Insilico Medicine says its AI-built lung drug pushed biological aging markers toward younger profiles in a fresh analysis of trial samples. Researchers measured serum from 42 people with idiopathic pulmonary fibrosis against six proteomic aging clocks. Patients on placebo tracked in the opposite direction.
The strongest signal came at week 4 in the 30 mg twice-daily arm, where predicted age fell by roughly three to four years, with one clock showing up to six years of reversal before effects leveled off by week 12. Most significant readouts clustered at that early time point, with 21 of 54 comparisons clearing the bar.
Separating real aging effects from lung repair took extra legwork. Researchers compared drug-driven protein shifts against age-linked trajectories from 55,319 UK Biobank participants. The 30 mg twice-daily arm ran counter to aging patterns, while placebo drifted toward older profiles. Several senescence markers, among them EREG, IGFBP4, MMP10 and MMP13, fell across every treated arm. The authors read this as a senomorphic signal, where a drug quiets the secretions of senescent cells rather than clearing them.
The dose that moved lung function most was not the one with the strongest age signal, evidence the effect runs deeper than treating fibrosis. Authors still caution the cohort is small and clocks cannot fully separate aging from illness. Rentosertib, the AI-designed TNIK inhibitor, has advanced to a phase 3 IPF program. Founder Alex Zhavoronkov planned to present the findings at a Nature conference in Paris on September 8.
