These findings were largely recapitulated in patient-derived PDA organoids, where GSTT1 and PROM1 co-expression predicted increased tumor sphere formation and enhanced response to the multi-kinase inhibitor Nintedanib. Together, these results identify a GSTT1 High CD133 High stem-like subpopulation in metastatic PDA and identify an FGFR-dependent signaling axis that sustains this state, representing a potential therapeutic vulnerability.
P=N/A, N=78, Completed, University of British Columbia | Trial completion date: Dec 2026 --> Aug 2025 | Trial primary completion date: Dec 2026 --> Aug 2025 | Recruiting --> Completed
1 month ago
Trial completion • Trial completion date • Trial primary completion date
SB-525334 blocked all effects of TGF-β1, whereas nintedanib was more effective in counteracting the stimulatory effects of TGF-β1 on cell length and α-SMA. Interestingly, nintedanib, per se, evoked small but consistent effects opposite to those of TGF-β1. In conclusion, integrating these experimental approaches provides a powerful platform for detailed investigation of EMT mechanisms and for the identification of novel drug candidates that counteract EMT.
The histological and biochemical findings of the present study indicate that nintedanib is a promising pharmacological agent for the prevention of post-laminectomy epidural fibrosis. Further studies with larger sample sizes and interval assessments are needed to clarify the effects of different dosages.
After the patient's condition stabilized, low-dose nintedanib was reinitiated, and the anticoagulant was switched to rivaroxaban orally after discharge...He was treated with nintedanib combined with enoxaparin sodium...Individualized risk assessment and precise plan adjustment are key to improving the prognosis of these complex patients and providing practical references for similar clinical cases. Further studies are required in the future to confirm the safety of nintedanib when used in combination with anticoagulants.
2 months ago
Journal • IO biomarker
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BRAF (B-raf proto-oncogene) • TP53 (Tumor protein P53)
In a Ba/F3 FLT3-ITD-F691L mouse model, nintedanib demonstrated superior anti-leukemic efficacy compared with gilteritinib and quizartinib. Furthermore, nintedanib potently inhibited primary AML blasts harboring FLT3-ITD while normal bone marrow remained intact. These findings identify nintedanib as a promising FLT3 inhibitor and support its further therapeutic investigation in FLT3-ITD-positive AML.