Sookmyung Women’s and Sungkyunkwan Researchers Identify Cdon Protein and AMC6156 Drug Candidate for Age-Related Muscle Loss

A joint research team from Sookmyung Women’s University and Sungkyunkwan University has identified a protein linked to muscle aging and a drug candidate designed to activate it. The researchers say Cdon plays a central role in maintaining adult muscle, while its expression falls markedly with aging, sarcopenia and muscle-wasting diseases.

When Cdon expression declined, genes associated with muscle atrophy became active. The change was accompanied by metabolic imbalance and smaller muscle fibers, leading the team to focus on Cdon’s role in maintaining muscle metabolism and homeostasis.

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We confirmed that the decline of the Cdon protein is a major indicator of muscle aging and demonstrated that regulating the Cdon axis through AMC6156 can restore muscle metabolism and mitochondrial homeostasis.

Using a search based on the Cdon promoter, the researchers identified the small-molecule compound AMC6156. They reported that the compound promotes muscle differentiation, increases muscle mass and function, and significantly eases age-related muscle atrophy.

The team also found that AMC6156 improved neuromuscular transmission and blood-glucose regulation while reducing fat accumulation in the liver. Researchers identified a mechanism involving activation of the AMPK signaling pathway, which they said restored mitochondrial metabolism and antioxidant function.

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We will accelerate the development of innovative new drugs to overcome age-related sarcopenia and metabolic diseases based on these research results.

The work was conducted with researchers from AnimusCure, a biotechnology venture whose chief executives include the two professors. The company plans to complete dosing for all patients in a phase 2 clinical trial in September, then analyze the data and assess the results. The trial will evaluate the appropriate dose and safety of AMC6156, as well as possible improvements in muscle mass, strength and physical function.

The researchers are also considering AMC6156 for combination treatment to offset muscle loss that can occur during GLP-1 obesity treatment, as well as for rare neuromuscular diseases. Professor Bae Gyu-un said, “We confirmed that the decline of the Cdon protein is a major indicator of muscle aging and demonstrated that regulating the Cdon axis through AMC6156 can restore muscle metabolism and mitochondrial homeostasis.”

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We will concentrate our research and development capabilities so that AMC6156 can establish itself as a new treatment in the field of age-related sarcopenia after rapid and rigorous data analysis and validation.