| |
| Names | |
|---|---|
| Preferred IUPAC name
(3R,4S,5S,6R)-5-Methoxy-4-[(2R,3R)-2-methyl-3-(3-methylbut-2-en-1-yl)oxiran-2-yl]-1-oxaspiro[2.5]octan-6-yl (2E)-3-{4-[2-(dimethylamino)ethoxy]phenyl}prop-2-enoate | |
| Other names
CKD-732; ZGN-433 | |
| Identifiers | |
 Y | |
3D model (JSmol) |
|
| ChemSpider |
|
PubChem CID |
|
| UNII |
Y |
CompTox Dashboard (EPA) |
|
| |
| |
| Properties | |
| C29H41NO6 | |
| Molar mass | 499.648 g·mol−1 |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa). | |
Beloranib is a former drug candidate for the treatment of obesity. It was discovered by CKD Pharmaceuticals and its clinical development was led by Zafgen.[1] Drug development was halted in 2016 after deaths during clinical trials.[2]
Beloranib, an analog of the natural chemical compound fumagillin, is an inhibitor of the enzyme METAP2.[3] It was originally designed as angiogenesis inhibitor for the treatment of cancer.[4] However, once the potential anti-obesity effects of METAP2 inhibition became apparent, the clinical development began to focus on these effects and beloranib has shown positive results in preliminary clinical trials for this indication.[5]
A Phase I trial was published in 2013,[6] finding a dose that led to weight loss in obese women in comparison to placebo. Results from a Phase II clinical trial for obesity were promising with clinically meaningful weight loss and improvements in cardiometabolic risk factors in the treated group.[7] Zafgen continued with a Phase III trial for Prader–Willi syndrome.[8]
In December 2015, Zafgen halted the Phase III clinical trial of beloranib for Prader–Willi syndrome after a second patient death in order to determine whether the deaths were treatment-related.[9] After discussions with the Food and Drug Administration indicated that the obstacles to gaining approval were insurmountable, product development for beloranib was ended.[2]
