The TrkA Antagonist AR786 Prevents Heterotopic Ossification

Soft tissue trauma can result in the pathologic formation of cartilage and bone outside of the skeleton, termed heterotopic ossification (HO). Therapeutic options for treatment of HO are lacking. We recently recognized the role of sensory nerve fibers in trauma‐induced HO through nerve growth factor (NGF) and tropomyosin receptor kinase A (TrkA) signaling whereby the deletion of NGF‐TrkA signaling impairs axonal invasion and blunts osteochondral differentiation after HO induction in a mouse model. Given this observation, we hypothesized that utilization of a small molecule antagonist for TrkA in clinical development, AR786, would demonstrate therapeutic benefit in the prevention of HO.