| Identification | Back Directory | [Name]
BVD523 | [CAS]
1956366-10-1 | [Synonyms]
BVD523
Ulixertinib HCl
Ulixertinib HCl salt
VRT752271 hydrochloride)
Ulixertinib hydrochloride
Ulixertinib hydrochloride (BVD-523 hydrochloride
Ulixertinib hydrochloride (Synonyms: BVD-523 hydrochloride
ULIXERTINIB HYDROCHLORIDE (SYNONYMS: BVD-523 HYDROCHLORIDE; VRT752271 HYDROCHLORIDE)
(S)-4-(5-chloro-2-(isopropylamino)pyridin-4-yl)-N-(1-(3-chlorophenyl)-2-hydroxyethyl)-1H-pyrrole-2-carboxamidehydrochloride | [Molecular Formula]
C21H23Cl3N4O2 | [MOL File]
1956366-10-1.mol | [Molecular Weight]
469.792 |
| Chemical Properties | Back Directory | [Melting point ]
231-232°C | [storage temp. ]
-20°C Freezer | [solubility ]
DMSO (Slightly), Methanol (Slightly) | [form ]
Solid | [color ]
White to Off-White |
| Hazard Information | Back Directory | [Description]
Ulixertinib is a reversible ERK1/2 inhibitor that demonstrates an IC50 value of <0.3 nM for ERK2.1 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).1 Ulixertinib has also been shown to inhibit A375 cell proliferation with an IC50 value of 180 nM.1 | [Uses]
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. | [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]. |
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