Enrasentan - CAS 167256-08-8
Catalog number: 167256-08-8
Category: Inhibitor
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Molecular Formula:
C29H30O8
Molecular Weight:
506.55
COA:
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Targets:
Endothelin Receptor
Description:
Enrasentan, an indene derivative, has been found to be an endothelin receptor antagonist that was once studied in reperfusion injury and heart failure therapy.
Purity:
98%
Appearance:
Powder
Synonyms:
Enrasentan; SB-217242; UNII-QG16H8A6ZH; SB 217242; SB217242; CHEMBL431651; (1S,2R,3S)-1-(1,3-benzodioxol-5-yl)-3-[2-(2-hydroxyethoxy)-4-methoxyphenyl]-5-propoxy-2,3-dihydro-1H-indene-2-carboxylic acid
Storage:
Store in a cool and dry place and at 0 - 4 °C for short term (days to weeks) or -20 °C for long term (months to years).
MSDS:
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Quality Standard:
In-house standard
Quantity:
Milligram-Grams
InChIKey:
GLCKXJLCYIJMRB-UPRLRBBYSA-N
InChI:
InChI=1S/C29H30O8/c1-3-11-34-19-6-7-20-22(14-19)27(21-8-5-18(33-2)15-24(21)35-12-10-30)28(29(31)32)26(20)17-4-9-23-25(13-17)37-16-36-23/h4-9,13-15,26-28,30H,3,10-12,16H2,1-2H3,(H,31,32)/t26-,27+,28+/m0/s1
Canonical SMILES:
CCCOC1=CC2=C(C=C1)C(C(C2C3=C(C=C(C=C3)OC)OCCO)C(=O)O)C4=CC5=C(C=C4)OCO5
1.Elevated pressure selectively blunts flow-evoked vasodilatation in rat mesenteric small arteries.
Christensen FH;Hansen T;Stankevicius E;Buus NH;Simonsen U Br J Pharmacol. 2007 Jan;150(1):80-7. Epub 2006 Nov 27.
BACKGROUND AND PURPOSE: ;The present study investigated mechanisms underlying impaired endothelium-dependent vasodilatation elicited by elevating the intraluminal pressure in rat mesenteric small arteries.;EXPERIMENTAL APPROACH: ;Arterial segments (internal diameter 316+/-2 microm, n=86) were mounted in a pressure myograph. The effect of elevating pressure from 50 to 120 mmHg for 1 h before resetting it to 50 mmHg was studied on endothelium-dependent vasodilatation.;KEY RESULTS: ;In arteries constricted with U46619 in the presence of indomethacin, shear stress generated by flow, evoked vasodilatation that was abolished by an inhibitor of nitric oxide (NO) synthase, asymmetric dimethylarginine (1 mM), whereas acetylcholine-induced vasodilatation was unchanged. After elevation of intraluminal pressure for 1 h and then resetting it to 50 mmHg, vasodilatation induced by shear stress and the NO donor, S-nitrosopenicillamine was inhibited, while vasodilatation induced by a guanylyl cyclase activator, BAY 412272, and acetylcholine was unaltered. Superoxide levels sensitive to polyethylene glycol superoxide dismutase were increased in segments exposed to elevated pressure. A superoxide scavenger, tempol (300 microM), a general endothelin receptor antagonist, SB 217242 and the selective ET(A) receptor antagonist, BQ 123 preserved shear stress-evoked vasodilatation.
2.Enrasentan improves survival, limits left ventricular remodeling, and preserves myocardial performance in hypertensive cardiac hypertrophy and dysfunction.
Willette RN;Anderson KM;Nelson AH;Olzinski AR;Woods T;Coatney RW;Aiyar N;Ohlstein EH;Barone FC J Cardiovasc Pharmacol. 2001 Oct;38(4):606-17.
Evidence suggests that endothelin receptor antagonists may have therapeutic potential for the chronic treatment of heart failure. In the current study, the effects of an orally active mixed endothelin-A/endothelin-B (ETA /ETB ) receptor antagonist (enrasentan) were assessed in a model of cardiac hypertrophy and dysfunction (spontaneously hypertensive stroke prone rats) maintained on a high-salt/high-fat diet. Echocardiography was used to quantify cardiac performance and left ventricular dimensions. Enrasentan (1,200 and 2,400 parts per million in the high-salt/high-fat diet) had no significant effects on body weight and systolic blood pressure. However, increases in heart rate were not observed in the enrasentan-treated groups at 12 weeks (p < 0.05). Enrasentan-treated groups exhibited significantly improved survival (90-95% vs. 30% [control rats] at 18 weeks; p < 0.001). Enrasentan treatments also increased stroke volume (at 8, 12, and 16 weeks) and cardiac index (at 8 and 16 weeks) 33-50% and 45-63%, respectively. Enrasentan treatments reduced the relative wall thickness (14-27% at 8 and 12 weeks), ratio of left ventricular mass to body weight (20% at 12 weeks), and ratio of terminal heart weight to body weight (16-23%, p < 0.
3.Comparison of the dual receptor endothelin antagonist enrasentan with enalapril in asymptomatic left ventricular systolic dysfunction: a cardiovascular magnetic resonance study.
Prasad SK;Dargie HJ;Smith GC;Barlow MM;Grothues F;Groenning BA;Cleland JG;Pennell DJ Heart. 2006 Jun;92(6):798-803. Epub 2005 Dec 9.
OBJECTIVE: ;To compare the effect of the dual endothelin A/B receptor antagonist enrasentan with enalapril on left ventricular (LV) remodelling.;METHODS: ;Multicentre, randomised, double blind, parallel group study of 72 asymptomatic patients with LV dysfunction. Patients received enrasentan (60-90 mg/day) or enalapril (10-20 mg/day). The primary end point was the change in LV end diastolic volume index (EDVI) after six months' treatment.;RESULTS: ;LV EDVI increased with enrasentan but decreased with enalapril (3.9 (1.8) v -3.4 (1.4) ml/m2, p = 0.001). Enrasentan increased resting cardiac index compared with enalapril (0.11 (0.07) v -0.10 (0.07) l/m2, p = 0.04), as well as LV mass index (0.67 (1.6) v -3.6 (1.6) g/m2, p = 0.04). Other variables were comparable between groups. Enalapril lowered brain natriuretic peptide more than enrasentan (-19.3 (9.4) v -5.8 (6.9) pg/ml, p = 0.005). Noradrenaline (norepinephrine) (p = 0.02) increased more with enrasentan than with enalapril. Enrasentan was associated with more serious adverse events compared with enalapril (six (16.7%) patients v one (2.8%), p = 0.02); the rate of progression of heart failure did not differ.;CONCLUSION: ;In asymptomatic patients with LV dysfunction, LV EDVI increased over six months with enrasentan compared with enalapril treatment, with adverse neurohormonal effects.
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CAS 167256-08-8 Enrasentan

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