Treprostinil sodium(LRX15)

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CAS NO:	289480-64-4
规格:	≥98%

包装与价格：

包装	价格(元)
5mg	询价
10mg	询价
25mg	询价
50mg	询价
100mg	询价
250mg	询价

理化性质和储存条件

	Name: Treprostinil sodium CAS#: 289480-64-4 (sodium) Chemical Formula: C23H33NaO5 Exact Mass: Molecular Weight: 412.5018
Storage	-20℃ for 3 years in powder form
Storage	-80℃ for 2 years in solvent
Technical Information	Synonym: UT-15; LRX 15 sodium; UT 15; LRX15 sodium; UT15;LRX-15 sodium; BW 15AU sodium; U-62840 sodium; Uniprost; Treprostinil; Orenitram; Remodulin. Chemical Name: 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 InChi Key: IQKAWAUTOKVMLE-ZSESPEEFSA-M InChi Code: InChI=1S/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 SMILES Code: O=C([O-])COC1=C2C[C@@]3([H])C[C@@H](O)[C@H](CC[C@@H](O)CCCCC)[C@@]3([H])CC2=CC=C1.[Na+]

实验参考方法

In Vitro	Treprostinil has high affinity for the DP1, EP2 and IP receptors (Ki=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[1].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[5].
In Vivo	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)[2]. 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[3].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[4]. Treprostinil is most efficacious in raising intracellular cAMP levels in murine and human hematopoietic stem and progenitor cells[5]. 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[6].

In Vitro

Treprostinil has high affinity for the DP1, EP2 and IP receptors (Ki=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[1].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[5].

In Vivo

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)[2]. 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[3].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[4]. Treprostinil is most efficacious in raising intracellular cAMP levels in murine and human hematopoietic stem and progenitor cells[5]. 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[6].