Erick Rodriguez-Palma, MSc, PhD

Fibromyalgia is a chronic pain condition marked by widespread hypersensitivity, with current treatments often limited by its complex mechanisms. Since Nav1.7 and Cav2.2 channels are key players in pain signaling, we hypothesize that increased phosphorylation of CRMP2, an auxiliary binding partner, at serine 522 (S522) amplifies the activity of these channels, leading to increased neuronal excitability and pain in fibromyalgia. Our research will investigate how CRMP2 modulates these channels and evaluate the therapeutic potential of a novel compound, A5-14, designed to inhibit CRMP2 S522 phosphorylation. By using both in vitro and in vivo models, we aim to determine the effect of A5-14 in reducing pain behaviors in male and female mice with fibromyalgia induced by chronic restraint stress. If successful, this study could lead to the development of a first-in-class, non-opioid therapeutic targeting CRMP2 phosphorylation for safer and more effective fibromyalgia treatment.