P2, N=25, Recruiting, Vall d'Hebron Institute of Oncology | Not yet recruiting --> Recruiting

P2, N=10, Active, not recruiting, UNICANCER | Trial completion date: Apr 2029 --> Mar 2026 | Trial primary completion date: Apr 2025 --> Mar 2026

Ve combined with Pa exerts a synergistic inhibitory effect on the growth and metastasis of FRO and ARO cells, while promoting apoptosis and cellular redifferentiation. This combination may provide a potential therapeutic strategy for ATC.

The vemurafenib combined with 131I revealed superior efficacy in improving survival and thyroid function recovery in lymph node metastatic BRAF-mutant thyroid cancer.

P2, N=84, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Feb 2026 --> Sep 2026 | Trial primary completion date: Feb 2026 --> Sep 2026

P1, N=70, Completed, F. Hoffmann-La Roche AG | Recruiting --> Completed

Compounds 20c and 21c exhibited potent inhibition of EGFR, with IC50 values of 71 and 64 nM, respectively, surpassing the reference erlotinib (IC50 = 80 nM). Moreover, compounds 20c and 21c exhibited BRAFV600E inhibitory action with IC50 values of 49 and 41 nM, respectively, which are somewhat less potent than the reference drug Vemurafenib...Compounds 20c and 21c showed a notable decrease in TNF-α and IL-6 levels compared with dexamethasone, suggesting an immunomodulatory effect. Molecular docking further validated the favorable orientation of 20c and 21c within the ATP-binding pocket of EGFR and BRAFV600E. These findings underscore compounds 20c and 21c as innovative dual-target scaffolds with significant promise for anticancer drug development.

This model successfully described the PK of encorafenib over time and across tumor types. No dose modifications are suggested on the basis of intrinsic or extrinsic factors evaluated.

P2, N=38, Terminated, Pfizer | Active, not recruiting --> Terminated; Study terminated due to inability to recruit the target number of patients. There were no safety and/or efficacy concerns involved in the decision to stop enrollment.

Furthermore, we show that secondary resistance induced by prolonged exposure of melanoma cells to BRAF inhibitor is associated with reduced FGD1 levels. These findings highlight the importance of FGD1 in melanoma progression and the acquisition of secondary resistance, positioning the FGD1-mediated signaling pathway as a putative therapeutic target.

Melanoma A375 (vemurafenib [VEM]-sensitive) and A375R (VEM-resistant) cells were exposed to eIF4Fi RocA at varying doses and durations in vitro...Combined CR-1-31-B, EZH2i, and AKT1i effectively overcame resistance to RocA and VEM resistance both in vitro and in vivo. The eIF4F complex inhibitor reactivates ERK1/2-EZH2 and AKT1 signaling pathways, resulting in resistance to both eIF4Fi and VEM. Combined administration of an eIF4Fi with EZH2 and AKT1 inhibitors effectively enhances sensitivity to both eIF4F complex and BRAF inhibitors.

P1, N=50, Recruiting, H. Lee Moffitt Cancer Center and Research Institute | Trial completion date: Jul 2026 --> Jul 2027