RESEARCH MONOGRAPH · KDC-MN-305

Vinpocetine

May 9, 2026 Kodiac biolabs Research Revised May 30, 2026 3 min read

Plain-language summary Intrigue 50 / 100

Vinpocetine (Cavinton) is a synthetic alkaloid derived from vincamine in the lesser periwinkle plant, developed at Gedeon Richter in Hungary in the 1960s. Approved across Europe for cerebrovascular insufficiency and used as a nootropic in the US (sold as a supplement). It works through several mechanisms at once: cerebral vasodilation, weak phosphodiesterase 1 inhibition, neuronal sodium channel block, and modest antioxidant activity, with the combined effect of improving blood flow to the brain. Clinical evidence in cognitive impairment and stroke recovery is mixed and dominated by older Eastern European trials with weak methodology. The FDA flagged it in 2019 over concerns about miscarriage in pregnant users. Not stocked by Kodiac. This monograph is provided for research and educational reference.

Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.

Synthetic vincamine derivative / cerebrovascular agent

A synthetic alkaloid derivative of vincamine from Vinca minor; a cerebrovascular agent and PDE1 inhibitor used as a nootropic.

Abstract

Vinpocetine ((3-alpha,16-alpha)-eburnamenine-14-carboxylic acid ethyl ester; CAS 42971-09-5; molecular formula C22H26N2O2; molecular weight 350.46) is a synthetic alkaloid derivative of vincamine from Vinca minor (lesser periwinkle), developed at Gedeon Richter (Hungary) in the 1960s and approved in many European countries as Cavinton for cerebrovascular insufficiency. Mechanism is multifactorial: cerebral vasodilation through smooth muscle relaxation, weak phosphodiesterase 1 (PDE1) inhibition, sodium channel block in neurons, and modest antioxidant activity. The combined effect produces improved cerebral blood flow and reduced ischemic neuronal injury in animal stroke models. Plasma half-life is approximately 1 to 2 hours; metabolism is hepatic via CYP2C9 and CYP3A4. Approved indications in Europe include cerebrovascular disorders, age-related cognitive decline, and tinnitus. In the US, the compound is sold as a dietary supplement with FDA reservations about that designation given its drug-like history. Used as a cerebrovascular nootropic and PDE1 inhibitor in research.

Mechanism of action

Cerebral vasodilation; weak PDE1 inhibition; sodium channel block; modest antioxidant activity. Improves cerebral blood flow.

Reported research dose ranges

Clinical 5 to 10 mg in the published literature. Rodent studies 1 to 10 mg/kg.

References

  1. Bonoczk P, et al. Role of sodium channel inhibition in neuroprotection: effect of vinpocetine. Brain Res Bull 2000.
  2. Patyar S, et al. Role of vinpocetine in cerebrovascular diseases. Pharmacol Rep 2011.
  3. Szilagyi G, et al. Effects of vinpocetine on the redistribution of cerebral blood flow and glucose metabolism in chronic ischemic stroke. J Neurol Sci 2005.

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KDC-MN-305

The full reference document is provided strictly for research use only. It reports research dose ranges from the published literature, not instructions for use in humans or animals.

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FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.