KROS - Keros Therapeutics Presents Preclinical Data from its KER-065 Program at the 28th International Annual Congress of the World Muscle Society | Benzinga
LEXINGTON, Mass., Oct. 04, 2023 (GLOBE NEWSWIRE) -- Keros Therapeutics, Inc. ("Keros") (NASDAQ:KROS), a clinical-stage biopharmaceutical company focused on developing and commercializing novel therapeutics to treat a wide range of patients with disorders that are linked to dysfunctional signaling of the transforming growth factor-beta ("TGF-ß") family of proteins, today announced results from preclinical studies evaluating the treatment effect of a research form of KER-065 ("RKER-065") in a mouse model of Duchenne muscular dystrophy ("DMD") and in prednisolone-treated mice, which were presented at the 28th International Annual Congress of the World Muscle Society ("WMS") on Wednesday, October 4, 2023.
"We are pleased to present promising preclinical data from our KER-065 program at WMS this year, showing that treatment with RKER-065 led to a robust increase in muscle mass, muscle function and bone mass in a mouse model of DMD and in prednisolone-treated mice," said Jasbir S. Seehra, Ph.D., President and Chief Executive Officer of Keros. "We believe these data support the potential of KER-065 to treat multiple pathophysiologies of DMD and other neuromuscular diseases, and we look forward to commencing a Phase 1 clinical trial of KER-065 in healthy volunteers in the first quarter of 2024."
RKER-065 treatment led to a robust increase in muscle mass, functional strength, and bone formation in a DMD mouse model
- RKER-065 ameliorated muscle and bone loss in a progressive murine model of Duchenne muscular dystrophy
Keros studied the effect of RKER-065 in a progressive and phenotypically severe DMD mouse model. DMD mice were dosed with vehicle or 10 mg/kg of RKER-065 once weekly for four or six weeks. A cohort of healthy mice received only vehicle.
In DMD mice, treatment with RKER-065 led to significant increases in body weight and lean mass by four weeks compared to vehicle-treated DMD mice. Additionally, an increase in forelimb grip strength was observed, which is supportive of improved muscle function. DMD mice treated with RKER-065 demonstrated significant increases in muscle mass in the pectoralis and tibialis anterior ("TA") as compared to vehicle-treated DMD mice. In addition, expression of utrophin, a functional analog of dystrophin, was higher in the TA of DMD mice treated with RKER-065 compared to vehicle-treated DMD mice.
Concomitant with neuromuscular decline, vehicle-treated DMD mice had significant decreases in bone mineral density ("BMD"), while DMD mice treated with RKER-065 showed no significant difference compared to healthy adult mice. RKER-065 treatment led to a significant increase in trabecular bone volume fraction by six weeks as compared to vehicle-treated DMD mice and ...