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ML-9 hydrochloride

  Cat. No.:  DC20457   Featured
Chemical Structure
105637-50-1
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More than 5000 active chemicals with high quality for research!
Field of application
ML-9 is a selective and potent inhibitor of Akt kinase, inhibits myosin light-chain kinase (MLCK) and stromal interaction molecule 1 (STIM1) activity. ML-9 inhibits inhibits MLCK, PKA and PKC activity with Ki values of 4, 32 and 54 μM, respectively. ML-9 induces autophagy by stimulating autophagosome formation and inhibiting their degradation.
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
Cas No.: 105637-50-1
Chemical Name: 1-[(5-chloro-1-naphthalenyl)sulfonyl]hexahydro-1H-1,4-diazepine, monohydrochloride
Synonyms: ml 9,ml-9,ml9
SMILES: Cl.ClC1C=CC=C2C=1C=CC=C2S(N1CCCNCC1)(=O)=O
Formula: C15H18Cl2N2O2S
M.Wt: 361.281
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Publication: [1]. Ito S, et al. ML-9, a myosin light chain kinase inhibitor, reduces intracellular Ca2+ concentration in guinea pig trachealis.Eur J Pharmacol. 2004 Feb 23;486(3):325-33. [2]. Shaikh S, et al. The STIM1 inhibitor ML9 disrupts basal autophagy in cardiomyocytes by decreasing lysosome content.Toxicol In Vitro. 2018 Apr;48:121-127. [3]. Kondratskyi A1, et al.Identification of ML-9 as a lysosomotropic agent targeting autophagy and cell death.Cell Death Dis. 2014 Apr 24;5:e1193.
Description: ML-9 is a selective and potent inhibitor of Akt kinase, inhibits myosin light-chain kinase (MLCK) and stromal interaction molecule 1 (STIM1) activity[3]. ML-9 inhibits inhibits MLCK, PKA and PKC activity with Ki values of 4, 32 and 54 μM, respectively[1]. ML-9 induces autophagy by stimulating autophagosome formation and inhibiting their degradation[3].
In Vitro: ML9 (0-100 μM; 0-24 hours) has no reduction in cardiomyocyte viability, 50-100 μM significantly induces cell death[2]. ML9 (50 μM; 1-4 hours) significantly increases cleaved caspase-3 levels, decreased STIM1 protein levels by about 42%[2]. Cell Viability Assay[1] Cell Line: Neonatal rat ventricular myocytes (NRVM) cells Concentration: 0, 10, 50 and 100 μM Incubation Time: 0, 1, 4, 8 and 24 hours Result: Decreased cell viability at 50-100 μM concentration. Apoptosis Analysis[1] Cell Line: Neonatal rat ventricular myocytes (NRVM) cells Concentration: 50 μM Incubation Time: 1, 4 and 8 hours Result: Induced cardiomyocyte death through necrosis and apoptosis.
References: [1]. Ito S, et al. ML-9, a myosin light chain kinase inhibitor, reduces intracellular Ca2+ concentration in guinea pig trachealis.Eur J Pharmacol. 2004 Feb 23;486(3):325-33. [2]. Shaikh S, et al. The STIM1 inhibitor ML9 disrupts basal autophagy in cardiomyocytes by decreasing lysosome content.Toxicol In Vitro. 2018 Apr;48:121-127. [3]. Kondratskyi A1, et al.Identification of ML-9 as a lysosomotropic agent targeting autophagy and cell death.Cell Death Dis. 2014 Apr 24;5:e1193.
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
2018-0101
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