erlotinib

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

The X-ray crystallographic analysis revealed the binding mode of 43 within the PHGDH active site. These findings provide a foundation for developing PHGDH-targeted anticancer therapies.

In vivo studies have shown that knockdown of SOX4 or administration of erlotinib significantly inhibited tumor growth and reduced the rate of lymph node metastasis. SOX4 promotes the growth and lymph node metastasis of LSCC by regulating PTBP2. The SOX4-PTBP2 axis may become a potential diagnostic and therapeutic target for LSCC.

P1, N=85, Terminated, Boundless Bio, Inc. | Trial completion date: Mar 2027 --> Mar 2026 | Active, not recruiting --> Terminated | Trial primary completion date: Sep 2026 --> Mar 2026; Decision was made to halt the study based on overall clinical experience and market considerations. This decision was not driven by any safety signal.

SUCLG2 overexpression conferred erlotinib resistance in vitro, whereas its depletion restored TKI sensitivity and impaired xenograft tumor growth, effects that were rescued by VEGFA reconstitution...In clinical specimens from CRPC patients and NEPC patient-derived xenografts, progressive nuclear co-accumulation of SUCLG2 and EGFR alongside elevated VEGFA expression correlated with disease advancement. Collectively, these findings define a non-canonical nuclear SUCLG2/EGFR/VEGFA signaling axis that mediates NEPC progression and therapeutic resistance, providing mechanistic rationale for combined SUCLG2 and EGFR inhibition as a strategy to overcome treatment resistance in this lethal malignancy.