Satellos Bioscience Announces 2023 Year End Financial Results and Operational Highlights

Satellos Bioscience Inc. (TSX: MSCL, OTCQB: MSCLF) (“Satellos” or the “Company”), a regenerative medicine company aimed at developing therapeutics that change the way degenerative muscle diseases are treated, announced today its financial results and operational highlights for the year ended December 31, 2023. All references to currency in this press release are in Canadian dollars unless otherwise noted.

“2023 has been a pivotal year in transitioning Satellos from a discovery-stage company to a preclinical company, positioning Satellos to further transition into a clinical-stage company during 2024 as we work to advance our lead drug candidate, SAT-3247, into first-in-human studies,” said Frank Gleeson, Co-founder and CEO, Satellos. “We’ve generated and publicly presented exciting preclinical data showing the broad potential of SAT-3247 to regenerate muscle tissue and disclosed its molecular drug target as AAK1. We look forward to initiating our clinical development program with a Phase 1 study of SAT-3247 mid-year.”

PROGRAM AND BUSINESS UPDATE:

Highlights for the year ended December 31, 2023, along with recent developments include:

Advanced SAT-3247

During Q1, 2024, the Company engaged a contract research organization (“CRO”) to design and implement its planned Phase 1 clinical trial for SAT-3247, initiated requisite GLP toxicology studies in two species with SAT-3247, made kilogram quantities of SAT-3247 under GLP conditions at the contract manufacturing organization it selected as its manufacturing partner, and initiated GMP manufacturing for SAT-3247. The Company continues to be on track to initiate and conduct a Phase 1 clinical trial in 2024 with SAT-3247.

Subsequent to the year end, on March 4, 2024, Satellos announced positive preclinical data presented at the Muscular Dystrophy Association Clinical and Scientific Conference. The preclinical data presented show the broad potential of SAT-3247 to improve skeletal muscle function as has been demonstrated in three mouse models of muscle degeneration: mdx model of Duchenne muscular dystrophy (DMD), FLExDUX4 model of facioscapulohumeral muscular dystrophy (FSHD), and a muscle injury model in wildtype mice. In all instances, treatment with SAT-3247 over a three-to-four-week period resulted in a statistically significant improvement in muscle force versus animals receiving placebo.