Nemadipine A
目录号 : GC44361An L-type calcium channel blocker
Cas No.:54280-71-6
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >98.00%
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- SDS (Safety Data Sheet)
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Nemadipine A is an L-type calcium channel blocker that induces morphological and growth defects in wild-type C. elegans and those with hypoexpression of egl-19, which encodes the only L-type calcium channel α1-subunit in the C. elegans genome. It also inhibits L-type calcium channels in chick ciliary neurons. Nemadipine A increases TRAIL-induced cytotoxicity and synergistically enhances caspase-8 and caspase-3 activation in a concentration-dependent manner in H1299 lung adenocarcinoma cells. It also decreases Survivin expression when used alone or in combination with TRAIL in A549 cells.
Cas No. | 54280-71-6 | SDF | |
Canonical SMILES | CC1=C(C(OCC)=O)C(C2=C(F)C(F)=C(F)C(F)=C2F)C(C(OCC)=O)=C(C)N1 | ||
分子式 | C19H18F5NO4 | 分子量 | 419.3 |
溶解度 | DMSO: 20 mg/ml,Ethanol: 15 mg/ml,Methanol: 100 mg/ml | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 2.3849 mL | 11.9246 mL | 23.8493 mL |
5 mM | 0.477 mL | 2.3849 mL | 4.7699 mL |
10 mM | 0.2385 mL | 1.1925 mL | 2.3849 mL |
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2.
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Arrhythmogenic effects of mutated L-type Ca 2+-channels on an optogenetically paced muscular pump in Caenorhabditis elegans
Sci Rep 2015 Sep 24;5:14427.PMID:26399900DOI:10.1038/srep14427.
Cardiac arrhythmias are often associated with mutations in ion channels or other proteins. To enable drug development for distinct arrhythmias, model systems are required that allow implementing patient-specific mutations. We assessed a muscular pump in Caenorhabditis elegans. The pharynx utilizes homologues of most of the ion channels, pumps and transporters defining human cardiac physiology. To yield precise rhythmicity, we optically paced the pharynx using channelrhodopsin-2. We assessed pharynx pumping by extracellular recordings (electropharyngeograms--EPGs), and by a novel video-microscopy based method we developed, which allows analyzing multiple animals simultaneously. Mutations in the L-type VGCC (voltage-gated Ca(2+)-channel) EGL-19 caused prolonged pump duration, as found for analogous mutations in the Cav1.2 channel, associated with long QT syndrome. egl-19 mutations affected ability to pump at high frequency and induced arrhythmicity. The pharyngeal neurons did not influence these effects. We tested whether drugs could ameliorate arrhythmia in the optogenetically paced pharynx. The dihydropyridine analog Nemadipine A prolonged pump duration in wild type, and reduced or prolonged pump duration of distinct egl-19 alleles, thus indicating allele-specific effects. In sum, our model may allow screening of drug candidates affecting specific VGCCs mutations, and permit to better understand the effects of distinct mutations on a macroscopic level.