Blocking MERTK calms lung scarring by dampening pro-fibrotic macrophages
- MERTK, a receptor tyrosine kinase, is elevated in lung macrophages of IPF patients and tracks with poorer lung function.
- In bleomycin-injured mice, the selective inhibitor UNC5293 curbed fibrosis and improved lung mechanics, even when dosing began during the fibrotic phase.
- The dual MERTK/FLT3 inhibitor MRX2843 reduced histological fibrosis; the proposed mechanism is suppressed M2 macrophage polarisation and osteopontin signalling.
💡 Points Based on the abstract
I'd want to see this before getting excited: the fibrotic-phase dosing is the part that counts, since prophylactic bleomycin data is cheap and notoriously over-optimistic. But bleomycin fibrosis resolves spontaneously in mice, and MRX2843's FLT3 activity muddies target attribution. Phagocytic MERTK is also tied to tissue clearance, so I'd ask about exposure and safety margins first.