Stereochemistry | ABSOLUTE |
Molecular Formula | C29H30O8 |
Molecular Weight | 506.5437 |
Optical Activity | UNSPECIFIED |
Defined Stereocenters | 3 / 3 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
CCCOC1=CC2=C(C=C1)[C@@H]([C@H]([C@@H]2C3=CC=C(OC)C=C3OCCO)C(O)=O)C4=CC=C5OCOC5=C4
InChI
InChIKey=GLCKXJLCYIJMRB-UPRLRBBYSA-N
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
Enrasentan is an orally active mixed endothelin A/B receptor antagonist with a 100-fold greater affinity for the endothelin A receptor. In an animal model of hypertension and cardiac hypertrophy the drug has reduced blood pressure, prevented cardiac hypertrophy and preserved myocardial function. In rats with hyperinsulinemia and hypertension enrasentan normalized blood pressure and prevented cardiac and renal damage. In rats with stroke the drug reduced the ischemic area in the brain. Enrasentan had been in phase II clinical trial for the treatment of heart failure but the results suggested that enrasentan does not appear to have favorable effects on ventricular remodeling.
Originator
Approval Year
Sourcing
PubMed
Patents
Sample Use Guides
The functional activity of enrasentan was evaluated in vitro in rat isolated aorta. In this model enrasentan (10 to 1000 nM) produced concentration-dependent, parallel rightward shifts in the ET-1 concentration-response curve. The Kb value for inhibition of ET-1-induced contraction for enrasentan was 4.4 ± 0.6 nM. The drug was devoid of agonistic activity. In human isolated pulmonary artery enrasentan produced a 7-fold shift to the right of the ET-1 concentration-response curve, with a calculated Kb value of 5.2 nM.