Ginkgolide C

Ginkgolide C at a Glance

Ginkgolide C is a minor diterpene trilactone of Ginkgo biloba and the weakest PAF receptor antagonist of the ginkgolide series — roughly an order of magnitude less potent than ginkgolide B.

It is included in standardised ginkgo extracts as part of the terpene lactone fraction, and its evidence is preclinical.

What It's Used For

Ginkgolide C is one of the diterpene trilactones (the “ginkgolides”, A/B/C/J) that, with bilobalide, make up the terpene-lactone fraction of Ginkgo biloba leaf — see the ginkgolides class page. Within that series it is the minor, weakest congener: an extra 7β-hydroxyl makes it a substantially poorer platelet-activating-factor (PAF) antagonist than ginkgolide B, and it is also the poorest-absorbed of the group. The load-bearing point is that ginkgo’s human evidence rests on the standardized EGb 761 extract (and, for the class, an injectable ginkgolide mixture used in stroke), not on isolated ginkgolide C ^{6Reference 6DeFeudis FV · 2000Ginkgo biloba extract (EGb 761) and CNS functionsView study →}.

Its own literature is thin and preclinical, with a single genuinely ginkgolide-C-specific efficacy signal: in-vitro anti-adipogenic activity via AMPK.

Evidence by IndicationStrength of support · Beta

Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. No isolate human data, so scores stay low by design.

01Anti-adipogenic / metabolicShaky26%One 3T3-L1 AMPK study ^{1Reference 1Liou CJ et al. · 2015Ginkgolide C suppresses adipogenesis in 3T3-L1 adipocytes via the AMPK signalling pathwayView study →}

02PAF antagonism (anti-platelet)Shaky22%Class SAR + human PK; weak congener ^{2,3Reference 2Liu XW et al. · 2018Human pharmacokinetics of ginkgo terpene lactones and the impact of carboxylation in blood on their PAF-antagonistic activityView study →Reference 3Strømgaard K et al. · 2003Preparation of 7-substituted ginkgolide derivatives: potent platelet-activating-factor receptor antagonistsView study →}

03Glycinergic / CNS (mechanistic)Shaky14%Receptor SAR, no functional outcome ^{4Reference 4Chatterjee SS et al. · 2003Structure-activity studies with Ginkgo biloba extract constituents as receptor-gated chloride-channel blockers and modulatorsView study →}

Mechanisms

Pharmacokinetics

Ginkgolide C is a cage diterpene trilactone (C₂₀H₂₄O₁₁). It is the worst-absorbed of the ginkgolides: human data show apparent oral bioavailability of only 6–15% for ginkgolides C and J, versus >100% for A and B ^{2Reference 2Liu XW et al. · 2018Human pharmacokinetics of ginkgo terpene lactones and the impact of carboxylation in blood on their PAF-antagonistic activityView study →}. Terminal half-life is ~4–7 h with predominantly renal (glomerular-filtration) excretion, and the lactone ring hydrolyses/carboxylates in blood — lowering both exposure and PAF activity ^{2Reference 2Liu XW et al. · 2018Human pharmacokinetics of ginkgo terpene lactones and the impact of carboxylation in blood on their PAF-antagonistic activityView study →}. BBB penetration of the ginkgolides is limited and efflux-dominated, so the CNS relevance of its glycine/PAF activity is questionable ^{5Reference 5Ude C et al. · 2011AnimalPlasma and brain levels of terpene trilactones in rats after an oral single dose of standardised Ginkgo biloba extract EGb 761View study →}. Net: a minor, poorly-absorbed congener.

Clinical trials

There are no trials of isolated ginkgolide C. Ginkgo’s human evidence rests on the standardized EGb 761 extract; the ginkgolide-class human data (ischemic stroke) come from an injectable ginkgolide mixture, not this isolate. Human PK for ginkgolide C exists only as part of terpene-lactone profiling after extract dosing ^{2Reference 2Liu XW et al. · 2018Human pharmacokinetics of ginkgo terpene lactones and the impact of carboxylation in blood on their PAF-antagonistic activityView study →}.

Last checked: July 2026.

Toxicity & Safety

There are no toxicology signals for ginkgolide C itself, and the only practical concern is class-level and mechanism-based — a theoretical additive bleeding risk with antiplatelet or anticoagulant drugs — which its weak PAF potency and poor absorption make small.

Safety at a Glance

✅ Low / no toxicityBleeding risk

• No isolate toxicology signals. At the sub-percent levels found in standardized ginkgo extracts, the ginkgolides are well tolerated.
• Avoid the isolate in pregnancy and lactation. No reproductive data.
• Theoretical additive bleeding risk. PAF antagonism may add to antiplatelet and anticoagulant drugs, though ginkgolide C’s contribution is small.
• Not the same as ginkgolic acids. The allergenic ginkgo constituents are a separate issue and should not be confused with this compound.

Full Safety & Interactions Detail

Ginkgolide C carries a low flag: no isolate toxicology signals, and at the sub-percent levels present in standardized extracts the ginkgolides are well tolerated. The only practical caution is class-level and mechanism-based — PAF antagonism may add to antiplatelet/anticoagulant drugs (bleeding risk) — though ginkgolide C’s contribution is small given its weak PAF potency and poor absorption. It is not to be confused with the allergenic ginkgolic acids.

Dosage

There is no established human dose for isolated ginkgolide C, and none should be implied. It occurs only as a minor fraction of the ~5–7% terpene-trilactone content of standardized EGb 761 leaf extract (typically dosed 120–240 mg extract/day); all efficacy figures above are in-vitro concentrations, not doses.

References

1. Liou CJ, et al. (2015). Ginkgolide C suppresses adipogenesis in 3T3-L1 adipocytes via the AMPK signalling pathway. Evidence-Based Complementary and Alternative Medicine. https://pubmed.ncbi.nlm.nih.gov/26413119/
2. Liu XW, Yang JL, Niu W, et al. (2018). Human pharmacokinetics of ginkgo terpene lactones and the impact of carboxylation in blood on their PAF-antagonistic activity. Acta Pharmacologica Sinica. https://pubmed.ncbi.nlm.nih.gov/30054600/
3. Strømgaard K, et al. (2003). Preparation of 7-substituted ginkgolide derivatives: potent platelet-activating-factor receptor antagonists. Journal of Medicinal Chemistry. https://pubmed.ncbi.nlm.nih.gov/12570381/
4. Chatterjee SS, et al. (2003). Structure-activity studies with Ginkgo biloba extract constituents as receptor-gated chloride-channel blockers and modulators. Pharmacopsychiatry. https://pubmed.ncbi.nlm.nih.gov/13130392/
5. Ude C, Paulke A, Nöldner M, et al. (2011). Plasma and brain levels of terpene trilactones in rats after an oral single dose of standardised Ginkgo biloba extract EGb 761. Planta Medica. https://pubmed.ncbi.nlm.nih.gov/20814851/
6. DeFeudis FV, Drieu K (2000). Ginkgo biloba extract (EGb 761) and CNS functions. Current Drug Targets. https://pubmed.ncbi.nlm.nih.gov/11475535/

View all 6 references▾