IngredientsVinpocetine is a synthetic ethyl ester of apovincamine, a vinca alkaloid obtained from the leaves of the Lesser Periwinkle (Vinca minor). Its systematic chemical name is ethyl apovincaminate, and it is also referred to by its IUPAC designation as (3α,16α)-eburnamenine-14-carboxylic acid ethyl ester (CAS Registry Number 42971-09-5). Vinpocetine is a white crystalline solid with a molecular mass of 350.45 g/mol. It has an estimated boiling point of 420°C, a melting point of 147–153°C, a log KOW of 4.31, and vapor pressure of 3.02 × 10−7 mm Hg at 25°C.
Vinca minor L. is the botanical source from which vincamine — the precursor to vinpocetine — is extracted from leaves. In the United States, the plant is commonly referred to as myrtle or creeping myrtle. The shrub is used as ground cover and bears single, violet-purple flowers. The 2.5 cm long fruit contain numerous tiny seeds. The plant differs from its relative Vinca major by having smaller, leathery leaves with a hairless margin. Vinca minor (genus Vinca), a member of the Apocynaceae family, contains vincamine along with several other vinca alkaloids.
Vinpocetine is a synthetic derivative of the natural compound vincamine found in the lesser periwinkle plant, also known as Vinca minor. Vincamine itself also has pharmacological activity; unlike vinpocetine, its precursor vincamine carries the ATC code C04AX, indicating it is classified as a substance for the treatment of cardiovascular conditions and belongs to the group of peripheral vasodilators.
Vinpocetine — the active ingredient of Cavinton® — has over five decades of clinical use. Drug names include Cavinton, Vicebrol, and Vincetan. Vinpocetine was first synthesized in the late 1960s from vincamine and has been sold under commercial names, such as Cavinton and Intelectol, since the late 1970s. In pharmaceutical settings it is available as oral tablets and intravenous infusions. In the dietary supplement market, it is sold as oral capsules and tablets, frequently in combination with other nootropic ingredients. Due to issues such as hepatic first-pass effect, low bioavailability, and poor patient compliance with multiple dosing, the secondary development of vinpocetine to address these limitations became a prominent area of research.
The World Health Organization's Anatomical Therapeutic Chemical (ATC) classification assigns vinpocetine the code N06BX18, meaning it is classified as a drug with an influence on the nervous system (N), falling under the group of psychoanaleptics (06) and the subgroup of psychostimulants, agents used for attention deficit hyperactivity disorder and nootropics (B).
Vinpocetine is often marketed as a dietary supplement although, as a synthetic substance, it is unauthorized in food supplements in the EU, where the European Medicines Agency considers it an approved drug, and the U.S. FDA has suggested it does not qualify as a legal dietary supplement ingredient but still allows it to be sold with a pregnancy warning. On September 6, 2016, FDA published a Federal Register notice seeking comment on its tentative conclusions that vinpocetine (1) does not meet the definition of a dietary ingredient, and (2) is excluded from the definition of a dietary supplement under the Federal Food, Drug, and Cosmetic Act because vinpocetine was authorized for investigation as a new drug before it was marketed as a dietary supplement or as a food. In Europe, vinpocetine is prescribed as a treatment for cerebrovascular disorders such as strokes and may help with cognitive impairment and memory loss in people with early dementia.
Vinpocetine, a semisynthetic derivative of vincamine — the Vinca minor alkaloid — was synthesized in Hungary in the mid-1960s. Vinpocetine was discovered in the 1960s, with the first clinical studies conducted in the 1970s, and it was followed by the introduction of the drug Cavinton in 1978 by Gedeon Richter Nyrt in Hungary. An Investigational New Drug (IND) application was filed in the U.S. in 1981.
Since the late 1970s, vinpocetine has been widely available as a pharmaceutical agent in Hungary, Germany, Poland, Russia, China, and Japan for use in cerebrovascular and cognitive disorders. The parent compound vincamine had been used somewhat earlier in European medicine as a peripheral vasodilator. Vinpocetine was developed expressly to improve upon vincamine's pharmacological profile while retaining its cerebrovascular activity.
Vinpocetine is a purely synthetic compound and thus carries no ethnobotanical or traditional folk-medicine history in its own right. The periwinkle plant (Vinca minor), from which vincamine is extracted, has been used in European herbal traditions over centuries for various purposes, but vinpocetine as a discrete chemical entity did not exist before its mid-20th-century laboratory synthesis. Its "traditional" context is therefore a modern pharmaceutical one: vinpocetine, a derivative of the alkaloid vincamine, has been clinically used in many countries for treatment of cerebrovascular disorders such as stroke and dementia for more than 30 years.
Though original indications for vinpocetine promoted its use in the elderly, several products are currently available that are specifically marketed toward students as brain supplements for increasing cognitive performance. Additionally, vinpocetine is used among healthy athletes within the bodybuilding community for reported enhancement of visual acuity, memory, and focus, in addition to rapid reductions in body fat.
Products containing vinpocetine are marketed for uses that include improvement of brain function, rapid weight loss and/or fat loss, increases in energy, and improvement in visual acuity, memory, and focus. Vinpocetine is also reportedly marketed for prevention of motion sickness and treatment of menopausal symptoms, chronic fatigue syndrome, seizure disorders, and hearing and eye disorders.
Vinpocetine itself is the pharmacologically active entity, as its precursor vincamine and its major metabolite apovincaminic acid (AVA) have distinct and generally weaker activity profiles. The main metabolite measured in humans is apovincaminic acid. Vinpocetine is rapidly and extensively metabolized mainly to its deesterified derivative, apovincaminic acid, and other minor metabolites.
Vinpocetine is a semi-synthetic indole alkaloid with a high degree of lipid solubility that easily crosses the blood–brain barrier into brain tissue and is therefore widely used in cerebrovascular diseases such as stroke and cognitive impairment. Vinpocetine readily crosses the blood-brain barrier (BBB) to enter brain tissue. The presence of vinpocetine in cerebrospinal fluid confirms that the drug is able to pass through the blood-brain barrier and reach the central nervous system, which is a possible site of action.
Phosphodiesterase type 1 (PDE1) is proven to be the first identified target of action of vinpocetine, a designation established in the 1990s. Vinpocetine enhances neuronal plasticity by regulating PDE1 to increase the level of the second messengers cAMP (cyclic adenosine monophosphate) and cGMP (cyclic guanosine monophosphate), improving the ability of neural reorganization in the brain. By catalyzing the hydrolysis of cAMP and cGMP, PDEs limit intracellular levels of cyclic nucleotides and thus regulate the amplitude, duration, and compartmentation of cyclic nucleotide signaling. Three PDE1 isoforms have been identified (PDE1A, PDE1B, and PDE1C), all expressed within the central nervous system, with PDE1-B mainly distributed in the cortex.
Vinpocetine inhibits 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 recovers cognitive functions and spatial memory through inhibition of hippocampal and cortical PDE1 with augmentation of cyclic adenosine monophosphate and cyclic guanosine monophosphate ratio, enhancement of cholinergic neurotransmission, and inhibition of neuronal inflammatory mediators.
Vinpocetine (VPN) is a synthetic ethyl-ester derivative of the alkaloid apovincamine from Vinca minor leaves. VPN is a selective inhibitor of phosphodiesterase type 1 (PDE1) that has potential neurological effects through inhibition of voltage-gated sodium channels and reduction of neuronal calcium influx. This mechanism is considered relevant both to its neuroprotective and antiepileptic properties. Preclinical data suggest vinpocetine's potency as a sodium channel blocker is comparable to that of established antiepileptic drugs.
Vinpocetine inhibits the expression of NF-κB-dependent inflammatory molecules by directly inhibiting IKK (inhibitor kinase) activity, attenuating IKK-mediated phosphorylation of IκB and increasing the stability of IκB, which leads to IκB binding to NF-κB. This mechanism has been described as independent of PDE inhibition. Recent studies have revealed a number of novel functions of vinpocetine, including anti-inflammation, antagonizing injury-induced vascular remodeling and high-fat-diet-induced atherosclerosis, as well as attenuating pathological cardiac remodeling.
The maximum increase of cerebral blood flow (25%) was measured at 32 minutes after the start of an intravenous infusion of vinpocetine in a study of patients with cerebrovascular disorders. Vinpocetine has several pharmacological and biochemical actions, including stimulating cerebral vasodilation, increasing tolerance of cerebral tissue to hypoxic and ischemic insults, anticonvulsant activity, inhibitory effects on phosphodiesterase, improving hematologic flow properties, and inhibiting thrombocyte aggregation.
Vinpocetine improves psychomotor performances through modulation of the brain monoamine pathway, mainly on dopamine and serotonin, which play an integral role in attenuation of depressive symptoms.
In vitro, antioxidant and hydroxyl radical scavenging properties have been observed. Additional preclinical studies observed that vinpocetine enhanced the brain's mitochondrial function, reduced oxidative stress, and lowered toxicity, all of which may prevent dementia and protect brain health.
Vinpocetine antagonizes platelet-derived growth factor-induced extracellular matrix synthesis, suppresses intracellular reactive oxygen species production, and inhibits extracellular signal-regulated kinase 1/2 activation and vascular smooth muscle cell growth. Vinpocetine may hamper atherosclerosis progression by antagonizing lipid uptake, hyperlipidemia, oxidative stress, and inflammation synergistically due to its multi-action mechanisms.
According to human studies, vinpocetine is readily absorbed from the gastrointestinal tract and has good blood–brain barrier penetration. Oral administration results in maximum plasma concentration 1–1.5 hours after administration, with values of 20–62 ng/mL. The bioavailability of the drug, calculated from the ratio of the areas under the concentration-time curves, was found to be 56.6 ± 8.9%. The peak plasma levels are reached at about one hour after oral administration.
The distribution volume is 3.2 ± 0.9 L/kg, which reflects high distribution of the drug and binding in tissue. The therapeutic dosage regimen may range from 5–10 mg orally, three times a day, due to a short half-life of 1 to 2 hours. However, half-life estimates vary across studies. In one study utilizing intravenous infusion in patients with cerebrovascular disorders, the elimination half-life of the parent drug in plasma was 4.7 ± 2.13 h, and total clearance of vinpocetine was 0.79 ± 0.11 h−1 kg−1.
Human hepatocyte studies have demonstrated that human metabolism of vinpocetine occurs almost exclusively in the liver. The main metabolite measured in humans is apovincaminic acid. The total plasma clearance of vinpocetine is 0.88 ± 0.20 L/hour per kg. Both vinpocetine and apovincaminic acid show linear pharmacokinetics at the doses studied, with no accumulation or autoinduction.
Only the concentrations of the metabolite (apovincaminic acid) could be used for standard bioequivalence determinations in some studies because the concentrations of the parent drug in plasma were too low to be accurately measured by routine methods.
Vinpocetine's most well-documented clinical use has been in acute ischemic stroke, where it has been characterized as a neuroprotective agent. Over ten trials, including more than five randomized controlled trials, have been conducted in the past, and researchers have provided systematic reviews on vinpocetine's effectiveness.
The Cochrane collaboration conducted a systematic review of vinpocetine in acute ischemic stroke (Bereczki and Fekete, 2008). Only truly randomized, unconfounded clinical trials that compared the effect of vinpocetine to either placebo or another reference treatment for acute stroke — where treatment started no later than 14 days after stroke onset — were eligible for inclusion, with data synthesis performed using Cochrane Review Manager software. Among the identified studies on vinpocetine in stroke, only one fulfilled the selection criteria for inclusion in the review. No death occurred in the study groups and no statistically significant difference was found in dependency between the treatment and the placebo groups. No adverse effects were reported. Based on only one small randomized controlled unconfounded study, the authors concluded there was not enough evidence to decide whether the administration of vinpocetine does or does not decrease case fatality and dependency in acute stroke.
A more recent clinical study of note involved a multi-center trial examining vinpocetine's effects on NF-κB-dependent inflammation in acute ischemic stroke. For this multi-center study, 60 patients with anterior cerebral circulation occlusion and onset of stroke exceeding 4.5 hours but lasting less than 48 hours were randomly divided into two groups receiving either standard management alone (controls) or standard management plus vinpocetine (30 mg per day intravenously for 14 consecutive days). Compared to controls, patients treated with vinpocetine had better recovery of neurological function and improved clinical outcomes during the acute phase and at 3-month follow-up, with findings identifying vinpocetine as an inflammation modulator. However, the final verdict on its effectiveness still remains unclear. The positive results of the Chinese CAVIN trial for intravenous vinpocetine in acute ischemic stroke are considered promising but require independent validation, as rigorous, multicenter, double-blind, placebo-controlled randomized trials are urgently needed in diverse populations to confirm or refute these findings.
Evidence strength: Weak to preliminary for clinical benefit in ischemic stroke. The Cochrane review found insufficient evidence from randomized controlled trials. More recent clinical data are promising but from small studies and require replication in larger, blinded trials.
The most comprehensive assessment of vinpocetine for cognitive impairment and dementia is the Cochrane systematic review by Szatmári and Whitehouse (2003). All identified studies were performed before and in the early 1990s and used various terms and criteria for cognitive decline and dementia. The three studies included in the review involved a total of 583 people with dementia treated with vinpocetine or placebo. The reports of these studies did not make possible any differentiation of effects for degenerative or vascular dementia.
The results show benefit associated with treatment with vinpocetine 30 mg/day and 60 mg/day compared with placebo, but the number of patients treated for six months or more was small. Only one study extended treatment to one year. Adverse effects were inconsistently reported and without regard for relationship to dose.
Although the basic science is interesting, the evidence for a beneficial effect of vinpocetine on patients with dementia is inconclusive and does not support clinical use. The drug seems to have few adverse effects at the doses used in the studies. Large studies evaluating the use of vinpocetine for people suffering from well-defined types of cognitive impairment are needed to explore possible efficacy of this treatment.
Clinical data on the effects of vinpocetine in Alzheimer's disease were more extensively studied before the 1990s, and some studies at that time suggested positive associations with the use of vinpocetine. However, a review by the Cochrane Database of Systematic Reviews found many inconsistencies in the evidence, and therefore the overall evidence for the effectiveness of vinpocetine in Alzheimer's disease remains inconclusive (up to 2003).
Basic science studies have been invoked to claim a variety of potentially important effects in the brain. However, despite these many proposed mechanisms and targets, the relevance of this basic science to clinical studies is unclear.
Evidence strength: Inconclusive. The principal Cochrane review found signals of benefit in small, methodologically limited trials but concluded the evidence does not support clinical use. The existing trials are dated, use heterogeneous diagnostic criteria, and are insufficiently powered.
Vinpocetine is reported to be effective as adjuvant therapy in the management of epilepsy, reducing seizure frequency by 50% in a dose of 2 mg/kg/day. A multicenter, double-blind, randomized, placebo-controlled trial of sustained-release vinpocetine as adjunctive treatment of focal-onset seizures (Garza-Morales et al., published in Epilepsia, 2015) was catalogued in the Cochrane CENTRAL registry. Antiepileptic effects have been attributed to suppression of abnormal neuronal excitability via sodium channel regulation and dopamine release in striatal nerve endings. The anti-epileptic mechanisms of vinpocetine are through blockade of presynaptic sodium channels, mediated glutamate release inhibition, and inhibition of TNF-α and IL-1β.
Evidence strength: Preliminary. Limited clinical trial data exist; mechanistic rationale from preclinical studies is plausible but robust, large-scale randomized controlled trial evidence in humans remains scarce.
Previous clinical trials have reported that vinpocetine can be used for the treatment of cognitive dysfunction, however its efficacy is still inconclusive. A protocol for a systematic review and meta-analysis registered with PROSPERO (CRD42018115224) was developed to evaluate the efficacy and safety of vinpocetine for the treatment of post-stroke cognitive dysfunction. All randomized controlled trials of vinpocetine for post-stroke cognitive dysfunction were to be considered for inclusion without language restriction.
Evidence strength: Emerging but inconclusive. Formal systematic review work is underway, and the existing individual trials are methodologically heterogeneous. No definitive conclusions can yet be drawn.
Cardiovascular diseases involve a variety of cell types and intercellular communications. The multiple actions of vinpocetine in different cell types may permit synergistic beneficial effects. For example, vinpocetine may hamper atherosclerosis progression by antagonizing lipid uptake, hyperlipidemia, oxidative stress, and inflammation synergistically due to its multi-action mechanisms. These findings are largely from preclinical (in vitro and animal model) studies. There are still limitations in previous studies, as the molecular mechanisms responsible for some novel functions of vinpocetine are not fully understood mechanistically — for example, anti-oxidation and anti-lipid accumulation.
Evidence strength: Preclinical only. Evidence for cardiovascular benefits in humans is absent; current data are exclusively from cell culture and animal models.
Another area where vinpocetine has been researched is ophthalmological disorders of vision and visual field. A body of evidence has shown that vinpocetine possesses diverse therapeutic effects on a myriad of diseases, including age-related macular degeneration. These studies are predominantly preclinical.
Evidence strength: Preclinical/preliminary. Robust human clinical trial data in ophthalmology are lacking.
Preclinical studies suggest that vinpocetine may reduce inflammation, improve biological aspects of memory, and perhaps improve memory or prevent cognitive impairment. It is not yet known, however, whether these effects will transfer to humans. The inclusion of vinpocetine in dietary supplements has recently come under scrutiny due to the lack of defined dosage parameters and yet unproven short- and long-term benefits and risks to human health.
Evidence strength: Very weak. No adequately powered, well-controlled clinical trials have established cognitive enhancement in healthy individuals.
There are few robust clinical studies to support the use of vinpocetine in stroke, dementia, or other diseases of the CNS. Most clinical studies have used between 5 and 30 mg vinpocetine given up to 3 times daily due to a short half-life (2 to 4 hours).
In the Cochrane systematic review on dementia (Szatmári and Whitehouse, 2003): the doses examined in the included trials were 30 mg/day and 60 mg/day.
In the NF-κB stroke study: patients received 30 mg per day intravenously for 14 consecutive days.
In pharmacokinetic studies of healthy volunteers: the pharmacokinetics of vinpocetine (Cavinton) and its main metabolite apovincaminic acid were studied in five healthy male volunteers after the administration of 3 × 5 mg and 3 × 10 mg daily doses of vinpocetine for seven days.
In the epilepsy context: a dose of 2 mg/kg/day was reported in a study examining adjuvant therapy in epilepsy management.
A study of commercially available dietary supplements found a highly variable range of 0.6–5.1 mg per serving. A broader analytical study found seventeen out of twenty-three supplements labeled as containing vinpocetine had quantities ranging from 0.3 to 32 mg per recommended daily serving. This wide variation underscores the lack of standardization in the supplement market.
Vinpocetine showed linear pharmacokinetics at the therapeutic dose, suggesting no drug accumulation.
Due to its generally favorable safety profile, increasing efforts have been put into exploring the novel therapeutic effects and mechanisms of action of vinpocetine in various cell types and disease models. It is considered to be a safe compound with no serious side effects reported in humans when administered as a single agent. The drug seems to have few adverse effects at the doses used in the reviewed clinical studies.
This is the most significant established safety signal for vinpocetine. On June 3, 2019, FDA issued a safety warning for women of childbearing age about vinpocetine. According to data reviewed by FDA, consumption of vinpocetine is associated with adverse reproductive effects — in other words, vinpocetine may cause a miscarriage or harm fetal development. Accordingly, FDA advised pregnant women and women who could become pregnant not to take vinpocetine.
This warning was based substantially on the NTP (National Toxicology Program) developmental toxicology studies. Because of the limited literature indicating that vinpocetine may not be safe for use during pregnancy and the possibility for widespread exposure to women of childbearing age, the NTP conducted prenatal developmental toxicology studies in time-mated Sprague Dawley rats and New Zealand White rabbits, which received vinpocetine (99.3% pure) by gavage from implantation through the day before expected parturition.
A study with pregnant rats evaluated the effects of vinpocetine on maternal health and embryo and fetal development following oral administration at doses of 5, 20, and 60 mg/kg/day from gestation days 6 through 20. Increased embryo/fetal loss occurred in the 60-mg/kg/day dose group. Administration of vinpocetine also decreased fetal weight at all tested doses and induced fetal malformations in the two highest dose groups.
Vinpocetine at doses up to 300 mg/kg/day in rabbits resulted in fewer live fetuses, attributable to the induction of both early and late resorptions. There are no studies that examined vinpocetine exposure and adverse reproductive or prenatal outcomes in humans.
In 2019, the FDA issued a safety warning for women of childbearing age regarding possible risks associated with vinpocetine, due to indications of adverse effects on reproductive health (i.e., reproductive and developmental toxicity in animals), including miscarriage and harm to fetal development, but the FDA has not yet issued a final decision on the matter.
Vinpocetine may have antiplatelet and anticoagulant effects, and therefore should be used with caution or avoided in individuals with bleeding disorders or a history of bleeding events. Vinpocetine may increase the risk of bleeding or interact with other anticoagulant medications, leading to serious bleeding complications.
Studies were carried out to evaluate the effects of vinpocetine on three main regulators of pharmacokinetic drug interactions: cytochromes P450 (CYPs), P-glycoprotein (P-gp), and Pregnane X receptor (PXR). P-gp inhibition due to drug–drug and food–drug interactions can significantly alter the pharmacokinetics and pharmacodynamics of other drugs, especially those with a narrow therapeutic index. Therefore, further investigation into the potential implications of these findings is warranted. Despite vinpocetine's wide use, formal pharmacokinetic drug interaction studies were not historically reported in the literature, and the risk of adverse effects is on the rise due to increasing use of dietary supplements in combination with conventional drugs.
A significant consumer safety issue specific to the supplement market has been documented. Twenty-three supplements labeled as containing vinpocetine were available for sale at two large supplement retail chains; 17 contained vinpocetine, with quantities ranging from 0.3 to 32 mg per recommended daily serving. No vinpocetine was detected in six of the sampled supplements. Consumers cannot obtain accurate information from supplement labels regarding the presence or quantity of vinpocetine.
FDA has tentatively concluded that vinpocetine does not meet the definition of a dietary ingredient and is excluded from the definition of a dietary supplement under the Federal Food, Drug, and Cosmetic Act because vinpocetine was authorized for investigation as a new drug before it was marketed as a dietary supplement or as a food. Despite this, vinpocetine is often marketed as a dietary supplement, although as a synthetic substance it is unauthorized in food supplements in the EU, where the European Medicines Agency considers it an approved drug.
In the United States, vinpocetine has never been approved by the US Food and Drug Administration as either a dietary supplement ingredient or a prescription drug.
Health conditions that Vinpocetine may help support.
Vinpocetine, a semi-synthetic vinca alkaloid derived from vincamine, enhances cerebral blood flow by inhibiting phosphodiesterase type 1, reducing blood viscosity, and improving red blood cell deformability. It has been used as a prescription drug in Eastern Europe since the 1970s for cerebrovascular insufficiency. A pilot RCT (12-week oral vinpocetine) found improved cerebrovascular reserve capacity and cognitive status in patients with chronic cerebral hypoperfusion.
Vinpocetine is a synthetic derivative of the Vinca minor alkaloid vincamine, studied clinically for cognitive impairment and age-related cerebrovascular decline. Its primary mechanism involves inhibition of phosphodiesterase type 1 (PDE1), which elevates cAMP/cGMP, improves cerebral blood flow, and supports neuronal plasticity. A Cochrane review of three randomized controlled trials (583 patients) found signals of benefit at 30–60 mg/day but concluded the evidence is inconclusive due to small sample sizes, short duration, and inconsistent adverse-effect reporting. Vinpocetine has not been approved by any regulatory body for treating cognitive impairment.
Vinpocetine, a synthetic derivative of the periwinkle alkaloid vincamine, enhances cerebral blood flow and neuronal glucose metabolism via PDE1 inhibition. Three controlled studies in older adults with memory problems found it significantly outperformed placebo on tests of attention, concentration, and memory. It is a licensed prescription drug for cerebrovascular disorders in multiple European and Asian countries.
Vinpocetine is a synthetic derivative of vincamine (from Vinca minor) used as a prescription pharmaceutical for cerebrovascular disorders in Japan, Russia, and parts of Europe. It improves cerebral blood flow, glucose uptake, and oxygen utilization in the brain. Multiple double-blind RCTs show improvements in memory and cognitive function in patients with mild to moderate cognitive impairment.
Vinpocetine, a synthetic derivative of vincamine from the periwinkle plant, increases cerebral blood flow and metabolism. Three RCTs in older adults with memory problems associated with poor brain circulation found significantly greater improvement on global cognitive tests including memory versus placebo. It has been used clinically in Europe for vascular cognitive impairment for decades.
Vinpocetine is a semi-synthetic alkaloid derived from vincamine (from periwinkle, Vinca minor) that increases cerebral blood flow and glucose metabolism. Studies show improvements in memory, attention, and alertness in healthy adults and those with cerebrovascular-related cognitive decline.
Vinpocetine is a semi-synthetic derivative of the periwinkle alkaloid vincamine that dilates cerebral blood vessels, improves cerebral blood flow, exhibits potent anti-inflammatory effects at the microglial level, and has been used clinically for cognitive impairment and nervous system disorders.
Vinpocetine, a semi-synthetic derivative of vincamine from the periwinkle plant, has been used traditionally in Europe (particularly Germany) to treat tinnitus associated with poor cochlear blood flow. It acts as a sodium channel blocker and cerebrovascular vasodilator. Preliminary clinical data indicate benefit for tinnitus with a vascular or ischemic origin, and a Phase 2 open-label study showed hearing improvement.
Vinpocetine, a semisynthetic alkaloid derived from Vinca minor, has been clinically used to treat vertigo and dizziness for over 30 years via cerebral blood flow enhancement and neuroprotection. A clinical study (n=44, 15 mg/day) showed improvement of vertigo in 100% and dizziness in 71% of patients. The EDELWEISS open-label parallel-group study (n=139, 8 months) demonstrated significant reduction in vertigo/dizziness severity and improved statodynamic function with vinpocetine plus vestibular exercises.
Body systems that Vinpocetine may help support.
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