Key Longevity Targets
Molecular targets with documented roles in aging biology. Click any target to explore compounds with PubMed evidence.
Nutrient sensing & autophagy regulator
NAD⁺-dependent deacetylase, aging regulator
Mitochondrial deacetylase, metabolic health
Energy sensor, activates longevity pathways
Transcription factor linked to centenarians
Telomere maintenance & cellular senescence
Growth hormone axis, lifespan modulation
Tumor suppressor & senescence gatekeeper
Master antioxidant regulator
DNA repair, NAD⁺ consumption
Anti-aging hormone, kidney-brain axis
NAD⁺ biosynthesis rate-limiting enzyme
Longevity Pathways
Six core biological pathways implicated in aging and lifespan regulation.
Cellular recycling activated by MTOR inhibition. Central to caloric restriction mimetics.
NAD⁺ decline drives aging via SIRT1/SIRT3 inactivation. Boosting NAD⁺ restores mitochondrial function.
Senescent cells accumulate with age and drive inflammation. Senolytics selectively clear them.
AMPK activates when energy is low, mimicking exercise and caloric restriction at the molecular level.
Telomere shortening limits cellular lifespan. Telomerase activation is studied in longevity contexts.
Most-Studied Longevity Compounds
Natural compounds with the strongest PubMed evidence for longevity-relevant targets.
The Molecular Biology of Longevity
Longevity research has identified several interconnected molecular pathways that regulate the rate of biological aging. The mTOR pathway acts as a central nutrient sensor — when inhibited, it activates autophagy, the cellular recycling process linked to lifespan extension in yeast, worms, flies, and mice.
The NAD⁺/Sirtuin axis connects metabolic health to epigenetic aging. NAD⁺ levels decline approximately 50% between age 40 and 60, impairing SIRT1 and SIRT3 activity. These sirtuins regulate hundreds of proteins involved in DNA repair, mitochondrial biogenesis, and inflammation.
Cellular senescence — the accumulation of non-dividing cells that secrete pro-inflammatory signals (the SASP) — is now recognized as a primary driver of age-related tissue dysfunction. Senolytic compounds such as quercetin and fisetin are being studied for their ability to selectively clear these cells.
BiohacksAI tracks all compounds with documented interactions at these targets, ranked by bioassay confidence from PubMed data. All data is computational and for research purposes only — not medical advice.
Frequently Asked Questions
Data derived from PubChem BioAssay, PubMed/MEDLINE (NLM), and the BiohacksAI compound corpus. BiohacksAI does not provide medical advice. Patent pending (EVE-PAT-2026-001). © 2026 Organiq Sweden AB.