erlotinib

Post hoc attribution analyses highlighted candidate TGF-β-associated epithelial-to-mesenchymal transition signatures in Erlotinib-associated Resistant-labeled states and cytoskeletal/metabolic response-associated signatures in BET-inhibitor-associated Resistant-labeled states. These results suggest that scRADAR provides an interpretable framework for single-cell drug-response phenotype prediction and for generating hypotheses about resistance-associated programs from heterogeneous tumor transcriptomes.

Compounds 4c, 4e, 4f, 4h, 4i and 4j showed promising anticancer activities against MCF-7 cells, with lower IC50 values (IC50 = 5.65 μM to 7.51 μM) than erlotinib (IC50 = 10.50 μM)...In silico molecular modelling studies also indicated that the 4i-EGFR complex was less stable than the 4h-EGFR complex throughout the simulation time. Furthermore, the disruption of cellular redox homeostasis, as evidenced by reduced ROS generation, mitochondrial membrane depolarization, and the induction of apoptosis in treated cells, suggests a possible secondary anticancer mechanism.

We established a novel lactylation-related risk signature that effectively stratifies CRC patients by prognosis and TME characteristics. By elucidating the crosstalk between metabolic dysregulation, stromal barriers, and immune exclusion, this study provides potential biomarkers and stratified therapeutic strategies-ranging from standard chemotherapy to targeted metabolic and stromal interventions-to optimize precision medicine for CRC patients.

P2, N=60, Not yet recruiting, University of Texas Southwestern Medical Center | Trial completion date: Dec 2030 --> Aug 2030 | Trial primary completion date: Dec 2030 --> Jun 2030

HHT has been identified as an impediment to cell invasion and metastasis in PC via the EphB4/SRI/EMT axis. Additionally, HHT enhances the efficacy of ERT in inhibiting the migration of PC cells.

NSC265450 and NSC70845 were the most potent antiproliferative agents with IC50 < 4 nM against overexpressed EGFR-TK cancer cell lines, HeLa and A549, displayed significantly much greater potencies than NSC116555, erlotinib and doxorubicin. Furthermore, molecular docking and molecular dynamics results predicted the binding action of the series to the ATP binding site of EGFR-TK; intermolecular interactions to key regions of the protein and amino acid residues are described. Prediction of pharmacokinetic and toxicity profiles of the series, and calculations of known drug indexes suggest the molecules are pharmaceutically compatible as therapeutic drug candidates.

The prepared NCM-ERL-Liposomes showed enhanced internalization, triggered caspase-3/7-mediated apoptosis (1.42-fold increase), and suppressed p-EGFR/p-STAT3, indicating adequate payload protection and targeted intracellular release. These results establish a translational platform that requires PK/PD studies in resistant NSCLC models to support precision oncology therapeutics.

Initial studies were done by molecular docking of five analogs of quinazoline- quinazolinone hybrids, erlotinib, and doxorubicin against the epidermal growth factor receptor. The insertion of a nitro group at the 7 position of quinazolinone enhanced the cytotoxic efficacy against MCF-7 cells, likely attributable to electronic influences. Consequently, this compound could serve as a lead compound in the search for new classes of effective anticancer agents.

hrFP-E is equipped with a nitroreductase (NTR)-sensitive motif activated in hypoxic regions to release a FAK degrader (FP) and an EGFR inhibitor (Erlotinib)...This platform is inherently modular and compatible with alternative oncogenic drivers and disease-specific gates. Our work establishes mechano-chemical therapeutics, spatiotemporally controlled degraders that rewire tumor mechanics alongside growth signaling, as a generalizable strategy for solid tumor treatment.

The E + B combination showed modest anti-tumor activity in patients with heavily pretreated EGFR-amplified solid cancers. While NGS may help identify new applications for existing drugs, additional investigations are warranted to validate the efficacy and benefit of E + B in this population.

Two epidermal growth factor receptor inhibitors (EGFRi) commonly used in cancer therapy and known to cause GI side effects, erlotinib and lapatinib, emerged as strong inducers of EEC differentiation, dramatically increasing chromogranin A (CHGA) expression compared to controls, while maintaining ISC function and organoid growth. These findings provide important insight into EEC differentiation that could inform treatment strategies for EAD, metabolic diseases, and GI diseases. Inhibition of EGFR signaling promotes human ISC-to-EEC differentiation through activation of STAT1 signaling.

P=N/A, N=42, Terminated, National Cancer Institute (NCI) | Completed --> Terminated; This particular part of the study could not be completed as endoscopy reports post completion of erlotinib trial were distributed across community and other hos