erlotinib

The docking protocol was validated by redocking (RMSD = 0.98 Å), and erlotinib (-8.96 kcal/mol) reproduced known interactions with ASP855, ALA859, and PHE723...In conclusion, PLA-EO exhibits selective cytotoxicity in ovarian cancer cells via ER stress pathways, supported by in silico evidence of EGFR targeting. The combined phytochemical, cellular, and docking results highlight P. loeflingii as a promising source of bioactive essential oils, warranting further in vivo validation.

Furthermore, evaluation of 7c in HCC827 (exon 19 deletion) mutation, which is a cell model highly sensitive to tyrosine kinase inhibitors, showed that the tested compound exhibited lower inhibition than erlotinib...Furthermore, 7c caused an increase in the levels of caspase 3 (4.68 folds) and caspase 9 (4.54 folds) in HCT-116 cells. Additionally, in silico studies of 7c showed a plausible binding mode that correlates with its potent inhibitory activity against the two enzymes, whereas ADME prediction revealed a favorable oral absorption.

Erlotinib induces oxidative and inflammatory optic nerve injury, while TPP co-treatment offers significant neuroprotection. These findings support TPP as a potential adjunct to reduce EGFR-TKI-related ocular toxicity and highlight importance of redox modulation in limiting treatment-associated side effects.

Notably, compound 3f displayed potent EGFR inhibition at submicromolar levels, with an IC50 of 0.121 ± 0.004 μM, which was comparable to the reference inhibitor, erlotinib...Based on predictions of toxicity, compound 3f was predicted to possess a favorable safety profile across 30 potential toxicities. Encouraged by its strong anticancer efficacy and safety profile, compound 3f represents a compelling lead candidate for further development as a targeted treatment for breast cancer.

P2, N=60, Not yet recruiting, University of Texas Southwestern Medical Center | N=30 --> 60

Further, EGFR inhibitor erlotinib synergized with the RAS(ON) multi-selective inhibitor RMC-7977 in KRASQ61H-mutant PDAC cell lines and in cell lines with highly active EGFR by mitigating ERK rebound activity. KRASi-resistant cell lines featured sustained ERK/MAPK dependence despite decreased ERK activity. Together, these findings enhance the understanding of intrinsic and acquired resistance to KRASi and identify therapeutic vulnerabilities that can potentially be exploited for KRASi combination therapies in pancreatic cancer patients.

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).

Medications such as CGP-082996, Dasatinib, Erlotinib, and Salubrinal were more sensitive to high-risk group, whereas drugs such as FTI-277, DMOG, and Crizotinib were more sensitive to low-risk group. UGT1A6 and IRGM were significantly upregulated in tumor group as revealed by qRT-PCR. This study constructed a new prognostic model for CRC patients based on RRAGs, and a series of analysis results is conducive to providing more theoretical references and new insights into precision treatment of CRC patients.

Bevacizumab plus erlotinib demonstrated promising efficacy in tumors with Krebs cycle gene mutations, warranting further investigation beyond FH-deficient RCC.

Our real-world study demonstrated survival outcomes that were comparable to those observed in clinical trials for patients with EGFR-mutant NSCLC treated with EGFR-TKIs. Detection of the acquired T790M mutation and subsequent osimertinib treatment had significant prognostic value.

Meanwhile, exosomal transfer of VPS9D1-AS1 sequestered miR-532-3p to up-regulate catenin beta 1 (CTNNB1). Taken together, exosomal transfer of VPS9D1-AS1 induced M2 polarization to promote erlotinib resistance of LUAD cells through activating Wnt/β-catenin pathway.

Moreover, the combination with epidermal growth factor receptor inhibitors like Osimertinib and Erlotinib enhances outcomes, but the combination with immunotherapy (Nivolumab) provided negligible benefit. Teliso-V is highly effective in MET-high NSCLC with tolerable side effects. Its combination with AI holds the hope of early diagnosis, individualized treatment, and intelligent ADCs of the future, but for this to manifest, clinical data and biomarker improvements must materialize.