Through this mechanism, befotertinib acts as a functional inhibitor of ABCG2, restoring intracellular drug accumulation and enhancing cytotoxic responses. Collectively, these findings indicate that befotertinib may serve as a chemosensitizing agent to overcome MDR in NSCLC with high ABCG2 expression, supporting further evaluation in combination therapeutic strategies.

Larger multicenter studies, functional experimental models, and pharmacogenetic investigations are needed to elucidate predictive factors, clarify molecular mechanisms, and develop preventive or therapeutic strategies. Understanding these pigmentary changes may also provide valuable insights into drug activity and pave the way toward personalized medicine.

We show that PTK6 is targeted by PRMT1 and mutation of PTK6 R131/R136 or R132, or treatment with the type 1 PRMT inhibitor GSK3368715, leads to decreased arginine methylation, increased PTK6 protein stability and impaired PTK6 association with its substrates...These results indicate that arginine methylation is a key regulatory switch for PTK6 signaling and protein turnover and may be central for the execution of its diverse context-specific functions. Mutation of PTK6 arginine residues has been reported in some cancers, which may contribute to disease-specific PTK6 expression and signaling.

This case demonstrates the effectiveness of first-generation TKIs in treating metastatic EGFR-positive NSCLC, particularly in countries that cannot afford recent targeted therapies. In addition, it describes a rare adverse effect that was well tolerated and managed successfully.

P1, N=18, Recruiting, Washington University School of Medicine | Trial primary completion date: Nov 2028 --> May 2031 | Trial completion date: Oct 2033 --> Apr 2036

P2, N=30, Not yet recruiting, Stuthi Perimbeti

P3, N=5000, Not yet recruiting, Exelixis

CRc rates were higher with venetoclax-based intensive (88.2%) or non-intensive (63.6%) CMT than with CMT alone (p = 0.001). In conclusion, this study offers a potential treatment paradigm for AML patients with co-occurring FLT3-ITD, NPM1 and DNMT3A mutations.

Using two mouse studies modeling multi-organ metastases and breast tumor formation in the brain, we observed that RET inhibition significantly prevented the circulating tumor cells from forming brain metastases and suppressed the growth of intracranially implanted tumor cells. Together, our findings demonstrated that RET functions as a novel mediator of BCBM and that RET inhibitors showed promising efficacy for BCBM.

This exploratory study identified WDR17 as a candidate biomarker associated with TKI resistance in lung adenocarcinoma, potentially involved in maintaining protein homeostasis and metabolic balance. These preliminary findings warrant validation in larger, independent cohorts.

P2, N=100, Recruiting, Exelixis | Not yet recruiting --> Recruiting

This validated LC-MS/MS method provides a rapid, sensitive, and cost-effective approach for erdafitinib quantification in preclinical plasma samples. Its application to pharmacokinetic studies supports drug development by enabling accurate assessment of exposure and disposition, thereby advancing pharmacological understanding and facilitating translation to clinical oncology research.