gefitinib

In vivo, mouse xenograft models confirmed that Remodelin significantly enhanced the antitumor efficacy of gefitinib. These findings suggest the potential of NAT10 as a therapeutic target to overcome EGFR-TKI resistance and improve treatment outcomes in patients with NSCLC.

Additionally, Nano-Gefitinib significantly increased M1 macrophage phenotype, evidenced by the upregulation in the immunoexpression of the CD68, in addition to increasing CD8 and caspase-3 and decreasing CD4, with VEGF immunoreactivity in the combination group. Gefitinib biosomes encouraged macrophage polarization, apoptosis, and reduced inflammation, with a subsequent decrease in tumor volume.

Our findings reveal that the HIF1A-SLC16A3-lactate axis orchestrates ferroptosis suppression and therapeutic resistance in LUAD. Targeting SLC16A3 represents a promising metabolic strategy for overcoming EGFR-TKI resistance by reactivating ferroptosis.

High-risk patients exhibited poor survival, enhanced immune infiltration, and potential sensitivity to AKT inhibitors, with several drugs, including gefitinib and paclitaxel, identified as promising candidates. Additional prognostic genes (DFFB, PSMB6, GLP1R, HDAC9, BACH2) displayed expression patterns largely consistent across HPA, TCGA, and RT-qPCR, with minor discrepancies likely due to sample size. This study integrates multi-omics and deep learning with experimental validation, providing insights into programmed cell death regulation and offering robust biomarkers and therapeutic targets for GC.

Comparative docking with five reference drugs (Alpelisib, Buparlisib, Lapatinib, Gefitinib, and Afatinib) identified nine flavonoids; Sphaerobioside, Avicularin, Nicotiflorin, Myricetin, Quercitrin, Rutin, Isoquercetin, Didymin, and Robinin as promising candidates with favorable binding affinities and stable receptor interactions...Collectively, these findings highlight the multitarget inhibitory potential of selected flavonoids and demonstrate how integrated computational profiling can accelerate the discovery and optimization of natural product-based anticancer agents. The online version contains supplementary material available at 10.1007/s40203-025-00489-0.

Patients received RAM (10 mg/kg every 2 wk) plus GEF (250 mg once daily) until disease progression (period 1); patients with disease progression who acquired a T790M mutation received RAM plus osimertinib (80 mg once daily) (period 2). Treatment-emergent T790M rate post progression was 81.3%. RELAY+ revealed a favorable benefit-risk profile for RAM plus GEF in East Asian patients with untreated EGFR-mutated metastatic NSCLC, supporting RAM plus GEF as an alternative first-line treatment option, particularly in those with an L858R mutation.

Subsequently, the patient started gefitinib treatment, and 3 months later, the treatment effect assessment showed a partial response (PR) at regular follow-up according to RECIST evaluation criteria...Two months later, imaging examination showed that the lesions in various parts of the body were stable. Except for dryness of oral and nasal mucosa, the patient did not experience other serious adverse reactions.

The patient attained sustained disease control with a partial response lasting 22 months on first-line gefitinib. Following progression with persistent EGFR L858R mutation, second-line platinum-pemetrexed-bevacizumab chemotherapy achieved stable disease (SD) in the primary lesion and shrinkage of pleural nodules. Subsequent neoadjuvant therapy with albumin-bound paclitaxel, carboplatin, bevacizumab, and sintilimab induced marked tumor regression, permitting curative-intent R0 resection...The patient remained recurrence-free 25 months post-surgery. This case illustrates the potential of immunotherapy-based neoadjuvant regimens to convert unresectable PD-L1-high EGFR-mutant lung adenocarcinoma into operable disease and achieve durable pCR.

Taken together, these findings suggest that EPP inhibits angiogenesis through dual mechanisms: direct inactivation of VEGFR2 in endothelial cells and attenuation of the pro-angiogenic potential of PC9/GR cells via ANG-1 downregulation. This study highlights the therapeutic potential of EPP as a natural anti-angiogenic agent.

To our knowledge, BIQO-9 represents the first ROR1/PI3Kα/BRD4 multi-target inhibitor with therapeutic potential in NSCLC. Moreover, the combination of BIQO-9 and Gefitinib offers a promising novel strategy for NSCLC treatment.

This NMA revealed that cases with EGFR-mutated NSCLC may benefit from different first-line treatment regimens according to their clinicopathological characteristics. On the whole, osimertinib plus CT and amivantamab plus lazertinib emerged as the most noticeable treatment modalities for such cases. (PROSPERO ID: CRD42024506995).

Plasma ctDNA assessment facilitates the evaluation of treatment efficacy, monitoring disease progression, and informing second-line treatment options. ClinicalTrials.gov NCT04425187.