Vinpocetine 15 mg - Vincamine Derivative to Support Brain Function

Vinpocetine is derived from the natural alkaloid vincamine, extracted from the small vinca minor. It has virtually no side effects or contraindications, and has been the subject of more than 700 scientific publications in recent years, of which 200 report results from animal and human studies.

What benefits are associated with Vinpocetine's?

Vinpocetine's main benefit is that it supports brain metabolism, and therefore alertness, by increasing synthesis of adenosine triphosphate (ATP), the universal energy molecule. It's also frequently used for its vasodilatory properties in sensory, hearing and visual problems of vascular origin (vertigo, tinnitus, buzzing in the ear, noise pollution, retinopathies).

• Improves the brain's utilisation of oxygen.
• Reduces platelet aggregation.
• Recommended for mainly hypoxia-related problems (oxygen insufficiency) or ischaemic problems (insufficient blood flow).
• Increases the synthesis of several neurotransmitters affecting critical brain functions such as memorisation, concentration and mood.

What do the studies show about Vinpocetine?

According to Dr Jack Vernon, American tinnitus expert, “vinpocetine is a very promising substance”.

• The first studies conducted on this compound recommended its use for mainly hypoxia-related problems (oxygen insufficiency) or ischaemic problems (insufficient blood flow). In these conditions, vinpocetine exerts a significant neuro-protective effect, saving up to 50% of neurons which would almost certainly otherwise be lost.
• Several studies have shown a significant improvement in hearing following supplementation with 30-40 mg vinpocetine a day.
• A number of studies show a perceptible improvement in cognitive performance following supplementation, particularly in one of the most difficult areas to influence, synaptic plasticity, which, in a way, is the cellular model for learning capacity.
• Other studies have shown that vinpocetine improves a number of visual deficiencies, related in particular to macular decline, poor night vision and glaucoma.

1. Kiss B, Szpomy L. On the possible role of central monoaminergic systems in the central nervous systems actions of vinpocetine. Drug Dev Res. 1988;14:263–79.
2. Shibuya T, Sato K. Effects of vinpocetine on experimental brain ischemia, histological study of brain monoamines. Igaku No Ayumi. 1986;139:217–9.
3. Nicholson CD. Pharmacology of nootropics and metabolically active compounds in relation to their use in dementia. Psychopharmacology (Berl) 1990;101:147–59
4. Patyar, S., Prakash, A., Modi, M., Medhi, B., 2011. Role of vinpocetine in cerebrovascular diseases. Pharmacol. Rep. 63, 618–628.
5. Bonoczk, P., Gulyas, B., Adam-Vizi, V., Nemes, A., Karpati, E., Kiss, B., Kapas, M., Szantay, C., Koncz, I., Zelles, T., Vas, A., 2000. Role of sodium channel inhibition in neuroprotection: effect of vinpocetine. Brain Res. Bull. 53, 245–254.
6. Zhang, L., Yang, L., 2015. Anti-inflammatory effects of vinpocetine in atherosclerosis and ischemic stroke: a review of the literature. Molecules 20, 335–347.
7. Szilagyi, G., Nagy, Z., Balkay, L., Boros, I., Emri, M., Lehel, S., Marian, T., Molnar, T., Szakall, S., Tron, L., Bereczki, D., Csiba, L., Fekete, I., Kerenyi, L., Galuska, L., Varga, J., Bonoczk, P., Vas, A., Gulyas, B., 2005. Effects of vinpocetine on the redistribution of cerebral blood flow and glucose metabolism in chronic ischemic stroke patients: a PET study. J. Neurol. Sci. 229–230, 275–284.
8. Gulyas, B., Halldin, C., Sandell, J., Karlsson, P., Sovago, J., Karpati, E., Kiss, B., Vas, A., Cselenyi, Z., Farde, L., 2002a. PET studies on the brain uptake and regional distribution of [11C]vinpocetine in human subjects. Acta Neurol. Scand. 106, 325–332
9. Gulyas, B., Halldin, C., Sovago, J., Sandell, J., Cselenyi, Z., Vas, A., Kiss, B., Karpati, E., Farde, L., 2002b. Drug distribution in man: a positron emission tomography study after oral administration of the labelled neuroprotective drug vinpocetine. Eur. J. Nucl. Med. Mol. Imaging 29, 1031–1038.
10. Deshmukh, R., Sharma, V., Mehan, S., Sharma, N., Bedi, K.L., 2009. Amelioration of intracerebroventricular streptozotocin induced cognitive dysfunction and oxidative stress by vinpocetine – a PDE1 inhibitor. Eur. J. Pharmacol. 620, 49–56.
11. Herrera-Mundo, N., Sitges, M., 2013. Vinpocetine and alpha-tocopherol prevent the increase in DA and oxidative stress induced by 3-NPA in striatum isolated nerve endings. J. Neurochem. 124, 233–240
12. Giachini, F.R., Lima, V.V., Carneiro, F.S., Tostes, R.C., Webb, R.C., 2011. Decreased cGMP level contributes to increased contraction in arteries from hypertensive rats: role of phosphodiesterase 1. Hypertension 57, 655–663.
13. Jeon, K.-I., Xu, X., Aizawa, T., Lim, J.H., Jono, H., Kwon, D.-S., Abe, J.-I., Berk, B.C., Li, J.- D., Yan, C., 2010. Vinpocetine inhibits NF-kappaB-dependent inflammation via an IKK-dependent but PDE-independent mechanism. Proc. Natl. Acad. Sci. USA 107, 9795–9800.
14. Medina, A.E., 2010. Vinpocetine as a potent antiinflammatory agent. Proc. Natl. Acad. Sci. USA 107, 9921–9922.
15. Yi-shuai Zhang, Jian-dong Li, and Chen Yan. An update on Vinpocetine: New discoveries and clinical implications, Eur J Pharmacol. 2018 Jan 15; 819: 30–34.
16. Lohmann A, Dingler E, Sommer W, et al. Bioavailability of vinpocetine and interference of the time of application with food intake. Arzneimittelforschung. 1992;42:914-917.