81846-19-7
基本信息
曲羅尼爾
曲前列環(huán)素
曲前列尼爾
曲前列尼爾中間體1
曲前列環(huán)素/曲前列尼爾
曲前列尼爾(瑞莫杜林)
曲前列尼爾(瑞莫杜林) 1G
TREPROSTINIL前列環(huán)素
LRX 15
BW 15AU
U 62840
15AU-81
Uniprost
Rumodolin
REMODULIN
Orenitram
TREPROSTINIL
物理化學性質(zhì)
常見問題列表
DP/DP1 Receptor 0.6 nM (EC 50 ) |
IP Receptor 1.9 nM (EC 50 ) |
EP 2 Receptor 6.2 nM (EC 50 ) |
EP3 Receptor 68.9 nM (EC 50 ) |
EP 4 Receptor 181 nM (EC 50 ) |
EP 1 Receptor 285 nM (EC 50 ) |
TP Receptor 919 nM (EC 50 ) |
EP 2 Receptor 3.6 nM (Ki) |
EP 1 Receptor 212 nM (Ki) |
EP 4 Receptor 826 nM (Ki) |
EP3 Receptor 2505 nM (Ki) |
DP/DP1 Receptor 4.4 nM (Ki) |
IP Receptor 32.1 nM (Ki) |
FP Receptor 4680 nM (Ki) |
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.
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.