gefitinib

Compounds 12, 17, 27, 43, 45, and 49 demonstrated strong binding affinities and superior pharmacokinetic profiles compared to Gefitinib and Erlotinib. Overall, benzothiazole derivatives represent a promising scaffold for the design of EGFR inhibitors, potentially contributing to targeted anticancer therapy.

High-risk patients were found to be more sensitive to treatment drugs ABT.263, AZD.0530, gefitinib, imatinib, PAC.1, and shikonin. The predictive model we constructed can independently predict the prognosis of patients with CRC. Further experimental validation and mechanistic studies are warranted to elucidate the precise role of OS-related lncRNAs in CRC pathogenesis.

P=N/A, N=4864, Completed, Brigham and Women's Hospital | Active, not recruiting --> Completed | Trial completion date: Jan 2025 --> Nov 2025 | Trial primary completion date: Jan 2025 --> Nov 2025

Western blotting and immunohistochemistry (IHC) showed that both GEF-BET-Lipo and GEF-BET-Lf-Lipo treatments significantly reduced pSTAT3 expression and increased the levels of the apoptotic marker caspase-3. Overall, the findings support the enhanced antitumor potential of GEF-BET-Lf-Lipo against HCC in animals.

Furthermore, coadministration of tamoxifen and the EGFR TKI gefitinib potentially inhibited p-EGFR expression in EGFR-mutant lung adenocarcinoma. Regular follow-up with chest computed tomography is recommended for patients with breast cancer. For those diagnosed with both ER-positive breast cancer and EGFR-mutant lung adenocarcinoma, combined tamoxifen and EGFR TKI therapy may offer an effective targeted treatment strategy.

As an adjunct treatment during gefitinib therapy for lung adenocarcinoma patients with EGFR mutations, Qilian mixture safely improved short-term clinical symptoms and quality of life, with future research requiring a large sample size and pharmacological mechanism studies in intestinal flora changes and related signaling pathways.

Our study established a NM-related gene signature closely linked to immune microenvironment and drug sensitivity, highlighting potential biomarkers and therapeutic targets for prognosis and personalized therapy in HNSCC.

Furthermore, we predicted and experimentally confirmed that DNAJB6 silencing conferred gefitinib resistance in HepG2 cells. In conclusion, our findings highlighted the significance of DNAJB6 expression in determining LIHC prognosis and immunotherapy response, as well as its potential in developing novel anti-cancer drugs and enhancing immunotherapy.

Huaier aqueous extract reversed gefitinib resistance in NSCLC cells by promoting ACSL4-dependent ferroptosis, thereby providing a promising therapeutic strategy for improving EGFR-TKI efficacy.

P1, N=105, Active, not recruiting, Novartis Pharmaceuticals | Trial completion date: Mar 2026 --> Oct 2026 | Trial primary completion date: Mar 2026 --> Oct 2026

P3, N=545, Active, not recruiting, Eli Lilly and Company | Trial completion date: Dec 2025 --> Dec 2026

In terms of mechanism, METTL14 endow NSCLC cells with gefitinib sensitivity via intracellular and exosomal miR-101-3p, leading to modulating of GSK-3β/Akt pathway. Collectively, this study indicated that restored METTL14/miR-101-3p confers gefitinib sensitivity in GR NSCLC by targeting GSK-3β/Akt pathway, indicating METTL14/miR-101-3p may act as a potential biomarker and therapeutic target for gefitinib response in NSCLC.