| Description | MRT199665 is an effective and ATP-competitive, selective MARK/SIK/AMPK inhibitor (IC50s of 2/2/3/2 nM, 10/10 nM, and 110/12/43 nM for MARK1/MARK2/MARK3/MARK14, AMPKα1/AMPKα2, and SIK1/SIK2/SIK3, respectively). MRT199665 suppresses the phosphorylation of SIK substrate CRTC3 at S370. MRT199665 induces apoptosis in MEF2C-activated human acute myeloid leukemia (AML) cells. |
| In vitro | MRT199665 also causes a decrease in total MEF2C protein. MRT199665 (1 μM; pre-treated for 1 h) enhances LPS (100 ng/mL; stimulated for up to 24 h)-stimulated IL-10 mRNA and Nurr77 mRNA production, and IL-10 secretion. MRT199665 treatment can block MEF2C S222 phosphorylation in acute myeloid leukemia (AML) cells. MRT199665 (1 nM-100 μM; 48 hours) decreases leukemia growth. MRT199665 (10 nM-1000 nM; 12 hours) leads to a dose-dependent reduction in total and pS222 MEF2C [1][2]. |
| Target activity | MELK:29 nM, AMPK α2:10 nM, TBK1:5400 nM, SIK1:110 nM, BRSK2:10000 nM, MARK4:2 nM, IKKε:7700 nM, SIK2:12 nM, SIK3:43 nM, MARK3:3 nM, NUAK1:3 nM, NUAK2:120 nM, MARK1:2 nM, MARK2:2 nM, AMPK α1:10 nM |
| molecular weight | 469.58 |
| Molecular formula | C28H31N5O2 |
| CAS | 1456858-57-3 |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| References | 1. Clark K, et al. Phosphorylation of CRTC3 by the salt-inducible kinases controls the interconversion of classically activated and regulatory macrophages. Proc Natl Acad Sci U S A. 2012 Oct 16;109(42):16986-91. 2. Brown FC, et al. MEF2C Phosphorylation Is Required for Chemotherapy Resistance in Acute Myeloid Leukemia. Cancer Discov. 2018 Apr;8(4):478-497. 3. Hutchinson LD, et al. Salt-inducible kinases (SIKs) regulate TGFβ-mediated transcriptional and apoptotic responses.Cell Death Dis. 2020 Jan 22;11(1):49. |