Vincamine

CAS# 1617-90-9

Vincamine

Catalog No. BCN2606----Order now to get a substantial discount!

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Quality Control of Vincamine

Number of papers citing our products

Chemical structure

Vincamine

3D structure

Chemical Properties of Vincamine

Cas No. 1617-90-9 SDF Download SDF
PubChem ID 15376 Appearance Cryst.
Formula C21H26N2O3 M.Wt 354.44
Type of Compound Alkaloids Storage Desiccate at -20°C
Solubility DMSO : 25 mg/mL (70.53 mM; Need ultrasonic)
SMILES CCC12CCCN3C1C4=C(CC3)C5=CC=CC=C5N4C(C2)(C(=O)OC)O
Standard InChIKey RXPRRQLKFXBCSJ-GIVPXCGWSA-N
Standard InChI InChI=1S/C21H26N2O3/c1-3-20-10-6-11-22-12-9-15-14-7-4-5-8-16(14)23(17(15)18(20)22)21(25,13-20)19(24)26-2/h4-5,7-8,18,25H,3,6,9-13H2,1-2H3/t18-,20+,21+/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 Vincamine

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

Biological Activity of Vincamine

DescriptionVincamine is a plant alkaloid used clinically as a peripheral vasodilator that increases cerebral blood flow and oxygen and glucose utilization by neural tissue to combat the effect of aging. Vincamine has contractile and relaxant actions on the guinea pig trachealis, may be due to the generation of prostaglandins and to changes in the membrane Ca2+ fluxes and/or the intracellular Ca2+ distribution. Vincamine alleviates Amyloid-β 25-35 peptides-induced cytotoxicity in PC12 cells.
TargetsCalcium Channel | Potassium Channel | Beta Amyloid | PI3K | Akt | SOD
In vitro

Trachealis responses induced by vincamine and vinpocetine; inhibition by indomethacin and Ca2+ dependence.[Pubmed: 2744076]

Eur J Pharmacol. 1989 Mar 29;162(3):387-95.


METHODS AND RESULTS:
Vincamine in low concentrations induced a sustained contraction of the isolated guinea pig trachealis with long latency and slow onset and, in high concentrations, it induced relaxation which was potentiated in the precontracted trachealis. Vinpocetine had actions similar to those of Vincamine on trachealis, however its relaxant effect was more pronounced. The Vincamine-induced trachealis contraction was not changed by substance P desensitization, was reduced by tetrodotoxin, nifedipine and low Ca2+ high Mg2+ solution and increased in nominally Ca2+-free solution. The Vincamine-induced relaxation of precontracted trachealis was increased by guanethidine and was not affected by propranolol, high Mg2+-low Ca2+ solution and tetrodotoxin. Vincamine- and vinpocetine-induced trachealis contraction as well as vinpocetine-induced relaxation at basal tension were abolished by indomethacin. Vincamine in a low concentration shifted to the left the concentration-effect curve for CaCl2 in the K+-depolarized trachealis, and shifted it to the right at a high concentration.
CONCLUSIONS:
Our results indicate that the contractile and relaxant actions of Vincamine and vinpocetine on the guinea pig trachealis may be due to the generation of prostaglandins and to changes in the membrane Ca2+ fluxes and/or the intracellular Ca2+ distribution.

Protocol of Vincamine

Cell Research

Vincamine Alleviates Amyloid-β 25-35 Peptides-induced Cytotoxicity in PC12 Cells.[Pubmed: 28216895 ]

Pharmacogn Mag. 2017 Jan-Mar;13(49):123-128.

Vincamine is a plant alkaloid used clinically as a peripheral vasodilator that increases cerebral blood flow and oxygen and glucose utilization by neural tissue to combat the effect of aging. The main purpose of the present study is to investigate the influence of Vincamine on amyloid-β 25-35 (Aβ25-35) induced cytotoxicity, to gain a better understanding of the neuroprotective effects of this clinically used anti-Alzheimer's disease drug.
METHODS AND RESULTS:
Oxidative stress was assessed by measuring malondialdehyde, glutathione, and superoxide dismutase (SOD) levels. Cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell apoptosis detection was performed using an Annexin-V-FITC Apoptosis Detection Kit. The production of reactive oxygen species (ROS) was determined using an ROS Assay Kit. Western blot detection was carried out to detect the protein expression. Our studies showed that pretreatment with Vincamine could reduce Aβ25-35 induced oxidative stress. Vincamine markedly inhibited cell apoptosis dose-dependently. More importantly, Vincamine increased the phosphatidylinositol-3 kinase (PI3K)/Akt and Bcl-2 family protein ratios on preincubation with cells for 2 h.
CONCLUSIONS:
Above observation led us to assume that one possible mechanism of Vincamine protects Aβ25-35-induced cell death could be through upregulation of SOD and activation of the PI3K/Akt pathway.Vincamine ameliorates amyloid-β 25-35 (Aβ25-35) peptides induced cytotoxicity in PC12 cellsVincamine reduces Aβ 25-35 peptides induced apoptosis of PC12 cellsVincamine activates the phosphatidylinositol-3 kinase/Akt pathwayVincamine up-regulates the superoxide dismutase.

Vincamine Dilution Calculator

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Preparing Stock Solutions of Vincamine

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.8214 mL 14.1068 mL 28.2135 mL 56.427 mL 70.5338 mL
5 mM 0.5643 mL 2.8214 mL 5.6427 mL 11.2854 mL 14.1068 mL
10 mM 0.2821 mL 1.4107 mL 2.8214 mL 5.6427 mL 7.0534 mL
50 mM 0.0564 mL 0.2821 mL 0.5643 mL 1.1285 mL 1.4107 mL
100 mM 0.0282 mL 0.1411 mL 0.2821 mL 0.5643 mL 0.7053 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.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

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The Institute of Cancer Research

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The University of Tokyo
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Background on Vincamine

Vincamine is a peripheral vasodilator, that increases blood flow to the brain.

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References on Vincamine

Vincamine Alleviates Amyloid-beta 25-35 Peptides-induced Cytotoxicity in PC12 Cells.[Pubmed:28216895]

Pharmacogn Mag. 2017 Jan-Mar;13(49):123-128.

OBJECTIVE: Vincamine is a plant alkaloid used clinically as a peripheral vasodilator that increases cerebral blood flow and oxygen and glucose utilization by neural tissue to combat the effect of aging. The main purpose of the present study is to investigate the influence of Vincamine on amyloid-beta 25-35 (Abeta25-35) induced cytotoxicity, to gain a better understanding of the neuroprotective effects of this clinically used anti-Alzheimer's disease drug. MATERIALS AND METHODS: Oxidative stress was assessed by measuring malondialdehyde, glutathione, and superoxide dismutase (SOD) levels. Cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell apoptosis detection was performed using an Annexin-V-FITC Apoptosis Detection Kit. The production of reactive oxygen species (ROS) was determined using an ROS Assay Kit. Western blot detection was carried out to detect the protein expression. RESULTS: Our studies showed that pretreatment with Vincamine could reduce Abeta25-35 induced oxidative stress. Vincamine markedly inhibited cell apoptosis dose-dependently. More importantly, Vincamine increased the phosphatidylinositol-3 kinase (PI3K)/Akt and Bcl-2 family protein ratios on preincubation with cells for 2 h. CONCLUSION: Above observation led us to assume that one possible mechanism of Vincamine protects Abeta25-35-induced cell death could be through upregulation of SOD and activation of the PI3K/Akt pathway. SUMMARY: Vincamine ameliorates amyloid-beta 25-35 (Abeta25-35) peptides induced cytotoxicity in PC12 cellsVincamine reduces Abeta 25-35 peptides induced apoptosis of PC12 cellsVincamine activates the phosphatidylinositol-3 kinase/Akt pathwayVincamine up-regulates the superoxide dismutase. Abbreviation used: Abeta25-35: Amyloid-beta 25-35; AD: Alzheimer's disease; BCA: Bicinchoninic acid; GSH: glutathione; PBS: Phosphate buffered solution; SDS: Sodium dodecylsulphate; SOD: Superoxide dismutase.

Trachealis responses induced by vincamine and vinpocetine; inhibition by indomethacin and Ca2+ dependence.[Pubmed:2744076]

Eur J Pharmacol. 1989 Mar 29;162(3):387-95.

Vincamine in low concentrations induced a sustained contraction of the isolated guinea pig trachealis with long latency and slow onset and, in high concentrations, it induced relaxation which was potentiated in the precontracted trachealis. Vinpocetine had actions similar to those of Vincamine on trachealis, however its relaxant effect was more pronounced. The Vincamine-induced trachealis contraction was not changed by substance P desensitization, was reduced by tetrodotoxin, nifedipine and low Ca2+ high Mg2+ solution and increased in nominally Ca2+-free solution. The Vincamine-induced relaxation of precontracted trachealis was increased by guanethidine and was not affected by propranolol, high Mg2+-low Ca2+ solution and tetrodotoxin. Vincamine- and vinpocetine-induced trachealis contraction as well as vinpocetine-induced relaxation at basal tension were abolished by indomethacin. Vincamine in a low concentration shifted to the left the concentration-effect curve for CaCl2 in the K+-depolarized trachealis, and shifted it to the right at a high concentration. Our results indicate that the contractile and relaxant actions of Vincamine and vinpocetine on the guinea pig trachealis may be due to the generation of prostaglandins and to changes in the membrane Ca2+ fluxes and/or the intracellular Ca2+ distribution.

Description

Vincamine is a peripheral vasodilator, that increases blood flow to the brain.

Keywords:

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