A reference work, not a recommendation to use: this profile describes mechanism and evidence and does not replace medical advice. The claims come from marketing and forums and are tested here, not endorsed.

Mechanism of action

Evidence map: Ginkgo biloba

Each line stands for a published finding; line style and color show where it comes from. The filter hides weaker evidence levels. Sources: see references.

Standardized ginkgo leaf extract has been used for decades to improve blood flow and treat dementia. It contains numerous flavonoids and terpenoids; in studies that are mostly animal experiments, it acts on cerebral blood flow, neurotransmitter systems, the cellular redox state, and nitric oxide [1]. The terpene lactone bilobalide inhibited GABA-A receptors (α1β2γ2L) in the laboratory with an IC50 of 4.6 µM, almost as strongly as the classic blockers bicuculline and picrotoxinin [2].

For healthy people, the evidence is clearly negative: a meta-analysis of RCTs found effect sizes near zero for memory (13 studies), executive functions, and attention, regardless of age, duration, and amount [3]. A six-week RCT with 230 cognitively healthy people over 60 years showed no benefit in any test [4]. Ginkgo was also useless for prevention: in the GEM study with 3069 people aged 75 and older, no fewer people developed dementia with ginkgo than with placebo [5], and neither did they in the French GuidAge study with 2854 people with memory complaints [6].

In existing dementia, a Cochrane review with 82 studies found possible small to moderate benefits in global impression, cognition, and daily function after six months, but with low certainty and large heterogeneity; in mild cognitive impairment, there was hardly any effect [7]. A long-term feeding study by the US National Toxicology Program found more liver tumors in mice and changes in the liver and thyroid in rats; the extract was mutagenic in bacterial tests [8].

Synaptik serves solely to explain biochemistry and pharmacology and is not medical advice or a recommendation to take anything.

Mechanism of action only. Schematic cross-section of a GABAergic synapse, not to scale; below, the GABA-A receptor α1β2γ2 seen from above with its binding sites. Particle numbers, opening times, speeds and the bars of the live readout are outputs of an illustrative model, not measurements. In the side view the binding sites are placed schematically; the top view shows the interfaces.
Drug
View

GABA  Cl⁻  K⁺  drug (shape per site)  rings = binding sites

The terpene lactone bilobalide from ginkgo leaves inhibited recombinant α1β2γ2L receptors in frog oocytes with an IC50 of 4.6 µM, almost as potently as the classical blockers bicuculline and picrotoxinin. It acted mainly non-competitively, with a competitive component at high GABA concentrations [18]. The source does not define a binding site, so the particles stay near the receptor. Whether ginkgo extracts act like this in humans has not been shown.

Tap or focus a labelled part for a short explanation.

Also acting here, not drawn

  • Ashwagandha: extract; partial agonist only in frog oocytes, binding site unresolved
  • Cortexin: only a binding screen
  • Fasoracetam: only changed receptor expression
  • IDRA-21: GABA currents enhanced only in cell culture; mainly an AMPA modulator
  • Magnesium glycinate: concerns only the glycine part; the only evidence is a review on glycine
  • Nefiracetam: affinity reported only in a review
  • Selank: binding site unresolved

Targets

TargetTypeActionKey dataEvidence
GABA-A receptor (α1β2γ2L) by bilobalideReceptorAntagonistIC50 4.6 µM (laboratory) Laboratory[2]

Effect profile

Which signaling systems the compound affects according to current data. ↑ enhanced, ↓ dampened, ≈ modulated, ○ no effect; dots = evidence level.

  • Dopamineno data
  • Noradrenalineno data
  • Serotoninno data
  • Acetylcholineno data
  • Glutamate · AMPAno data
  • Glutamate · NMDAno data
  • GABA↓ · Bilobalide inhibits GABA-A receptors in the laboratory[2]
  • Histamineno data
  • Orexinno data
  • Adenosineno data
  • Opioidsno data
  • Melatoninno data
  • Neurotrophinsno data
  • Blood flow↑ · greater cerebral blood flow, nitric oxide altered (mainly animal data according to the review)[1]
  • Nitric oxideno data
  • Energy metabolismno data
  • Insulin · glucoseno data
  • Inflammation · oxidative↓ · Influence on the redox state of cells (mainly animal data according to the review)[1]
  • Stress axisno data
  • Testosterone axisno data
  • Endocannabinoidsno data
  • Autophagy · senescenceno data
  • Immune systemno data
  • Lipid metabolismno data
  • Coagulation · fibrinolysisno data
  • Methylationno data

Human studies

  • Meta-analysis in healthy people

    Meta-analysis of RCTs · healthy · n = 1132 · varied

    Measured: Memory, executive function, attention

    Result: Effect sizes near zero: memory d = −0.04, executive function d = −0.05, attention d = −0.08.[3]

    Human, randomised

  • Memory in healthy older adults

    RCT, double-blind, placebo-controlled · healthy (over 60 years) · n = 230 · 6 weeks

    Measured: neuropsychological tests, self- and informant ratings

    Result: No difference in any endpoint.[4]

    Human, randomised

  • GEM: dementia prevention

    RCT, double-blind, placebo-controlled · healthy or mild cognitive impairment (75 years and older) · n = 3069 · median 6.1 years

    Measured: new dementia, Alzheimer’s disease

    Result: No protection: HR 1.12 (95% CI 0.94–1.33) for dementia.[5]

    Human, randomised

  • GuidAge: Alzheimer’s prevention

    RCT, double-blind, placebo-controlled · People aged 70 and older with memory complaints · n = 2854 · 5 years

    Measured: Conversion to probable Alzheimer’s dementia

    Result: No significant difference (HR 0.84; 95% CI 0.60–1.18); funded by Ipsen.[6]

    Human, randomised

  • Cochrane review, cognitive impairment and dementia

    systematic review of 82 studies · Patients: subjective complaints, MCI, dementia · n = 10613 · mostly up to 6 months

    Measured: Global impression, cognition, daily living, adverse effects

    Result: MCI: hardly any effect; dementia: possible small to moderate benefits, low certainty.[7]

    Human, randomised

Risks and warnings

  • Bleeding

    In the GuidAge study with 2854 participants, strokes and other bleeding and cardiovascular events over five years did not differ from placebo [6].

    Human, randomised

  • Tumors in long-term animal experiments

    Mice developed more liver tumors after two years of administration, rats showed changes in the liver and thyroid; the extract was mutagenic in bacterial tests. Transferability to humans is unclear [8].

    Animal study

  • Adverse events

    In MCI and dementia, hardly any differences from placebo; in subjective complaints, possibly more adverse events in one study [7].

    Human, randomised

Fact check: common claims

  • refuted

    “Ginkgo improves memory and concentration in healthy people”

    Meta-analysis of RCTs with effect sizes near zero [3]; RCT in 230 healthy older adults without an effect [4].

  • refuted

    “Ginkgo prevents dementia”

    Two large, multiyear RCTs found no protection [5][6].

  • partly supported

    “Ginkgo helps in existing dementia”

    Cochrane: possible small to moderate benefits in dementia, but low certainty and large heterogeneity [7].

  • partly supported

    “Ginkgo improves cerebral blood flow”

    Described mainly in animal studies [1]; a benefit for cognition in healthy people does not follow from this [3].

Pharmacokinetics

Absorption
By mouth as a standardized extract.
Half-life
Not verified.
Metabolism
Not verified.
Entry into the brain
Not verified.

Legal status

Germany
Not verified.
EU
Not verified.
USA
Widely used as an herbal dietary supplement to support mental performance [8].
Other countries
Standardized extracts have been used therapeutically for decades, including in dementia [1]; country-specific information not checked.

Related compounds

Bacopa monnierisame classVinpocetinsame class (German only)

Open questions

  • Which components of the extract are responsible for the effects in animal experiments?
  • How relevant are the tumor findings in the long-term animal experiment for humans?
  • Are there subgroups with dementia who reliably benefit?

References

  1. Ahlemeyer B, Krieglstein J. Neuroprotective effects of Ginkgo biloba extract. Cell Mol Life Sci. 2003;60(9):1779–92. doi:10.1007/s00018-003-3080-1 · PubMed
  2. Huang SH, Duke RK, Chebib M, Sasaki K, Wada K, Johnston GA. Bilobalide, a sesquiterpene trilactone from Ginkgo biloba, is an antagonist at recombinant alpha1beta2gamma2L GABA(A) receptors. Eur J Pharmacol. 2003;464(1):1–8. doi:10.1016/s0014-2999(03)01344-x · PubMed
  3. Laws KR, Sweetnam H, Kondel TK. Is Ginkgo biloba a cognitive enhancer in healthy individuals? A meta-analysis. Hum Psychopharmacol. 2012;27(6):527–33. doi:10.1002/hup.2259 · PubMed
  4. Solomon PR, Adams F, Silver A, Zimmer J, DeVeaux R. Ginkgo for memory enhancement: a randomized controlled trial. JAMA. 2002;288(7):835–40. doi:10.1001/jama.288.7.835 · PubMed
  5. DeKosky ST, Williamson JD, Fitzpatrick AL, Kronmal RA, Ives DG, Saxton JA, et al. Ginkgo biloba for prevention of dementia: a randomized controlled trial. JAMA. 2008;300(19):2253–62. doi:10.1001/jama.2008.683 · PubMed
  6. Vellas B, Coley N, Ousset PJ, Berrut G, Dartigues JF, Dubois B, et al. Long-term use of standardised Ginkgo biloba extract for the prevention of Alzheimer’s disease (GuidAge): a randomised placebo-controlled trial. Lancet Neurol. 2012;11(10):851–9. doi:10.1016/S1474-4422(12)70206-5 · PubMed
  7. Wieland LS, Ludeman E, Chi Y, Feinberg TM, Chen IH, Chen KH, et al. Ginkgo biloba for cognitive impairment and dementia. Cochrane Database Syst Rev. 2026;2:CD013661. doi:10.1002/14651858.CD013661.pub2 · PubMed
  8. National Toxicology Program. Toxicology and carcinogenesis studies of Ginkgo biloba extract (CAS No. 90045-36-6) in F344/N rats and B6C3F1/N mice (gavage studies). Natl Toxicol Program Tech Rep Ser. 2013;(578):1–183. PubMed
How this profile was checked

Last reviewed: 2026-10-23. All sources with a DOI or PMID were resolved automatically via Crossref or doi.org and PubMed.

Translated from the German profile (version of 2026-10-23); translation checked on 2026-10-26.

Checked

  • All DOIs resolved via Crossref, PMIDs match the DOIs; [8] without a DOI, via PMID only.
  • From the abstracts: constituents, effects mainly in animal experiments [1]; IC50 4.6 µM [2]; d = −0.04/−0.05/−0.08, 1132 participants for memory [3]; 230 people, no difference [4]; 3069 people, HR 1.12 [5]; 2854 people, HR 0.84, no differences in bleeding, funding by Ipsen [6]; 82 studies, 10,613 participants, results by group [7]; composition, liver tumors in mice, thyroid, mutagenicity [8].
  • ClinicalTrials.gov: 145 entries for ginkgo (October 23, 2026).

Not verified

  • Approval status of standardized extracts in Germany and the EU (medicinal products) not checked in registers.
  • Interactions (e.g., with anticoagulants) were not researched separately; the bleeding risk is documented only via GuidAge.
  • Pharmacokinetics of ginkgolides and flavonoids in humans.

No dosages, no sources of supply. This information does not replace medical advice.

Spotted an error or missing something?

Request a compound, suggest an improvement or report an error. Every message is read.

Type of message

The website stores nothing. The button opens your email app with a pre-filled message.