EGFR T790M

P2, N=173, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Apr 2026 --> Apr 2027 | Trial primary completion date: Apr 2026 --> Apr 2027

Orthogonal validation via amplicon sequencing confirmed the reference values with high concordance to dPCR. These findings provide evidence that nDNA-based RMs can serve as a biologically representative and reliable standard for validating assays at low VAFs, expanding to large-scale RM production and interlaboratory evaluation.

P2, N=46, Completed, Sun Yat-sen University | Recruiting --> Completed | N=30 --> 46

FGTKIs have altered the therapeutic concept for mutant NSCLC patients and offered unprecedented efficacy and durability compared to earlier-generation inhibitors.

P2, N=27, Active, not recruiting, University of California, San Francisco | Trial completion date: Oct 2026 --> Sep 2027

Molecular docking, molecular dynamics simulations, and MM-GBSA analyses supported stable binding of the active compounds within the catalytic sites of the investigated enzymes. Overall, these findings identify compounds 1, 9, 12, and 13 as promising multi-target anticancer leads warranting further optimization and development.

Among the tested compounds, Tetrandrine, Dauricine, and Olmutinib exhibited robust binding affinities across both wild-type and mutant EGFR configurations, highlighting their potential as effective inhibitors. The integrated approach of combining molecular docking using CB-dock2, ADMET profiling, and Lipinski's rule of five provides a robust framework for preliminary drug candidate screening, potentially accelerating the development of more precise and effective EGFR-targeted therapies. The findings contribute to the growing body of research exploring alternative and more nuanced strategies for inhibiting EGFR-driven oncogenic mechanisms, highlighting the importance of computational methods in identifying novel molecular targets with improved specificity and reduced side effects.

A focused translational approach that combines structural insights with innovative therapeutic strategies is urgently needed to achieve lasting clinical benefits in EGFR-driven cancers.

P2, N=23, Recruiting, Taipei Veterans General Hospital, Taiwan | Not yet recruiting --> Recruiting | Trial completion date: Jun 2027 --> Dec 2027 | Trial primary completion date: Jun 2026 --> Dec 2026

P2, N=124, Active, not recruiting, SWOG Cancer Research Network | Trial completion date: Mar 2026 --> Dec 2026 | Trial primary completion date: Mar 2026 --> Dec 2026

In this exploratory study, we analyzed CD73 expression and related immune markers during sequenced EGFR-TKI treatment, including osimertinib, to identify potential biomarkers for CD73-based therapeutic opportunities in EGFR-resistant tumors...We demonstrated differential expression patterns among the immune markers and higher levels of CD73 in cases with non-T790M-resistance to EGFR-TKIs. Although a limited number of cases were included in these analyses, the results might point to a potential role of immune markers inducing an immunosuppressive environment and thereby contribute to development of resistance to TKIs, which in turn could have future therapeutic implications.

These findings uncover a novel CCL2-STAT3-ZEB1 signaling axis that drives acquired osimertinib resistance in NSCLC. Dual targeting of STAT3 and EGFR may represent a promising therapeutic approach to improve clinical outcomes.