BGE-105: Apelin receptor APJ agonist
A key pathway that promotes muscle regeneration and repair
Apelin is a small secreted peptide hormone that regulates multiple aspects of muscle physiology, including cell growth and survival, regeneration, and repair. Analysis of our proprietary longitudinal human cohorts revealed that higher apelin signaling activity correlates with improved muscle function, reduced frailty, and longer lifespan. In mice, apelin levels decline with age; by contrast, activation of apelin signaling reverses age-related sarcopenia.
BGE-105 is an oral agonist of the apelin receptor APJ. By targeting this fundamental mechanism of aging, BGE-105 could treat multiple acute and chronic indications: improving muscle strength in frail patients, accelerating rehabilitation following fractures, and increasing mobility after extended bed rest.
BGE-105 activates apelin / APJ signaling, which has
been shown to improve muscle strength and repair
and increase energy
BGE-105 activates apelin / APJ signaling,
which has been shown to improve muscle
strength and repair and increase energy
BGE-105 activates
apelin / APJ signaling,
which has been shown to
improve muscle strength
and repair and increase
energy
- LOW level of apelin production
- LOW pathway activity
- HIGH level of apelin production
- HIGH pathway activity
- LOW level of apelin production
- HIGH pathway activity
BioAge collaborator spotlight
Maintaining muscle mass and strength is key to maintaining physical function, independence, and quality of life in the elderly. In our mouse models, apelin reverses age-associated sarcopenia, and it is tremendously exciting to trial in humans an oral apelin receptor agonist, BGE-105, that recapitulates the positive effects of apelin peptide.
Cédric Dray, PhD
Faculty of Science & Engineering
Paul Sabatier University - Toulouse III
We plan to initially develop BGE-105 for
ICU diaphragm atrophy given significant unmet
need–with an ultimate path to treat frailty.
We plan to initially develop BGE-105 for
ICU diaphragm atrophy given significant
unmet need–with an ultimate path
to treat frailty.
We plan to initially
develop BGE-105 for
ICU diaphragm
atrophy given
significant unmet
need–with an
ultimate path
to treat frailty.
Patients undergoing mechanical ventilation (MV) in the ICU undergo rapid diaphragmatic atrophy (DA) given muscle disuse
40-75% of patients undergoing MV develop clinically significant DA
It typically begins to develop within 24 hours of MV, with most profound changes occurring within 3 days
DA is the leading cause of difficulty weaning from MV, and is associated with poor clinical outcomes and increased resource utilization, including:
Longer time on MV
Longer time in the ICU
Higher mortality
Currently there is no therapeutic for prevention or treatment of DA, although ventilation approaches aim to minimize lung stress and limit diaphragm injury
BioAge advisor spotlight
Diaphragmatic atrophy during mechanical ventilation is associated with delayed recovery from respiratory failure and significant morbidity. Activating the apelin pathway has the potential to prevent muscle atrophy, accelerate recovery, and improve long-term functional outcomes in these patients.
Ewan Goligher, MD, PhD, FRCPC
Division of Critical Care Medicine
Toronto General Hospital
