales, anxiety score, and disability scale; there was no relevant difference in tinnitus-related outcomes between the two treatment groups; 20 adverse events were documented in the EGb 761® group.
An exploratory study examining EGb 761® for chronic tinnitus over 24 weeks reported that at week 24, significant improvements were observed in all tinnitus-related outcomes compared to baseline; patients with high baseline anxiety or stress as well as those with normacusis improved more; the overall response rate was 18.8%; the results indicate that EGb 761® improved complaints in patients with chronic tinnitus, appearing to be particularly beneficial for patients with normal hearing and/or concomitant anxiety and/or stress.
Evidence strength: Preliminary and mixed. Some RCTs show statistically significant improvements in tinnitus-related quality of life measures with EGb 761®, but effect sizes are modest and the overall response rate in the 24-week study was below 20%. The EMA-sanctioned indication for tinnitus in elderly patients with long-standing symptoms is based on traditional use rather than established efficacy from high-quality RCTs.
This anti-inflammatory agent has been used for cerebrovascular disorders, peripheral circulatory insufficiency, geriatric complaints, and Alzheimer's disease. Controlled double-blind clinical studies have demonstrated the effectiveness of Ginkgo biloba in treating peripheral arterial insufficiency. Ginkgo biloba leaf extract is the most widely sold phytomedicine in Europe, where it is used to treat the symptoms of early-stage Alzheimer's disease, vascular dementia, peripheral claudication, and tinnitus of vascular origin.
Standardized extracts have been demonstrated in controlled clinical studies to improve cognitive functions, Alzheimer disease, vascular dementia, and peripheral vascular disorders; therapeutic effects have been confirmed in several meta-analyses and clinical use of standardized extracts is recommended by a number of learned societies as well as the WHO.
Evidence strength: The evidence for symptomatic benefit in intermittent claudication (peripheral arterial disease) is among the more consistently positive areas in the clinical literature, with support from multiple RCTs and meta-analyses, though the magnitude of benefit (increased pain-free walking distance) is generally modest.
Whereas cardiovascular diseases and cerebrovascular disorders are depicted in the Chinese Pharmacopoeia for Ginkgo leaf tablets, the European Herbal Monograph describes the use of G. biloba leaf extract-based herbal medicinal products for the improvement of (age-associated) cognitive impairment and of quality of life in mild dementia. G. biloba has been shown to protect against oxidative stress, inhibit platelet-activating factor (PAF), suppress inflammation, affect vascular smooth muscle, inhibit amyloid aggregation, and modulate gene expression.
Evidence strength: The cardiovascular evidence is largely mechanistic and derived from in vitro or animal studies, with limited robust human clinical trial data specifically evaluating hard cardiovascular endpoints (e.g., myocardial infarction, stroke prevention). Mechanistic plausibility is well established; clinical proof-of-concept in humans remains incomplete.
Research on flavonoid glycosides beyond the Ginkgo context — in particular flavone C-glycosides — reveals additional areas of investigated activity. The dietary flavonoids, especially their glycosides, are the most vital phytochemicals in diets and are of great general interest due to their diverse bioactivity. According to a review by Xiao et al. (2016), C-glycosyl flavonoids generally showed greater antioxidant and anti-diabetes effects than their equivalent O-glycosyl flavonoids and aglycones in vitro. However, these findings are in vitro only, and direct human clinical evidence for the anti-diabetic effects of flavone C-glycosides specifically is not yet established.
Among the flavonoid C-glycosides, flavone C-glycosides — especially vitexin, isoorientin, orientin, isovitexin, and their multiglycosides — are more frequently mentioned than others. These compounds are present in common dietary sources including passion flower (Passiflora spp.), hawthorn (Crataegus spp.), and various cereal plants, but their clinical evidence base is far less developed than that for ginkgo-derived flavoglycosides.
The following dosages are taken directly from cited sources and reflect only what has been reported in clinical studies or regulatory documents. They are not recommendations.
Ginkgo biloba leaves contain the potentially harmful phenolic acid ginkgolic acid, which may cause embryotoxicity, cytotoxicity, and neurotoxicity. These components are linked to adverse reactions such as allergies and toxic effects; according to the monograph of the German Commission E and WHO, the maximum safe concentration of ginkgolic acid is 5 µg/g. Ginkgo leaf also contains ginkgolic acid, a strong allergen; in assured extracts, levels are specified to be less than 5 parts per million. Products that are not standardized or verified may contain significantly higher levels.
Ginkgo may increase the risk of bleeding in people who are taking anticoagulant drugs such as warfarin, and may also interact with other drugs. Taking Ginkgo biloba with warfarin is specifically associated with increased risk for major bleeding events compared to warfarin alone. Preparations containing ginkgo might increase susceptibility to bleeding; the medicinal product should be discontinued as a precaution two weeks prior to surgery.
However, the picture from controlled studies is nuanced. Some writers hold the view that the combination of Ginkgo biloba with anticoagulant or antiplatelet drugs represents a serious health risk; such concerns are largely based on the assumption that ginkgo has clinically relevant antiplatelet activity, as well as accounts of bleeding episodes associated with ginkgo consumption; a review of controlled clinical studies and case reports found that results from controlled studies consistently indicate that ginkgo does not significantly impact haemostasis nor adversely affect the safety of co-administered aspirin or warfarin.
A large observational analysis of 2,647 prescriptions found that out of prescriptions meeting inclusion criteria, 342 exhibited drug interactions with a prevalence rate of 12.94%; Ginkgo biloba extract frequently interacts with antiplatelets, anticoagulants, and NSAIDs, with clopidogrel and aspirin exhibiting the highest prevalence rates of 2.61% each; however, interactions with anticoagulants including direct oral anticoagulants and acenocoumarol were not statistically significant. Significant correlations were found between Ginkgo biloba extract drug interactions and the bleeding risk (OR: 1.08, p < 0.001) and abnormal coagulation (OR: 1.49, p < 0.001).
Concomitant use of Ginkgo biloba preparations and efavirenz (a non-nucleoside reverse transcriptase inhibitor) is not recommended. The interaction is attributed partly to the effects of ginkgo constituents on cytochrome P450 enzymes responsible for efavirenz metabolism.
In patients with epilepsy, onset of further seizures promoted by intake of ginkgo preparations cannot be excluded; it has been argued that this might be associated with the 4'-O-methylpyridoxine content. This is a compound present in ginkgo seeds (and potentially in trace amounts in leaf preparations) that acts as a vitamin B6 antagonist.
Specific medications including clopidogrel, aspirin, celecoxib, loxoprofen, nifedipine, and omeprazole were significantly associated with the risk of bleeding and abnormal coagulation (p < 0.05) when used with Ginkgo biloba extract. Ginkgo biloba contains components that could cause drug interactions through multiple mechanisms, including effects on cytochrome isozymes and P-glycoprotein (P-gp).
The pharmacologic advantage of ginkgo seems to be a very tolerable side-effect profile, with a side-effect frequency at the placebo level. In the 2018 tinnitus RCT, 20 adverse events were documented in the EGb 761® group compared with 36 adverse events in the pentoxifylline group, and no serious adverse events were reported for EGb 761®. Ginkgo may be unsafe for use during pregnancy.
It is important to exercise caution when administering EGb to patients with bleeding disorders or those using NSAIDs, antiplatelet drugs, or anticoagulants.
Health conditions that Flavoglycosides may help support.
Body systems that Flavoglycosides may help support.
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