Skye Bioscience Demonstrates Prominent Role of Peripheral CB1 Inhibition and Achieves Significant Weight Loss with Novel CB1-inhibiting Antibody, Nimacimab, in Preclinical Model
Peripherally-restricted nimacimab achieves significant dose-dependent weight loss, fat mass reduction, lean mass preservation, and glycemic control in diet-induced obesity model
Preliminary data shows that nimacimab achieves desired metabolic outcomes without central inhibition and its risk of neuropsychiatric adverse events
Excerpt from the Press Release:
SAN DIEGO, Nov. 04, 2024 (GLOBE NEWSWIRE) — Skye Bioscience, Inc. (Nasdaq: SKYE) (“Skye”), a clinical-stage biopharmaceutical company focused on unlocking new therapeutic pathways for metabolic health, today announced preliminary data from a diet-induced obesity (DIO) model in mice. Skye’s CB1-inhibiting antibody, nimacimab, achieved significant dose-dependent weight loss of up to 16% compared to vehicle, highlighting a novel peripherally-driven mechanism for inducing weight loss and other metabolic benefits.
Skye developed a DIO model using a transgenic mouse expressing the human CB1 receptor (hCB1R). After establishing this newly-developed model, the goal of this initial study was to assess the effects of its peripherally-targeting CB1 inhibitor on weight loss and other metabolic parameters. Five groups of mice were treated for 35 days with vehicle, 10 nmol/kg semaglutide, or nimacimab at 7.5 mg/kg, 24 mg/kg or 75 mg/kg, respectively. Key initial findings include:
- Dose-dependent weight loss with nimacimab of 4.5%, 11.4% and 16.0% compared to vehicle
- Significant fat mass loss with lean mass preservation
- Dose-dependent improvement in glucose tolerance.
Chris Twitty, PhD, Chief Scientific Officer of Skye, commented, “This is the first-ever reported assessment of an antibody-based peripherally-restricted CB1 inhibitor using a DIO model. These results are preliminary and we continue to refine this model, however, the data are very encouraging and provide the first direct evidence supporting our hypothesis that peripheral CB1 inhibition is the primary driver of weight loss whereas central CB1 inhibition contributes minimally to efficacy yet promotes neuropsychiatric adverse events.
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