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| Cas No.: | 1236699-92-5 |
| Chemical Name: | Pimasertib |
| Synonyms: | Pimasertib; MSC1936369B; AS-703026; AS 703026, Pimasertib; MSC1936369B; AS-703026; AS 703026 |
| SMILES: | FC1=C(C=CC(I)=C1)NC2=CN=CC=C2C(NC[C@@H](CO)O)=O |
| Formula: | C15H15FIn3O3 |
| M.Wt: | 431.206 |
| Sotrage: | 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO |
| Description: | Pimasertib (AS703026) is a highly selective, potent, ATP non-competitive allosteric inhibitor of MEK1/2, used for cancer treatment. |
| In Vivo: | Pimasertib (15, 30 mg/kg) significantly inhibits the growth of tumor in the human H929 MM xenograft model in CB17 SCID mice[1]. Pimasertib (10 mg/kg, p.o.) inhibits tumor growth of cetuximab-resistant tumor attributed by K-ras mutation[2]. |
| In Vitro: | Pimasertib (5, 0.5, and 0.1 μM) specifically blocks ERK1/2 activation in MM cells, cultured alone or with BMSCs. Pimasertib inhibits the growth of MM cell lines in a dose-dependent manner, with IC50s ranging from 0.005 to 2 μM. The IC50s of Pimasertib against INA-6, U266, H929 cells are 10 nM, 5 nM, 200 nM respectively. Pimasertib induces apoptosis and modulates the cell cycle profile. Pimasertib targets MM cells in the BM microenvironment[1]. Pimasertib (10 μmol/L) inhibits ERK pathway, proliferation, and transformation in cetuximab-resistant D-MUT cells[2]. Pimasertib in combination with PLX4032 significantly induces apoptosis of RPMI-7951 cells, whereas each drug used alone does not. Pimasertib synergizes with small interfering RNA-mediated downregulation of BRAF to produce results similar to those of combined treatment with PLX4032 and Pimasertib[3]. |
MSDS
COA
| LOT NO. | DOWNLOAD |
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| 2018-0101 |
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