BRAFV600E/ABL2-IN-1 

BRAF^V600E/ABL2-IN-1 is a BRAF^V600E (IC₅₀ = 0.088 μM)/ABL2 (IC₅₀ = 0.3 μM) dual inhibitor. BRAF^V600E/ABL2-IN-1 can diminish P-glycoprotein expression. BRAF^V600E/ABL2-IN-1 effectively inhibits p-CrkL (Abl2 signaling) and p-ERK1/2 (BRAF^V600E pathway) in A375-R melanoma cells. BRAF^V600E/ABL2-IN-1 causes cell cycle arrest at the G1 phase, inhibiting progression to the S phase and subsequent phases and G2/M phase. BRAF^V600E/ABL2-IN-1 significantly increases the percentage of late apoptotic cells. BRAF^V600E/ABL2-IN-1 can be used for the study of melanoma^[1].

BRAF^V600E/ABL2-IN-1 (Compound 8h) (0.01-100 μM，48 h) 在黑色素瘤细胞系中对 SK-MEL5 细胞表现出最佳活性，GI₅₀ 为 0.54 μM，对黑色素瘤 (SK-MEL-5；TGI = 19.95 μM) 和结肠癌 (HT29；TGI = 26.30 μM) 均表现出显著的细胞抑制活性^[1]。
BRAF^V600E/ABL2-IN-1 (0.125-1 μM，72 h) 可显著下调 SK-MEL-5 细胞中 P-gp 的表达^[1]。
BRAF^V600E/ABL2-IN-1 (0.4-100 μM) 在 A375 细胞 (BRAF^V600E 突变体) 中的 IC₅₀ 值为 6.888 μg/mL (~12.3 μM)，在 A375-R 细胞 (维莫非尼耐药) 中的 IC₅₀ 值为 11.242 μg/mL (~20.1 μM)，在 WI-38 细胞中的 IC₅₀ 值为 28.776 μM^[1]。
BRAF^V600E/ABL2-IN-1 显著降低A375- R 细胞中 p-CrkL (ABL2 下游) 和 p-ERK1/2 (BRAF 下游) 的磷酸化水平，而总蛋白水平保持不变。p-CrkL 降低了 67.7%，p-ERK1/2 降低了 63.0%[1]。 BRAF^V600E/ABL2-IN-1 (0.54 μM, 48 h) 通过诱导 G1 期阻滞和细胞凋亡抑制 SK-MEL-5 细胞的增殖^[1]。

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

559.86

C₂₄H₂₀BrClN₄O₃S

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• [1]. Badawy MAS, et al. Targeting melanoma resistance: Novel oxindole and non-oxindole-based benzimidazole derivatives as potent dual inhibitors of BRAFV600E and ABL2 kinases. Eur J Med Chem. 2025 Dec 15;300:118096.  [Content Brief]