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Ginkgo biloba
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Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
Not available
Mechanism
Two key active ingredients in ginkgo biloba are terpene lactones (notably ginkgo…
Food interactions
2 warnings
Human targets
8 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
80%
Studies assessed the pharmacokinetic parameters of terpene lactones, the main component of ginkgo biloba.…
Half-life
80 mg
Unpublished human data reports that after oral administration of 80 mg EGb 761, the half-life was four hours for ginkgolides A and six hours for ginkgolides B.…
Protein binding
No data available.
Volume of distribution
No data available.
Metabolism
In earlier studies, detectable urinary metabolites in healthy volunteers who ingested EGb were various benzoic acids, such as 4-hydroxybenzoic…
Elimination
72 hours
At 72 hours following oral administration in rats, about 38% of the ginkgo biloba extract was excreted via expiration, 22% was excreted in urine, and 29% was excreted in feces.…
Clearance
No data available.
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Nutraceutical
Biologic
About this compound
Ginkgo biloba extract contains a group of terpene lactones (notably, ginkgolides and diterpenes) and ginkgo flavone glycosides (notably, ginkgetin, bilobetin, and sciadopitysin) that have antioxidant and vasoactive properties.[A232389] Most of the studies that investigate the effect of ginkgo biloba use the standardized extract of Ginkgo biloba (EGb) 761 (EGb761), which was developed by a German pharmaceutical company in 1964.[A232404] EGb761 contains 6% terpene lactones and 24% flavonoid glycosides.[A232379] Flavonoids include quercetin, rutin, kaempferol, and isorhamnetin. Lactones include ginkgolide A, ginkgolide B, ginkgolide C, bilobalide, and ginkgotoxin, a lactone that is structurally related to [pyridoxine].[L32789] Ginkgo biloba is an herbal plant that is now cultivated worldwide. It is originally native to China, and ginkgo biloba extract has been used in traditional Chinese medicine for centuries.[A232389]
After its nootropic properties were discovered, ginkgo biloba has gained attention as a therapeutic ingredient for memory and concentration enhancement in cognitive impairment and neurogenerative diseases, such as dementia.[A232384] Ginkgo biloba was investigated in preliminary studies for a variety of therapeutic purposes such as improving cardiovascular health, sexual dysfunction, psychiatric disorders, skin disorders, and glaucoma. Ginkgo biloba is found in a number of homeopathic and over-the-counter herbal products and dietary supplements, but it has no approved therapeutic indications by regulatory bodies, such as the FDA, EMA, and Health Canada.[A232379] Ginkgo folium, the leaf extract of Ginkgo biloba, is considered an anti-dementia drug by the World Health Organization.[A232389]
After its nootropic properties were discovered, ginkgo biloba has gained attention as a therapeutic ingredient for memory and concentration enhancement in cognitive impairment and neurogenerative diseases, such as dementia.[A232384] Ginkgo biloba was investigated in preliminary studies for a variety of therapeutic purposes such as improving cardiovascular health, sexual dysfunction, psychiatric disorders, skin disorders, and glaucoma. Ginkgo biloba is found in a number of homeopathic and over-the-counter herbal products and dietary supplements, but it has no approved therapeutic indications by regulatory bodies, such as the FDA, EMA, and Health Canada.[A232379] Ginkgo folium, the leaf extract of Ginkgo biloba, is considered an anti-dementia drug by the World Health Organization.[A232389]
Properties:
solid
DrugBank indication
Ginkgo biloba does not currently have any approved therapeutic indications, and there is insufficient evidence to support its unapproved use.
[A232379]
It is available in over-the-counter herbal products mostly for oral use, to improve memory and cognitive problems.
[A232379]
It is available in over-the-counter herbal products mostly for oral use, to improve memory and cognitive problems.
Also known as(98)
Common ginkgo leaf
Ginkgo
Ginkgo biloba extract
Ginkgo biloba leaf
Ginkgo biloba leaf dry extract
Ginkgo biloba leaf tincture
Ginkgo extract
Ginkgo folium
Dosage forms(37)
Cream (Topical)
Solution / drops — 20 ml
Solution / drops — 50 ml
Tablet (Oral) — 80 mg
Tablet (Oral)
Tablet, film coated (Oral) — 240 MG
Tablet, film coated (Oral) — 40 MG
Tablet, film coated (Oral) — 80 MG
Drug interactions(735)
Known interactions with other medications. Always consult a healthcare professional.
Lomitapide
Moderate
The metabolism of Lomitapide can be decreased when combined with Ginkgo biloba.
Aminosalicylic acid
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Aminosalicylic acid.
Mesalazine
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Mesalazine.
Sulfasalazine
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Sulfasalazine.
Diflunisal
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Diflunisal.
Salicylic acid
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Salicylic acid.
Balsalazide
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Balsalazide.
Olsalazine
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Olsalazine.
Bismuth subsalicylate
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Bismuth subsalicylate.
Dersalazine
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Dersalazine.
Phenyl aminosalicylate
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Phenyl aminosalicylate.
Methyl salicylate
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Methyl salicylate.
Nitroaspirin
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Nitroaspirin.
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Aloxiprin.
Guacetisal
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Guacetisal.
Carbaspirin calcium
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Carbaspirin calcium.
Choline salicylate
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Choline salicylate.
Thiosalicylic acid
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Thiosalicylic acid.
Acetylsalicylic acid
Unknown severity
The risk or severity of bleeding can be increased when Ginkgo biloba is combined with Acetylsalicylic acid.
Dipyridamole
Moderate
The therapeutic efficacy of Ginkgo biloba can be decreased when used in combination with Dipyridamole.
Ginkgo biloba may increase the neuromuscular blocking activities of Ephedrine.
Bambuterol
Moderate
Ginkgo biloba may increase the neuromuscular blocking activities of Bambuterol.
Clevidipine
Moderate
Ginkgo biloba may increase the neuromuscular blocking activities of Clevidipine.
Ginkgo biloba may increase the neuromuscular blocking activities of Sar9, Met (O2)11-Substance P.
Mirabegron
Moderate
Ginkgo biloba may increase the neuromuscular blocking activities of Mirabegron.
Moxisylyte
Moderate
Ginkgo biloba may increase the neuromuscular blocking activities of Moxisylyte.
Ginkgo biloba may increase the neuromuscular blocking activities of Procaine.
Ginkgo biloba may increase the neuromuscular blocking activities of Cocaine.
Trimethaphan
Moderate
Ginkgo biloba may increase the neuromuscular blocking activities of Trimethaphan.
Doxacurium
Moderate
Ginkgo biloba may increase the neuromuscular blocking activities of Doxacurium.
Chloroprocaine
Moderate
Ginkgo biloba may increase the neuromuscular blocking activities of Chloroprocaine.
Tubocurarine
Moderate
Ginkgo biloba may increase the neuromuscular blocking activities of Tubocurarine.
Aclidinium
Moderate
Ginkgo biloba may increase the neuromuscular blocking activities of Aclidinium.
Butyrylthiocholine
Moderate
Ginkgo biloba may increase the neuromuscular blocking activities of Butyrylthiocholine.
Oxybuprocaine
Moderate
Ginkgo biloba may increase the neuromuscular blocking activities of Oxybuprocaine.
Benzonatate
Moderate
Ginkgo biloba may increase the neuromuscular blocking activities of Benzonatate.
The serum concentration of Efavirenz can be decreased when it is combined with Ginkgo biloba.
Ginkgo biloba may increase the anticoagulant activities of Lepirudin.
Bivalirudin
Moderate
Ginkgo biloba may increase the anticoagulant activities of Bivalirudin.
Ginkgo biloba may increase the anticoagulant activities of Alteplase.
Ginkgo biloba may increase the anticoagulant activities of Urokinase.
Ginkgo biloba may increase the anticoagulant activities of Reteplase.
Anistreplase
Moderate
Ginkgo biloba may increase the anticoagulant activities of Anistreplase.
Tenecteplase
Moderate
Ginkgo biloba may increase the anticoagulant activities of Tenecteplase.
Ginkgo biloba may increase the anticoagulant activities of Abciximab.
Drotrecogin alfa
Moderate
Ginkgo biloba may increase the anticoagulant activities of Drotrecogin alfa.
Streptokinase
Moderate
Ginkgo biloba may increase the anticoagulant activities of Streptokinase.
Dicoumarol
Moderate
Ginkgo biloba may increase the anticoagulant activities of Dicoumarol.
Argatroban
Moderate
Ginkgo biloba may increase the anticoagulant activities of Argatroban.
Ginkgo biloba may increase the anticoagulant activities of Ardeparin.
Showing 50 of 735 interactions
Food & lifestyle interactions
Advice
Avoid herbs and supplements with anticoagulant/antiplatelet activity. Additive anticoagulant/antiplatelet activity may increase the risk of bleeding. Examples include garlic, ginger, bilberry, danshen, piracetam, and ginkgo biloba.
Advice
Take with or without food. Food insignificantly decreases the rate of absorption.
Toxicity & overdose
Oral LD50 of standardized extract in mice is 7730 mg/kg, which corresponds to 2300 mg/kg of active ingredients, 1900 mg/kg of flavone glycosides, and 464 mg/kg of terpene lactones. Intravenous LD50 is 1100 mg/kg.
[L32779]
No case of overdose has been reported so far.
[L10247]
Cyanogenic glycosides found in raw ginkgo seeds are potentially toxic compounds; thus, contact or ingestion of ginkgo seeds can lead to serious reactions such as allergic skin reaction, including acute generalized exanthematous pustulosis, and convulsions. Ginkgo toxicity can manifest as bleeding, seizure, and serotonin syndrome.
As there is no known antidote for ginkgo toxicity, treatment includes discontinuation of ginkgo and symptomatic and supportive care.
[A232379]
Seizures may be attributed to ginkgotoxin, which can cause seizures at high doses.
[L32798]
[L32779]
No case of overdose has been reported so far.
[L10247]
Cyanogenic glycosides found in raw ginkgo seeds are potentially toxic compounds; thus, contact or ingestion of ginkgo seeds can lead to serious reactions such as allergic skin reaction, including acute generalized exanthematous pustulosis, and convulsions. Ginkgo toxicity can manifest as bleeding, seizure, and serotonin syndrome.
As there is no known antidote for ginkgo toxicity, treatment includes discontinuation of ginkgo and symptomatic and supportive care.
[A232379]
Seizures may be attributed to ginkgotoxin, which can cause seizures at high doses.
[L32798]
How it works
Mechanism of action
Two key active ingredients in ginkgo biloba are terpene lactones (notably ginkgolides and diterpenes) and ginkgo flavone glycosides (notably ginkgetin, bilobetin, and sciadopitysin), which are present at varying concentrations. Ginkgo biloba extract EGb 761 is the standardized extract of ginkgo biloba used in studies, which contains 6% terpenoids and 24% flavonoid glycosides. Animal studies have shown that ginkgo biloba works on several neurotransmitter pathways and brain structures. Flavones were shown to inhibit lipid peroxidation; inhibit the uptake of serotonin, dopamine, and norepinephrine; and inhibit platelet aggregation.[A232404] Terpene lactones may also act as potent antagonists of the platelet-activating factor and may possess anti-ischemic and fibrinolytic effects.[A232379] They were also shown to downregulate adrenal peripheral benzodiazepine receptors and increase adrenocorticotropic hormone levels.[A232404] Ginkgo biloba also reversibly inhibits monoamine oxidase A; and modestly inhibits anticholinesterase activity,[A232379][A232389] leading to enhanced cholinergic transmission in the brain.[A232394]
Several studies suggest that ginkgo biloba exerts neuroprotective effects by reducing free radical production in the prefrontal cortex, which may explain its improvement on short-term memory. Ginkgo biloba extract acts as a free radical scavenger, protecting neurons from oxidative damage and apoptosis related to aging, cerebral ischemia, and neurodegenerative disorders.[A232379] Ginkgo biloba also inhibits amyloid-β neurotoxicity and protects against hypoxic challenges and increased oxidative stress.[A232389] One study showed that bilobalide, a terpene lactone, delays the onset of hypoxic glycolysis.[A232404] Ginkgo biloba has the potential to regulate metabolism, stabilize the membrane, and promote vasodilation. In the arterial endothelium, EGb stimulated the release of endogenous relaxing factors, such as endothelium-derived relaxing factor and prostacyclin. In the inflammatory environment that causes tissue damage, EGb promoted nitric oxide production, leading to enhanced peripheral and cerebral blood flow.[A232379]
Several studies suggest that ginkgo biloba exerts neuroprotective effects by reducing free radical production in the prefrontal cortex, which may explain its improvement on short-term memory. Ginkgo biloba extract acts as a free radical scavenger, protecting neurons from oxidative damage and apoptosis related to aging, cerebral ischemia, and neurodegenerative disorders.[A232379] Ginkgo biloba also inhibits amyloid-β neurotoxicity and protects against hypoxic challenges and increased oxidative stress.[A232389] One study showed that bilobalide, a terpene lactone, delays the onset of hypoxic glycolysis.[A232404] Ginkgo biloba has the potential to regulate metabolism, stabilize the membrane, and promote vasodilation. In the arterial endothelium, EGb stimulated the release of endogenous relaxing factors, such as endothelium-derived relaxing factor and prostacyclin. In the inflammatory environment that causes tissue damage, EGb promoted nitric oxide production, leading to enhanced peripheral and cerebral blood flow.[A232379]
Pharmacodynamics
Ginkgo biloba is a herbal ingredient with demonstrated antioxidant, vasoactive, antiapoptotic, anti-inflammatory, antiplatelet, and fibrinolytic properties.[A232389][A232399] Ginkgo biloba has been investigated for use in a variety of medical conditions, but the most extensively studied area is in the context of cognitive impairment and neurodegenerative disorders. Ginkgo biloba was examined as a potential nootropic agent or cognitive enhancer but research findings supporting the therapeutic efficacy of ginkgo biloba extract (EGb) in dementia remain controversial. Some clinical studies of dementia that were up to one year long showed that EGb improves the cognitive performance and social functioning of patients. However, other studies did not support its clinical benefit for patients with cognitive impairment and dementia. Numerous meta-analysis studies showed insufficient evidence of the effectiveness of EGb in reducing both all-cause dementia incidence and Alzheimer's disease-associated dementia incidence in elderly patients with normal cognition or with mild cognitive impairment. Additionally, there is no up-to-date evidence that demonstrates the benefit of the long-term use of standardized EGb in reducing the risk of progression to Alzheimer's disease. A 2012 meta-analysis did not support the use of EGb in enhancing cognitive function in healthy adults.[A232379]
In the context of cardiovascular diseases, a limited number of studies showed that EGb improved mortality or neurological recovery in the post-stroke period, reduced cognitive and neurological impairment after acute ischemic stroke, and improved blood flow in the coronary artery in patients with coronary artery disease. However, a systemic review found no statistical or clinically significant benefit of EGb for patients with peripheral arterial disease or hypertension. Overall, there is a lack of strong evidence in the use of EGb for the treatment or prevention of cardiovascular diseases.[A232379]
In a small trial, the use of EGb as an adjunctive treatment with citalopram improved depressive symptoms and cognitive function in patients with depression.[A232379] Ginkgo biloba was also investigated as a potential treatment for antidepressant-induced sexual dysfunction.[A2434] Another study showed EGb improving the symptoms of tardive dyskinesia. There is insufficient evidence to prove the effectiveness of EGb in these psychiatric disorders. Limited studies have investigated the role of ginkgo biloba in the treatment of vertigo, tinnitus, vitiligo, macular degeneration, and glaucoma, as well as the prevention of acute mountain sickness. As results are either preliminary or controversial, more quality research is warranted.[A232379]
In the context of cardiovascular diseases, a limited number of studies showed that EGb improved mortality or neurological recovery in the post-stroke period, reduced cognitive and neurological impairment after acute ischemic stroke, and improved blood flow in the coronary artery in patients with coronary artery disease. However, a systemic review found no statistical or clinically significant benefit of EGb for patients with peripheral arterial disease or hypertension. Overall, there is a lack of strong evidence in the use of EGb for the treatment or prevention of cardiovascular diseases.[A232379]
In a small trial, the use of EGb as an adjunctive treatment with citalopram improved depressive symptoms and cognitive function in patients with depression.[A232379] Ginkgo biloba was also investigated as a potential treatment for antidepressant-induced sexual dysfunction.[A2434] Another study showed EGb improving the symptoms of tardive dyskinesia. There is insufficient evidence to prove the effectiveness of EGb in these psychiatric disorders. Limited studies have investigated the role of ginkgo biloba in the treatment of vertigo, tinnitus, vitiligo, macular degeneration, and glaucoma, as well as the prevention of acute mountain sickness. As results are either preliminary or controversial, more quality research is warranted.[A232379]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Studies assessed the pharmacokinetic parameters of terpene lactones, the main component of ginkgo biloba. Following oral administration of ginkgo biloba solution, the mean absolute bioavailability was 80% for ginkgolide A, 88% for ginkgolide B and 79% for biloalide.
[L10247]
In an early rat study, about 60% of radiolabeled EGb 761 was absorbed with a Tmax of 1.5 hours. The highest amount of radioactivity was measured in the stomach and small intestine.
[L32779]
In another study, after a single oral dose of 120 mg EGb 761 in healthy volunteers, Cmax was 22.22 ± 4.57 ng/mL for ginkgolide A, 8.27 ± 1.82 ng/mL for ginkgolide B, and 54.42 ± 13.62 ng/mL for biloalide.
AUC0-∞ was 121.35 ± 22.92 ng × h/mL for ginkgolide A, 59.88 ± 11.39 ng × h/mL for ginkgolide B, and 217.24 ± 44.07 ng × h/mL for biloalide. Tmax ranged from 1.17 to 1.54 hours for those three compounds.
[L10247]
[L10247]
In an early rat study, about 60% of radiolabeled EGb 761 was absorbed with a Tmax of 1.5 hours. The highest amount of radioactivity was measured in the stomach and small intestine.
[L32779]
In another study, after a single oral dose of 120 mg EGb 761 in healthy volunteers, Cmax was 22.22 ± 4.57 ng/mL for ginkgolide A, 8.27 ± 1.82 ng/mL for ginkgolide B, and 54.42 ± 13.62 ng/mL for biloalide.
AUC0-∞ was 121.35 ± 22.92 ng × h/mL for ginkgolide A, 59.88 ± 11.39 ng × h/mL for ginkgolide B, and 217.24 ± 44.07 ng × h/mL for biloalide. Tmax ranged from 1.17 to 1.54 hours for those three compounds.
[L10247]
Half-life
Unpublished human data reports that after oral administration of 80 mg EGb 761, the half-life was four hours for ginkgolides A and six hours for ginkgolides B. The half-life of bilobalide was three hours after administration of 120 mg EGb 761 extract.
[L32779]
[L32779]
Protein binding
No data available.
Volume of distribution
No data available.
Metabolism
In earlier studies, detectable urinary metabolites in healthy volunteers who ingested EGb were various benzoic acids, such as 4-hydroxybenzoic acid conjugate, 4-hydroxyhippuric acid, 3-methoxy-4-hydroxyhippuric acid, 3,4-dihydroxybenzoic acid, 4-hydroxybenzoic acid, hippuric acid, and 3-methoxy-4-hydroxybenzoic acid (vanillic acid).
[L32789]
[L32789]
Route of elimination
At 72 hours following oral administration in rats, about 38% of the ginkgo biloba extract was excreted via expiration, 22% was excreted in urine, and 29% was excreted in feces. About 70% of ginkgolides A, 50% of ginkgolides B, and 30% of bilobalide were excreted unchanged in the urine.
[L32779]
[L32779]
Clearance
No data available.
Drug targets(8)
Proteins and enzymes this drug interacts with in the body
Sodium-dependent noradrenaline transporter
SLC6A2
inhibitor
Specific functionactin binding
Cellular location
Cell membrane
General function & pharmacology
Mediates sodium- and chloride-dependent transport of norepinephrine (also known as noradrenaline), the primary signaling neurotransmitter in the autonomic sympathetic nervous system .
PMID:2008212 PMID:8125921 PMID:38750358
Is responsible for norepinephrine re-uptake and clearance from the synaptic cleft, thus playing a crucial role in norepinephrine inactivation and homeostasis (By similarity). Can also mediate sodium- and chloride-dependent transport of dopamine PMID:11093780 PMID:8125921 PMID:39395208 PMID:39048818
PMID:2008212 PMID:8125921 PMID:38750358
Is responsible for norepinephrine re-uptake and clearance from the synaptic cleft, thus playing a crucial role in norepinephrine inactivation and homeostasis (By similarity). Can also mediate sodium- and chloride-dependent transport of dopamine PMID:11093780 PMID:8125921 PMID:39395208 PMID:39048818
Phospholipase A2, membrane associated
PLA2G2A
inhibitor
Specific functioncalcium ion binding
Cellular location
Secreted
General function & pharmacology
Secretory calcium-dependent phospholipase A2 that primarily targets extracellular phospholipids with implications in host antimicrobial defense, inflammatory response and tissue regeneration .
PMID:10455175 PMID:10681567 PMID:2925633
Hydrolyzes the ester bond of the fatty acyl group attached at sn-2 position of phospholipids (phospholipase A2 activity) with preference for phosphatidylethanolamines and phosphatidylglycerols over phosphatidylcholines .
PMID:10455175 PMID:10681567
Contributes to lipid remodeling of cellular membranes and generation of lipid mediators involved in pathogen clearance. Displays bactericidal activity against Gram-positive bacteria by directly hydrolyzing phospholipids of the bacterial membrane .
PMID:10358193 PMID:11694541
Upon sterile inflammation, targets membrane phospholipids of extracellular mitochondria released from activated platelets, generating free unsaturated fatty acids such as arachidonate that is used by neighboring leukocytes to synthesize inflammatory eicosanoids such as leukotrienes. Simultaneously, by compromising mitochondrial membrane integrity, promotes the release in circulation of potent damage-associated molecular pattern molecules that activate the innate immune response .
PMID:25082876
Plays a stem cell regulator role in the intestinal crypt.
Within intracellular compartment mediates Paneth cell differentiation and its stem cell supporting functions by inhibiting Wnt signaling pathway in intestinal stem cell (ICS). Secreted in the intestinal lumen upon inflammation, acts in an autocrine way and promotes prostaglandin E2 synthesis that stimulates Wnt signaling pathway in ICS cells and tissue regeneration (By similarity). May play a role in the biosynthesis of N-acyl ethanolamines that regulate energy metabolism and inflammation.
Hydrolyzes N-acyl phosphatidylethanolamines to N-acyl lysophosphatidylethanolamines, which are further cleaved by a lysophospholipase D to release N-acyl ethanolamines .
PMID:14998370
Independent of its catalytic activity, acts as a ligand for integrins .
PMID:18635536 PMID:25398877
Binds to and activates integrins ITGAV:ITGB3, ITGA4:ITGB1 and ITGA5:ITGB1 .
PMID:18635536 PMID:25398877
Binds to a site (site 2) which is distinct from the classical ligand-binding site (site 1) and induces integrin conformational changes and enhanced ligand binding to site 1 .
PMID:25398877
Induces cell proliferation in an integrin-dependent manner PMID:18635536
PMID:10455175 PMID:10681567 PMID:2925633
Hydrolyzes the ester bond of the fatty acyl group attached at sn-2 position of phospholipids (phospholipase A2 activity) with preference for phosphatidylethanolamines and phosphatidylglycerols over phosphatidylcholines .
PMID:10455175 PMID:10681567
Contributes to lipid remodeling of cellular membranes and generation of lipid mediators involved in pathogen clearance. Displays bactericidal activity against Gram-positive bacteria by directly hydrolyzing phospholipids of the bacterial membrane .
PMID:10358193 PMID:11694541
Upon sterile inflammation, targets membrane phospholipids of extracellular mitochondria released from activated platelets, generating free unsaturated fatty acids such as arachidonate that is used by neighboring leukocytes to synthesize inflammatory eicosanoids such as leukotrienes. Simultaneously, by compromising mitochondrial membrane integrity, promotes the release in circulation of potent damage-associated molecular pattern molecules that activate the innate immune response .
PMID:25082876
Plays a stem cell regulator role in the intestinal crypt.
Within intracellular compartment mediates Paneth cell differentiation and its stem cell supporting functions by inhibiting Wnt signaling pathway in intestinal stem cell (ICS). Secreted in the intestinal lumen upon inflammation, acts in an autocrine way and promotes prostaglandin E2 synthesis that stimulates Wnt signaling pathway in ICS cells and tissue regeneration (By similarity). May play a role in the biosynthesis of N-acyl ethanolamines that regulate energy metabolism and inflammation.
Hydrolyzes N-acyl phosphatidylethanolamines to N-acyl lysophosphatidylethanolamines, which are further cleaved by a lysophospholipase D to release N-acyl ethanolamines .
PMID:14998370
Independent of its catalytic activity, acts as a ligand for integrins .
PMID:18635536 PMID:25398877
Binds to and activates integrins ITGAV:ITGB3, ITGA4:ITGB1 and ITGA5:ITGB1 .
PMID:18635536 PMID:25398877
Binds to a site (site 2) which is distinct from the classical ligand-binding site (site 1) and induces integrin conformational changes and enhanced ligand binding to site 1 .
PMID:25398877
Induces cell proliferation in an integrin-dependent manner PMID:18635536
Glycine receptor subunit alpha-1
GLRA1
antagonist
Specific functionextracellularly glycine-gated chloride channel activity
Cellular location
Postsynaptic cell membrane
General function & pharmacology
Subunit of heteromeric glycine-gated chloride channels .
PMID:14551753 PMID:23994010 PMID:25730860 PMID:37821459
Plays an important role in the down-regulation of neuronal excitability .
PMID:8298642 PMID:9009272
Contributes to the generation of inhibitory postsynaptic currents .
PMID:25445488
Channel activity is potentiated by ethanol .
PMID:25973519
Potentiation of channel activity by intoxicating levels of ethanol contribute to the sedative effects of ethanol (By similarity)
PMID:14551753 PMID:23994010 PMID:25730860 PMID:37821459
Plays an important role in the down-regulation of neuronal excitability .
PMID:8298642 PMID:9009272
Contributes to the generation of inhibitory postsynaptic currents .
PMID:25445488
Channel activity is potentiated by ethanol .
PMID:25973519
Potentiation of channel activity by intoxicating levels of ethanol contribute to the sedative effects of ethanol (By similarity)
Gamma-aminobutyric acid receptor subunit alpha-1
GABRA1
negative modulator
Specific functionGABA-A receptor activity
Cellular location
Postsynaptic cell membrane
General function & pharmacology
Alpha subunit of the heteropentameric ligand-gated chloride channel gated by Gamma-aminobutyric acid (GABA), a major inhibitory neurotransmitter in the brain .
PMID:23909897 PMID:25489750 PMID:29950725 PMID:30602789
GABA-gated chloride channels, also named GABA(A) receptors (GABAAR), consist of five subunits arranged around a central pore and contain GABA active binding site(s) located at the alpha and beta subunit interface(s) .
PMID:29950725 PMID:30602789
When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient .
PMID:23909897 PMID:29950725 PMID:30602789
Alpha-1/GABRA1-containing GABAARs are largely synaptic (By similarity). Chloride influx into the postsynaptic neuron following GABAAR opening decreases the neuron ability to generate a new action potential, thereby reducing nerve transmission (By similarity). GABAARs containing alpha-1 and beta-2 or -3 subunits exhibit synaptogenic activity; the gamma-2 subunit being necessary but not sufficient to induce rapid synaptic contacts formation .
PMID:23909897 PMID:25489750
GABAARs function also as histamine receptor where histamine binds at the interface of two neighboring beta subunits and potentiates GABA response (By similarity).
GABAARs containing alpha, beta and epsilon subunits also permit spontaneous chloride channel activity while preserving the structural information required for GABA-gated openings (By similarity). Alpha-1-mediated plasticity in the orbitofrontal cortex regulates context-dependent action selection (By similarity). Together with rho subunits, may also control neuronal and glial GABAergic transmission in the cerebellum (By similarity)
PMID:23909897 PMID:25489750 PMID:29950725 PMID:30602789
GABA-gated chloride channels, also named GABA(A) receptors (GABAAR), consist of five subunits arranged around a central pore and contain GABA active binding site(s) located at the alpha and beta subunit interface(s) .
PMID:29950725 PMID:30602789
When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient .
PMID:23909897 PMID:29950725 PMID:30602789
Alpha-1/GABRA1-containing GABAARs are largely synaptic (By similarity). Chloride influx into the postsynaptic neuron following GABAAR opening decreases the neuron ability to generate a new action potential, thereby reducing nerve transmission (By similarity). GABAARs containing alpha-1 and beta-2 or -3 subunits exhibit synaptogenic activity; the gamma-2 subunit being necessary but not sufficient to induce rapid synaptic contacts formation .
PMID:23909897 PMID:25489750
GABAARs function also as histamine receptor where histamine binds at the interface of two neighboring beta subunits and potentiates GABA response (By similarity).
GABAARs containing alpha, beta and epsilon subunits also permit spontaneous chloride channel activity while preserving the structural information required for GABA-gated openings (By similarity). Alpha-1-mediated plasticity in the orbitofrontal cortex regulates context-dependent action selection (By similarity). Together with rho subunits, may also control neuronal and glial GABAergic transmission in the cerebellum (By similarity)
Gamma-aminobutyric acid receptor subunit beta-2
GABRB2
negative modulator
Specific functionchloride channel activity
Cellular location
Postsynaptic cell membrane
General function & pharmacology
Beta subunit of the heteropentameric ligand-gated chloride channel gated by gamma-aminobutyric acid (GABA), a major inhibitory neurotransmitter in the brain .
PMID:19763268 PMID:27789573 PMID:29950725 PMID:8264558
GABA-gated chloride channels, also named GABA(A) receptors (GABAAR), consist of five subunits arranged around a central pore and contain GABA active binding site(s) located at the alpha and beta subunit interface(s) .
PMID:29950725
When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient (By similarity). Chloride influx into the postsynaptic neuron following GABAAR opening decreases the neuron ability to generate a new action potential, thereby reducing nerve transmission (By similarity). GABAARs containing alpha-1 and beta-2 or -3 subunits exhibit synaptogenic activity; the gamma-2 subunit being necessary but not sufficient to induce rapid synaptic contacts formation .
PMID:23909897 PMID:25489750
Extrasynaptic beta-2 receptors contribute to the tonic GABAergic inhibition (By similarity).
Beta-containing GABAARs can simultaneously bind GABA and histamine where histamine binds at the interface of two neighboring beta subunits, which may be involved in the regulation of sleep and wakefulness (By similarity)
PMID:19763268 PMID:27789573 PMID:29950725 PMID:8264558
GABA-gated chloride channels, also named GABA(A) receptors (GABAAR), consist of five subunits arranged around a central pore and contain GABA active binding site(s) located at the alpha and beta subunit interface(s) .
PMID:29950725
When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient (By similarity). Chloride influx into the postsynaptic neuron following GABAAR opening decreases the neuron ability to generate a new action potential, thereby reducing nerve transmission (By similarity). GABAARs containing alpha-1 and beta-2 or -3 subunits exhibit synaptogenic activity; the gamma-2 subunit being necessary but not sufficient to induce rapid synaptic contacts formation .
PMID:23909897 PMID:25489750
Extrasynaptic beta-2 receptors contribute to the tonic GABAergic inhibition (By similarity).
Beta-containing GABAARs can simultaneously bind GABA and histamine where histamine binds at the interface of two neighboring beta subunits, which may be involved in the regulation of sleep and wakefulness (By similarity)
Metabolizing enzymes(5)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CYP2C9Cytochrome P450 2C9
inhibitor
CYP3A4Cytochrome P450 3A4
inhibitor
inducer
CYP1B1Cytochrome P450 1B1
inhibitor
CYP1A1Cytochrome P450 1A1
inhibitor
CYP1A2Cytochrome P450 1A2
inhibitor
Scientific references(7)
Cohen A.J., Bartlik B.
Ginkgo biloba for antidepressant-induced sexual dysfunction.
Journal of Sex & Marital Therapy
199824(2):139-143. doi: 10.1080/00926239808404927
Nguyen T., Alzahrani T.
CHEMICAL CONSTITUENTS OF GINKGO BILOBA. Ginkgo Biloba. 2000;:142-182.
doi: 10
1201/9780203304945-15
Brondino N., De Silvestri A., Re S., Lanati N., Thiemann P., Verna A., Emanuele E., Politi P.
A Systematic Review and Meta-Analysis of Ginkgo biloba in Neuropsychiatric Disorders: From Ancient Tradition to Modern-Day Medicine.
Evid Based Complement Alternat Medicine
20132013:915691. doi: 10.1155/2013/915691. Epub 2013 May 28
Silberstein R.B., Pipingas A., Song J., Camfield D.A., Nathan P.J., Stough C.
Examining brain-cognition effects of ginkgo biloba extract: brain activation in the left temporal and left prefrontal cortex in an object working memory task.
Evid Based Complement Alternat Medicine
20112011:164139. doi: 10.1155/2011/164139. Epub 2011 Aug 18
Diamond B.J., Bailey M.R.
Ginkgo biloba: indications, mechanisms, and safety.
Psychiatr Clinical North American
2013 Mar36(1):73-83. doi: 10.1016/j.psc.2012.12.006
Diamond B.J., Shiflett S.C., Feiwel N., Matheis R.J., Noskin O., Richards J.A., Schoenberger N.E.
Ginkgo biloba extract: mechanisms and clinical indications.
Arch Phys Medicine Rehabil
2000 May81(5):668-78. doi: 10.1016/s0003-9993(00)90052-2
Field B.H., Vadnal R.
Ginkgo biloba and Memory: An Overview.
Nutr Neurosci
19981(4):255-67. doi: 10.1080/1028415X.1998.11747236
ATC classification(2 codes)
ATC N06DX02
ATC N06DA53
Affected organisms(1)
Humans and other mammals
Commercial products(17)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Ginkgo biloba
Additional database identifiers
Drugs Product Database (DPD)
1522
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11048
GenAtlas
SLC6A2
GeneCards
SLC6A2
GenBank Gene Database
M65105
GenBank Protein Database
189258
Guide to Pharmacology
926
UniProt Accession
SC6A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9031
GenAtlas
PLA2G2A
GeneCards
PLA2G2A
GenBank Gene Database
M22430
GenBank Protein Database
190889
Guide to Pharmacology
1417
UniProt Accession
PA2GA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4326
GenAtlas
GLRA1
GeneCards
GLRA1
GenBank Gene Database
X52009
GenBank Protein Database
31851
Guide to Pharmacology
423
UniProt Accession
GLRA1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4075
GenAtlas
GABRA1
GeneCards
GABRA1
GenBank Gene Database
X13584
GenBank Protein Database
31631
Guide to Pharmacology
404
UniProt Accession
GBRA1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4082
GenAtlas
GABRB2
GeneCards
GABRB2
GenBank Gene Database
S67368
GenBank Protein Database
455946
UniProt Accession
GBRB2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4087
GeneCards
GABRG2
GenBank Gene Database
X15376
GenBank Protein Database
31637
UniProt Accession
GBRG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6833
GenAtlas
MAOA
GeneCards
MAOA
GenBank Gene Database
M68840
GenBank Protein Database
187353
Guide to Pharmacology
2489
UniProt Accession
AOFA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7873
GenAtlas
NOS2A
GeneCards
NOS2
GenBank Gene Database
L09210
GenBank Protein Database
292242
Guide to Pharmacology
1250
UniProt Accession
NOS2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2597
GenAtlas
CYP1B1
GeneCards
CYP1B1
GenBank Gene Database
U03688
GenBank Protein Database
501031
Guide to Pharmacology
1320
UniProt Accession
CP1B1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2595
GeneCards
CYP1A1
GenBank Gene Database
K03191
GenBank Protein Database
181276
Guide to Pharmacology
1318
UniProt Accession
CP1A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_HUMAN
International reference pricing
9 formulations
Reference pricing from DrugBank. Prices are indicative and may not reflect current UK costs.
From $0.03/capsule
To $0.24/tablet
Pv ginkgo biloba capsule
$0.03/capsule
Ginkgo biloba 30 mg capsule
$0.04/capsule
Ginkgo biloba 50 mg tablet
$0.09/tablet
Ginkgo biloba 60 mg capsule
$0.10/capsule
Ra ginkgo biloba 40 mg tablet
$0.11/tablet
Source: DrugBank. Used under CC BY-NC 4.0 academic licence for non-commercial purposes.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 27 days ago(8 Mar 2026)