The company is working on a new approach to treating rheumatoid arthritis based on a common pathway in the cell that infiltrates bone and joints. Inflammatory arthritis disables thousands of people each year. It occurs in children and adults after trauma and infections but most cases are idiopathic. Millions of adults live with chronic RA, which has similar features.

Inflammatory arthritis often requires treatments with serious side effects. Later in arthritis, bone erosion is a major problem that causes severe pain and debilitation. There is no small molecule drug available to specifically treat arthritis bone erosion. We show that osteoclast maturation is suppressed by blocking ion channels. An ion-channel antagonist, ELP-004, suppressed osteoclast maturation and strongly suppressed bone erosion in collagen-induced arthritis (CIA) in mice, even after symptoms of arthritis were measurable.

We hypothesize that signals mediated by specific ion channels modulate the final differentiation of osteoclasts resulting in bone and joint degradation in acute arthritis. We propose that pharmacologically suppressing specific ion channels with ELP-004 will prevent bone erosion due to arthritic stimuli without major adverse effects. Preclinical toxicity assays show that ELP-004 has minimal toxicity to the immune and cardiovascular systems and has no measurable genotoxicity. Continued comprehensive pharmacokinetic and toxicokinetic testing in addition to mechanistic experiments with ion-channel signaling, immunology, and bone biology expertise is underway.