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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.

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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

aged
  • LOW level of apelin production
  • LOW pathway activity
young
  • HIGH level of apelin production
  • HIGH pathway activity
aged
bge-105
  • LOW level of apelin production
  • HIGH pathway activity
  • Improved muscle repair
  • Increased muscle mass and strength
  • Increased energy
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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

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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.

Normal
Diaphragmatic atrophy
  • 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

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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

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