TalatisamineCAS# 20501-56-8 |
2D Structure
Quality Control & MSDS
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Number of papers citing our products
Cas No. | 20501-56-8 | SDF | Download SDF |
PubChem ID | 441761 | Appearance | Powder |
Formula | C24H39NO5 | M.Wt | 421.57 |
Type of Compound | Alkaloids | Storage | Desiccate at -20°C |
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
SMILES | CCN1CC2(CCC(C34C2CC(C31)C5(CC(C6CC4C5C6O)OC)O)OC)COC | ||
Standard InChIKey | BDCURAWBZJMFIK-FLDLCTCNSA-N | ||
Standard InChI | InChI=1S/C24H39NO5/c1-5-25-11-22(12-28-2)7-6-18(30-4)24-14-8-13-16(29-3)10-23(27,19(14)20(13)26)15(21(24)25)9-17(22)24/h13-21,26-27H,5-12H2,1-4H3/t13-,14-,15+,16+,17-,18+,19-,20+,21?,22+,23+,24-/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. |
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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. |
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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. |
Description | Talatisamine is a newly identified K+ channel blocker with hypotensive and antiarrhythmic activities. Talatisamine (120 μM) and TEA (5mM) inhibits the enhanced I(K) caused by Aβ40 oligomers, attenuates cytotoxicity of Aβ oligomers by restoring cell viability and suppressing K(+) loss related apoptotic response. |
Targets | Bcl-2/Bax | Caspase | Beta Amyloid | Calcium Channel | Potassium Channel |
In vitro | The newly identified K+ channel blocker talatisamine attenuates beta-amyloid oligomers induced neurotoxicity in cultured cortical neurons.[Pubmed: 22561032]Neurosci Lett. 2012 Jun 19;518(2):122-7.Loss of cytosolic K(+) through up-regulated delayed rectifier K(+) channels play an important role in beta-amyloid (Aβ) induced neurotoxicity. Potent K(+) channel blocker, particular specific for I(K) channels has been suggested as an attractive candidate for the treatment of Alzheimer's disease (AD). Talatisamine is a novel I(K) channel blocker discovered by virtual screening and electrophysiological characterization. |
Kinase Assay | Discovery of talatisamine as a novel specific blocker for the delayed rectifier K+ channels in rat hippocampal neurons.[Pubmed: 18601983]Neuroscience. 2008 Aug 13;155(2):469-75.Blocking specific K+ channels has been proposed as a promising strategy for the treatment of neurodegenerative diseases. Using a computational virtual screening approach and electrophysiological testing, we found four Aconitum alkaloids are potent blockers of the delayed rectifier K+ channel in rat hippocampal neurons. |
Talatisamine Dilution Calculator
Talatisamine Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.3721 mL | 11.8604 mL | 23.7209 mL | 47.4417 mL | 59.3021 mL |
5 mM | 0.4744 mL | 2.3721 mL | 4.7442 mL | 9.4883 mL | 11.8604 mL |
10 mM | 0.2372 mL | 1.186 mL | 2.3721 mL | 4.7442 mL | 5.9302 mL |
50 mM | 0.0474 mL | 0.2372 mL | 0.4744 mL | 0.9488 mL | 1.186 mL |
100 mM | 0.0237 mL | 0.1186 mL | 0.2372 mL | 0.4744 mL | 0.593 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. |
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The newly identified K+ channel blocker talatisamine attenuates beta-amyloid oligomers induced neurotoxicity in cultured cortical neurons.[Pubmed:22561032]
Neurosci Lett. 2012 Jun 19;518(2):122-7.
Loss of cytosolic K(+) through up-regulated delayed rectifier K(+) channels play an important role in beta-amyloid (Abeta) induced neurotoxicity. Potent K(+) channel blocker, particular specific for I(K) channels has been suggested as an attractive candidate for the treatment of Alzheimer's disease (AD). Talatisamine is a novel I(K) channel blocker discovered by virtual screening and electrophysiological characterization. In the present study, we examined the neuroprotective effect of Talatisamine against Abeta oligomers induced cytotoxicity in primarily cultured cortical neurons. The neurotoxicity related to K(+) loss caused by Abeta40 oligomers included enhanced I(K) density, increased cell membrane permeability, reduced cell viability, and impaired mitochondrial transmembrane potential. Decreased Bcl-2 and increased Bax level, activation of Caspase-3 and Caspase-9 were also observed after Abeta40 oligomers incubation. Talatisamine (120 muM) and TEA (5mM) inhibited the enhanced I(K) caused by Abeta40 oligomers, attenuated cytotoxicity of Abeta oligomers by restoring cell viability and suppressing K(+) loss related apoptotic response. Our results suggested that Talatisamine may become a leading compound as I(K) channel blocker for neuroprotection.
Discovery of talatisamine as a novel specific blocker for the delayed rectifier K+ channels in rat hippocampal neurons.[Pubmed:18601983]
Neuroscience. 2008 Aug 13;155(2):469-75.
Blocking specific K+ channels has been proposed as a promising strategy for the treatment of neurodegenerative diseases. Using a computational virtual screening approach and electrophysiological testing, we found four Aconitum alkaloids are potent blockers of the delayed rectifier K+ channel in rat hippocampal neurons. In the present study, we first tested the action of the four alkaloids on the voltage-gated K+, Na+ and Ca2+ currents in rat hippocampal neurons, and then identified that Talatisamine is a specific blocker for the delayed rectifier K+ channel. External application of Talatisamine reversibly inhibited the delayed rectifier K+ current (IK) with an IC50 value of 146.0+/-5.8 microM in a voltage-dependent manner, but exhibited very slight blocking effect on the voltage-gated Na+ and Ca2+ currents even at the high concentration of 1-3 mM. Moreover, Talatisamine exerted a significant hyperpolarizing shift of the steady-state activation, but did not influence the steady state inactivation of IK and its recovery from inactivation, suggesting that Talatisamine had no allosteric action on IK channel and was a pure blocker binding to the external pore entry of the channel. Our present study made the first discovery of potent and specific IK channel blocker from Aconitum alkaloids. It has been argued that suppressing K+ efflux by blocking IK channel may be favorable for Alzheimer's disease therapy. Talatisamine can therefore be considered as a leading compound worthy of further investigations.