Health Care Professional Information

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

Kavinton, Rgh-4405, Tcv-3B, apovincaminic acid, Cavinton, vinpocetine, periwinkle

Brand Name


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.

Animal models suggest that vinpocetine has anti-inflammatory, antioxidant, antimitotic, anti-atherogenic, antithrombotic, and antiepileptic effects (1) (2) (3) (4) (5) (6) (7). Human studies show that vinpocetine enhances short-term memory (8), cognitive performance (9), and improves chronic cerebral dysfunction in elderly patients (10). It has also been studied as a potential treatment for Alzheimer's disease (11), but a systematic review did not find evidence of its benefits (12). Parenteral followed by oral administration of vinpocetine significantly maintained beneficial hemorheologic changes in stroke patients in one pilot study (13), but a systematic review did not find enough evidence to determine whether vinpocetine could benefit patients with acute ischemic stroke (14).

Vinpocetine inhibits the growth of breast cancer cells in vitro and in vivo (15). In animal studies, it potentiates the effects of radiation therapy in tumor cells (16). However, vinpocetine has not yet been studied in humans for its potential anticancer effects.

Vinpocetine should not be confused with chemotherapy drugs such as vincristine or vinblastine, which are also alkaloids derived from the periwinkle plant.

Purported Uses
  • Alzheimer's disease
  • Cognitive decline
  • Dementia
  • Memory loss
  • Stroke
  • Cancer treatment

Vinpocetine is a synthetic ethyl ester of apovincamine derived from an alkaloid in the common periwinkle plant (17).

Mechanism of Action

Vinpocetine has been shown to possess antioxidant and hydroxyl radical scavenging properties in vitro (18) (13). It inhibits phosphodiesterase 1 (PDE1) activity and improves cerebral blood flow by elevating cGMP and cAMP, increasing mitochondrial function, and 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 (18). It demonstrated antiepileptic effects by suppressing abnormal neuronal excitability through the regulation of sodium channels and release of dopamine in the striatal nerve endings (5) (6) (7). Vinpocetine antagonizes platelet-derived growth factor (PDGF)-induced extracellular matrix synthesis, suppresses intracellular reactive oxidative species (ROS) production, and inhibits extracellular signal-regulated kinase (ERK) 1/2 activation and vascular smooth muscle cell growth (4). Anti-atherogenic effects occur through inhibition of monocyte adhesion, oxidative stress, and inflammatory responses mediated by protein kinase B (Akt)/nuclear factor kappa B (NF-ĸB)-dependent pathways (3). Vinpocetine also demonstrates anti-inflammatory effects by inhibiting tumor necrosis factor-alpha (TNF-α)-induced NF-κB activities (19) as well as Akt and STAT3 activation (15). Administration of vinpocetine to chronic stroke patients increased glucose uptake and release in unaffected areas of the brain (12).

In vitro and in vivo studies indicate vinpocetine antitumor activity against human breast cancer cells occurs through G0/G1-phase cell cycle arrest and mitochondrial pathways of apoptosis (15). Vinpocetine can also increase the effects of radiation by increasing tumor oxygenation (16).


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 an empty stomach. Plasma levels of vinpocetine peak approximately 1–1.5 hours after ingestion. T 1/2 is 1–2 hours, with non-detectable plasma levels 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 (20).

Various novel formulations of vinpocetine are currently being developed to attempt more efficient delivery and bioavailability (21) (22).


Patients with low blood pressure, a history of heart problems or strokes, or those on blood-thinning medications should consult their physician before using this product.

Adverse Reactions

Rare: Flushing, rashes, gastrointestinal problems (23), hypotension (24)

Case Report: A 73 year-old man developed agranulocytosis after using vinpocetine for 50 days. His symptoms resolved after discontinuing vinpocetine (25).

Herb-Drug Interactions
  • Anticoagulants/antiplatelet agents: Vinpocetine may have additive effects and can increase risk of bleeding (13) (14) (26).
  • Antihypertensive agents: Vinpocetine may increase hypotensive effects (24).
Herb Lab Interactions
Literature Summary and Critique

Feher 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 who had an occurrence of stroke >3 months prior to enrollment were administered high-dose parenteral vinpocetine, gradually increasing to 1 mg/kg/day. Hemorheological parameters including plasma fibrinogen, whole blood viscosity, red blood cell aggregation, deformability, and hematocrit were assessed at 1 and 3 months. Additionally, 20 patients received 30 mg of vinpocetine orally for 3 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 with initial values (P<.05). In the oral treatment arm, whole blood and plasma viscosities were significantly lower compared with placebo at 3 months (P<.05). With the exception of red blood cell aggregation, most parameters studied 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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  1. Wang H, Zhang K, Zhao L, et al. Anti-inflammatory effects of vinpocetine on the functional expression of nuclear factor-kappa B and tumor necrosis factor-alpha in a rat model of cerebral ischemia-reperfusion injury. Neurosci Lett. Apr 30 2014;566:247-251. doi: 10.1016/j.neulet.2014.02.045
  2. Zaki HF, Abdelsalam RM. Vinpocetine protects liver against ischemia-reperfusion injury. Can J Physiol Pharmacol. Dec 2013;91(12):1064-1070. doi: 10.1139/cjpp-2013-0097
  3. Zhuang J, Peng W, Li H, et al. Inhibitory effects of vinpocetine on the progression of atherosclerosis are mediated by Akt/NF-kappaB dependent mechanisms in apoE-/- mice. PLoS One. 2013;8(12):e82509. doi: 10.1371/journal.pone.0082509
  4. Cai Y, Knight WE, Guo S, et al. Vinpocetine suppresses pathological vascular remodeling by inhibiting vascular smooth muscle cell proliferation and migration. J Pharmacol Exp Ther. Nov 2012;343(2):479-488. doi: 10.1124/jpet.112.195446
  5. 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. doi: 10.1016/j.neuint.2005.12.019
  6. Sitges M, Aldana BI, Chiu LM, et al. 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. doi: 10.1007/s11064-008-9805-7
  7. 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.
  8. Bhatti JZ, Hindmarch I. Vinpocetine effects on cognitive impairments produced by flunitrazepam. Int Clin Psychopharmacol. Oct 1987;2(4):325-331.
  9. 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.
  10. 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.
  11. 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.
  12. Szatmari SZ, Whitehouse PJ. Vinpocetine for cognitive impairment and dementia. Cochrane Database Syst Rev. 2003(1):CD003119. doi: 10.1002/14651858.CD003119
  13. 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. doi: 10.1016/j.phymed.2008.10.014
  14. Bereczki D, Fekete I. Vinpocetine for acute ischaemic stroke. Cochrane Database Syst Rev. 2008(1):CD000480. doi: 10.1002/14651858.CD000480.pub2
  15. Huang EW, Xue SJ, Zhang Z, et al. Vinpocetine inhibits breast cancer cells growth in vitro and in vivo. Apoptosis. Oct 2012;17(10):1120-1130. doi: 10.1007/s10495-012-0743-0
  16. 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. Dec 2005;46(4):373-378.
  17. Feigin VL, Doronin BM, Popova TF, et al. Vinpocetine treatment in acute ischaemic stroke: a pilot single-blind randomized clinical trial. Eur J Neurol. Jan 2001;8(1):81-85.
  18. Deshmukh R, Sharma V, Mehan S, et al. 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. doi: 10.1016/j.ejphar.2009.08.027
  19. 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. doi: 10.1073/pnas.0914414107
  20. 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. doi: 10.1055/s-0031-1296915
  21. Moghaddam AA, Aqil M, Ahmad FJ, et al. Nanoethosomes mediated transdermal delivery of vinpocetine for management of Alzheimer's disease. Drug Deliv. Apr 10 2014. doi: 10.3109/10717544.2013.846433
  22. Lin C, Chen F, Ye T, et al. A novel oral delivery system consisting in “drug-in cyclodextrin-in nanostructured lipid carriers” for poorly water-soluble drug: Vinpocetine. Int J Pharm. Apr 25 2014;465(1-2):90-96. doi: 10.1016/j.ijpharm.2014.02.013
  23. Vinpocetine [monograph]. Altern Med Rev. Jun 2002;7(3):240-243.
  24. Imamoto T, Tanabe M, Shimamoto N, et al. Cerebral circulatory and cardiac effects of vinpocetine and its metabolite, apovincaminic acid, in anesthetized dogs. Arzneimittelforschung. 1984;34(2):161-169.
  25. Shimizu Y, Saitoh K, Nakayama M, et al. Agranulocytosis induced by vinpocetine. Medicine Online [serial online]. Accessed April 21, 2014.
  26. Kuzuya F. Effects of vinpocetine on platelet aggregability and erythrocyte deformability. Ther Hung. 1985;33(1):22-34.

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 and has been studied as a treatment for Alzheimer's disease and for disorders of the nervous and circulatory systems. However, 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 the periwinkle plant.

Purported Uses
  • Alzheimer's disease
    Small studies have shown benefit with 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 benefits with vinpocetine in stroke patients, but larger studies are needed.
  • Cancer treatment
    Laboratory studies suggest some anticancer and increased radiation effects on tumor cells, but this has not been studied in humans.
Research Evidence

Cerebrovascular Disease
A study of 40 patients who had a stroke more than 3 months before the study began were given an intravenous high dose of vinpocetine. In addition, 20 patients received oral vinpocetine for 3 months, while the other 20 received a placebo. Investigators found that intravenous vinpocetine for 7 days significantly improved blood flow properties. For those taking the oral treatment, blood flow properties were also significantly improved compared with placebo at 3 months. Most of the blood flow properties were worse in the control group during follow-up.

Patient Warnings

Patients with low blood pressure, a history of heart problems or strokes, or those on cardiovascular medications should consult their physician before using this product.

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.
Side Effects
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