Gilotrif (afatinib)

P1/2, N=45, Recruiting, West China Hospital | Not yet recruiting --> Recruiting | Trial completion date: Apr 2028 --> Sep 2028 | Initiation date: Apr 2025 --> Sep 2025 | Trial primary completion date: Apr 2027 --> Sep 2027

Likewise, a combination of selective inhibitors of KRAS (RMC-6236/daraxonrasib), EGFR family (afatinib), and STAT3 (SD36) induced the complete regression of orthotopic PDAC tumors with no evidence of tumor resistance for over 200 d posttreatment...Of importance, this combination therapy was well tolerated. In sum, these results should guide the development of new clinical trials that may benefit PDAC patients.

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.

Notably, no adverse events were observed, and the patient has maintained a partial response for over eight months. This case suggests that afatinib can be administered without major dose modification in HD patients, with PK data indicating minimal impact of dialysis and underscoring the importance of accumulating real-world evidence in this underrepresented population.

The study identified multiple genomic characteristics associated with primary and secondary resistance to first-line afatinib treatment in EGFR- and ERBB2-positive subpopulations.

Spatially distinct and simultaneous resistance mechanisms, namely, EGFR L718V mutation and SCLC transformation, contributed to osimertinib resistance. The detection of RB1 2.4 kb small deletion in RB1 gene highlights the importance of deep genomic profiling. Multi-site biopsy and molecular diagnostics are necessary to guide treatment decisions in EGFR-TKI-resistant NSCLC.

P2, N=0, Withdrawn, West China Hospital | N=98 --> 0 | Recruiting --> Withdrawn

CRM197 markedly inhibited cell proliferation, induced G₀/G₁ arrest, and outperformed cetuximab and matched or exceeded afatinib in vitro; in vivo, CRM197 reduced tumor volume and weight more effectively than afatinib, with extensive necrosis. These data establish CRM197 as a potent, multi‑targeted inhibitor of arsenic‑driven LSCC and highlight novel therapeutic targets for further drug development.

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).

This study represents the largest cohort of NSCLC patients with EGFR G719X + S768I co-mutations treated with first-line afatinib. Our findings confirmed the effectiveness and safety of afatinib in this patient population. Furthermore, the presence of the G719X + S768I co-mutations serves as an independent predictor of favorable PFS for NSCLC patients. This study will provide new clinical evidence supporting afatinib therapy for patients with EGFR G719X + S768I co-mutations, both in China and globally. This study fills an important gap in the existing literature by providing robust, large-scale clinical data, offering new insights for the treatment of NSCLC patients with these uncommon mutations.

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.

Low-risk patients were enriched in fatty acid metabolism and peroxisome pathways, exhibited higher immunotherapy responsiveness, and showed greater sensitivity to Gefitinib and Afatinib. High-risk patients exhibited activation of inflammatory and profibrotic pathways, an elevated TMB, immunosuppressive microenvironments, and greater sensitivity to Topotecan and Irinotecan. RT-qPCR validated the expression of HGRGs across selected cell lines. The prognostic model derived from five HGRGs demonstrates excellent clinical value in predicting prognosis and guiding therapeutic strategies in KIRC.