nintedanib

P=N/A, N=10646, Completed, Boehringer Ingelheim | Active, not recruiting --> Completed

Beyond their direct antimesenchymal actions, the current therapeutics pirfenidone and nintedanib also temper innate and adaptive immune signalling. Proof of concept for sharper immunomodulation now comes from recent phase III trials of nerandomilast, a highly selective phosphodiesterase-4B inhibitor that preserved forced vital capacity and downregulated TNF-α, IL-6 and IL-17 networks...This review synthesises current understanding of how immunity initiates, amplifies and perpetuates PF, linking genetic and mechanistic insights to emerging therapeutic opportunities. A deeper grasp of immune-epithelial-fibroblast crosstalk is essential for transforming disease-slowing care into genuinely disease-modifying intervention.

P=N/A, N=88, Active, not recruiting, Boehringer Ingelheim | Terminated --> Active, not recruiting | Trial completion date: Sep 2025 --> Apr 2026 | Trial primary completion date: Sep 2025 --> Apr 2026

Furthermore, Ofev inhibited fibroblast-to-myofibroblast transition by downregulating α-smooth muscle actin (α-SMA) expression and restored physiological type I/III collagen ratios, yielding regenerated skin morphologically and functionally comparable to normal tissue. Critically, this study provides the first direct evidence linking PFTs clearance to scar prevention, establishing a novel therapeutic paradigm for drug-resistant wound infections through the coordinated actions of detoxification, antimicrobial intervention, and fibrosis suppression.

P4, N=20, Not yet recruiting, The Affiliated Hospital of Qingdao University

P=N/A, N=586, Active, not recruiting, Boehringer Ingelheim | Trial completion date: Sep 2026 --> Jun 2026

Adding nintedanib to anti-PD-1 mAb therapy significantly inhibited in vivo tumor progression. These results indicate that nintedanib suppresses MDSCs and CAFs by inhibiting VEGFR-, PDGFR-, and FGFR-mediated signaling, thereby increasing effector T-cell infiltration into tumors and enhancing the anti-tumor effects of αPD-1 mAb therapy.

P1, N=57, Not yet recruiting, Endeavor Biomedicines, Inc.

We evaluated the antitumor effect of the combination therapy with osimertinib and either nintedanib (an indirect TGF-β inhibitor) or vactosertib (a specific TGF-β type I receptor kinase inhibitor). In conclusion, combination therapy with osimertinib and TGF-β inhibitors potentiates osimertinib-induced antitumor immunity. These findings highlight a novel therapeutic strategy for EGFR-mutated NSCLC and warrant further clinical investigation.

Standard-of-care treatments (pirfenidone, nintedanib) reduced FUS expression in PCLs. In contrast, ION363 promoted functional marker expression and improved morphology in patient-derived 3D alveolospheres. We conclude that FUS is a pivotal regulator of fibrotic signaling in IPF and that targeting FUS via ASO represents a promising therapeutic avenue for IPF.

His condition worsened despite high-dose steroids, cyclophosphamide, and plasma exchange; he required ECMO and died after 40 days...He was treated with steroids, rituximab, nintedanib, and mycophenolate...This case series highlights the full clinical spectrum, from pediatric onset to fulminant adult disease. Multidisciplinary care, awareness of atypical presentations, and continued research into disease mechanisms and therapeutics are essential to improving survival in MDA5-DM.

Combination of nivolumab and nintedanib was shown to be safe and feasible. Despite missing synergistic effects on efficacy for the overall population, promising OS was observed for patients with high PD-L1 expression and for patients with previous immunotherapy. Therefore, CPI responsiveness may have been restored in some cases. Inhibition of FGFR-mediated tumor progression seems relevant in tumors with lower levels of both PD-L1 and FGFR1 expression and might be effectively inhibited by nintedanib. The combination nivolumab/nintedanib might warrant further exploration in selected patients.