ML-7 HYDROCHLORIDE

ML-7 HYDROCHLORIDE
  • CAS No.:110448-33-4

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  1. This product is a chemical product/pharmaceutical intermediate. It is not a drug, an active pharmaceutical ingredient (API), or a pharmaceutical-grade material. It has not been granted a drug approval number or a Chemical Drug Substance Approval Notice, has not passed drug-related review and approval, and is not manufactured, tested, or released in accordance with pharmaceutical GMP.
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ML-7 HYDROCHLORIDE Basic information
Product Name:ML-7 HYDROCHLORIDE
Synonyms:ML-7, Hydrochloride - CAS 110448-33-4 - Calbiochem;ML;ML 7;CS-755;ML7;ML 7 HYDROCHLORIDE;1-(5-IODONAPHTHALENE-1-SULFONYL)-1H-HEXAHYDRO-1,4-DIAZEPINE HCL;1-(5-IODONAPHTHALENE-1-SULFONYL)-1H-HEXAHYDRO-1,4-DIAZEPINE HYDROCHLORIDE;1-(5-IODONAPHTHALENE-1-SULFONYL)HOMOPIPERAZINE, HCL;1-(5-IODONAPHTHALENE-1-SULFONYL)-1H-HEXAHYDRO-1,4-DIAZEPINE
CAS:110448-33-4
MF:C15H18ClIN2O2S
MW:452.74
EINECS:
Product Categories:All Inhibitors;Inhibitors;Protein Kinase Inhibitors and Activators
Mol File:110448-33-4.mol
ML-7 HYDROCHLORIDE Chemical Properties
Melting point 246-249°C dec.
storage temp. -20°C
solubility insoluble in EtOH; ≥15.95 mg/mL in DMSO; ≥8.82 mg/mL in H2O with gentle warming and ultrasonic
form powder
color white
Safety Information
WGK Germany 3
MSDS Information
ProviderLanguage
SigmaAldrich English
ML-7 HYDROCHLORIDE Usage And Synthesis
DescriptionML-7 inhibits smooth muscle myosin light chain kinase (MLCK) with a Ki value of 0.3 μM and displays reversible, ATP-competitive inhibition of Ca2+-calmodulin-dependent and -independent smooth muscle MLCKs. It exhibits a 10-fold more potent inhibition of MLCK than its parent compound ML-9 .
Chemical PropertiesOff-White to Yellow Fine Crystalline Solid
UsesA potent and selective inhibitor of myosin light chain kinase.
UsesML-7 has been used as a myosin light chain kinase (MLCK) inhibitor in various experiments.
Biochem/physiol ActionsSelective myosin light chain kinase inhibitor.
in vitrorats with myocardial infarction were intravenously infused with rhnrg-1. the cmlck expression and phosphorylated mlc-2v were up-regulated in rat treated with rhnrg-1 significantly. moreover, the restoration of rhnrg-1-induced sarcomeric organization in serum-free cultured neonatal rat cardiomyocytes with rhnrg-1 was inhibited by ml-7 [1].
in vivoadministration of ml-7 from 10 min before ischemia to the first 10 min of reperfusion led to a significant recovery of heart contractility. gel analyses of two-dimensional electrophoresis revealed eight proteins with decreased levels in i/r hearts. six proteins involved in energy metabolism, which were cytochrome b-c1 complex subunit 1, atp synthase beta subunit, cytochrome c oxidase subunit, mitochondrial nadhdehydrogenase, nadhdehydrogenase iron-sulfur protein 8, and succinyl-coa ligase subunit. the other two protein levels decreased in i/r hearts, which were peroxiredoxin-2 and tubulin. in addition, ml-7 treatment increased the level of succinyl-coa ligase, which was a key enzyme involved in the citric acid cycle [2].
references[1] gu x,liu x,xu d,li x,yan m,qi y,yan w,wang w,pan j,xu y,xi b,cheng l,jia j,wang k,ge j,zhou m. cardiac functional improvement in rats with myocardial infarction by up-regulating cardiac myosin light chain kinase with neuregulin. cardiovasc res.2010 nov 1;88(2):334-43. [2] lin hb,cadete vj,sawicka j,wozniak m,sawicki g. effect of the myosin light chain kinase inhibitor ml-7 on the proteome of hearts subjected to ischemia-reperfusion injury. j proteomics.2012 sep 18;75(17):5386-95.
ML-7 HYDROCHLORIDE Preparation Products And Raw materials

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