推荐产品
质量水平
方案
≥98%
SMILES字符串
Cl[H].COc1ccc(CCN(C)CCCC(C#N)(C(C)C)c2cc(OC)c(OC)c(OC)c2)cc1OC
InChI
1S/C28H40N2O5.ClH/c1-20(2)28(19-29,22-17-25(33-6)27(35-8)26(18-22)34-7)13-9-14-30(3)15-12-21-10-11-23(31-4)24(16-21)32-5;/h10-11,16-18,20H,9,12-15H2,1-8H3;1H
InChI key
OKCRIUNHEQSXFD-UHFFFAOYSA-N
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储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
个人防护装备
Eyeshields, Gloves, type N95 (US)
其他客户在看
Anamika Awasthi et al.
Bioorganic & medicinal chemistry letters, 15(24), 5412-5415 (2005-10-11)
Ab initio Hartree-Fock calculations have been performed at the 6-31G level to study the pharmacophoric features of verapamil. Both the unprotonated and the protonated forms of verapamil have been studied. The study predicts that the drug enters the body in
D N Serban et al.
Revista medico-chirurgicala a Societatii de Medici si Naturalisti din Iasi, 108(2), 445-451 (2005-02-04)
Membrane potential (MP) is essential in smooth muscle (SM) contractile activity, mainly by its effect upon L-type Ca2+ channels. We simultaneously recorded SM isometric tension and MP in de-endothelised rat aorta rings and examined their submaximal activation by K+, norepinephrine
Iliyana D Stefanova et al.
Molecular nutrition & food research, 51(4), 468-472 (2007-03-16)
Melanoidins obtained from L-arginine and D-glucose (MW > 3500 Da) were tested for their ability to influence the contractility of gastric smooth muscles. A study within the range 0.1-10 mg/mL revealed that at low concentrations, the melanoidins provoked concentration-dependent contraction
Shigehiro Hayashi et al.
Acta pharmacologica Sinica, 31(1), 19-26 (2009-11-17)
To quantitatively assess the effect of lowering external Ca(2+) ([Ca(2+)](o)) on both endothelium-dependent and -independent relaxations in rabbit aorta. Isometric contractions and relaxations of isolated aortae were recorded. When assessing the effect of reduced [Ca(2+)](o) on relaxations, the normal [Ca(2+)](o)
Xian Wang et al.
Biosensors & bioelectronics, 166, 112399-112399 (2020-07-22)
Heart failure fundamentally results from loss of cardio myocyte contractility. Developing new methods that quantify the contractile stress of the human cardiomyocyte would facilitate the study of the molecular mechanism of heart failure and advance therapy development, to improve the
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