bleomycin

P2, N=13, Recruiting, Institute of Oncology Ljubljana

P3, N=1334, Completed, Takeda | Active, not recruiting --> Completed

Further, treatment of mice with bleomycin-induced lung injury using CSP7, an anti-IL-17A antibody, or an IL-17RA blocking antibody attenuates total lung hydroxyproline and soluble collagen content, as well as levels of profibrogenic markers. These observations support the role of IL-17A/IL-17RA signaling in lung injury and post-injury remodeling.

AA (50 μg/animal) and LXA4 improved the antioxidant status and upregulated anti-inflammatory and anti-apoptotic genes IκB and Bcl2. These results suggest AA and LXA4 can prevent bleomycin-induced dysfunction of pancreatic β cells.

Increased levels of Gli3 repressor (Gli3-REP) and decreased GSK-3β phosphorylation further confirmed Hedgehog pathway inhibition. In conclusion, the current study provides the first evidence that CAN, CGA, and their combination modulate the Hedgehog pathway, suggesting their potential as novel therapeutic strategies for IPF.

P2, N=340, Active, not recruiting, Merck Sharp & Dohme LLC | Trial completion date: Feb 2027 --> Nov 2026 | Trial primary completion date: Feb 2027 --> Nov 2026

P=N/A, N=10, Enrolling by invitation, Institute of Oncology Ljubljana | Trial completion date: Nov 2025 --> Dec 2026 | Trial primary completion date: Sep 2025 --> Sep 2026

This study investigates the therapeutic efficacy of sacubitril/valsartan in a bleomycin-induced rat model of pulmonary fibrosis. Additionally, sacubitril/valsartan treatment resulted in a notable reduction in pulmonary levels of transforming growth factor-β (TGF-β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), indicating attenuation of both fibrotic and inflammatory responses. Collectively, these findings suggest that sacubitril/valsartan mitigates pulmonary fibrosis through modulation of the SNHG-16/miR-455 axis and inhibition of the Notch-2/Smad-3/TGF-β signaling cascade, highlighting its potential as a promising therapeutic strategy for the management of pulmonary fibrosis.

P1/2, N=82, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Jan 2026 --> Jan 2027 | Trial primary completion date: Jan 2026 --> Jan 2027

Additionally, TA mitigated the infiltration of fibroblasts and inflammatory cells and prevented alveolar thickening induced by Bleo. The findings demonstrated that TA exhibits a protective effect against PF induced by Bleo.

Seventy-two rats were divided into six groups: Control, BLM, BHD, prednisone acetate, SN, and PC. BHD, PC, and SN alleviated BLM-induced lung inflammation and collagen deposition, reduced Wnt3a, glycogen synthase kinase 3 beta, β-catenin, and transforming growth factor beta 1 (TGF-β1) mRNA/protein expression, and decreased the p-Smad3/Smad3 ratio. BHD and its fractions alleviate PF through dual inhibition of Wnt/β-catenin and TGF-β1/Smad pathways, with SN demonstrating the highest overall efficacy.

Here, using a bleomycin-induced experimental lung fibrosis model, we observed that RAP2A expression was markedly upregulated in pulmonary endothelial cells and correlated with disease severity...In vitro assays further demonstrated that RAP2A deficiency impaired tumor necrosis factor-α-induced endothelial adhesiveness without affecting basal endothelial integrity. Collectively, our findings identify endothelial RAP2A as a regulator of inflammatory endothelial activation in experimental lung fibrosis and suggest that targeting RAP2A-mediated signaling may represent a potential strategy to modulate endothelial-immune crosstalk during fibrotic lung injury.