ML-SA5

CAS: 2418670-70-7 F: C19H24ClN3O4S2 W: 457.99

ML-SA5 is a potent TRPML1 cation channel agonist that activates the entire endosomal TRPML1 (ML1) current in DMD myocyte

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Bioactivity	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].
Invitro	ML-SA5(1-100 μM, 24 h) has some cell-targeting specificity and induces substantial cell death in M12 and MeWo cells, but fully preserves normal melanocytes. It also causes a loss of mitochondrial membrane potential in M12 cells[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].
Name	ML-SA5
CAS	2418670-70-7
Formula	C19H24ClN3O4S2
Molar Mass	457.99
Appearance	Solid
Transport	Room temperature in continental US; may vary elsewhere.
Storage	4°C, sealed storage, away from moisture and light *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Reference	[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. [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.