Nebentan (YM598) 是一种有效的具有口服活性的非肽类内皮素受体 (ETA receptor) 拮抗剂，通过 Bosentan 修饰得到。Nebentan 抑制 [125I] 内皮素-1 与人内皮素 ETA 和 ETB 受体结合，Ki 分别为 0.697 nM 和 569 nM。Nebentan 可改善肺心病和心肌梗死的进展。
货号:ajcx29542
CAS:403604-85-3
分子式:C24H21N5O5S
分子量：491.52
溶解度:DMSO: 125 mg/mL (254.31 mM)
纯度：98%
存储：Store at -20°C
库存：现货

Background:

Nebentan (YM598) is a potent, selective and orally active non-peptide endothelin ETA receptor antagonist through the modification of Bosentan . Nebentan inhibits [125I] endothelin-1 binding to cloned human endothelin ETA and ETB receptor, with Ki of 0.697 nM and 569 nM, respectively[1]. YM598 can ameliorate the progression of cor pulmonale and myocardial infarction in vivo[2].

Nebentan inhibits the specific binding of [125I] endothelin-1 to endothelin ETA and ETB receptors in a concentration dependent manner,Ki values are 0.697 nM and 1.53 nM for human and rat endothelin ETA receptors, respectively. In contrast, YM598 exhibits low affinities for human and rat endothelin ETB receptors, with Ki values of 569 nM and 155 nM,respectively[1].In measurement of intracellular Ca2+ concentration, Nebentan concentration-dependently inhibits the increase in [Ca2+]i induced by 10 nM endothelin-1 in both CHO cells and A10 cells, the IC50 values are 26.2 nM for CHO cells and 26.7 nM for A10 cells, respectively[1].

Nebentan (oral administration; 0.1-1 mg/kg; 4 weeks) significantly inhibits the progression of pulmonary hypertension and the development of right ventricular hypertrophy[2].Nebentan (oral administration; 1 mg/kg; 30 weeks) significantly ameliorates the poor survival rate of CHF rats, it markedly reduces the hypertrophy of both ventricles as well as pulmonary congestion[2].

[1]. Hironori Yuyama, et al. Pharmacological Characterization of YM598, an Orally Active and Highly Potent Selective Endothelin ET(A) Receptor Antagonist. Eur J Pharmacol. 2003 Sep 30;478(1):61-71. [2]. Akira Fujimori, et al. YM598, an Orally Active ET(A) Receptor Antagonist, Ameliorates the Progression of Cardiopulmonary Changes and Both-Side Heart Failure in Rats With Cor Pulmonale and Myocardial Infarction. J Cardiovasc Pharmacol. 2004 Nov;44 Suppl 1:S354-7.