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ChemicalBook--->CAS DataBase List--->2109805-96-9

2109805-96-9

2109805-96-9 Structure

2109805-96-9 Structure
IdentificationBack Directory
[Name]

BAY707)
[CAS]

2109805-96-9
[Synonyms]

BAY707)
BAY-707 (BAY 707
BAY-707 free base
1H-Pyrrolo[2,3-b]pyridine-2-carboxamide, N-ethyl-4-[(3S)-3-methyl-4-morpholinyl]-
[Molecular Formula]

C15H20N4O2
[MDL Number]

MFCD31814430
[MOL File]

2109805-96-9.mol
[Molecular Weight]

288.34
Chemical PropertiesBack Directory
[density ]

1.225±0.06 g/cm3(Predicted)
[storage temp. ]

Store at -20°C
[solubility ]

DMSO:28.83(Max Conc. mg/mL);100.0(Max Conc. mM)
Ethanol:2.88(Max Conc. mg/mL);10.0(Max Conc. mM)
[form ]

Solid
[pka]

14.36±0.40(Predicted)
[color ]

Light yellow to khaki
Safety DataBack Directory
[Symbol(GHS) ]


GHS07
[Signal word ]

Warning
[Hazard statements ]

H302-H315-H319-H335
[Precautionary statements ]

P261-P305+P351+P338
Hazard InformationBack Directory
[Uses]

BAY-707 is a substrate-competitive, highly potent and selective inhibitor of MTH1(NUDT1) with an IC50 of 2.3 nM. BAY-707 has a good pharmacokinetic (PK) profile to other MTH1 compounds and is well-tolerated in mice, but shows a clear lack of in vitro or in vivo anticancer efficacy[1].
[Biological Activity]

BAY-707 is a substrate-competitive, highly selective inhibitor of MTH1(NUDT1) with IC50 of 2.3 nM. It has a favorable pharmacokinetic profile compared to other MTH1 compounds and is well tolerated in mice, but the experiments clearly lack in vitro or in vivo anticancer efficacy.
[in vivo]

Bay-077 (orally adminstation; 50-250 mg/kg; 2 weeks) exhibits superior biochemical potency, cellular target engagement, and a pharmacokinetic profile to other MTH1 tool compounds, But Bay-077 exerts no anticancer efficacy either in mono- or in combination therapies in CT26 and NCI-H460 mice model.
[target]

IC50: 2.3 nM (MTH1/NUDT1)

[storage]

Store at -20°C
[References]

[1] Ellermann M, et al. Novel Class of Potent and Cellularly Active Inhibitors Devalidates MTH1 as Broad-Spectrum Cancer Target.ACS Chem Biol. 2017 Aug 18;12(8):1986-1992. DOI:10.1021/acschembio.7b00370
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