lapatinib

The Lapatinib-Bevacizumab combination produced the most potent inhibition of cell viability, comparable to high-dose monotherapy. These findings suggest that combining kinase inhibitors with Bevacizumab may enhance antitumor activity, allow the use of lower drug doses, and overcome resistance, representing a promising therapeutic strategy for medullary thyroid carcinoma that warrants further investigation in clinical settings.

Collectively, KRT80 may be linked with metastasis of BC, and it may serve as a potential therapeutic target for mBC treatment.

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.

Not just increasing ALA-PpIX levels, Lap enhanced PpIX localization in the mitochondria and promoted mitochondria-mediated apoptosis after PDT in the H4 cell line with strong ABCG2 activities. Our results demonstrate that blocking ABCG2-mediated PpIX efflux is critical for the enhancement of ALA and, in tumor cells with ABCG2 activities, inhibiting PpIX bioconversion by DFO needs to be combined with PpIX efflux suppression for effective enhancement of ALA.

P3, N=608, Active, not recruiting, Daiichi Sankyo | Trial completion date: Jul 2025 --> Jan 2026

Co-treatment with lapatinib and doxorubicin exhibited synergistic cytotoxicity in both cancer cell lines and patient-derived organoids. These findings reveal a previously unrecognized role for lapatinib in targeting DNA repair machinery, supporting its repurposing as a chemosensitizing agent. Our study highlights DDB2 as a critical mediator of chemoresistance and proposes disruption of DDB2-dependent DNA repair as a novel strategy for chemosensitization.

This study reveals that KIF18A is upregulated in OS, particularly in metastatic cases, and is linked to poor clinical outcomes. Functional experiments confirm that KIF18A promotes proliferation, migration, and invasion of OS cells while suppressing apoptosis. In vivo experiments reveal that KIF18A knockdown strongly inhibits tumor growth. KIF18A expression correlates with dysregulation of key oncogenic pathways, an immunosuppressive microenvironment, and potential immunotherapy resistance. These results highlight KIF18A's role as a pivotal oncogene in OS progression and suggest its promise as both a prognostic biomarker and a therapeutic target.

Pharmacokinetic studies in Wistar rats showed a longer half-life (9.69 vs. 5.28 h), higher AUC0-∞ (452.880 vs. 159.715 µg/mL·h), and improved MRT (15.260 vs. 7.696 h). Focused colon retention (8.20 ± 1.38 µg/g), minimal toxicity, and confirmed safety and stability underscore its potential as an accurate, efficient treatment for colon cancer.

Lapatinib and neratinib are tyrosine kinase inhibitors (TKIs) approved for treating HER2-positive metastatic breast cancer, but their clinical use is limited by hepatotoxicity. This underscores the importance of targeting senescent cells or SASP factors to reduce liver toxicity and improve treatment outcomes, making the identification of effective senotherapeutics a vital research focus. There hasn't been any literature report demonstrating the effect of TKI-induced liver cell secretome on macrophage polarization.

Drug sensitivity assays confirmed lower lapatinib IC50 in overexpression models. High BRI3BP expression correlates with aggressive HCC phenotypes, poorer survival, and dysregulated oncogenic pathways, supporting its role as a prognostic biomarker and candidate therapeutic target.

SPECT images of [99mTc]Tc-Lapa-HYNIC-TPPTS in HER2-positive model mice revealed that it can effectively locate tumors. This study is the first attempt at a 99mTc-labeled small-molecule inhibitor tracer targeting HER2, showing great potential for applications in the diagnosis of HER2-positive cancers.

Uptake of guideline-recommended regimens in each line of therapy was lower in recurrent patients although survival was similar to de novo patients. These findings highlight the need for consensus on treatment regimens for de novo and recurrent HER2+ patients, effective first-and second-line management, and novel therapies to improve outcomes. MICROABSTRACT Our study evaluated real-world treatment patterns, clinical outcomes, and healthcare utilization in HER2-positive metastatic breast cancer (mBC) in Alberta, Canada. Among 758 patients, survival was similar between new diagnoses and recurrent cases, despite lower uptake of guideline-recommended therapies in recurrent patients. Our findings highlight the need for consensus on treatment strategies and novel therapies to improve mBC outcomes.