ChemicalBook--->CAS DataBase List--->1558598-41-6

1558598-41-6

1558598-41-6 Structure

1558598-41-6 Structure
IdentificationBack Directory
[Name]

PFM01
[CAS]

1558598-41-6
[Synonyms]

PFM01
PFM01 >=98% (HPLC)
(5Z)-5-[(4-Hydroxyphenyl)methylene]-3-(2-methylpropyl)-2-thioxo-4-thiazolidinone
[Molecular Formula]

C14H15NO2S2
[MDL Number]

MFCD02220972
[MOL File]

1558598-41-6.mol
[Molecular Weight]

293.4
Chemical PropertiesBack Directory
[Boiling point ]

435.2±55.0 °C(Predicted)
[density ]

1.35±0.1 g/cm3(Predicted)
[storage temp. ]

2-8°C
[solubility ]

Soluble in DMSO
[form ]

powder
[pka]

8.59±0.30(Predicted)
[color ]

white to beige
[InChI]

1S/C14H15NO2S2/c1-9(2)8-15-13(17)12(19-14(15)18)7-10-3-5-11(16)6-4-10/h3-7,9,16H,8H2,1-2H3/b12-7-
[InChIKey]

GPURHDUTZUYAFI-GHXNOFRVSA-N
[SMILES]

OC1=CC=C(/C=C2SC(N(CC(C)C)C\2=O)=S)C=C1
Safety DataBack Directory
[Symbol(GHS) ]

Exclamation Mark (GHS07)
GHS07
[Signal word ]

Warning
[Hazard statements ]

H302-H315-H319
[Precautionary statements ]

P301+P312+P330-P305+P351+P338
[WGK Germany ]

WGK 3
[Storage Class]

11 - Combustible Solids
[Hazard Classifications]

Acute Tox. 4 Oral
Eye Irrit. 2
Skin Irrit. 2
Hazard InformationBack Directory
[Uses]

PFM01, N-alkylated Mirin derivative, is a MRE11 endonuclease inhibitor. PFM01 can regulate double-strand break repair (DSBR) by nonhomologous end-joining (NHEJ) versus homologous recombination (HR)[1][2].
[Biochem/physiol Actions]

PFM01 is a cell-permeable N-alkylated Mirin (Sigma Cat. No. 475954) derivative that selectively inhibits against MRE11 endo-, but not exo-, nuclease activity. PFM01 targets MRE11 at a site near the dimer interface, distinct from that occupied by Mirin and PFM39 to allow disruption of the ssDNA-binding groove and selective inhibition against MRE11 endo-, but not exo-, nuclease activity. While both endonuclease and exonuclease activities are required for MRE11-mediated homologous recombination (HR) repair, only FM01 (100 μM), but not the exonuclease inhibitors Mirin (500 μM) and PFM39 (100 μM), rescues G2-phase double-strand break (DSB) repair defect in HR protein BRCA2-deficient HSC62-hTERT fibroblasts following ionizing irradiation (IR) by blocking HR initiation and thereby allowing non-homologous end joining (NHEJ) to proceed.
[storage]

Store at -20°C
[References]

[1] Shibata A, et, al. DNA double-strand break repair pathway choice is directed by distinct MRE11 nuclease activities. Mol Cell. 2014 Jan 9; 53(1): 7-18. DOI:10.1016/j.molcel.2013.11.003
[2] V?lkening L, et, al. RAD50 regulates mitotic progression independent of DNA repair functions. FASEB J. 2020 Feb; 34(2): 2812-2820. DOI:10.1096/fj.201902318R
Spectrum DetailBack Directory
[Spectrum Detail]

PFM01(1558598-41-6)1HNMR
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