GRI Bio has announced positive topline results from its phase 2a clinical trial evaluating GRI-0621 in idiopathic pulmonary fibrosis (IPF). The study met its primary and secondary endpoints, showing the drug was well tolerated over 12 weeks and demonstrated signs of disease-modifying activity.
The company reported no drug-related severe or serious adverse events. Common side effects included dry skin, dry lips and muscle or joint pain. Importantly, there were no increases in cough or gastrointestinal disorders compared to placebo. Eighty per cent of subjects were taking background pirfenidone or nintedanib.
GRI-0621 also showed improvements in forced vital capacity (FVC). At 12 weeks, 39% of treated subjects experienced an increase in FVC, while 80% of those on placebo saw a decline.
Toby Maher, Professor of Clinical Medicine at the Keck School of Medicine, USC Los Angeles, said: “Treatment of patients with IPF in the GRI-0621 phase 2a trial was observed to be safe and well tolerated through the completion of the 12-week study. Secondary endpoints related to the effect of GRI-0621 on biomarkers associated with disease progression provided evidence that GRI-0621 maintains a net anti-fibrotic effect compared to standard of care.”
Biomarker data suggested fibrosis resolution and repair of the alveolar basement membrane. Collagen turnover rates shifted from fibrogenic in placebo-treated subjects to fibrolytic in those receiving GRI-0621. Gene expression analysis also indicated activation of lung repair mechanisms.
Marc Hertz, Chief Executive Officer of GRI Bio, explained: “The positive phase 2a results represent an important milestone for our IPF program and a compelling early signal of GRI-0621’s disease-modifying potential.
“In addition to a favourable safety and tolerability profile, GRI-0621 demonstrated meaningful improvement in biomarkers suggesting fibrosis resolution and repair of the alveolar basement membrane. These results reinforce our belief in GRI-0621’s differentiated mechanism and support its potential to go beyond slowing disease progression by directly impacting core drivers of IPF.”
