They want to provide this for people who are bedridden or otherwise unable to exercise.

LAMZ augments muscle and bone by mimicking calcium signaling to induce PGC-1α. Schematic of LAMZ function in the augmentation of muscle and bone. Exercise increases the calcium concentration in muscle and bone cells, inducing calcium signaling. Under this signaling, PGC-1α and Mef2c are activated and reciprocally drive their expression. Mitochondriogenic, myogenic and osteogenic genes are induced as well, together augmenting the muscle and bone. Thus, LAMZ facilitates the calcium signaling pathway and restores locomotor fitness.

They have established a novel, three–part drug screening system and discovered a locomomimetic drug, LAMZ. LAMZ enhances myogenesis and osteoblastogenesis via stimulation of calcium-PGC-1α signaling. It can be administered by multiple routes and improves both muscle and bone mass, resulting in increased capacity for locomotion. Therefore, LAMZ has potential as a therapeutic drug for patients with impaired locomotion, such as those with sarcopenia and osteoporosis.

Medication is safer than exercise, but there are no drugs that reinforce both muscle and bone when administered alone. Multiple medications increase the risk of adverse events; thus, there is a need for individual drugs targeting both tissues. To this end, we established a novel sequential drug screening system and identified an aminoindazole derivative, locamidazole (LAMZ), which promotes both myogenesis and osteoblastogenesis while suppressing osteoclastogenesis. Administration of this drug enhanced locomotor function, with muscle and bone significantly strengthened. Mechanistically, LAMZ induced Mef2c and PGC-1α in a calcium signaling–dependent manner. As this signaling is activated upon physical exercise, LAMZ mimics physical exercise. Thus, LAMZ is a promising therapeutic drug for locomotor diseases, including sarcopenia and osteoporosis.