| Chemical Properties | Back Directory | [Melting point ]
114-116 °C | [Boiling point ]
309.0±42.0 °C(Predicted) | [density ]
1.45±0.1 g/cm3(Predicted) | [storage temp. ]
-10 to -25°C | [solubility ]
DMSO: 2mg/mL, clear (Warmed) | [form ]
Solid | [color ]
White to off-white | [InChI]
1S/C15H10F6OS2/c16-14(17,18)23-12-5-1-10(2-6-12)9-22-11-3-7-13(8-4-11)24-15(19,20)21/h1-8H,9H2 | [InChIKey]
OJUUGOMDHJFXJH-UHFFFAOYSA-N | [SMILES]
FC(F)(F)SC1=CC=C(COC2=CC=C(C=C2)SC(F)(F)F)C=C1 |
| Hazard Information | Back Directory | [Uses]
MY10 is a potent and orally active receptor protein tyrosine phosphatase (RPTPβ/ζ) inhibitor. MY10 reduces NF-κB p65 expression. MY10 activates tyrosine phosphorylation of c-Met. MY10 prevents the alcohol-induced downregulation of Ptprz1 and Alk expression. MY10 attenuates binge-like ethanol consumption and ethanol reward. MY10 can be used in the study of neurological and vascular diseases[1][2][3][4][5]. | [Biological Activity]
MY10 is a cell penetrant potent and selective inhibitor of Receptor Protein Tyrosine Phosphatase (RPTP) β/ζ. It interacts with the cytoplasmatic D1 domain of RPTPβ/ζ. MY10 reduces alcohol intake in rats. | [in vivo]
MY10 (100 mg/kg, p.o., 1 h before the voluntary alcohol consumption) reduces the alcohol consumption in rats[5].
| Animal Model: | Adult male Wistar rats (male, 375-440 g) in alcohol operant self- administration paradigm and Drinking In the Dark - Multiple Scheduled Access (DID-MSA) paradigm[5] | | Dosage: | 20, 60, 100 mg/kg (in 10% dehydrated ethanol, 20% polysorbate 80, and 70% PEG 300 vehicle) | | Administration: | Administered by oral gavage, once 1 hour before the voluntary alcohol consumption, for 3 days. | | Result: | Caused a significant 26.1% reduction in alcohol consumption at 100 mg/kg (in the alcohol operant self-administration paradigm).
Caused a 28.1% decrease in cumulative alcohol intake (in the DID-MSA paradigm).
Decreased the alcohol preference.
Had no effect on saccharin intake.
Prevented the alcohol-induced down-regulation of Prprzl and Alk gene expression.
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| [References]
[1] Fernández-Calle R, et, al. Pharmacological inhibition of Receptor Protein Tyrosine Phosphatase β/ζ (PTPRZ1) modulates behavioral responses to ethanol. Neuropharmacology. 2018 Jul 15;137:86-95. DOI:10.1016/j.neuropharm.2018.04.027
[2] Del Campo M, et al. Role of Receptor Protein Tyrosine Phosphatase β/ζ in Neuron-Microglia Communication in a Cellular Model of Parkinson's Disease. Int J Mol Sci. 2021 Jun 22;22(13):6646. DOI:10.3390/ijms22136646
[3] Fernández-Calle R, et al. Role of RPTPβ/ζ in neuroinflammation and microglia-neuron communication. Sci Rep. 2020 Nov 20;10(1):20259. DOI:10.1038/s41598-020-76415-5
[4] Kastana P, et al. Genetic deletion or tyrosine phosphatase inhibition of PTPRZ1 activates c-Met to up-regulate angiogenesis and lung adenocarcinoma growth. Int J Cancer. 2023 Sep 1;153(5):1051-1066. DOI:10.1002/ijc.34564
[5] Calleja-Conde J, et al. Inhibition of Receptor Protein Tyrosine Phosphatase β/ζ Reduces Alcohol Intake in Rats. Alcohol Clin Exp Res. 2020 May;44(5):1037-1045. DOI:10.1111/acer.14321 |
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| Company Name: |
Merck KGaA
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| Tel: |
21-20338288 |
| Website: |
www.sigmaaldrich.cn |
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