Vinpocetine CAS NO.42971-09-5

Hubei CuiRan Biotechnology Co., Ltd is a leading company in the research, development, manufacture and marketing of High Quality Phytochemicals and Extracts(especially Active Ingredients from Traditional Chinese Medicine，Traditional Chinese Medicine), Natural Active Pharmaceutical Ingredients worldwide. From small quantities for R&D or reference standard, to large quantities for customizing or manufacturing, Biopurify emphasizes on consistent and reliable services for his customers. 
With excellent quality products and good service, we have clients from more than dozens countries and regions, and we pride ourselves in providing our customers with a total satisfaction experiences.
We are doing our best to be your reliable partner for high quality Phytochemicals and Reference Standards from china.
 
Our main services:
A. Supply active ingredients and reference standards ofTraditional Chinese Medicine, from mgs to kgs scale.
B. Custom extraction and purification, target Herb Active Ingredients
C. Custom synthesis and semi-synthesis for Natural Active Ingredients
D. CR, CM and PD services from lab scale, pilot scale to commercial scale(GMP is also available)
E.Traditional Chinese Medicine compounds library
 

1.Provide traditional Chinese medicine reference materials and natural active ingredients;
2.More than 2200 compounds are available for selection, continuously building high-quality natural product libraries for drug research and development;
3.Provide various screening libraries and more inhibitor products;
4.Provide separation and structural determination of natural products;
5.Laboratory scale pilot to commercial scale collaborative research and process development services.More than 180 experiences in phytochemistry (still increasing)
Each product has passed very strict testing (NMR/MS/HPLC)
Agents from many countries

General tips：For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging：1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition：Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Chemical Properties of Vinpocetine

Cas No.	42971-09-5
PubChem ID	443955	Appearance	Cryst.
Formula	C22H26N2O2	M.Wt	350.45
Type of Compound	Alkaloids	Storage	Desiccate at -20°C
Solubility	DMSO : 6.25 mg/mL (17.83 mM; Need ultrasonic)
SMILES	CCC12CCCN3C1C4=C(CC3)C5=CC=CC=C5N4C(=C2)C(=O)OCC
Standard InChIKey	DDNCQMVWWZOMLN-IRLDBZIGSA-N
Standard InChI	InChI=1S/C22H26N2O2/c1-3-22-11-7-12-23-13-10-16-15-8-5-6-9-17(15)24(19(16)20(22)23)18(14-22)21(25)26-4-2/h5-6,8-9,14,20H,3-4,7,10-13H2,1-2H3/t20-,22+/m1/s1
General tips	For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging	1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment.
Shipping Condition	Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Vinpocetine

The herbs of Catharanthus roseus (L.) G. Don

Biological Activity of Vinpocetine

Description	Vinpocetine is a selective inhibitor of voltage-sensitive sodium channel for the treatment of stroke, vascular dementia and Alzheimer's disease. Vinpocetine can attenuate neointimal formation in diabetic rats and inhibit HG-induced VSMCs proliferation, chemokinesis and apoptotic resistance by preventing ROS activation and affecting MAPK, PI3K/Akt, and NF-κB signaling.Vinpocetine has anti-inflammatory activity, can treat inflammation and pain induced by a gram-negative bacterial component by targeting NF-κB activation and NF-κB-related cytokine production in macrophages.
Targets	NF-kB | Beta Amyloid | Caspase | IL Receptor | TNF-α | Akt | JNK | Bcl-2/Bax | ROS | PI3K | IkB | MAPK | IKK
In vivo	Vinpocetine modulates metabolic activity and function during retinal ischemia.[Pubmed: 25696811] Am J Physiol Cell Physiol. 2015 May 1;308(9):C737-49. Vinpocetine protects against a range of degenerative conditions and insults of the central nervous system via multiple modes of action. Little is known, however, of its effects on metabolism. This may be highly relevant, as Vinpocetine is highly protective against ischemia, a process that inhibits normal metabolic function. METHODS AND RESULTS: This study uses the ischemic retina as a model to characterize Vinpocetine's effects on metabolism. Vinpocetine reduced the metabolic demand of the retina following ex vivo hypoxia and ischemia to normal levels based on lactate dehydrogenase activity. Vinpocetine delivered similar effects in an in vivo model of retinal ischemia-reperfusion, possibly through increasing glucose availability. Vinpocetine's effects on glucose also appeared to improve glutamate homeostasis in ischemic Müller cells. Other actions of Vinpocetine following ischemia-reperfusion, such as reduced cell death and improved retinal function, were possibly a combination of the drug's actions on metabolism and other retinal pathways. Vinpocetine's metabolic effects appeared independent of its other known actions in ischemia, as it recovered retinal function in a separate metabolic model where the glutamate-to-glutamine metabolic pathway was inhibited in Müller cells. CONCLUSIONS: The results of this study indicate that Vinpocetine mediates ischemic damage partly through altered metabolism and has potential beneficial effects as a treatment for ischemia of neuronal tissues. Vinpocetine attenuates MPTP-induced motor deficit and biochemical abnormalities in Wistar rats.[Pubmed: 25514048] Neuroscience. 2015 Feb 12;286:393-403. Up-regulation in phosphodiesterase 1 (PDE1) expression and decreased levels of cyclic nucleotides (cAMP and cGMP) have been reported in patients and experimental animal models of Parkinson's disease (PD). Phosphodiesterase (PDE) inhibitors have been reported to be beneficial in cognitive and motor deficit states. METHODS AND RESULTS: The present study is designed to investigate the effect of Vinpocetine, a PDE1 inhibitor in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced experimental PD-like symptoms in rats. To produce stable motor deficit, MPTP was repeatedly administered intranigrally (bilaterally) at an interval of 1 week (days 1, 7 and 14). Following development of stable motor deficit, which was observed after the third infusion of MPTP (day 14) in rats, the animals were treated with Vinpocetine (5-, 10- and 20-mg/kg, i.p.) from days 15 to 28. Movement abnormalities were assessed by a battery of behavioral tests. Moreover, levels of malondialdehyde, nitrite and reduced glutathione were measured in striatal brain homogenate to confirm the role of oxidative and nitrosative stress in PD. Repeated intranigral administration of MPTP produced stable motor deficits, reduced the cyclic nucleotides and dopamine levels and caused elevation in oxidative-nitrosative stress markers. Chronic administration of Vinpocetine (for 14 days) significantly and dose dependently attenuated movement disabilities and oxidative-nitrosative stress in MPTP-treated rats. Moreover, Vinpocetine treatment enhances cyclic nucleotide levels and restores the dopamine level in MPTP-treated rats. CONCLUSIONS: The observed results of the present study are indicative of the therapeutic potential of Vinpocetine in PD. Vinpocetine attenuates neointimal hyperplasia in diabetic rat carotid arteries after balloon injury.[Pubmed: 24819198] PLoS One. 2014 May 12;9(5):e96894. Diabetes exacerbates abnormal vascular smooth muscle cell (VSMC) accumulation in response to arterial wall injury. Vinpocetine has been shown to improve vascular remolding; however, little is known about the direct effects of Vinpocetine on vascular complications mediated by diabetes. The objective of this study was to determine the effects of Vinpocetine on hyperglycemia-facilitated neointimal hyperplasia and explore its possible mechanism. METHODS AND RESULTS: Nondiabetic and diabetic rats were subjected to balloon injury of the carotid artery followed by 3-week treatment with either Vinpocetine (10 mg/kg/day) or saline. Morphological analysis and proliferating cell nuclear antigen (PCNA) immunostaining were performed on day 21. Rat VSMCs proliferation was determined with 5-ethynyl-20-deoxyuridine cell proliferation assays. Chemokinesis was monitored with scratch assays, and production of reactive oxygen species (ROS) was assessed using a 2',7'-dichlorodihydrofluorescein diacetate (H2DCFDA) flow cytometric assay. Apoptosis was detected by annexin V-FITC/PI flow cytometric assay. Cell signaling was assessed by immunblotting. Vinpocetine prevented intimal hyperplasia in carotid arteries in both normal (I/M ratio: 93.83 ± 26.45% versus 143.2 ± 38.18%, P<0.05) and diabetic animals (I/M ratio: 120.5 ± 42.55% versus 233.46 ± 33.98%, P<0.05) when compared to saline. The in vitro study demonstrated that Vinpocetine significantly inhibited VSMCs proliferation and chemokinesis as well as ROS generation and apoptotic resistance, which was induced by high glucose (HG) treatment. Vinpocetine significantly abolished HG-induced phosphorylation of Akt and JNK1/2 without affecting their total levels. For downstream targets, HG-induced phosphorylation of IκBα was significantly inhibited by Vinpocetine. Vinpocetine also attenuated HG-enhanced expression of PCNA, cyclin D1 and Bcl-2. CONCLUSIONS: Vinpocetine attenuated neointimal formation in diabetic rats and inhibited HG-induced VSMCs proliferation, chemokinesis and apoptotic resistance by preventing ROS activation and affecting MAPK, PI3K/Akt, and NF-κB signaling.

Protocol of Vinpocetine

Animal Research

Vinpocetine reduces lipopolysaccharide-induced inflammatory pain and neutrophil recruitment in mice by targeting oxidative stress, cytokines and NF-κB.[Pubmed: 25980587] Vinpocetine inhibits amyloid-beta induced activation of NF-κB, NLRP3 inflammasome and cytokine production in retinal pigment epithelial cells.[Pubmed: 25041941] Exp Eye Res. 2014 Oct;127:49-58. Chronic inflammation is a key pathogenic process in age-related macular degeneration (AMD). Amyloid-beta (Aβ) is a constituent of AMD drusen and promotes the activation of NLRP3 inflammasome which facilitates the production of cytokines. METHODS AND RESULTS: We investigated the role of transcription factor NF-κB in the activation of inflammasome in the RPE and the effect of Vinpocetine, a dietary supplement with inhibitory effect on NF-κΒ. ARPE19/NF-κB-luciferase reporter cells treated with Aβ demonstrated enhanced NF-κB activation that was significantly suppressed by Vinpocetine. Intraperitoneal injection of Vinpocetine (15 mg/kg) inhibited NF-κB nuclear translocation and reduced the expression and activation of NLRP3, caspase-1, IL-1β, IL-18, and TNF-α in the RPE of adult rats that received intraocular Αβ, as measured by retinal immunohistochemistry and Western blot. Cytokine level in the vitreous was assayed using multiplex suspension arrays and revealed significantly lower concentration of MIP-3α, IL-6, IL-1α, IL-1β, IL-18, and TNF-α in Vinpocetine treated animals. These results suggest that the NF-κB pathway is activated by Aβ in the RPE and signals the priming of NLRP3 inflammasome and the expression of pro-inflammatory cytokines including the inflammasome substrates IL-1β and IL-18. NF-κB inhibition may be an effective approach to stem the chronic inflammatory milieu that underlies the development of AMD. CONCLUSIONS: Vinpocetine is a potentially useful anti-inflammatory agent that is well-tolerated in long term use. Chem Biol Interact. 2015 Jul 25;237:9-17. In response to lipopolysaccharide (LPS), tissue resident macrophages and recruited neutrophils produce inflammatory mediators through activation of Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathway. These mediators include inflammatory cytokines and reactive oxygen species that, in turn, sensitize nociceptors and lead to inflammatory pain. Vinpocetine is a nootropic drug widely used to treat cognitive and neurovascular disorders, and more recently its anti-inflammatory properties through inhibition of NF-κB activation have been described. METHODS AND RESULTS: In the present study, we used the intraplantar and intraperitoneal LPS stimulus in mice to investigate the effects of Vinpocetine pre-treatment (3, 10, or 30mg/kg by gavage) in hyperalgesia, leukocyte recruitment, oxidative stress, and pro-inflammatory cytokine production (TNF-α, IL-1β, and IL-33). LPS-induced NF-κB activation and cytokine production were investigated using RAW 264.7 macrophage cell in vitro. Vinpocetine (30mg/kg) significantly reduces hyperalgesia to mechanical and thermal stimuli, and myeloperoxidase (MPO) activity (a neutrophil marker) in the plantar paw skin, and also inhibits neutrophil and mononuclear cell recruitment, superoxide anion and nitric oxide production, oxidative stress, and cytokine production (TNF-α, IL-1β and IL-33) in the peritoneal cavity. At least in part, these effects seem to be mediated by direct effects of Vinpocetine on macrophages, since it inhibited the production of the same cytokines (TNF-α, IL-1β and IL-33) and the NF-κB activation in LPS-stimulated RAW 264.7 macrophages. CONCLUSIONS: Our results suggest that Vinpocetine represents an important therapeutic approach to treat inflammation and pain induced by a gram-negative bacterial component by targeting NF-κB activation and NF-κB-related cytokine production in macrophages.

Preparing Stock Solutions of Vinpocetine

	1 mg	5 mg	10 mg	20 mg	25 mg
1 mM	2.8535 mL	14.2674 mL	28.5347 mL	57.0695 mL	71.3369 mL
5 mM	0.5707 mL	2.8535 mL	5.7069 mL	11.4139 mL	14.2674 mL
10 mM	0.2853 mL	1.4267 mL	2.8535 mL	5.7069 mL	7.1337 mL
50 mM	0.0571 mL	0.2853 mL	0.5707 mL	1.1414 mL	1.4267 mL
100 mM	0.0285 mL	0.1427 mL	0.2853 mL	0.5707 mL	0.7134 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

 

References on Vinpocetine

Vinpocetine attenuates MPTP-induced motor deficit and biochemical abnormalities in Wistar rats.[Pubmed:25514048]

Neuroscience. 2015 Feb 12;286:393-403.

Up-regulation in phosphodiesterase 1 (PDE1) expression and decreased levels of cyclic nucleotides (cAMP and cGMP) have been reported in patients and experimental animal models of Parkinson's disease (PD). Phosphodiesterase (PDE) inhibitors have been reported to be beneficial in cognitive and motor deficit states. The present study is designed to investigate the effect of Vinpocetine, a PDE1 inhibitor in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced experimental PD-like symptoms in rats. To produce stable motor deficit, MPTP was repeatedly administered intranigrally (bilaterally) at an interval of 1 week (days 1, 7 and 14). Following development of stable motor deficit, which was observed after the third infusion of MPTP (day 14) in rats, the animals were treated with Vinpocetine (5-, 10- and 20-mg/kg, i.p.) from days 15 to 28. Movement abnormalities were assessed by a battery of behavioral tests. Moreover, levels of malondialdehyde, nitrite and reduced glutathione were measured in striatal brain homogenate to confirm the role of oxidative and nitrosative stress in PD. Repeated intranigral administration of MPTP produced stable motor deficits, reduced the cyclic nucleotides and dopamine levels and caused elevation in oxidative-nitrosative stress markers. Chronic administration of Vinpocetine (for 14 days) significantly and dose dependently attenuated movement disabilities and oxidative-nitrosative stress in MPTP-treated rats. Moreover, Vinpocetine treatment enhances cyclic nucleotide levels and restores the dopamine level in MPTP-treated rats. The observed results of the present study are indicative of the therapeutic potential of Vinpocetine in PD.

Vinpocetine inhibits amyloid-beta induced activation of NF-kappaB, NLRP3 inflammasome and cytokine production in retinal pigment epithelial cells.[Pubmed:25041941]

Exp Eye Res. 2014 Oct;127:49-58.

Chronic inflammation is a key pathogenic process in age-related macular degeneration (AMD). Amyloid-beta (Abeta) is a constituent of AMD drusen and promotes the activation of NLRP3 inflammasome which facilitates the production of cytokines. We investigated the role of transcription factor NF-kappaB in the activation of inflammasome in the RPE and the effect of Vinpocetine, a dietary supplement with inhibitory effect on NF-kappaBeta. ARPE19/NF-kappaB-luciferase reporter cells treated with Abeta demonstrated enhanced NF-kappaB activation that was significantly suppressed by Vinpocetine. Intraperitoneal injection of Vinpocetine (15 mg/kg) inhibited NF-kappaB nuclear translocation and reduced the expression and activation of NLRP3, caspase-1, IL-1beta, IL-18, and TNF-alpha in the RPE of adult rats that received intraocular Alphabeta, as measured by retinal immunohistochemistry and Western blot. Cytokine level in the vitreous was assayed using multiplex suspension arrays and revealed significantly lower concentration of MIP-3alpha, IL-6, IL-1alpha, IL-1beta, IL-18, and TNF-alpha in Vinpocetine treated animals. These results suggest that the NF-kappaB pathway is activated by Abeta in the RPE and signals the priming of NLRP3 inflammasome and the expression of pro-inflammatory cytokines including the inflammasome substrates IL-1beta and IL-18. NF-kappaB inhibition may be an effective approach to stem the chronic inflammatory milieu that underlies the development of AMD. Vinpocetine is a potentially useful anti-inflammatory agent that is well-tolerated in long term use.

Vinpocetine reduces lipopolysaccharide-induced inflammatory pain and neutrophil recruitment in mice by targeting oxidative stress, cytokines and NF-kappaB.[Pubmed:25980587]

Chem Biol Interact. 2015 Jul 25;237:9-17.

In response to lipopolysaccharide (LPS), tissue resident macrophages and recruited neutrophils produce inflammatory mediators through activation of Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-kappaB) signaling pathway. These mediators include inflammatory cytokines and reactive oxygen species that, in turn, sensitize nociceptors and lead to inflammatory pain. Vinpocetine is a nootropic drug widely used to treat cognitive and neurovascular disorders, and more recently its anti-inflammatory properties through inhibition of NF-kappaB activation have been described. In the present study, we used the intraplantar and intraperitoneal LPS stimulus in mice to investigate the effects of Vinpocetine pre-treatment (3, 10, or 30mg/kg by gavage) in hyperalgesia, leukocyte recruitment, oxidative stress, and pro-inflammatory cytokine production (TNF-alpha, IL-1beta, and IL-33). LPS-induced NF-kappaB activation and cytokine production were investigated using RAW 264.7 macrophage cell in vitro. Vinpocetine (30mg/kg) significantly reduces hyperalgesia to mechanical and thermal stimuli, and myeloperoxidase (MPO) activity (a neutrophil marker) in the plantar paw skin, and also inhibits neutrophil and mononuclear cell recruitment, superoxide anion and nitric oxide production, oxidative stress, and cytokine production (TNF-alpha, IL-1beta and IL-33) in the peritoneal cavity. At least in part, these effects seem to be mediated by direct effects of Vinpocetine on macrophages, since it inhibited the production of the same cytokines (TNF-alpha, IL-1beta and IL-33) and the NF-kappaB activation in LPS-stimulated RAW 264.7 macrophages. Our results suggest that Vinpocetine represents an important therapeutic approach to treat inflammation and pain induced by a gram-negative bacterial component by targeting NF-kappaB activation and NF-kappaB-related cytokine production in macrophages.

Vinpocetine attenuates neointimal hyperplasia in diabetic rat carotid arteries after balloon injury.[Pubmed:24819198]

PLoS One. 2014 May 12;9(5):e96894.

BACKGROUND: Diabetes exacerbates abnormal vascular smooth muscle cell (VSMC) accumulation in response to arterial wall injury. Vinpocetine has been shown to improve vascular remolding; however, little is known about the direct effects of Vinpocetine on vascular complications mediated by diabetes. The objective of this study was to determine the effects of Vinpocetine on hyperglycemia-facilitated neointimal hyperplasia and explore its possible mechanism. MATERIALS AND METHODS: Nondiabetic and diabetic rats were subjected to balloon injury of the carotid artery followed by 3-week treatment with either Vinpocetine (10 mg/kg/day) or saline. Morphological analysis and proliferating cell nuclear antigen (PCNA) immunostaining were performed on day 21. Rat VSMCs proliferation was determined with 5-ethynyl-20-deoxyuridine cell proliferation assays. Chemokinesis was monitored with scratch assays, and production of reactive oxygen species (ROS) was assessed using a 2',7'-dichlorodihydrofluorescein diacetate (H2DCFDA) flow cytometric assay. Apoptosis was detected by annexin V-FITC/PI flow cytometric assay. Cell signaling was assessed by immunblotting. RESULTS: Vinpocetine prevented intimal hyperplasia in carotid arteries in both normal (I/M ratio: 93.83 +/- 26.45% versus 143.2 +/- 38.18%, P<0.05) and diabetic animals (I/M ratio: 120.5 +/- 42.55% versus 233.46 +/- 33.98%, P<0.05) when compared to saline. The in vitro study demonstrated that Vinpocetine significantly inhibited VSMCs proliferation and chemokinesis as well as ROS generation and apoptotic resistance, which was induced by high glucose (HG) treatment. Vinpocetine significantly abolished HG-induced phosphorylation of Akt and JNK1/2 without affecting their total levels. For downstream targets, HG-induced phosphorylation of IkappaBalpha was significantly inhibited by Vinpocetine. Vinpocetine also attenuated HG-enhanced expression of PCNA, cyclin D1 and Bcl-2. CONCLUSIONS: Vinpocetine attenuated neointimal formation in diabetic rats and inhibited HG-induced VSMCs proliferation, chemokinesis and apoptotic resistance by preventing ROS activation and affecting MAPK, PI3K/Akt, and NF-kappaB signaling.

Vinpocetine modulates metabolic activity and function during retinal ischemia.[Pubmed:25696811]

Am J Physiol Cell Physiol. 2015 May 1;308(9):C737-49.

Vinpocetine protects against a range of degenerative conditions and insults of the central nervous system via multiple modes of action. Little is known, however, of its effects on metabolism. This may be highly relevant, as Vinpocetine is highly protective against ischemia, a process that inhibits normal metabolic function. This study uses the ischemic retina as a model to characterize Vinpocetine's effects on metabolism. Vinpocetine reduced the metabolic demand of the retina following ex vivo hypoxia and ischemia to normal levels based on lactate dehydrogenase activity. Vinpocetine delivered similar effects in an in vivo model of retinal ischemia-reperfusion, possibly through increasing glucose availability. Vinpocetine's effects on glucose also appeared to improve glutamate homeostasis in ischemic Muller cells. Other actions of Vinpocetine following ischemia-reperfusion, such as reduced cell death and improved retinal function, were possibly a combination of the drug's actions on metabolism and other retinal pathways. Vinpocetine's metabolic effects appeared independent of its other known actions in ischemia, as it recovered retinal function in a separate metabolic model where the glutamate-to-glutamine metabolic pathway was inhibited in Muller cells. The results of this study indicate that Vinpocetine mediates ischemic damage partly through altered metabolism and has potential beneficial effects as a treatment for ischemia of neuronal tissues.

Vinpocetine is as potent as phenytoin to block voltage-gated Na+ channels in rat cortical neurons.[Pubmed:7737339]

Eur J Pharmacol. 1995 Feb 6;273(3):303-6.

The effects of Vinpocetine and phenytoin on voltage-gated Na+ channels were examined on cultured cerebrocortical neurones of the rat using a conventional whole-cell patch-clamp method. Vinpocetine and phenytoin decreased Na+ currents in a concentration-dependent manner, with IC50 values of 44.2 +/- 14.6 and 50.5 +/- 17.4 microM, respectively. Both compounds shifted the voltage dependence of the steady-state inactivation of the channel in the hyperpolarising direction. This pronounced Na+ channel blocking activity may contribute to the neuroprotective and anticonvulsant effects of Vinpocetine.

Effects of vinpocetine on cyclic nucleotide metabolism in vascular smooth muscle.[Pubmed:6322804]

Biochem Pharmacol. 1984 Feb 1;33(3):453-7.

A novel vasodilating agent, Vinpocetine (14-ethoxycarbonyl-(3 alpha,16 alpha-ethyl)-14,15-eburnamenine) inhibits Ca2+-dependent phosphodiesterase, selectively, among the three forms of cyclic nucleotide phosphodiesterase identified in the rabbit aorta. The concentration of Vinpocetine producing 50% inhibition of Ca2+-dependent phosphodiesterase activity was approximately 21 microM, both in the presence and absence of Ca2+-calmodulin (CaM). Increasing the concentration of CaM in the presence of Ca2+ did not prevent Vinpocetine-induced inhibition of Ca2+-dependent phosphodiesterase, thereby indicating that Vinpocetine inhibited the enzyme by interacting with the enzyme and not with CaM. To determine the influence of Vinpocetine-induced inhibition of Ca2+-dependent phosphodiesterase on cyclic nucleotide metabolism in vascular smooth muscle, cyclic nucleotide levels in isolated rabbit aortic strips were also investigated. Addition of Vinpocetine produced dose-dependent increases in only the cyclic GMP levels and there was no significant effects on the cyclic AMP levels. These results provide pharmacological evidence that Ca2+-dependent phosphodiesterase mainly hydrolyzes cyclic GMP in vascular smooth muscle. Vinpocetine may induce vascular relaxation by increasing cyclic GMP contents in vascular smooth muscle through selective inhibition of Ca2+-dependent phosphodiesterase.

Description

Vinpocetine (Ethyl apovincaminate) is a derivative of the alkaloid Vincamine that blocks voltage-gated Na+ channels. The IC50 value of Vinpocetine on direct IKK inhibition in the cell-free system is 17.17 μM. Vinpocetine is a phosphodiesterase (PDE) inhibitor and inhibits NF-κB-dependent inflammatory responses by directly targeting IκB kinase complex (IKK), and has been widely used for the treatment of cerebrovascular disorders.

Keywords:

Vinpocetine,42971-09-5,Natural Products,PDE, buy Vinpocetine , Vinpocetine supplier , purchase Vinpocetine , Vinpocetine cost , Vinpocetine manufacturer , order Vinpocetine , high purity Vinpocetine