“Ginkgo Biloba as a Thrombolytic Agent: Can It Replace Aspirin in Long-Term Therapy?”

Ginkgo biloba’s Possible Mechanism as Thrombolytic Agent

Ginkgo biloba has extended effect on blood clotting as compared to only platelet inhibiting action of aspirin. Laboratory and clinical studies suggest that the main constituents are Biflavones; specifically Ginkgetin and isoginkgetin can directly interfere with thrombin activity, and slow down the conversion of fibrinogen into fibrin and in that way it reduces clot formation. In addition to this, Ginkgo extracts have been shown to enhance plasminogen activation, which promotes the breakdown of existing fibrin clots. This effect of Ginkgo is very similar to that of established thrombolytic agents such as urokinase. Another important mechanism involves ginkgolide B; it is a strong antagonist of platelet-activating factor (PAF), which reduces platelet aggregation and prevents the early steps of blood clot development. Apart from these direct clot-related actions, Ginkgo also supports vascular health by improving nitric oxide synthesis and lowering the expression of adhesion molecules on blood vessel walls. These actions collectively reduce inflammation and make the vessels less prone to clot formation. Altogether, Ginkgo not only prevent the formation of new clots but also assists in breaking down those that have already formed, making it a unique and versatile agent when compared to aspirin.

Evidence from Clinical Studies

Some clinical studies have investigated, can Ginkgo biloba could match or at least non-inferior to aspirin in long-term vascular studies, particularly in stroke recovery and microcirculation disorders associated with diabetes.

In one real-world study from Xuanwu Hospital, China, 99 patients were enrolled to evaluate the effect of Ginkgo biloba extract (GBE) compared with aspirin. Patients with internal jugular venous stenosis received GBE alone, while those with acute ischemic stroke (AIS) were treated either with aspirin alone (100 mg/day) or in combination with GBE. The study found that GBE selectively inhibited arachidonic acid induced platelet aggregation and mildly prolonged clotting times. In AIS patients, adding GBE to aspirin enhanced inhibition of platelet aggregation more than aspirin alone, but this was also linked to a higher rate of minor bleeding events, though no major bleeding occurred. Beyond its antiplatelet effect, GBE also showed neuroprotective benefits, including improved neuronal survival and cognition after stroke, suggesting it may contribute to both vascular and cognitive recovery.

In another randomized, double-blind, placebo-controlled trial over four weeks, researchers compared taking a relatively high dose of standardized Ginkgo biloba extract (EGb 761, 300 mg/day) alongside a daily 325 mg aspirin regimen versus aspirin with placebo in older adults (average age 69 years) who had peripheral artery disease or cardiovascular risk factors. They tested platelet function using both the PFA-100 analyzer (with ADP as the agonist) and traditional aggregation assays (using ADP, epinephrine, collagen, and ristocetin). The results showed no statistically or clinically significant differences in platelet aggregation or function between the two groups, and reports of bleeding or bruising were rare and similar suggesting that, over four weeks, adding Ginkgo biloba didn’t alter aspirin’s effect on clotting or increase bleeding risk compared with aspirin alone.

One randomized, double-blind, placebo-controlled, crossover trial, 50 healthy volunteers received either Ginkgo biloba extract (EGb 761, 2×120 mg/day), aspirin (500 mg/day), or placebo for seven days, with a washout phase between treatments. Platelet aggregation was tested using arachidonic acid, ADP, collagen, and epinephrine as agonists. The results showed that aspirin strongly inhibited arachidonic acid–induced platelet aggregation, while Ginkgo biloba produced only a small and inconsistent effect, mainly reducing ADP-induced aggregation in some individuals. No clinically relevant bleeding events were observed. The findings suggest that, compared with aspirin, Ginkgo biloba has only weak and variable antiplatelet activity and is unlikely to serve as an effective substitute for aspirin in healthy individuals.

Even if above trials shows mixed results with some are showing strong beneficial effect of Ginkgo over aspirin; still Ginkgo biloba does not have large-scale clinical studies as compared to aspirin, specifically in acute coronary syndromes and cardiovascular mortality. Most of the available trials are smaller and focus on minor outcomes such as cerebral blood flow or platelet aggregation or cognitive measures rather than major endpoints like survival or major cardiac events. This space highlights the need for larger randomized trials before Ginkgo can be considered an alternative to aspirin in mainstream cardiovascular care.