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Nootropics Powder 99% Purity Vinpocetine powder CAS: 42971-09-5
Common Name(s): Vinpocetine , Cavinton , apovincaminic acid kavinton
The scientific literature contains numerous studies and investigations on the pharmacological and biochemical actions of vinpocetine, including antioxidant effects, menopause, antiulcer activity, and phosphodiesterase-1 inhibition. Vinpocetine is best known for its neuroprotective effects. However, there are limited clinical studies to support the use of vinpocetine for many of these potential uses.
Follow suggested manufacturers' product guidelines. Most clinical studies used vinpocetine 10 mg 3 times daily, orally or parenterally.
The drug should not be used in patients with severe, general, cerebral hypertensive crises, or in elderly or senile patients with acute cardio-cerebral or cerebro-cardiac syndrome, postinfarction cardiosclerosis, or marked disorders of heart rhythm.
Avoid use during pregnancy and lactation because of lack of clinical studies.
Caution is warranted in patients on blood-thinning medications because vinpocetine decreases platelet aggregation. In 1 study, bioavailability increased 60% to 100% when vinpocetine was taken with food.
One review article documents patients reporting flushing, rashes, and minor GI problems.
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. 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.
Vinpocetine is also a phosphodiesterase (PDE) type-1 inhibitor, (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.
Independent of vinpocetine's action on PDE, vinpocetine inhibits IKK preventing IκB degradation and the following translocation of NF-κB to the cell nucleus.
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. Such an effect is consistent with the biogenic pharmacology of reserpine, a structural relative of vinpocetine.However, this effect tends to be reversible upon cessation of vinpocetine administration, with full remission typically occurring within 3–4 weeks.
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