曲前列尼尔钠 |
时间:2023-07-18 来源:化工号 作者:C23H35NaO5 |
中文名 | 曲前列尼尔钠
| 英文名 | Treprostinil Sodium
| 别名 | 曲前列素 曲列前素 曲前列尼尔酸 曲前列尼尔钠 曲前列环素钠盐 曲前列尼尔钠9(瑞莫杜林)
| 英文别名 | Remodulin UNII-7JZ75N2NT6 Treprostinil Sodium UT 15 (pharMaceutical) Treprostinil Sodium API Treprostinil sodium salt Treprostinil sodium (LRX15) Treprostinil Sodium (UT-15) 289480-64-4 Treprostinil Sodium ({(1S,2S,3aR,9aR)-2-hydroxy-1-[(3R)-3-hydroxyoctyl]-2,3,3a,4,9,9a-hexahydro-1H-cyclopenta[b]naphthalen-5-yl}oxy)acetic acid sodium ({(1S,2S,3aR,9aR)-2-hydroxy-1-[(3R)-3-hydroxyoctyl]-2,3,3a,4,9,9a-hexahydro-1H-cyclopenta[b]naphthalen-5-yl}oxy)acetate sodium ({(1R,2R,3aS,9aS)-2-hydroxy-1-[(3S)-3-hydroxyoctyl]-2,3,3a,4,9,9a-hexahydro-1H-cyclopenta[b]naphthalen-5-yl}oxy)acetate Acetic acid, (((1R,2R,3aS,9aS)-2,3,3a,4,9,9a-hexahydro-2-hydroxy-1-((3S)-3-hydroxyoctyl)-1H-benz(f)inden-5-yl)oxy)-, monosodium salt
| CAS | 289480-64-4
| 化学式 | C23H35NaO5
| 分子量 | 414.52 | InChI | InChI=1/C23H34O5.Na/c1-2-3-4-7-17(24)9-10-18-19-11-15-6-5-8-22(28-14-23(26)27)20(15)12-16(19)13-21(18)25;/h5-6,8,16-19,21,24-25H,2-4,7,9-14H2,1H3,(H,26,27);/q;+1/p-1/t16-,17-,18+,19-,21+;/m0./s1 | 沸点 | 587.1°C at 760 mmHg | 闪点 | 199.3°C | 蒸汽压 | 1.25E-14mmHg at 25°C | 存储条件 | Inert atmosphere,Store in freezer, under -20°C | 体外研究 | Treprostinil has high affinity for the DP1, EP2 and IP receptors (K i =4.4, 3.6 and 32 nM, respectively), low affinity for EP1 and EP4 receptors and even lower affinity for EP3, FP and TP receptors. Activation of IP, DP1 and EP2 receptors, as with treprostinil, can all result in vasodilatation of human pulmonary arteries.Treprostinil inhibits viability of cultured endothelial colony forming cells. Endothelial colony forming cells proliferation is stimulated by conditioned media from Treprostinil pretreated mesenchymal stem cells. | 体内研究 | Inhaled treprostinil sodium, a prostacyclin analog, is the most recent agent to receive FDA approval for the treatment of a fatal orphan disease: pulmonary arterial hypertension (PAH). Treprostinil preserves the sinusoidal endothelial cell lining and reduces platelet deposition early post-transplantation compared to placebo. Hepatic tissue blood flow is significantly compromised in the placebo group, whereas treprostinil maintains blood flow similar to normal levels.Treprostinil treatment significantly increases the vessel-forming ability of endothelial colony forming cells combined with mesenchymal stem cells in Matrigel implanted in nude mice. Silencing VEGF-A gene in mesenchymal stem cells also blocks the pro-angiogenic effect of Treprostinil. Treprostinil is most efficacious in raising intracellular cAMP levels in murine and human hematopoietic stem and progenitor cells. Treatment with Treprostinil significantly reduces the recruitment of cells compared to normoxic mice. Treprostinil also reduces right ventricular systolic pressure and slightly reduces the vascular remodelling but fails to reverse the right ventricular hypertrophy. |
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