Elevai Biosciences Highlights Preclinical Data Showing Potential of In-Licensed Asset “EL-22” for The Treatment of Obesity

• 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.