First-in-class program for the treatment of early onset obesity

Obesity is a complex disease with various contributing environmental and genetic factors. Amongst them, single nucleotide polymorphisms (SNPs) in multiple genes have been shown to increase the risk of disease. This is the case for SNPs of the melanocortin-4 receptor (MC4R), a GPCR playing a key role in energy homeostasis, affecting both energy intake and expenditure. Mutations of the MC4R have been described as causing early onset severe obesity which is the most common monogenic form of obesity in humans.

Program description

MC4R pharmacochaperone

  • Discovery
  • Candidate
  • Preclinical
  • Clinical

Pioneering works from the laboratory of Michel Bouvier in Montreal, Canada, showed that a significant number of MC4R mutants results in mistrafficked receptors that can no longer reach the plasma membrane, resulting in reduction or loss of the leptin-melanocortin pathway activation.
Thanks to the uniqueness of BRET-based biosensors, the same team has also demonstrated that small molecules called chaperone molecules or pharmacochaperones were able to enter the cell and interact with mutated MC4Rs to recapitulate an appropriate membrane expression.

We have entered into a research collaboration with Michel Bouvier’s lab with the objective to discover and develop novel small molecule pharmacochaperones of mutated MC4Rs for the treatment of early onset obesity. The bioSens-All™ technology, originating from the same lab in Montreal University, constitutes the pillar of this collaborative effort.
MC4R program is currently at the hit-to-lead stage.

Other programs

mGluR3 PAM


mGluR4/7/8 PAM