Diabetic nephropathy is a complication of diabetes that occurs in microvascular cells in the kidney that are continually exposed to excessive blood sugar. Extracellular matrix accumulation and inflammatory cells are deposited in the glomerulus and renal tubular interstitial tissue, resulting in albuminuria and decreased renal function. Approximately 20-30% of patients with diabetes develop chronic kidney disease in which structural or functional abnormalities of the kidneys (glomerular filtration rate less than 60 ml/min/1.73 m2) persist for three months or longer.

Chronic kidney disease, which causes serious social problems due to its high mortality rate, is administered with blood pressure-lowering agents for hypertensive patients and hypoglycemic agents for diabetic patients depending on the cause. However, for patients with end-stage renal disease with the lowest glomerular filtration rate (less than 20 ml/min/1.73 m2), the treatment option mentioned above is limited, and there is no approved treatment that directly suppresses renal inflammation and fibrosis, prominent and pathological manifestation of chronic kidney disease.

• FM101 mediates biased modulation upon binding A3AR, which suppresses AMP activation leading to an anti-inflammatory/fibrotic effect.
• By inhibiting beta-arrestin, FM101 prevents receptor desensitization and internalization to mediate long term therapeutic effects.