| Candidate ID: | R0506 |
| Source ID: | DB01381 |
| Source Type: | approved; investigational; nutraceutical |
| Compound Type: |
biotech
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| Compound Name: |
Ginkgo biloba
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| Synonyms: |
Common ginkgo leaf; Ginkgo; Ginkgo biloba extract; Ginkgo biloba leaf; Ginkgo biloba leaf dry extract; Ginkgo biloba leaf tincture; Ginkgo extract; Ginkgo folium; Ginkgo leaf; Ginkgo macrophylla leaf; Maidenhair extract; Maidenhair tree leaf; Pterophyllus salisburiensis leaf; Salisburia adiantifolia leaf; Salisburia biloba leaf; Salisburia ginkgo leaf; Salisburia macrophylla leaf; Tanakan; Yinxingye
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| Molecular Formula: |
--
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| SMILES: |
--
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| DrugBank Description: |
_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. 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. EGb761 contains 6% terpene lactones and 24% flavonoid glycosides. 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 . _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.
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. _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. _Ginkgo folium_, the leaf extract of _Ginkgo biloba_, is considered an anti-dementia drug by the World Health Organization.
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| CAS Number: |
90045-36-6
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| Molecular Weight: |
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| DrugBank Indication: |
_Ginkgo biloba_ does not currently have any approved therapeutic indications, and there is insufficient evidence to support its unapproved use. It is available in over-the-counter herbal products mostly for oral use, to improve memory and cognitive problems.
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| DrugBank Pharmacology: |
_Ginkgo biloba_ is a herbal ingredient with demonstrated antioxidant, vasoactive, antiapoptotic, anti-inflammatory, antiplatelet, and fibrinolytic properties. _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.
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.
In a small trial, the use of EGb as an adjunctive treatment with citalopram improved depressive symptoms and cognitive function in patients with depression. _Ginkgo biloba_ was also investigated as a potential treatment for antidepressant-induced sexual dysfunction. 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.
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| DrugBank MoA: |
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. Terpene lactones may also act as potent antagonists of the platelet-activating factor and may possess anti-ischemic and fibrinolytic effects. They were also shown to downregulate adrenal peripheral benzodiazepine receptors and increase adrenocorticotropic hormone levels. _Ginkgo biloba_ also reversibly inhibits monoamine oxidase A; and modestly inhibits anticholinesterase activity, leading to enhanced cholinergic transmission in the brain.
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. _Ginkgo biloba_ also inhibits amyloid-β neurotoxicity and protects against hypoxic challenges and increased oxidative stress. One study showed that bilobalide, a terpene lactone, delays the onset of hypoxic glycolysis. _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.
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| Targets: |
Sodium-dependent noradrenaline transporter inhibitor; Phospholipase A2, membrane associated inhibitor; Glycine receptor subunit alpha-1 antagonist; Gamma-aminobutyric acid receptor subunit alpha-1 negative modulator; Gamma-aminobutyric acid receptor subunit beta-2 negative modulator; Gamma-aminobutyric acid receptor subunit gamma-2 negative modulator; Amine oxidase [flavin-containing] A inhibitor; Nitric oxide synthase, inducible inhibitor
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| Inclusion Criteria: |
Therapeutic strategy associated
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