Didn’t say by how much unless I skimmed over it.

Not proven yet. The study found a coordinated shift in blood proteins associated with younger predicted biological age in treated IPF patients. It cannot prove the drug reversed the aging process itself, because all study participants had IPF — a disease that alters the very protein patterns the clocks are trained on. The critical next test, which Nobel laureate Michael Levitt explicitly named, is a trial in healthy volunteers without IPF. If the biological age signal persists in people without the disease confound, the case for systemic geroprotective activity becomes substantially stronger. The ongoing Phase III trial in IPF (320 patients, 47 centers in China) is designed to assess lung function, not aging per se — but its larger sample may provide additional proteomic data over a longer time horizon.

What makes rentosertib different from other longevity drugs like rapamycin or metformin?

Rapamycin, metformin, and the senolytic combination dasatinib plus quercetin are repurposed drugs: they were developed for other indications (organ transplant, diabetes, and cancer, respectively) and discovered through subsequent research to interact with aging-relevant pathways. None was designed with aging biology as the primary specification. Rentosertib was. Insilico’s AI platform scored TNIK — the drug’s molecular target — against the 12 hallmarks of aging framework, found it relevant to six hallmarks, and designed a molecule specifically to inhibit it. That makes rentosertib, if its geroprotective effects are confirmed in further studies, the first drug created from scratch specifically for the biology of aging to produce a clinical signal in humans.