MRT199665

MRT199665 is a potent and ATP-competitive, selective MARK/SIK/AMPK inhibitor with 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[1]. MRT199665 causes apoptosis in MEF2C-activated human acute myeloid leukemias (AML) cells[2]. MRT199665 inhibits the phosphorylation of SIK substrate CRTC3 at S370[3].

Product Specifications

CAS Number

[1456858-57-3]

UNSPSC

12352005

Target

AMPK; Apoptosis; MARK; Salt-inducible Kinase (SIK)

Type

Reference compound

Related Pathways

Apoptosis; Cell Cycle/DNA Damage; Epigenetics; Immunology/Inflammation; PI3K/Akt/mTOR

Applications

Cancer-Kinase/protease

Field of Research

Cancer

Assay Protocol

https://www.medchemexpress.com/mrt199665.html

Concentration

10mM

Purity

99.74

Solubility

DMSO : 100 mg/mL (ultrasonic)

Smiles

O=C1C(C)(C)C2=CN=C(NC3=CC=CC(CN4CCCC4)=C3)N=C2N1[C@H]5CCC6=C5C=CC=C6O

Molecular Formula

C28H31N5O2

Molecular Weight

469.58

References & Citations

[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.