Extract
Clinical studies and real-world experience show that pirfenidone is effective in decelerating disease progression in idiopathic pulmonary fibrosis (IPF) patients. However, many of the details that define its molecular mechanisms are still unknown. Yes, it works, but how exactly? And why should we care? Identifying the missing pieces and completing the puzzle will be helpful for the development of more specific and hopefully better therapeutics, and instrumental in developing effective combination therapies that have a better safety profile while simultaneously allowing for disease progression to be halted, or perhaps even an improvement in lung function.
Abstract
An editorial discussing the recent article by Ma and co-workers that contributes another puzzle piece to the mechanism of action for pirfenidone with elegant in vitro and in situ studies, and importantly, using a clinically relevant drug concentration https://bit.ly/40Vi0zr
Footnotes
Conflict of interest: M. Lehmann reports grants from Boehringer Ingelheim, outside the submitted work.
Conflict of interest: M. Kolb reports grants from Boehringer Ingelheim, Pieris and Roche, consulting fees from Boehringer Ingelheim, Roche, Horizon, Cipla, Abbvie, Bellerophon, Algernon, CSL Behring, United Therapeutics, LabCorp and ShouTi, lecture honoraria from Roche, Novartis and Boehringer Ingelheim, payment for expert testimony from Roche, advisory board participation for United Therapeutics and LabCorp, and reports an allowance as Chief Editor of the ERJ.
- Received February 9, 2023.
- Accepted February 10, 2023.
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