• Preclinical results of EL-22 from a 2022 study demonstrated physiological (serum creatine kinase level), physical (body weight change), and functional (rotarod test) improvements in the dystrophic features of mdx mice, a mouse model of Duchenne muscular dystrophy (DMD)1.
• Elevai believes that EL-22 has the potential to treat obesity in combination with popular weight loss therapeutics, including GLP-1 receptor agonists, by preserving muscle mass while decreasing fat mass.
• Elevai plans to submit an Investigational New Drug (IND) application in 2025 that utilizes the licensed asset EL-22, previously called BLS-M221.
  

NEWPORT BEACH, Calif., May 02, 2024 (GLOBE NEWSWIRE) -- Elevai Labs, Inc. (NASDAQ:ELAB) ("Elevai" or the "Company"), today highlights results from our licensor's 2022 preclinical studies evaluating the treatment effect of its recently in-licensed asset, EL-22. EL-22 will primarily be commercialized by Elevai Biosciences, Inc., a biopharmaceutical division of the Company focusing on the development and acquisition of cutting-edge aesthetic medicines. Based on our licensor's 2022 preclinical data, Elevai believes that EL-22 has the potential to treat obesity in combination with GLP-1 receptor agonists by preserving muscle mass while decreasing fat mass.

"With the growing prevalence of obesity, and popularity of drugs like Ozempic and Mounjaro, we believe there is a need for a treatment option that leads to weight loss without the associated loss of muscle. Based on the preclinical data generated by our licensor, we believe that EL-22 has the potential to treat obesity while supporting and preserving existing muscle," said Jordan R. Plews, Ph.D., Chief Executive Officer of Elevai. "EL-22 is an engineered probiotic expressing myostatin on its surface, which triggers a mucosal immune response resulting in the body's own anti-myostatin antibodies. Myostatin has been shown to play an important role in regulating muscle and the preclinical data show potential proof-of-mechanism of EL-22 to preserve muscle fibers in mouse models of Duchenne muscular dystrophy by reducing the effects of myostatin."

Specifically, in the preclinical studies1:

• EL-22 showed a statistically significant increase in anti-myostatin IgG antibody concentration, where myostatin is a key negative regulator of muscle growth.
• Statistically significant decrease in creatine kinase levels, which indicates a decrease of muscle destruction.
• EL-22 administered to mdx mice, a mouse model of Duchenne muscular dystrophy, had improved physical activity and gross motor function, as demonstrated by a longer duration during rotarod tests.
  

Based on the highlighted preclinical data, Elevai believes that EL-22 has the potential to treat obesity in combination with GLP-1 by preserving muscle mass while decreasing fat mass. The Company intends to complete an IND submission in 2025 and to initiate clinical trials in the U.S. to evaluate the myostatin approach in combination with one or more GLP-1 receptor agonists in obesity.