Health Care Professional Information

Scientific Name
(14-ethoxycarbonyl-(3a,16a-ethyl)-14,15eburnamine)
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Common Name

Kavinton, Rgh-4405, Tcv-3B

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Brand Name

Cavinton

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Clinical Summary

Vinpocetine is derived from vincamine, an alkaloid found in the common periwinkle plant. Originally developed in Europe where it is marketed as a drug called Cavinton, vinpocetine is sold in the United States as a dietary supplement to improve brain function. Studies show that vinpocetine enhances short-term memory (2), cognitive performance (3), and improves chronic cerebral dysfunction in elderly patients (4). It has also been studied as a potential treatment for Alzheimer's disease (5) but a systematic review did not find evidence of its benefits (6).
Parenteral administration followed by oral administration of vinpocetine significantly maintained beneficial hemorheologic changes in stroke patients in a recent clinical trial (1).

In animal studies, vinpocetine potentiates the effects of radiation therapy in tumor cells (7). There is no evidence of vinpocetine's anticancer effects in humans.
Vinpocetine should not be confused with chemotherapy drugs such as vincristine or vinblastine, which are also alkaloids derived from the periwinkle plant.

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Purported Uses
  • Alzheimer's disease
  • Cognitive decline
  • Dementia
  • Stroke
  • Vasoconstriction
  • Cancer treatment
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Constituents

Vinpocetine is a synthetic ethyl ester of apovincamine derived from an alkaloid from the common periwinkle plant (1).

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Mechanism of Action

Vinpocetine has been shown to possess antioxidant and hydroxyl radical scavenging properties in vitro (8) (9). It inhibits phosphodiesterase 1 (PDE1) activity and improves cerebral blood flow by elevating cGMP and cAMP, by increasing mitochondrial function and also by improving glucose and oxygen utilization by the brain. Vinpocetine helps improve spatial memory in rats through its ability to prevent neuronal damage and to favorably modulate cholinergic function (8). In an animal study, it increased cerebral microcirculation and blood flow by inhibiting platelet aggregation. Administration of vinpocetine to chronic stroke patients increased glucose uptake and release in unaffected areas of the brain (6). Vinpocetine does not possess systemic circulatory effects or any effects on heart rate or blood pressure (10). It demonstrated antiepileptic effects by suppressing the abnormal neuronal excitability through the regulation of sodium channels and release of dopamine in the striatal nerve endings (11) (12) (13). Vinpocetine can increase the effects of radiation by increasing tumor oxygenation (7). It also shows anti-inflammatory effects by inhibiting TNF-alpha-induced NF-kappaB activities (14).

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Pharmacokinetics

Vinpocetine is absorbed in the small intestine and transported to the liver via portal circulation. Absorption is 60% when taken with food and 7% on empty stomach. Plasma levels of vinpocetine peak approximately 1 to 1.5 hours after ingestion. The elimination half-life is 1 to 2 hours and it is non-detectable in plasma 2-3 hours after ingestion. From the liver vinpocetine is distributed via systemic circulation to various tissues including the brain. In the liver, it is metabolized to the inactive apovincaminic acid, which is the major metabolite excreted in the urine (10).

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Adverse Reactions

Rare: Flushing, rashes, gastrointestinal problems (15), hypotension (16) (17)
Case Report: A 73 year-old man developed agranulocytosis after using vinpocetine for 50 days. His symptoms resolved after discontinuing vinpocetine (18).

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Herb-Drug Interactions
  • Anticoagulants/antiplatelet agents: Vinpocetine may have additive effects and can increase risk of bleeding.
  • Antihypertensive agents: Vinpocetine may increase hypotensive effects.
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Herb Lab Interactions
  • May decrease red blood cell aggregation (9).
  • May reduce plasma and whole blood viscosity (9).
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Literature Summary and Critique

Feher G, Koltai K, Kesmarky G, et al. Effect of parenteral or oral vinpocetine on the hemorheological parameters of patients with chronic cerebrovascular diseases. Phytomedicine. 2009;16(2-3):111-7.
In this study 40 patients with ischemic cardiovascular disease were administered high-dose parenteral vinpocetine gradually increasing to 1mg/kg/day. Patients underwent stroke > three months prior to the beginning of the study. Hemorheological parameters including plasma fibrinogen, whole blood viscosity, red blood cell aggregation, deformability, and hematocrit were assessed at one and three months. Additionally, 20 patients received 30mg of vinpocetine orally for three months with those receiving placebo serving as controls. High-dose parenteral administration of vinpocetine for 7 days significantly reduced whole blood and plasma viscosity and red blood cell aggregation in comparison to initial values (p<0.05). In the oral treatment arm of the study, whole blood and plasma viscosities were significantly lower compared to the placebo group at 3 months (p<0.05). Most of the parameters studied, with the exception of red blood cell aggregation, worsened in the control group during follow up.
The authors suggest that long-term oral administration of vinpocetine along with parenteral administration helps maintain the beneficial hemorheological changes.

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Dosage (Inside MSKCC Only)
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References
  1. Feigin VL, Doronin BM, Popova TF, Gribatcheva EV, Tchervov DV. Vinpocetine treatment in acute ischaemic stroke: a pilot single-blind randomized clinical trial. Eur J Neurol. Jan 2001;8(1):81-85.
  2. Bhatti JZ, Hindmarch I. Vinpocetine effects on cognitive impairments produced by flunitrazepam. Int Clin Psychopharmacol. Oct 1987;2(4):325-331.
  3. Hindmarch I, Fuchs HH, Erzigkeit H. Efficacy and tolerance of vinpocetine in ambulant patients suffering from mild to moderate organic psychosyndromes. Int Clin Psychopharmacol. Spring 1991;6(1):31-43.
  4. Balestreri R, Fontana L, Astengo F. A double-blind placebo controlled evaluation of the safety and efficacy of vinpocetine in the treatment of patients with chronic vascular senile cerebral dysfunction. J Am Geriatr Soc. May 1987;35(5):425-430.
  5. Akhondzadeh S, Abbasi SH. Herbal medicine in the treatment of Alzheimer's disease. Am J Alzheimers Dis Other Demen. Mar-Apr 2006;21(2):113-118.
  6. Szatmari SZ, Whitehouse PJ. Vinpocetine for cognitive impairment and dementia. Cochrane Database Syst Rev. 2003(1):CD003119.
  7. Amano M, Monzen H, Suzuki M, et al. Increase in tumor oxygenation and potentiation of radiation effects using pentoxifylline, vinpocetine and ticlopidine hydrochloride. J Radiat Res (Tokyo). Dec 2005;46(4):373-378.
  8. Deshmukh R, Sharma V, Mehan S, Sharma N, Bedi KL. Amelioration of intracerebroventricular streptozotocin induced cognitive dysfunction and oxidative stress by vinpocetine — a PDE1 inhibitor. Eur J Pharmacol. Oct 12 2009;620(1-3):49-56.
  9. Feher G, Koltai K, Kesmarky G, et al. Effect of parenteral or oral vinpocetine on the hemorheological parameters of patients with chronic cerebrovascular diseases. Phytomedicine. Mar 2009;16(2-3):111-117.
  10. Vlase L, Bodiu B, Leucuta SE. Pharmacokinetics and comparative bioavailability of two vinpocetine tablet formulations in healthy volunteers by using the metabolite apovincaminic acid as pharmacokinetic parameter. Arzneimittelforschung. 2005;55(11):664-668.
  11. Sitges M, Chiu LM, Nekrassov V. Single and combined effects of carbamazepine and vinpocetine on depolarization-induced changes in Na+, Ca2+ and glutamate release in hippocampal isolated nerve endings. Neurochem Int. Jul 2006;49(1):55-61.
  12. Sitges M, Aldana BI, Chiu LM, Nekrassov V. Characterization of phenytoin, carbamazepine, vinpocetine and clorgyline simultaneous effects on sodium channels and catecholamine metabolism in rat striatal nerve endings. Neurochem Res. Mar 2009;34(3):470-479.
  13. Trejo F, Nekrassov V, Sitges M. Characterization of vinpocetine effects on DA and DOPAC release in striatal isolated nerve endings. Brain Res. Aug 3 2001;909(1-2):59-67.
  14. Jeon KI, Xu X, Aizawa T, et al. Vinpocetine inhibits NF-kappaB-dependent inflammation via an IKK-dependent but PDE-independent mechanism. Proc Natl Acad Sci U S A. May 25 2010;107(21):9795-9800.
  15. Vinpocetine. Monograph. Altern Med Rev. Jun 2002;7(3):240-243.
  16. Imamoto T, Tanabe M, Shimamoto N, Kawazoe K, Hirata M. Cerebral circulatory and cardiac effects of vinpocetine and its metabolite, apovincaminic acid, in anesthetized dogs. Arzneimittelforschung. 1984;34(2):161-169.
  17. Manconi E, Binaghi F, Pitzus F. A double-blind clinical trial of vinpocetine in the treatment of cerebral insufficiency of vascular and degenerative origin. Curr Ther Res. 1986;40:702-709.
  18. Shimizu Y, Saitoh K, Nakayama M, et al. Agranulocytosis induced by vinpocetine. Medicine Online [serial online]. http://www.priory.com/med/vinpocetine.htm. Accessed March 7, 2011.
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Consumer Information

How It Works

Bottom Line: Vinpocetine may be useful against some cerebrovascular disorders. It has not been shown to treat or prevent cancer.

Vinpocetine is made from a compound found in the common periwinkle plant. It was developed in Europe as a drug but sold in the United States as a dietary supplement to improve brain function. Vinpocetine was shown to increase blood flow to the brain by inhibiting clumping of blood platelets. It has also been studied as a treatment for Alzheimer's disease and for disorders of the nervous and circulatory systems. But more studies are needed before it can be recommended. Vinpocetine should not be confused with the chemo drugs vincristine and vinblastine, which are also made from compounds of periwinkle plant.

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Purported Uses
  • Alzheimer's disease
    Small studies have shown benefit of vinpocetine, but well designed clinical trials are needed.
  • Cognitive decline
    Vinpocetine was useful in improving cognitive decline. More studies are needed.
  • Dementia
    A systematic review of studies did not find any effectiveness of Vinpocetine for dementia.
  • Memory loss
    A few clinical trials have shown benefit. Large scale studies are needed.
  • Stroke
    Some studies have shown effectiveness of vinpocetine in stroke patients.
  • Cancer treatment
    In animal studies, vinpocetine increased the effects of radiation on tumor cells. But there is no evidence of vinpocetine's anticancer effects in humans.
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Research Evidence

Cerebrovascular Disease:
In this study 40 patients who had a stroke three months prior to the study, were given high-dose parenteral vinpocetine up to 1mg/kg/day. Additionally, 20 patients received 30mg of vinpocetine orally for three months with those receiving placebo serving as controls. Plasma fibrinogen, whole blood viscosity, red blood cell aggregation and deformability and hematocrit were assessed at one and three months. High-dose parenteral administration of vinpocetine for 7 days significantly reduced whole blood and plasma viscosity and red blood cell aggregation in comparison to initial values. In the oral treatment arm of the study, whole blood and plasma viscosities were significantly lower compared to the placebo group at 3 months (p<0.05) Most of the parameters studied, with the exception of red blood cell aggregation, showed worsening in the control group during follow up.

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Do Not Take If
  • You are using blood-thinning drugs (Vinpocetine may increase their effects).
  • You are taking medication to lower high blood pressure (Vinpocetine may enhance their effects).
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Side Effects
  • Flushing, rashes, gastrointestinal problems
  • Low blood pressure
  • Decreased white blood cell count
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Last updated: September 27, 2012
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