Seragon Biosciences administers SRN-901 orally to middle-aged mice, achieving a 34.4% extension of remaining lifespan and improved physical endurance. The compound integrates mTOR inhibition, autophagy activation, NAD+ enhancement, and senolytic stimulation to restore youthful gene expression and metabolic profiles, offering a promising approach to mitigate age-related decline and extend disease-free lifespan.
Key points
Oral SRN-901 extends remaining lifespan by 34.4% and more than doubles endurance in middle-aged mice.
Drug combines mTOR inhibition, autophagy activation, NAD+ enhancement, and senolytic stimulation to restore youthful gene expression.
Multi-omics profiling and machine learning bioinformatics reveal pathway modulation, improved metabolic markers, and reduced senescence.
Why it matters:
This study demonstrates a multi-targeted drug that robustly extends lifespan and healthspan, paving the way for next-generation longevity therapies.
Q&A
What is mTOR?
How does SRN-901 differ from rapamycin?
What does healthspan mean?
How does machine learning assist in this study?
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Academy
Key Mechanisms in Anti-Aging Research
Longevity interventions aim to slow or reverse biological aging by targeting cellular pathways that drive age-associated decline. Four major strategies have emerged:
- mTOR inhibition
- Autophagy activation
- NAD+ enhancement
- Senolytic stimulation
mTOR Inhibition
mTOR (mechanistic Target of Rapamycin) is a central protein kinase that integrates nutrient and growth signals to control protein synthesis and cell growth. In aging cells, overactive mTOR accelerates damage accumulation. By using compounds that inhibit mTOR, such as rapamycin or novel agents like SRN-901, cells reduce unnecessary growth signaling, conserve resources, and trigger survival pathways. This shift promotes cellular maintenance and longevity across various models.
Autophagy Activation
Autophagy is the process by which cells digest and recycle damaged proteins and organelles. Efficient autophagy prevents toxic build-up that contributes to cell aging. Activators of autophagy enhance this “cellular cleanup,” improving mitochondrial function and stress resilience. Drugs that simultaneously inhibit mTOR often stimulate autophagy, creating a synergistic effect that supports tissue health and delays age-related diseases.
NAD+ Enhancement
NAD+ (nicotinamide adenine dinucleotide) is a coenzyme essential for energy production and DNA repair. Levels of NAD+ decline with age, impairing metabolic and repair pathways. Supplements or compounds that boost NAD+ availability restore sirtuin activity—enzymes that regulate gene expression related to longevity. Enhanced NAD+ metabolism supports both cellular energy balance and genome stability, key factors in extending healthy lifespan.
Senolytic Compounds
Senescent cells have stopped dividing but secrete harmful inflammatory factors that damage neighboring cells. Senolytics selectively eliminate these cells, reducing chronic inflammation and tissue dysfunction. By combining senolytic agents with other interventions, researchers aim to clear age-related debris while bolstering repair mechanisms, promoting a rejuvenated cellular environment.
Integrating Strategies
Modern anti-aging candidates like SRN-901 combine multiple mechanisms—mTOR inhibition, enhanced autophagy, NAD+ boosting, and senolytic action—into a single therapy. This multi-targeted design leverages synergy between pathways to drive more pronounced improvements in lifespan and healthspan.