[CAS NO. 2061980-01-4]  XMU-MP-1

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PRODUCTS SPECIFICATIONS [2061980-01-4]

Catalog
SLK-S8334
Brand
Selleck
CAS
2061980-01-4

DESCRIPTION [2061980-01-4]

Overview

MDLMFCD30377214
Molecular Weight416.48
Molecular FormulaC17H16N6O3S2
SMILESO=S(C1=CC=C(NC2=NC=C(C(N(C)C3=C4SC=C3)=N2)N(C)C4=O)C=C1)(N)=O

For research use only.

Storage

3 years,-20°C,powder
1 years,-80°C,in solvent

Shipping

Room temperature shipping(Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

1 mg5 mg10 mg
1 mM2.4011 mL12.0054 mL24.0108 mL
5 mM0.4802 mL2.4011 mL4.8022 mL
10 mM0.2401 mL1.2005 mL2.4011 mL
50 mM0.0480 mL0.2401 mL0.4802 mL

Description

XMU-MP-1 is an inhibitor of with IC50 values of 71.1±12.9 nM and 38.1±6.9 nM against MST1 and MST2, respectively.

Targets

MST2 [1]
(Cell-free assay)
MST1 [1]
(Cell-free assay)
38.1 nM71.1 nM

In vitro

XMU-MP-1 blocks MST1/2 kinase activities, thereby activating the downstream effector Yes-associated protein and promoting cell growth. XMU-MP-1 inhibits phosphorylation of MOB1 in a dose-dependent manner. Furthermore, with increasing ATP concentration, XMU-MP-1 exhibits a proportional increase in IC50 against MST1/2, as well as an attenuated inhibition of the MST2-mediated phosphorylation of MOB1. At concentrations ranging from 0.1 to 10 μM, XMU-MP-1 reduces the phosphorylation of endogenous MOB1, LATS1/2, and YAP in human liver carcinoma (HepG2) cells in a dose-dependent manner. Similarly, XMU-MP-1 treatment inhibits hydrogen peroxide (H2O2)-stimulated MOB1 phosphorylation and MST1/2 autophosphorylation in a variety of cell lines, including mouse macrophage-like cells (RAW264.7), human osteosarcoma (U2OS), human colorectal adenocarcinoma (SW480), immortalized human retinal pigment epithelial cells (RPE1), human pleomorphic hepatocellular carcinoma (SNU-423), and HepG2, as well as primary mouse hepatocytes, without affecting the phosphorylation of JNK (c-Jun N-terminal kinase), which is a positive control for H2O2 stimulation. XMU-MP-1 treatment increases YAP nuclear translocation.

In vivo

XMU-MP-1 displays excellent in vivo pharmacokinetics and is able to augment mouse intestinal repair, as well as liver repair and regeneration, in both acute and chronic liver injury mouse models at a dose of 1 to 3 mg/kg via intraperitoneal injection. XMU-MP-1 exhibits favorable pharmacokinetics in rats with a half-life of 1.2 hours and a bioavailability of 39.5%. The maximal phosphorylation inhibition of MOB1 and YAP is achieved between 1.5 and 6 hours after intraperitoneal dosing with XMU-MP-1 (1 mg/kg). XMU-MP-1 protects mice from DSS-induced colitis and ameliorates chronic liver injury.