| Identification | Back Directory | [Name]
REMODULIN | [CAS]
289480-64-4 | [Synonyms]
UT 15 (pharMaceutical)
Treprostinil Sodium API
Treprostinil sodium salt
Treprostinil Sodium (UT-15)
289480-64-4 Treprostinil Sodium | [Molecular Formula]
C23H34O5 | [MDL Number]
MFCD00888847 | [MOL File]
289480-64-4.mol | [Molecular Weight]
390.517 |
| Chemical Properties | Back Directory | [storage temp. ]
Inert atmosphere,Store in freezer, under -20°C | [solubility ]
DMSO : ≥ 26 mg/mL (63.03 mM) | [form ]
solid | [color ]
White | [InChIKey]
XUACDQZEUSYNGG-DJYDVLTONA-N | [SMILES]
C([C@H]1[C@@H](C[C@]2([H])CC3=C(C=CC=C3C[C@]12[H])OCC(=O)O)O)C[C@@H](O)CCCCC.[NaH] |&1:1,2,4,14,23,r| |
| Hazard Information | Back Directory | [Description]
Treprostinil sodium is a chemically stable prostacyclin analogue that shares at least some of the pharmacologic actions of epoprostenol. The sodium salt of treprostinil is currently approved for the treatment of PAH for either parenteral (Remodulin) or inhaled (Tyvaso) routes of administration. Acute hemodynamic effects with treprostinil are similar to those observed with intravenous epoprostenol in patients with IPAH; however, treprostinil is stable at room temperature and neutral pH and has a longer half-life, 2–3 hours, when administered subcutaneously. Like epoprostenol, treprostinil is infused continuously by a portable pump and can be administered subcutaneously or intravenously. Treprostinil was approved in 2002 for subcutaneous infusion and in 2004 for intravenous injection[1]. | [Uses]
Treprostinil Sodium is a potent agonist of DP1, EP2 and IP receptors. | [Definition]
ChEBI: Treprostinil sodium is an organic sodium salt. It contains a treprostinil. | [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]. | [IC 50]
IP Receptor: 1.9 nM (EC50); TP Receptor: 919 nM (EC50); IP Receptor: 32.1 nM (Ki); FP Receptor: 4680 nM (Ki); DP1: 0.6±0.1 nM (EC50); EP2: 6.2±1.2 nM (EC50); DP1: 4.4 nM (Ki); EP2: 3.6 nM (Ki); EP4: 826 nM (Ki); EP3: 2505 nM (Ki); EP1: 212 nM (Ki); EP1: 285 nM (EC50); EP3: 68.9 nM (EC50); EP4: 181 nM (EC50) | [storage]
Store at -20°C | [References]
[1] Zhi-Cheng Jing. “Efficacy and safety of oral treprostinil monotherapy for the treatment of pulmonary arterial hypertension: a randomized, controlled trial.” Circulation 127 5 (2013): 624–33.
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