BioAge Labs has reported positive data from a Phase Ib clinical trial of apelin receptor APJ agonist BGE-105 to treat muscle atrophy.

The placebo-controlled, double-blind trial has been designed for assessing BGE-105’s pharmacodynamics and safety.

In the study, 21 volunteers underwent bed rest for ten days while receiving BGE-105 or placebo infusions.

The findings showed that treatment with BGE-105 resulted in a statistically significant improvement in muscle size, quality, and protein synthesis, compared to a placebo, in healthy volunteers aged 65 years or above, during ten days of strict bed rest.

Volunteers receiving treatment with BGE-105 demonstrated a 100% improvement in thigh circumference.

In addition, a 58% improvement in vastus lateralis cross-sectional area was found in ultrasound measurements and a 73% improvement in vastus lateralis thickness.

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The company stated that the apelin agonist was well tolerated in the study.

BioAge CEO and co-founder Kristen Fortney said: “The data from this Phase Ib study provides clinical validation of BioAge’s AI-driven discovery platform and demonstrates the power of our human-first approach to identify medically relevant drug targets.

“Our analysis of BioAge’s human aging cohorts revealed that the apelin pathway is a strong predictor of healthy longevity and muscle function, and now this has translated directly into our clinical finding that apelin pathway activation with BGE-105 improves muscle physiology in older adults.

“Today’s announcement is a milestone in BioAge’s mission to create a pipeline of drugs that treat disease and extend healthy lifespan by targeting the mechanisms of ageing.”

The company stated that the data from the Phase Ib clinical trial supports advancement to the Phase II study of BGE-105 for preventing adverse muscle atrophy–related outcomes in older patients, who are under ventilation in the intensive care unit (ICU).

Scheduled to commence next year, the Phase II study is designed to evaluate BGE-105’s ability to prevent ICU diaphragmatic atrophy and critical illness myopathy.