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muscle guy posingAfter piracetam, vinpocetine (ethyl-apovincaminate, 14,-ethoxycarbonyl-(3alpha, 16alpha-ethyl)-14, 15-eburnamine) is perhaps the most well-known nootropic and is regarded by some as more important [1]. First synthesized about forty years ago, vinpocetine is a derivative of vincamine, which is found in the periwinkle plant (Vinca minor). Other compounds in the vinca alkaloid family include vinburnine, vintoperol and brovincane [2]. After being synthesized in Hungary, the neuroprotective and nootropic properties of vinpocetine were discovered, and appeared under the name Cavinton in 1978. Since that point, it has been used in over 40 countries including Japan, Hungary, Germany, Poland and Russia, primarily for the treatment and prevention of stroke and other cerebrovascular diseases [3-4]. This article will discuss the experimental and clinical research, safety and ideal use of this compound.


In 1955, Vincamine was first extracted in large quantities from the leaves of the periwinkle plant, and in 1959 it was used to treat cerebrovascular disorders. Various active derivatives have been discovered and it is thought that the fused, five-membered eburnane ring system is responsible for the pharmacological activity of these compounds [2]. Vinpocetine is a cis (3S, 16S)-derivative of vincamine, and is the strongest derivative discovered so far. A related compound, vintoperol (the trans (3S, 16R)-derivative), increases blood flow in the lower extremities (whereas vinpocetine primarily enhances cerebral blood flow), but produces some toxic side effects [5].

Animal Studies

Extensive animal research has been conducted on vinpocetine’s therapeutic effects. It has been found to have neuroprotective and memory-enhancing effects and other beneficial properties.

Much of the research has focused on vinpocetine’s effects on hypoxia (low oxygen supply) and ischemia (low blood supply), both of which are commonly seen during strokes. In a rat model of central ischemia, 77% of hippocampal neurons were damaged, and administration of vinpocetine reduced this damage to 37%. This effect has been replicated, both in rats and other animals, and in other areas of the brain [1, 6]. Vinpocetine’s neuroprotective effect in rats subjected to middle cerebral artery (MCA) occlusion was found to be over twice as effective as other neuroprotectants (nimodipine, MK-801) [7].

Vinpocetine is also neuroprotective in many other situations. It protects against excitotoxicity induced by glutamate and N-methyl-D-aspartate (NMDA), and is equally as effective as nimodipine [7]. In rats subjected to radiation, it increases cerebral blood flow and improves central energy metabolism [8]. In cells treated with beta-amyloid, vinpocetine improved mitochondrial function, oxidative stress, and other signs of toxicity [9].

In animal models, vinpocetine also improves learning and memory. In one study, vinpocetine improved recall on a passive avoidance test [1]. In others, it protected against the deficits caused by scopolamine and hypoxia induced by various means [10].

Vinpocetine may have effects on a wider population than just those that are subjected to brain damage or other injury. To test this, vinpocetine’s effects on astrocytes under normal conditions were measured. Vinpocetine significantly increased mitochondrial function and reduced lactate dehydrogenase release while increasing intracellular ATP and phosphocreatine (PCr) concentrations and cell proliferation [11]. If these effects hold true in in vivo situations, vinpocetine has the potential to improve brain function in normal individuals.

Human Studies

There is a significant body of evidence indicating that vinpocetine has beneficial effects in humans. Some of the research is discussed by McDaniel et al. [1]. In three controlled trials involving individuals with memory dysfunction of various origins, vinpocetine improved attention, concentration and memory. In two of these studies, vinpocetine caused a 3.1-5.1 improvement relative to placebo on the Mini-Mental Status Questionnaire (scale of 39), which measures spatial and temporal orientation skills, mathematical ability, short-term memory and knowledge of synonyms and antonyms. In one study, 87% of patients were rated as improved (11% with placebo), while in another, 21% were rated as strongly improved (7% with placebo).

These results are similar to those found by other researchers. A meta-analysis of six studies in patients with “degenerative senile cerebral dysfunction” (total of 731 patients) found that vinpocetine had a highly significant effect on tests of speech and movement capacity, muscular coordination and strength, and perceptual ability [6]. However, the research on patients with Alzheimer’s has not been promising. A one-year open-label study with 15 patients found no improvement [1, 6]. Given the small number of patients, the statistical power of this study was small. Still, it may be that vinpocetine is primarily useful in situations with less cognitive impairment.

Vinpocetine could have multiple benefits for stroke patients. These include increased cerebral blood flow, decreased platelet aggregability, and direct neuroprotective effects [12]. PET studies in chronic stroke patients indicate that vinpocetine increases cerebral glucose uptake and metabolism. In a trial with 15 chronic ischemic stroke patients, two weeks of vinpocetine treatment significantly increased cerebral blood flow [6]. Other studies have demonstrated improved cerebral glucose metabolism, oxygenation, and blood flow in stroke patients as well [13]. However, there is not yet enough research to demonstrate improved outcomes in stroke patients given vinpocetine [6].

Vinpocetine has also been examined in the treatment of hearing loss. It is associated with significant improvement of tinnitus (ear ringing) after acoustic trauma, indicating that it may protect against noise-induced hearing loss [6]. It also improved hearing function in patients with tuberculosis [14]. These results are in line with experimental studies, which have found vinpocetine to prevent ototoxicity.

Little research has examined vinpocetine’s effects in healthy humans. In one study, 20 healthy females (age 25-40) were given either 10, 20, or 40 mg of vinpocetine or placebo for a three day periods in crossover fashion. On the third day of each period, the subjects underwent a variety of psychological tests. On the Sternberg Memory Scanning Test, in which subjects decide whether a digit was contained in a previously displayed set of 1-3 digits, 40 mg vinpocetine significantly increased performance compared to the other groups. No effects were found on other psychological parameters, including performance on a choice reaction time task [1, 15]. It is difficult to draw conclusions from this study because of the short treatment periods, but it does suggest that vinpocetine can improve cognition in at least some ways in healthy individuals.

In another study, two weeks of a combined supplement of ginkgo and vinpocetine improved reaction time and working memory in healthy adults [16]. However, one cannot know whether this effect was due to ginkgo, vinpocetine, or the combination.

Dosage & Safety

Like other nootropics, vinpocetine is exceptionally safe. Side effects are not noted with a greater incidence than placebo in most studies, and no significant side effects have been noted with dosages up to 360 mg daily [1, 17]. Some studies have reported flushing, rashes, or minor gastrointestinal discomfort, but these were not a cause for patient dropouts [6]. The only concern is that vinpocetine decreases platelet aggregation, so it should not be used—or only used with a high amount of caution—with blood thinners [1, 6].

The study in healthy humans gives us a good idea of what vinpocetine’s ideal dosage should be, which is definitely over 20 mg daily (since 20 mg was not effective, whereas 40 mg was). Similarly, a meta-analysis of Italian and German studies found that 30 mg daily was superior to 15 mg daily [10]. A study in patients with cognitive impairment found that 30 mg daily and 60 mg daily were both effective [1]. These studies place the probable ideal dosage of vinpocetine at 30-40 mg daily. Indeed, most studies use a dosage of 30 mg daily [6].

Like the other nootropics we have discussed, vinpocetine displays a bell-shaped dose-response curve [1]. For this reason, one should use an effective dose and no more.

Vinpocetine’s absorption in a fasted state is approximately 6.7% [12]. However, if it is taken with food, this increases to 60-100% [10]. For this reason, it is essential to take vinpocetine with a meal. The primary metabolites are apovincaminic acid and ethanol (not enough to cause a noticeable effect) [18]. Due to vinpocetine’s low oral bioavailability, transdermal administration has been explored. A delivery system consisting of 1% vinpocetine, 4% oleic acid, 20% PEG-40 hydrogenated castor oil, 10% purified diethylene glycol monoethyl ether, and 65% distilled water (w/w) has been described [19]. However, given that vinpocetine’s desirable dosage can easily be reached at an affordable price, transdermal administration should not be necessary.

After consumption, vinpocetine reaches the bloodstream within a few minutes, crosses the blood-brain barrier, and is present in the brain in 10 minutes [20]. Vinpocetine tends to concentrate itself in the brain, with the concentration about twice the expected level, indicating preferential uptake [6, 13]. After oral administration to healthy volunteers in one study, maximum CNS levels were seen 100 minutes after administration, and at the 110 minute point a gradual decrease began [13, 21]. According to another article, maximum levels are reached an hour after administration, and the majority is eliminated by the 8 hour point [10]. The reported half-life ranges from 1-2 to almost 5 hours [10, 18]. In any case, it is generally recommended to take vinpocetine three times a day to maintain adequate levels of the compound.


The present research with vinpocetine is promising, and it makes a worthwhile addition to a nootropic stack. Unlike many other nootropics, research exists indicating that it improves cognition in some ways in healthy individuals. The ideal dosage is 10-15 mg three times daily. Part II will explore vinpocetine’s mechanism of action.

For questions or comments regarding this article, email [email protected].


1. Nutrition. 2003 Nov-Dec;19(11-12):957-75. “Brain-specific” nutrients: a memory cure? McDaniel MA, Maier SF, Einstein GO.

2. J Chromatogr A. 2003 May 9;996(1-2):195-203. Lipophilicity of vinpocetine and related compounds characterized by reversed-phase thin-layer chromatography. Karoly M, Vamos J, Nemes A, Racz A, Noszal B.

3. Altern Med Rev. 2002 Jun;7(3):240-3. Vinpocetine. Monograph. [No authors listed]

4. Acta Neurol Scand. 2002 Dec;106(6):325-32. PET studies on the brain uptake and regional distribution of [11C]vinpocetine in human subjects. Gulyas B, Halldin C, Sandell J, Karlsson P, Sovago J, Karpati E, Kiss B, Vas A, Cselenyi Z, Farde L.

5. Acta Pharm Hung. 2002;72(1):25-36. [Investigation of vasoactive agents with indole skeletons at Richter Ltd.] [Article in Hungarian]. Karpati E, Biro K, Kukorelli T.

6. Eur J Pharmacol. 2003 Apr 25;467(1-3):103-9. Pharmacological evidence for a correlation between hippocampal CA1 cell damage and hyperlocomotion following global cerebral ischemia in gerbils. Katsuta K, Umemura K, Ueyama N, Matsuoka N.

7. Acta Pharm Hung. 2002;72(2):84-91. [Neuroprotective effects of vinpocetine in vivo and in vitro. Apovincaminic acid derivatives as potential therapeutic tools in ischemic stroke] [Article in Hungarian]. Dezsi L, Kis-Varga I, Nagy J, Komlodi Z, Karpati E.

8. Eksp Klin Farmakol. 2003 Sep-Oct;66(5):14-6. [Effect of vinpocetine on cerebral circulation in rats after exposure to radiation] [Article in Russian]. Vereshchagin VK.

9. Free Radic Res. 2000 Nov;33(5):497-506. Vinpocetine attenuates the metabolic dysfunction induced by amyloid beta-peptides in PC12 cells. Pereira C, Agostinho P, Oliveira CR.

10. Brain Res Bull. 2000 Oct;53(3):245-54. Role of sodium channel inhibition in neuroprotection: effect of vinpocetine. Bonoczk P, Gulyas B, Adam-Vizi V, Nemes A, Karpati E, Kiss B, Kapas M, Szantay C, Koncz I, Zelles T, Vas A.

11. Neurotoxicology. 2002 May;23(1):19-31. Piracetam and vinpocetine exert cytoprotective activity and prevent apoptosis of astrocytes in vitro in hypoxia and reoxygenation. Gabryel B, Adamek M, Pudelko A, Malecki A, Trzeciak HI.

12. Chem Pharm Bull (Tokyo). 2003 Aug;51(8):914-22. Investigation and physicochemical characterization of vinpocetine-sulfobutyl ether beta-cyclodextrin binary and ternary complexes. Ribeiro L, Loftsson T, Ferreira D, Veiga F.

13. J Neurol Sci. 2002 Nov 15;203-204:259-62. Clinical and non-clinical investigations using positron emission tomography, near infrared spectroscopy and transcranial Doppler methods on the neuroprotective drug vinpocetine: a summary of evidences. Vas A, Gulyas B, Szabo Z, Bonoczk P, Csiba L, Kiss B, Karpati E, Panczel G, Nagy Z.

14. Vestn Otorinolaringol. 2003;(3):35-40. [Cavinton prevention of neurosensory hypoacousis in patients with different forms of tuberculosis] [Article in Russian]. Maliavina US, Ovchinnikov IuM, Fasenko VP, Maliev BM, Kalinina MV, Dadasheva BB.

15. Eur J Clin Pharmacol. 1985;28(5):567-71. Psychopharmacological effects of vinpocetine in normal healthy volunteers. Subhan Z, Hindmarch I.

16. Hum Psychopharmacol. 2001 Jul;16(5):409-416. Cognitive effects of a Ginkgo biloba/vinpocetine compound in normal adults: systematic assessment of perception, attention and memory. Polich J, Gloria R.

17. World J Urol. 2001 Nov;19(5):344-50. Phosphodiesterase 1 inhibition in the treatment of lower urinary tract dysfunction: from bench to bedside. Truss MC, Stief CG, Uckert S, Becker AJ, Wefer J, Schultheiss D, Jonas U.

18. Nucl Med Biol. 2002 Oct;29(7):753-9. Cerebral uptake of [ethyl-11C]vinpocetine and 1-[11C]ethanol in cynomolgous monkeys: a comparative preclinical PET study. Gulyas B, Vas A, Halldin C, Sovago J, Sandell J, Olsson H, Fredriksson A, Stone-Elander S, Farde L.

19. Pharmazie. 2004 Apr;59(4):274-8. Preparation and evaluation of microemulsion of vinpocetine for transdermal delivery. Hua L, Weisan P, Jiayu L, Hongfei L.

20. Orv Hetil. 2003 Nov 16;144(46):2271-6. [Human positron emission tomography with oral 11C-vinpocetine] [Article in Hungarian]. Vas A, Christer H, Sovago J, Johan S, Cselenyi Z, Kiss B, Karpati E, Lars F, Gulyas B.

21. Eur J Nucl Med Mol Imaging. 2002 Aug;29(8):1031-8. Epub 2002 May 07. Drug distribution in man: a positron emission tomography study after oral administration of the labelled neuroprotective drug vinpocetine. Gulyas B, Halldin C, Sovago J, Sandell J, Cselenyi Z, Vas A, Kiss B, Karpati E, Farde L.

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