化学性质:
规格 | 1mg 5mg 10mg 25mg |
CAS | 195 |
别名 | BVD-523,VRT-752271 |
化学名 | 4-[5-chloro-2-[(1-methylethyl)amino]-4-pyridinyl]-N-[(1S)-1-(3-chlorophenyl)-2-hydroxyethyl]-1H-pyrrole-2-carboxamide, monohydrochloride |
分子式 | C21H22Cl2N4O2 • HCl |
分子量 | 469.8 |
溶解度 | ≤1mg/ml in ethanol;30mg/ml in DMSO;30mg/ml in dimethyl formamide |
储存条件 | Store at -20°C |
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
Shipping Condition | Evaluation sample solution : ship with blue ice |
产品描述:
Ulixertinib, also named as BVD-523, is a novel and reversible inhibitor of ERK1/2. Ulixertinib potently and selectively inhibits the activity of ERK1 and ERK2 kinases in a reversible, ATP-competitive fashion [1].
The Ras-dependent extracellular signal-regulated kinase (ERK)1/2 mitogen-activated protein (MAP) kinase pathway plays a central role in cell proliferation control. In normal cells, sustained activation of ERK1/ERK2 is necessary for G1- to S-phase progression and is associated with induction of positive regulators of the cell cycle and inactivation of antiproliferative genes. The RAF-MEK-ERK1/2 signal pathway plays a dominant role in promoting cell survival [2].
In vitro: In two lymphoma cell lines (SUDHL-10 and Raji), treatment with ulixertinib significantly reduced the expression of ERK1/2 phosphorylation in a dose-dependent manner. Treatment with 0.4 nM ulixertinib decreased the percentage of G2-M phase cells in the SUDHL-10 cells. In the Raji cells, treated with ulixertinib at 0.4 and 1.0 nM increased the percentage of G0-G1 phase cells and decreased S phase cells [1]. Treatment of ulixertinib at the dose of 0.1, 0.4 and 1.0 nM for 48 h dose-dependently increased the number of early apoptotic SUDHL- 10 and Raji cells [1]. In SUDHL-10 and Raji cells, ulixertinib reduced mRNA and protein expression of VEGFR2 and Bcl-2 genes and increased the expression of Bax and caspase-3 genes [1].
In vivo: BVD-523 inhibited tumor growth in BRAF-mutant melanoma and colorectal xenografts as well as in KRAS-mutant colorectal and pancreatic models. BVD-523 treatment in combination with dabrafenib inhibited tumor growth in a BRAF-mutant melanoma model [3]. Single-agent BVD-523 inhibited the growth of a patient-derived tumor xenograft harboring cross-resistance to dabrafenib, trametinib, and the combination treatment following clinical progression on a MEK inhibitor [3].
Clinical trials: In patients (pts) with advanced solid tumors, BVD-523 (ulixertinib) achieved pharmacologically relevant exposure and manageable tolerability at its MTD of 600 mg twice a day [4].
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