Should you have any questions, please contact email@example.com.
Our approach exploits the longstanding symbiotic relationship between the mitochondria and human cells, enabling us to take advantage of millennia of evolutionary pressure. Even though our peptides are sourced from the mitochondrial genome, certain of these peptides produce effects that are not limited to local regulation within the mitochondria but may play important signaling and regulatory roles in diverse biological pathways unrelated to what have historically been considered mitochondrial functions.Our Approach
Our approach enables us to potentially target large unmet medical needs in a range of conditions such as nonalcoholic steatohepatitis (NASH), obesity, and idiopathic pulmonary fibrosis (IPF).Our Programs
In 2021, we announced positive topline data from our Phase 1a/1b study of CB4211, which is under development for the treatment of NASH and obesity. This study met its primary endpoints as CB4211 was well-tolerated and appeared safe with no serious adverse events. Evaluation of the exploratory endpoints in the 1b portion of the trial showed significant reductions from baseline in key biomarkers of liver damage, ALT and AST, and in glucose levels in the CB4211 group compared to placebo after four weeks of treatment, with a trend towards lower body weight. In addition, there was a measurable reduction in the level of liver fat.
CB4211 is a first-in-class therapeutic that is a novel and improved analog of MOTS-c, a naturally occurring mitochondrial derived peptide (MDP). MOTS-c was discovered in 2012 by CohBar founder Dr. Pinchas Cohen and his academic collaborators and has been shown to play an important role in the regulation of metabolism. Consistent with our recent clinical data, CB4211 has demonstrated significant therapeutic potential in preclinical models of NASH and obesity.View Candidate
In August 2020, we presented data on the efficacy of CB5138 Analog peptides in preclinical models of IPF at the American Thoracic Society Virtual Annual Meeting. In a widely used therapeutic mouse model of IPF, CB5138 Analogs significantly reduced lung fibrosis, as evidenced by decreases in the Ashcroft Score, fibrosis-related changes in lung weight, collagen deposition in lung tissue and collagen secretion into lung fluid.View Candidate