BRAFV600E/ABL2-IN-2

BRAFV600E/ABL2-IN-2 (Compound 8h) (0.01-100 μM; 48 h) inhibits the proliferation of cancer cell lines in the NCI-60 cell panel, with the strongest inhibitory activity against SK-MEL-5 melanoma cells (GI₅₀ = 0.54 μM)^[1].
BRAFV600E/ABL2-IN-2 (10 μM) potently inhibits BRAF^WT, PI3K and VEGFR2 kinases, and exhibits moderate inhibitory activity against FGFR1, CDK4 and CDK6 kinases^[1].
BRAFV600E/ABL2-IN-2 (72 h) downregulates P-glycoprotein expression by 67.38% in SK-MEL-5 melanoma cells^[1].
BRAFV600E/ABL2-IN-2 inhibits the proliferation of both parental and vemurafenib-resistant A375 melanoma cells, with an IC₅₀ of 12.3 μM against A375 cells and 20.1 μM against A375-R cells. It exhibits low cytotoxicity toward normal human WI-38 lung fibroblasts, with an IC₅₀ of 28.78 μM^[1].
BRAFV600E/ABL2-IN-2 inhibits the ABL2-mediated p-CrkL and BRAFV600E-mediated p-ERK1/2 signaling pathways in Vemurafenib (HY-12057)-resistant A375-R melanoma cells without altering total protein levels^[1].
BRAFV600E/ABL2-IN-2 (0.54 μM) induces G1 phase cell cycle arrest in SK-MEL-5 melanoma cells and reduces their progression to the S and G2/M phases^[1].
BRAFV600E/ABL2-IN-2 (0.54 μM; 24 h) induces significant early and late apoptosis in SK-MEL-5 melanoma cells, with a total apoptotic rate of 45.28%^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.