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2418670-70-7

2418670-70-7 Structure

2418670-70-7 Structure
IdentificationBack Directory
[Name]

1,4-Benzenedisulfonamide, N4-[3-chloro-2-(1-piperidinyl)phenyl]-N1,N1-dimethyl-
[CAS]

2418670-70-7
[Synonyms]

ML-SA5
1,4-Benzenedisulfonamide, N4-[3-chloro-2-(1-piperidinyl)phenyl]-N1,N1-dimethyl-
[Molecular Formula]

C19H24ClN3O4S2
[MDL Number]

MFCD32679424
[MOL File]

2418670-70-7.mol
[Molecular Weight]

457.99
Chemical PropertiesBack Directory
[Boiling point ]

600.4±65.0 °C(Predicted)
[density ]

1.395±0.06 g/cm3(Predicted)
[storage temp. ]

-20°C
[solubility ]

DMSO: 2mg/mL, clear
[form ]

Solid
[pka]

7.99±0.10(Predicted)
[color ]

White to light brown
Safety DataBack Directory
[Symbol(GHS) ]


GHS07
[Signal word ]

Warning
[Hazard statements ]

H319-H335-H315-H302
[Precautionary statements ]

P264-P280-P305+P351+P338-P337+P313P-P264-P280-P302+P352-P321-P332+P313-P362-P264-P270-P301+P312-P330-P501
Hazard InformationBack Directory
[Description]

ML-SA5 is a novel mucolipin 1 (ML1) agonist, inducing lysosomal Ca2+ release, ameliorating muscular dystrophies and activating TFEB to correct lysosomal insufficiency in mdx mice.
[Uses]

ML-SA5 is a potent TRPML1 cation channel agonist that activates the entire endosomal TRPML1 (ML1) current in DMD myocytes with an EC50 of 285 nM and is more potent than ML-SA1. ML-SA5 has anticancer activity and can inhibit tumour growth[1].
[in vivo]

ML-SA5 (i.p., 2-5 mg/kg, daily, 2 weeks) reduces muscle necrosis in MDX mice by more than 70% and reduces central nucleated fibers, suggesting that ML-SA5 can improve muscle atrophy in mdx mice in vivo by promoting myosin repair, but has no effect in ML1 knockout mice. Moreover, ML-SA5 reduces skeletal and cardiac muscle damage in mdx mice through ML1 upregulation[2].

[References]

[1] Wanlu Du, et al. Lysosomal Zn2+?release triggers rapid, mitochondria-mediated, non-apoptotic cell death in metastatic melanoma. Cell Rep. 2021 Oct 19;37(3):109848. DOI:10.1016/j.celrep.2021.109848
[2] Lu Yu, et al. Small-molecule activation of lysosomal TRP channels ameliorates Duchenne muscular dystrophy in mouse models. Sci Adv. 2020 Feb 7;6(6):eaaz2736. DOI:10.1126/sciadv.aaz2736
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