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Clinical data
AHFS/Drugs.comInternational Drug Names
  • not recommended
Routes of
Oral, intravenous
ATC code
Legal status
Legal status
  • OTC US, RX only Europe, not sold in Australia, Canada or New Zealand
Pharmacokinetic data
Bioavailability56.6 +/- 8.9%
Elimination half-life2.54 +/- 0.48 hours
CAS Number
PubChem CID
E number{{#property:P628}}
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Chemical and physical data
Molar mass350.454 g/mol
3D model (JSmol)
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Vinpocetine (brand names: Cavinton, Intelectol; chemical name: ethyl apovincaminate) is a semisynthetic derivative of the vinca alkaloid vincamine (sometimes described as "a synthetic ethyl ester of apovincamine"),[1] an extract from the lesser periwinkle plant. Vinpocetine was first isolated from the plant in 1975 by the Hungarian chemist Csaba Szántay. The mass production of the synthetic drug was started in 1978 by the Hungarian pharmaceutical company Richter Gedeon.

Vinpocetine is reported to have cerebral blood-flow enhancing[2] and neuroprotective effects,[3] and is used as a drug in Eastern Europe for the treatment of cerebrovascular disorders and age-related memory impairment.[4]

Vinpocetine is not approved in the United States for pharmaceutical use, but it can be sold as a dietary supplement. Vinpocetine is widely marketed as a supplement for vasodilation and as a nootropic for the improvement of memory and cerebral metabolism. Vinpocetine has been identified as a potent anti-inflammatory agent that might have a potential role in the treatment of Parkinson's disease and Alzheimer's disease.[5][6]

Controlled clinical trials

As of 2003 only three controlled clinical trials had tested "older adults with memory problems".[7] However, a 2003 Cochrane review determined that the results were inconclusive.[8]

Prior to 2003, a different study from 1985[9] had tested young, healthy adults, but this study had 12 subjects and used a short treatment period.[7]

Use as a vasodilator

Vinpocetine is widely used in the body building community as a vasodilator. Although no studies have been conducted on the effectiveness of vinpocetine on performance enhancement during exercise, both beneficial and adverse effects have been reported on body building forums.[citation needed]

Anticonvulsant potential

Kindling models in rats has shown Vinpocetine to exhibit anticonvulsant properties, the most pronounced anticonvulsant effects were observed in Pentylenetetrazole (PTZ)-kindled rats although there was also an effect on amygdala-kindled and neocortically-kindled rats.[10] Vinpocetine has also been shown to abolished [3H]Glu release after in vivo exposure to 4-aminopyridine (4-AP) which suggests an important mechanism for vinpocetine anticonvulsant potential.[11]

Anti-inflammatory action

Vinpocetine has been identified as a novel anti-inflammatory agent.[5][6] Vinpocetine inhibits the up-regulation of NF-κB by TNFα in various cell tests. Reverse transcription polymerase chain reaction also shows that it reduced the TNFα-induced expression of the mRNA of proinflammatory molecules such as interleukin-1 beta, monocyte chemoattractant protein-1 (MCP-1), and vascular cell adhesion molecule-1 (VCAM-1). In mice, vinpocetine reduced lipopolysaccharide inoculation induced polymorphonuclear neutrophil infiltration into the lung.[5][6] Neuroinflammatory processes can result in neuronal death in Parkinson's disease (PD) and Alzheimer's disease (AD). It has been suggested that "it would be interesting to test whether vinpocetine’s antiinflammatory properties would have a protective effect in models of neurodegenerative conditions such as AD and PD."[6]

Mechanism of action

Vinpocetine has been shown to selectively inhibit voltage-sensitive Na+ channels, resulting in a dose-dependent decrease in evoked extracellular Ca+ ions in striatal nerve endings.[12] The Na+ channel inhibiting properties of vinpocetine are thought to contribute to a general neuroprotective effect through blockade of excitotoxicity and attenuation of neuronal damage induced by cerebral ischemia/reperfusion.[13]

Vinpocetine is also a phosphodiesterase (PDE) type-1 inhibitor,[14] (with an IC50 of approximately 10−5 M.) leading to increases in intracellular levels of cyclic guanosine 3'5'-monophosphate (cGMP), an action that causes the vasorelaxant effects of vinpocetine on cerebral smooth muscle tissue.[15][16]

Independent of vinpocetine's action on PDE, vinpocetine inhibits IKK preventing IκB degradation and the following translocation of NF-κB to the cell nucleus.[5][6]

Increases in neuronal levels of DOPAC, a metabolic breakdown product of dopamine, have been shown to occur in striatal isolated nerve endings as a result of exposure to vinpocetine.[17] Such an effect is consistent with the biogenic pharmacology of reserpine, a structural relative of vinpocetine, which depletes catecholamine levels and causes depression as a side effect of the cardiovascular and anti-psychotic effects.[17] However, this effect tends to be reversible upon cessation of Vinpocetine administration, with full remission typically occurring within 3–4 weeks.

Side effects

Vinpocetine is generally well-tolerated in humans.[18] No serious side effects have thus far been noted in clinical trials,[19] although none of these trials were long-term.[8] Some users have reported headaches, especially at doses above 15 milligrams per day, as well as occasional upset stomach. Adverse drug-herb interactions have not been prevalent, and vinpocetine appears safe to take with other medications, including diabetes drugs, as well as blood thinners like Coumadin.[18] However, it should be carefully noted that the safety of vinpocetine in pregnant women has not been evaluated. Vinpocetine has been implicated in one case to induce agranulocytosis,[20] a condition in which granulocytes are markedly decreased. Some people have anecdotally noted that their continued use of vinpocetine reduces immune function. Commission E warned that vinpocetine reduced immune function and could cause apoptosis (cellular death) in the long term.[21]


  1. Lörincz C, Szász K, Kisfaludy L (1976). "The synthesis of ethyl apovincaminate". Arzneimittel-Forschung. 26 (10a): 1907. PMID 1037211.
  2. PMID 15760651 (PMID 15760651)
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  3. PMID 12498034 (PMID 12498034)
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  4. "Vinpocetine. Monograph" (PDF). Alternative Medicine Review. 7 (3): 240–3. 2002. PMID 12126465.
  5. 5.0 5.1 5.2 5.3 PMID 20448200 (PMID 20448200)
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  6. 6.0 6.1 6.2 6.3 6.4 PMID 20495091 (PMID 20495091)
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  7. 7.0 7.1 McDaniel MA, Maier SF, Einstein GO (2003). "'Brain-specific' nutrients: a memory cure?". Nutrition. 19 (11–12): 957–75. doi:10.1016/S0899-9007(03)00024-8. PMID 14624946.
  8. 8.0 8.1 Szatmari SZ, Whitehouse PJ (2003). Szatmári, Szabolcs, ed. "Vinpocetine for cognitive impairment and dementia". Cochrane Database of Systematic Reviews (1): CD003119. doi:10.1002/14651858.CD003119. PMID 12535455.
  9. Subhan Z, Hindmarch I (1985). "Psychopharmacological effects of vinpocetine in normal healthy volunteers". European Journal of Clinical Pharmacology. 28 (5): 567–71. doi:10.1007/BF00544068. PMID 3899677.
  10. Schmidt, J (1990). "Comparative studies on the anticonvulsant effectiveness of nootropic drugs in kindled rats". Biomedica biochimica acta. 49 (5): 413–9. PMID 2271012.
  11. Sitges, M; Sanchez-Tafolla, BM; Chiu, LM; Aldana, BI; Guarneros, A (2011). "Vinpocetine inhibits glutamate release induced by the convulsive agent 4-aminopyridine more potently than several antiepileptic drugs". Epilepsy research. 96 (3): 257–66. doi:10.1016/j.eplepsyres.2011.06.006. PMID 21737246.
  12. Sitges M, Galván E, Nekrassov V (2005). "Vinpocetine blockade of sodium channels inhibits the rise in sodium and calcium induced by 4-aminopyridine in synaptosomes". Neurochemistry International. 46 (7): 533–40. doi:10.1016/j.neuint.2005.02.001. PMID 15843047.
  13. Adám-Vizi V (2000). "[Neuroprotective effect of sodium channel blockers in ischemia: the pathomechanism of early ischemic dysfunction]". Orvosi Hetilap (in Hungarian). 141 (23): 1279–86. PMID 10905082.
  14. Hagiwara M, Endo T, Hidaka H (1984). "Effects of vinpocetine on cyclic nucleotide metabolism in vascular smooth muscle". Biochemical Pharmacology. 33 (3): 453–7. doi:10.1016/0006-2952(84)90240-5. PMID 6322804.
  15. Truss MC, Uckert S, Stief CG, Forssmann WG, Jonas U (1996). "Cyclic nucleotide phosphodiesterase (PDE) isoenzymes in the human detrusor smooth muscle. II. Effect of various PDE inhibitors on smooth muscle tone and cyclic nucleotide levels in vitro". Urological Research. 24 (3): 129–34. doi:10.1007/BF00304075. PMID 8839479.
  16. Gurkovskaia AV, Gokina NI, Buryĭ VA, Shuba MF (1987). "[Electrophysiological analysis of the action of kavinton on the smooth muscles]". Biulleten' Eksperimental'noĭ Biologii I Meditsiny (in Russian). 103 (1): 68–71. PMID 3801654.
  17. 17.0 17.1 Trejo F, Nekrassov V, Sitges M (2001). "Characterization of vinpocetine effects on DA and DOPAC release in striatal isolated nerve endings". Brain Research. 909 (1–2): 59–67. doi:10.1016/S0006-8993(01)02621-X. PMID 11478921.
  18. 18.0 18.1 "Is Vinpocetine the Answer to Brain Fog, Cognitive and Memory Problems?". Retrieved 2011-06-30.
  19. "Vinpocetine Side Effects and Warnings". foundhealth. Retrieved 2011-07-02.
  20. Shimizu Y, Saitoh K, Nakayama M, et al. Agranulocytosis induced by vinpocetine. Medicine Online, Retrieved March 08, 2008.
  21. The Complete German Commission E Monographs, Therapeutic Guide to Herbal Medicines, 1st ed. 1998, Integrative Medicine Communications, pub; Bk&CD-Rom edition, 1999.[page needed]

External links

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