GlobeNewswire·Sep 8, 2026, 8:15 AM ET

GRI Bio Presents New Phase 2a Data at ERS 2026 Defining GRI-0621's Mechanism of Action in IPF Across Nine Mechanistic Pillars

GRI

New whole blood RNA sequencing data identified coordinated changes in genes governing immune re-balancing, myofibroblast inhibition, fibrolysis, basement membrane repair, re-epithelialization, antitussive effects, & GI protection.
Signals from four independent measurement modalities (RNA sequencing, serum ECM biomarkers, spectral flow cytometry, & clinical readouts) supported all nine pre-specified mechanistic pillars defining a repair phenotype.
Approximately 2x to 2.5x more GRI-0621-treated patients experienced an FVC increase compared with placebo, with a placebo-adjusted FVC change of +99 mL overall & +139 mL on background antifibrotic therapy at Week 12.
The Phase 2a study involved 35 IPF patients randomized 2:1 to receive GRI-0621 or placebo, with 80% receiving background pirfenidone or nintedanib.
Mechanistic findings included a Th2-to-Th1 shift, suppression of TGF-β & ROCK2 pathways, net fibrolysis of type III & VI collagen, net repair of type IV collagen basement membrane, & AT2-to-AT1 re-epithelialization.
GRI-0621 demonstrated an antitussive effect with 0% treatment-emergent cough versus 25% on placebo, alongside reduced dyspnea (4% vs 17%) & diarrhea (17% vs 33%).
Safety data showed no serious treatment-emergent adverse events (0% vs 8% on placebo) & no drug-related serious adverse events, with all reported adverse events being Grade 1–2.
Ten post hoc robustness sensitivity analyses remained directionally positive, with FVC estimates converging on +40 to +65 mL overall & +67 to +89 mL for patients on background standard-of-care therapy.
The totality of Phase 2a findings supports advancing GRI-0621 into a longer-duration 52-week study & further evaluation in the IPF program.
Data were presented at the 2026 European Respiratory Society Congress in Barcelona, Spain, via one late-breaking oral presentation & three posters.