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Merck
CN

SML1117

ML345

≥98% (HPLC)

别名:

5-Fluoro-2-[5-(morpholine-4-sulfonyl)-2-morpholin-4-yl-phenyl]-benzo[d]isothiazol-3-one, CID 57390068

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关于此项目

经验公式(希尔记法):
C21H22FN3O5S2
化学文摘社编号:
分子量:
479.54
UNSPSC Code:
51111800
PubChem Substance ID:
NACRES:
NA.77
Assay:
≥98% (HPLC)
Form:
powder
Quality level:
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产品名称

ML345, ≥98% (HPLC)

SMILES string

O=S(C1=CC(N(C2=O)SC3=C2C=C(F)C=C3)=C(N4CCOCC4)C=C1)(N5CCOCC5)=O

InChI

1S/C21H22FN3O5S2/c22-15-1-4-20-17(13-15)21(26)25(31-20)19-14-16(32(27,28)24-7-11-30-12-8-24)2-3-18(19)23-5-9-29-10-6-23/h1-4,13-14H,5-12H2

InChI key

FVKOFZKSMMIUTL-UHFFFAOYSA-N

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 5 mg/mL, clear (warmed)

storage temp.

2-8°C

Quality Level

Biochem/physiol Actions

ML345 is a cell penetrant, potent and moderately selective insulin degrading enzyme (IDE) inhibitor.
ML345 has effective concentration (EC50) value of 188 nM.
ML345 is a cell penetrant, potent and moderately selective insulin degrading enzyme (IDE) inhibitor that targets Cys819 in IDE. IDE is involved in β-chain of insulin degradation and linked to β-amyloid degradation. Recent findings indicate that IDE inhibition is a valid strategy for diabetes mellitus type 2 (DMT2) treatment.

pictograms

Exclamation mark

signalword

Warning

hcodes

Hazard Classifications

Acute Tox. 4 Oral

存储类别

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Selective Targeting of Extracellular Insulin-Degrading Enzyme by Quasi-Irreversible Thiol-Modifying Inhibitors
Abdul. A SO, et al.
ACS chemical biology null
Selective Targeting of Extracellular Insulin-Degrading Enzyme by Quasi-Irreversible Thiol-Modifying Inhibitors
Abdul. A SO, et al.
ACS Chemical Biology null
Helen A Rowland et al.
Neuronal signaling, 7(4), NS20230016-NS20230016 (2023-10-09)
Alzheimer's disease (AD) is characterised by the aggregation and deposition of amyloid-β (Aβ) peptides in the human brain. In age-related late-onset AD, deficient degradation and clearance, rather than enhanced production, of Aβ contributes to disease pathology. In the present study

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