Lung function decline in patients with idiopathic pulmonary fibrosis (IPF) was slowed by the investigational drug pamrevlumab, according to the results from a Phase 2b clinical trial.
The results were presented at the European Respiratory Society (ERS) International Congress 2017 held Sept. 9-13 in Milan, Italy. A second presentation reported on studies in rodents.
FibroGen’s pamrevlumab (FG-3019) is an antibody that targets a protein called connective tissue growth factor (CTGF), which is responsible for wound healing and fibrotic activity in the body. The drug is being evaluated in fibrotic diseases and cancer because it is designed to stop the progression of fibrosis (tissue scarring).
The Phase 2b, randomized, double-blind, placebo-controlled study (NCT01890265) tested the safety and effectiveness of pamrevlumab in treating IPF. It included 103 IPF patients and lasted 48 weeks.
Forced vital capacity (FVC; a measure of lung function) assesses changes in lung volume, and measures the amount of air that can be forcibly exhaled from the lungs, after taking the deepest breath possible. It was compared between patients taking pamrevlumab and patients taking a placebo.
The primary endpoint of the trial was met, where the average decline in FVC was 2.85% (129 mL) in the pamrevlumab group, significantly smaller than the average decline of 7.17% (308 mL) in the placebo group, after 48 weeks.
“It is exciting to see positive results for this new therapeutic agent specifically targeting a key mechanism in the fibrotic disease process. In contrast to other agents, pamrevlumab brings a unique therapy to the treatment of IPF,” Luca Richeldi, an MD and PhD, head of the Division of Pulmonary Medicine at Agostino Gemelli University Hospital of the Catholic University of the Sacred Heart in Rome, Italy, said in a press release.
No safety risks were identified during the study. Pamrevlumab was well tolerated when used in combination with the current standard of care.
“This clinical data advances our scientific understanding of anti-CTGF therapy and clinical findings for patients living with IPF,” said Peony Yu, MD, chief medical officer at FibroGen. “The IPF population has a critical need for a safer and more efficacious treatment with a distinctive mechanism.”
A second ESR presentation reported on pamrevlumab tested in rodents with induced lung fibrosis. Lower lung densities (an indication of less fibrosis) and a greater inhibition of progressive lung remodeling were seen in rodents treated with pamrevlumab, compared to those treated with IPF-approved therapies Ofev (nintedanib) or Esbriet (pirfenidone).
The use of pamrevlumab combined with either Ofev or Esbriet was found to be not statistically significantly better than the use of pamrevlumab alone.
“The superior activity of pamrevlumab in the late intervention of progressive fibrosis in a direct back-to-back comparison with two recently approved treatments for pulmonary fibrosis are intriguing and opens a new venue for development of anti-fibrotic therapy strategies,” said Amir Abdollahi, MD and PhD, head of the Division of Molecular and Translational Radiation Oncology at the National Center for Tumor Diseases, Heidelberg Institute of Radiation Oncology, Heidelberg University Medical School and German Cancer Research Center.
“This data warrants further investigation of anti-CTGF therapy in IPF, and also in other fibrotic diseases such as radiation-induced fibrosis in cancer therapy,” Abdollahi concluded.