| Stereochemistry | ACHIRAL |
| Molecular Formula | C29H43NO4S |
| Molecular Weight | 501.721 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CC(C)C1=CC(C(C)C)=C(CC(=O)NS(=O)(=O)OC2=C(C=CC=C2C(C)C)C(C)C)C(=C1)C(C)C
InChI
InChIKey=PTQXTEKSNBVPQJ-UHFFFAOYSA-N
InChI=1S/C29H43NO4S/c1-17(2)22-14-25(20(7)8)27(26(15-22)21(9)10)16-28(31)30-35(32,33)34-29-23(18(3)4)12-11-13-24(29)19(5)6/h11-15,17-21H,16H2,1-10H3,(H,30,31)
Avasimibe (CI 1011) is a potent ACAT (Acyl-CoA:cholesterol acyltransferase) inhibitor. Avasimibe inhibits both ACAT1 and ACAT2 isoforms. Avasimibe was in development by Parke-Davis (now Pfizer) in the US for the treatment of atherosclerosis and hyperlipidaemia. Avasimibe was in phase III studies and more than 1300 patients had been treated for up to one year, however, in October 2003, Pfizer announced that development had been discontinued.
CNS Activity
Originator
Approval Year
Doses
AEs
Sourcing
PubMed
Patents
Sample Use Guides
Following an 8-week placebo and dietary-controlled baseline period, patients with combined hyperlipidemia and hypoalphalipoproteinemia were randomly assigned to double-blind treatment with placebo, 50, 125, 250, or 500 mg Avasimibe (CI 1011) administered as capsules once daily for 8 weeks. At all evaluated doses, avasimibe treatment resulted in prompt and significant reductions in plasma levels of total triglycerides and very low-density lipoprotein cholesterol, apparently independent of dose. All doses of avasimibe were well tolerated with no resulting significant abnormalities of biochemical, hematological, or clinical parameters.
Route of Administration:
Oral
ACTIVE MOIETY
SALT/SOLVATE (PARENT)
