Vinpocetine

Vinpocetine is a compound from the Periwinkle plant that is used as a cognitive protective and anti-aging agent. One of the more common of the nootropics, Vinpocetine may enhance blood flow and is touted to increase memory; this latter claim has not been investigated

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Vinpocetine is a compound derived via the Vincamine compound from Periwinkle plants, which have been used since medieval times for the treatment of headaches.

The active compound, vinpocetine, is known as a neurological protecting agent. It is able to increase blood flow to the brain while simultaneously decreasing blood viscosity. When in the brain it; increases brain activity, provides anti-oxidant protection, protects against stroke, and increases glucose consumption by neurons.

It also inhibits the enzyme phosphodiesterase type 1, which leads to some systemic benefits such as increased energy, urinary tract protection, and increased learning (in the neurologically compromised).

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Also Known As

Vincamine, Vinca Minor, Periwinkle Extract, Cavinton (Brand Name)


Things to Note

Although not a classical stimulant, Vinpocetine/Vincamine increase brain activity and may induce a slight state of mental alertness.

Is a Form of


Caution Notice

Examine.com Medical Disclaimer

With Vincamine supplementation, doses of 30-60mg have been used in humans effectively (Although animal toxicity studies pinpoint harm at a much higher level). Due to a short half life of vincamine, multiple doses may be needed throughout the day.

Vinpocetine is usually used in doses of 15mg 2-3 times over the course of a day.


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A large amount in interventions published in Russian prevent the Rubric from showing more representative data; Vinpocetine does not appear to be a well studied compound in humans according to English literature, but more-so at an in vitro stage.


Kurtis Frank

The Human Effect Matrix looks at human studies (excluding animal/petri-dish studies) to tell you what effect Vinpocetine has in your body, and how strong these effects are.
GradeLevel of Evidence
ARobust research conducted with repeated double blind clinical trials
BMultiple studies where at least two are double-blind and placebo controlled
CSingle double blind study or multiple cohort studies
DUncontrolled or observational studies only
Level of Evidence
EffectChange
Magnitude of Effect Size
Scientific ConsensusComments
CPulse Rate

Minor

A decrease in pulse rate has been noted with vinpocetine

CReaction Time

Minor

High doses (40mg) may reduce reaction time during tested, with lower doses not being potent enough to influence reaction time

CMemory

Minor

An increase in acute memory formation has been noted in female volutneers given 40mg Vinpocetine

DSubjective Well-being

Minor

An increase in well being has been noted to be secondary to the reduced rate of cognitive decline

DFunctionality in Elderly or Injured

Minor

An improvement in balance has been noted with vinpocetine ingestion in the elderly, which may be related to the attenuation of cognitive decline

DCognitive Decline

Minor

The rate of cognitive decline appears to be attenuated with vinpocetine administration, this may be related to blood flow

DIsaac speech activity test

Minor

Improvements in speech performance have been noted in the elderly, which may be more indicative of the reductions in cognitive decline


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Table of Contents:


Edit1. Sources and Composition

1.1. Sources

Vinpocetine is derived from the compound Vincamine, which is the principle active ingredient of the plant Vinca Minor L(periwinkle). Vincamine comprises about 25-65% of the total alkaloids (not weight) in the plant and should not be confused with the toxic alkaloids from Vinca Rosea.[1] This plant, Periwinkle, has traditionally been used in Europe as a folk remedy for headaches and is generally (anecdotally) seen as safe.

Vincamine is rapidly and easily digested. A dose of 15mg gives rise to serum levels of 5ug for up to 6 hours, whereas 30mg ingested vincamine can potentially reach the same concentration threshold but for longer periods of time.[2] It has a relatively short half-life in humans, ranging from 1-2.5 hours with doses between 30 and 60mg.[3]

1.2. Structure

Vinpocetine is an alkaloid with slight modifications from the Vincamine molecule, both pictured below.


Edit2. Vinpocetine

As the active compound of Vincamine, most clinical benefits are attributed to the active vinpocetine content of vincamine.

Vinpocetine is able to effectively penetrate the blood-brain barrier. Once located in the brain it increases blood flow to neural tissue (in hypertensive situations)[4] and, although heterogeneous, is more active in the thalamus, basal ganglia, and visual cortex.[5] Vinpocetine can also reduce blood viscosity, leading to its usage as an anti-stroke protective agent.[6]

Vinpocetine is also a phosphodiesterase 1 inhibitor, which has been linked to potentially increasing learning in the neurologically compromised lab animal[7][8] possibly via both increasing neural plasticity and increasing levels of cGMP and cAMP in the hippocampus, the latter of which was observable in normal lab animals as well.[9]

2.1. Pharmacokineics

Vinpocetine appears to have a biphasic half-life, with the alpha half-life of 0.136 hours (rapid metabolism) whereas the beta half-life is more prolonged at 4.83 hours.[10]

It appears to have a bioavailability of 56.6+/-8.9%, and is rapidly absorbed by tissues.[10]

No detectable unchanged vinpocetine is excreted in the urine[10], as it is excreted after ester cleavage.[11]

2.2. Enzymatic Interactions

Vinpocetine appears to have selective inhibitory potential on the PDE1 enzyme,[12] and can inhibit the PDE1 in a concentration-dependent manner between 10-100uM with a Ki of 50.5 ± 9.5uM.[13]


Edit3. Interactions with Neurology

3.1. Processing Speed

Vinpocetine has been shown to increase reaction speed to identifying stimuli in healthy females in the age group of 25-40, where 10,20, and 40mg decreased reaction times to 95% of control, 93% of control, and 70% of control; respectively.[14] Increased reaction speed, as well as increased processing speed, have been seen in a rehabilitative setting with NFL football players (although highly confounded with Acetyl-L-Carnitine, Fish Oil, Alpha-Lipoic Acid and Huperzine-A).[15]

3.2. Inflammation

Vinpocetine is an effective neurological anti-inflammatory agent[16] via inhibitions of pro-inflammatory signalling proteins.[17] Which is one of the mechanisms it is suspected in being an anti-neurodegenerative agent.


Edit4. Safety and Toxicity

When used in hospital settings as IV administration, there have been reports of adverse effects such as death from drastic drops in blood pressure and pulse rate.[18][19]

Toxicity studies on Vincamine have shown acute oral toxicity in the range of 460-1,200mg/kg bodyweight in experimental animals, and doses of 15-30mg/kg bodyweight have shown no side effects in the same animals.

No such adverse effects have been reported with normal dosages of vinpocetine or vincamine taken orally.

Contact dermatitis to vincamine has been reported.[20]

References

  1. Summary of Data for Chemical Selection: Vincamine
  2. The effect of an acute infusion of vincamine and ethyl apovincaminate on cerebral blood flow in healthy volunteers
  3. Millart H, et al. Pharmacokinetic study of two pharmaceutical preparations containing alkaloid vincamine administered orally to human subjects. Int J Clin Pharmacol Ther Toxicol. (1983)
  4. Nevzorova VA, Zakharchuk NV, Plotnikova IV. {The state of cerebral blood flow in hypertensive crises and possibilities of its correction}. Kardiologiia. (2007)
  5. Vas A, et al. 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. J Neurol Sci. (2002)
  6. Feher G, et al. Effect of parenteral or oral vinpocetine on the hemorheological parameters of patients with chronic cerebrovascular diseases. Phytomedicine. (2009)
  7. Filgueiras CC, Krahe TE, Medina AE. Phosphodiesterase type 1 inhibition improves learning in rats exposed to alcohol during the third trimester equivalent of human gestation. Neurosci Lett. (2010)
  8. Medina AE, Krahe TE, Ramoa AS. Restoration of neuronal plasticity by a phosphodiesterase type 1 inhibitor in a model of fetal alcohol exposure. J Neurosci. (2006)
  9. van Staveren WC, et al. The effects of phosphodiesterase inhibition on cyclic GMP and cyclic AMP accumulation in the hippocampus of the rat. Brain Res. (2001)
  10. Vereczkey L, et al. Pharmacokinetics of vinpocetine in humans. Arzneimittelforschung. (1979)
  11. Vereczkey L. Pharmacokinetics and metabolism of vincamine and related compounds. Eur J Drug Metab Pharmacokinet. (1985)
  12. Ahn HS, et al. Effects of selective inhibitors on cyclic nucleotide phosphodiesterases of rabbit aorta. Biochem Pharmacol. (1989)
  13. Yu MC, et al. Luteolin, a non-selective competitive inhibitor of phosphodiesterases 1-5, displaced {3H}-rolipram from high-affinity rolipram binding sites and reversed xylazine/ketamine-induced anesthesia. Eur J Pharmacol. (2010)
  14. Subhan Z, Hindmarch I. Psychopharmacological effects of vinpocetine in normal healthy volunteers. Eur J Clin Pharmacol. (1985)
  15. Amen DG, et al. Reversing brain damage in former NFL players: implications for traumatic brain injury and substance abuse rehabilitation. J Psychoactive Drugs. (2011)
  16. Medina AE. Vinpocetine as a potent antiinflammatory agent. Proc Natl Acad Sci U S A. (2010)
  17. Jeon KI, et al. Vinpocetine inhibits NF-kappaB-dependent inflammation via an IKK-dependent but PDE-independent mechanism. Proc Natl Acad Sci U S A. (2010)
  18. Hutter K, Deli L, Csomós I. {Successful resuscitation from sudden death caused by Cavinton}. Orv Hetil. (1980)
  19. Dany F, et al. {Cardiac toxicity of vincamine: a seven cases report of ventricular arrhythmias by parenteral administration of vincamine (author's transl)}. Therapie. (1981)
  20. van Hecke E. Contact sensitivity to vincamine tartrate. Contact Dermatitis. (1981)
  21. Lim CC, Cook PJ, James IM. The effect of an acute infusion of vincamine and ethyl apovincaminate on cerebral blood flow in healthy volunteers. Br J Clin Pharmacol. (1980)
  22. Chukanova EI. Efficacy of cavinton in the treatment of patients with chronic blood flow insufficiency. Russian multicenter clinical-epidemiological program "CALIPSO". Zh Nevrol Psikhiatr Im S S Korsakova. (2010)
  23. Vorob'eva OV, Tamarova ES. Efficacy of vinpotropile in the therapy of initial signs of cerebrovascular pathology. Zh Nevrol Psikhiatr Im S S Korsakova. (2010)
  24. Zakharov VV. Vinpotropil in the treatment of dyscirculatory encephalopathy with cognitive impairment without dementia. Zh Nevrol Psikhiatr Im S S Korsakova. (2010)

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