Both drugs have the potential to offer a disease-modifying approach to the lung disease.
Vicore Pharma and Endeavor BioMedicines have shared new data from two mid-stage clinical trials of two therapies that show promise in treating patients living with idiopathic pulmonary fibrosis (IPF).
Vicore’s buloxibutid and Endeavor’s ENV-101 could provide new ways of treating this chronic, progressive lung disease.
Affecting up to 20 people per 100,000 globally, IPF is a rare lung disease that causes the lungs to thicken and stiffen, causing permanent fibrosis and difficulty breathing.
Both treatments are being investigated to improve on the current standard-of-care therapies for IPF that could potentially slow the decline of lung function, without reversing or stopping it.
In a phase 2a AIR trial, buloxibutid, an angiotensin II type 2 receptor agonist taken orally twice a day, showed significantly improved lung function across 36 weeks with an average forced vital capacity (FVC) increase of 216ml from baseline, reversing the 180ml decline over the same period that would usually be observed in untreated IPF patients.
In addition, the drug was safe and well-tolerated over the 26-week period of treatment, with no new drug-related adverse events.
Meanwhile, Endeavor’s hedgehog (Hh) signalling pathway inhibitor presented data from another phase 2a trial, which showed that ENV-101 achieved a statistically significant increase in total lung capacity above baseline at 12 weeks, with an average 200ml improvement compared to a decrease of 56ml in an IPF group treated with placebo.
Usually involved in wound healing, the Hh pathway is thought to be activated in IPF, as well as progressive pulmonary fibrosis (PPF), causing the build-up of scar tissue in the lungs.
Both companies aim to move ahead with further trials. Vicore’s phase 2b trial will investigate FVC changes over 52 weeks, while Endeavor plans to begin the WHISTLE-PF trial, which includes a phase 2b cohort of IPF patients and a phase 2 PPF group.
If successful, both drugs could offer a disease-modifying approach to IPF.