GW 274150 - CAS 210354-22-6
Catalog number:
210354-22-6
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C8H17N3O2S
Molecular Weight:
219.30
COA:
Inquire
Targets:
Nitric oxide synthase (NOS)
Description:
GW 274150 is a potent, long-acting and highly selective inhibitor of iNOS which have a very high degree of selectivity for iNOS versus both eNOS (>100-fold) and nNOS (>80-fold). GW 274150 shows analgesic effects in rat models of inflammatory and neuropath
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Appearance:
Solid powder
Synonyms:
(2S)-2-amino-4-[2-(1-aminoethylideneamino)ethylsulfanyl]butanoic acid GW 274150 GW274150
Solubility:
Soluble to 10 mM in H2O
Storage:
Store in a cool and dry place and at 0 - 4℃ for short term (days to weeks) or -65℃ for long term (months to years).
MSDS:
Inquire
Shelf Life:
2 years
Boiling Point:
392.3±52.0 °C | Condition: Press: 760 Torr
Density:
1.30±0.1 g/cm3
InChIKey:
MOLOJNHYNHBPCW-ZETCQYMHSA-N
InChI:
1S/C8H17N3O2S/c1-6(9)11-3-5-14-4-2-7(10)8(12)13/h7H,2-5,10H2,1H3,(H2,9,11)(H,12,13)/t7-/m0/s1
Canonical SMILES:
CC(=NCCSCCC(C(=O)O)N)N
1.Role of inducible nitric oxide synthase in the reduced responsiveness of the myocardium to catecholamines in a hyperdynamic, murine model of septic shock.
Barth E1, Radermacher P, Thiemermann C, Weber S, Georgieff M, Albuszies G. Crit Care Med. 2006 Feb;34(2):307-13.
OBJECTIVES: Excess nitric oxide production is a key mediator of hypotension and catecholamine-resistance in septic shock. Although nitric oxide synthase blockade has been shown to restore hemodynamics, conflicting results on myocardial function were reported. Inducible nitric oxide synthase (iNOS) knockout (iNOS-/-) mice showed improved heart function, but these results were obtained during hypodynamic shock characterized by reduced cardiac output. Therefore, we investigated heart function and catecholamine responsiveness in a clinically relevant, murine model of cecal ligation and puncture (CLP)-induced septic shock.
2.Activation of hypoxia-inducible factor-1 ameliorates postischemic renal injury via inducible nitric oxide synthase.
Zhang XL1, Yan ZW, Sheng WW, Xiao J, Zhang ZX, Ye ZB. Mol Cell Biochem. 2011 Dec;358(1-2):287-95. doi: 10.1007/s11010-011-0979-y. Epub 2011 Jul 14.
Hypoxia-inducible factor-1 (HIF-1) could ameliorate renal ischemia reperfusion injury (IRI), but the underlying mechanism remains elusive. In the current study, we aim to investigate the possible role of prolyl hydroxylases inhibitor dimethyloxalylglycine (DMOG) in inducing delayed preconditioning-like effects against IRI. Mice were divided into four groups (n = 6): sham group; IRI group; DMOG group: pretreated with DMOG 24 h before IRI; and GW274150 + DMOG group: pretreated with DMOG followed by iNOS inhibitor GW274150 treatment 24 h before IRI. The results showed that the protein level of HIF-1a and the expression of its targets inducible nitric oxide synthase (iNOS), erythropoietin, and heme oxygenase-1 were obviously increased after administration of DMOG. Histological analysis of renal function showed improvement in tubulointerstitial injury due to ischemia by delayed preconditioning with DMOG. GW274150 antagonized the delayed renal protection afforded by DMOG as reflected by deteriorated renal dysfunction, aggravated histological injury, increased renal cell apoptosis, and increased vimentin expression in the kidney.
3.Ultrasonographic measures of synovitis in an early phase clinical trial: a double-blind, randomised, placebo and comparator controlled phase IIa trial of GW274150 (a selective inducible nitric oxide synthase inhibitor) in rheumatoid arthritis.
Seymour M1, Pétavy F, Chiesa F, Perry H, Lukey PT, Binks M, Donatien PD, Freidin AJ, Eckersley RJ, McClinton C, Heath K, Prodanovic S, Radunovic G, Pilipovic N, Damjanov N, Taylor PC. Clin Exp Rheumatol. 2012 Mar-Apr;30(2):254-61. Epub 2012 Apr 13.
OBJECTIVES: To test the sensitivity to change of ultrasonographic endpoints in early phase clinical trials in subjects with active rheumatoid arthritis (RA).
4.Inhibition of inducible nitric oxide synthase in respiratory diseases.
Hesslinger C1, Strub A, Boer R, Ulrich WR, Lehner MD, Braun C. Biochem Soc Trans. 2009 Aug;37(Pt 4):886-91. doi: 10.1042/BST0370886.
Nitric oxide (NO) is a key physiological mediator and disturbed regulation of NO release is associated with the pathophysiology of almost all inflammatory diseases. A multitude of inhibitors of NOSs (nitric oxide synthases) have been developed, initially with low or even no selectivity against the constitutively expressed NOS isoforms, eNOS (endothelial NOS) and nNOS (neuronal NOS). In the meanwhile these efforts yielded potent and highly selective iNOS (inducible NOS) inhibitors. Moreover, iNOS inhibitors have been shown to exert beneficial anti-inflammatory effects in a wide variety of acute and chronic animal models of inflammation. In the present mini-review, we summarize some of our current knowledge of inhibitors of the iNOS isoenzyme, their biochemical properties and efficacy in animal models of pulmonary diseases and in human disease itself. Moreover, the potential benefit of iNOS inhibition in animal models of COPD (chronic obstructive pulmonary disease), such as cigarette smoke-induced pulmonary inflammation, has not been explicitly studied so far.
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CAS 210354-22-6 GW 274150

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