gefitinib

This case demonstrates the effectiveness of first-generation TKIs in treating metastatic EGFR-positive NSCLC, particularly in countries that cannot afford recent targeted therapies. In addition, it describes a rare adverse effect that was well tolerated and managed successfully.

P1/2, N=6, Completed, Stanford University | N=12 --> 6

Antioxidant N-acetylcysteine (NAC) treatment markedly restored GSH content and suppressed lipid ROS overproduction to relieve AO-triggered ferroptosis. The introduction of the iron scavenger deferoxamine or the ferroptosis inhibitor ferrostatin-1 weakened AO-induced ferroptosis in breast cancer cells...Selective EGFR inhibitor gefitinib exacerbated AO-mediated ferroptosis and autophagy, while genetic overexpression of EGFR completely reversed these AO-mediated phenotypes...Our study revealed that AO facilitated autophagy-dependent ferroptosis in breast cancer cells through the downregulation of EGFR. This work provides a new perspective on the antitumor activity of AO, which is valuable for further investigations of the practical application of AO in breast cancer.

P2, N=156, Completed, European Organisation for Research and Treatment of Cancer - EORTC | Active, not recruiting --> Completed | Trial completion date: Dec 2027 --> Aug 2025

HDI inhibits breast cancer growth and lung metastasis by dual targeting of PTK2B and CCN2, thereby suppressing KRAS-p38 MAPK signaling, reversing EMT, and modulating TIMP2/MMP2-mediated extracellular matrix remodeling. Asperulosidic acid is identified as an important active constituent contributing to these effects. The favorable safety profile of HDI and its synergistic interaction with gefitinib support its potential application as a multitarget adjuvant therapy for metastatic breast cancer, particularly TNBC.

This is the first report of pulmonary adenocarcinoma with both high serum β-hCG levels and an EGFR mutation.

Notably, compound 5 exhibits superior anti-proliferative activity against HepG2 cells compared to doxorubicin (DOX) and Gefitinib, with markedly reduced cytotoxicity toward normal cells. In vivo efficacy was confirmed in a zebrafish xenograft model, where compound 5 significantly suppressed tumor proliferation. These findings establish compound 5 as a potent EGFR G4 DNA stabilizer that exerts multi-level anti-tumor effects through targeted modulation of this macromolecular structure, offering a promising lead for EGFR G4-directed liver cancer therapy.

P3, N=393, Completed, Yuhan Corporation | Active, not recruiting --> Completed

In EGFR-driven NSCLC models, the IVSA siRNA dramatically reduced tumour size and suppressed EGFR expression more effectively than traditional treatments such as gefitinib or osimertinib. In these models, the IVSA siRNA resulted in significant tumour suppression and enhanced survival outcomes. These findings underscore the versatility and potency of the IVSA platform as a universal therapeutic approach for EGFR-targeted siRNA delivery, providing a promising new avenue for treating a range of EGFR-positive cancers.

Furthermore, patients in the low-risk group may demonstrate greater sensitivity to crizotinib while exhibiting reduced responsiveness to gefitinib. Two robust molecular subtypes of LUAD were identified through consensus clustering. By constructing prognostic models centered on APRGs, this investigation systematically elucidated the immune microenvironment and molecular underpinnings of LUAD, contributing fresh perspectives on disease mechanisms and potential treatment avenues.

This study offers comprehensive insights into the molecular underpinnings of TC progression, highlighting the diagnostic and therapeutic potential of these hub genes and their associated regulatory networks. These findings lay a foundation for developing novel therapeutic strategies targeting these genes in TC management.

Despite standard treatments like 5-fluorouracil, therapeutic success is frequently challenged by systemic toxicity, drug resistance, and high recurrence rates...Using a molecular hybridization strategy based on lead pharmacophores Gefitinib and Tozadenant, three chemical series were developed and validated through a multi-disciplinary pipeline including molecular docking and iterated biological testing...Moreover, the in vivo validation using AOM-induced CRC mouse models illustrated the effective restoration of the colonic crypt architecture, suppression of EGFR overexpression, and exhibition of favorable safety profiles regarding liver serum enzyme levels. This research provides a robust therapeutic framework for multi-target drug discovery in advanced colorectal cancer management.