OA inflammatory phenotype: symptom and joint structure modification
Osteoarthritis (OA) is a heterogeneous disease: our and other scientists’ experience suggests that patients belong to different subsets corresponding to so-called disease phenotypes. The scientific community is working to clearly identify these phenotypes, to find molecular targets and pathways specific for them (thus characterizing endotypes), and to eventually obtain a true disease-modifying drug. It is indeed possible that a single “magic bullet”, suitable for all OA patients, does not exist and we will have to find drugs that may be different for each phenotype.
The investigation of the OA inflammatory phenotype is the approach we are following with CR10049.
Inflammatory OA is triggered by an inflammatory reaction. As such, selective anti-inflammatory agents could be disease-modifying in this patient subpopulation. CR10049 is the lead of a series of small molecules with potent activity on undisclosed kinases that play a role in both OA pain (symptom-modifying) and inflammatory joint degeneration (structure-modifying).
Pre-clinical evaluation in small (rat, MIA and MMT) and large (rabbit, ACLT) OA animal models showed that CR10049 completely abrogates pain behavior and improved several histological late-stage parameters of the OA joint.
One such drug would be a major breakthrough in the treatment of inflammatory OA.