Ulixertinib (hydrochloride) is supplied as a crystalline solid. A stock solution may be made by dissolving the ulixertinib (hydrochloride) in the solvent of choice, which should be purged with an inert gas. Ulixertinib (hydrochloride) is soluble in organic solvents such as ethanol, DMSO, and dimethylformamide (DMF). The solubility of this compound in ethanol is approximately 1 mg/ml and approximately 30 mg/ml in DMSO and DMF. Ulixertinib(hydrochloride) is sparingly soluble in aqueous buffers. For maximum solubility in aqueous buffers,ulixertinib (hydrochloride) should first be dissolved in DMSO and then diluted with the aqueous buffer of choice. Ulixertinib (hydrochloride) has a solubility of approximately 0.25 mg/ml in a 1:3 solution of DMSO: PBS (pH 7.2) using this method.
Ulixertinib is a reversible ERK1/2 inhibitor that demonstrates an IC50 value of <0.3 nM for ERK2. In A375 melanoma cells with b-RafV600E mutation, it has been reported to reduce the levels of phosphorylated ERK2 and the downstream kinase RSK (IC50s = 4.1 and 0.14 μM, respectively). Ulixertinib has also been shown to inhibit A375 cell proliferation with an IC50 value of 180 nM.
Ulixertinib Hydrochloride is an acid salt of Ulixertinib (U700830), a potent and reversible ERK1/ERK2 inhibitor with IC50 of <0.3 nM for ERK2. Inhibits cell proliferation. Anti-cancer.
Ulixertinib hydrochloride is a potent in vitro inhibitor of ERK1/2 kinase that contacts myogenic precursor cells in farmed animals, thereby promoting fusion and myogenic maturation for industrial meat production.
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].
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].
