Cellular Rejuvenation

Cellular aging manifests through multiple hallmarks — senescent cell accumulation, mitochondrial dysfunction, proteostatic collapse, stem cell exhaustion, telomere attrition — each requiring distinct intervention strategies. Senolytic drugs that selectively clear senescent cells have shown dramatic healthspan extension in animal models, but the current pipeline of senolytic candidates is narrow, limited to a few compound families (dasatinib+quercetin, navitoclax, fisetin) with significant off-target effects. Beyond senolytics, interventions targeting other aging hallmarks — mitochondrial transfer, autophagy enhancement, NAD+ restoration — lack systematic approaches to candidate generation.

Current longevity drug discovery applies standard medicinal chemistry and phenotypic screening to identify compounds affecting aging biomarkers. This approach is slow, anchored to known compound families, and evaluates candidates against individual aging hallmarks rather than generating interventions that address the interconnected biology of aging. Computational aging models predict biological age but do not generate the molecular interventions needed to reduce it.