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Merck

SML1735

PFM01

≥98% (HPLC)

Synonyme(s) :

(5Z)-5-[(4-Hydroxyphenyl)methylene]-3-(2-methylpropyl)-2-thioxo-4-thiazolidinone, 5-(4-Hydroxybenzylidene)-3-isobutyl-2-thioxothiazolidin-4-one

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About This Item

Formule empirique (notation de Hill) :
C14H15NO2S2
Numéro CAS:
Poids moléculaire :
293.40
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:

Nom du produit

PFM01, ≥98% (HPLC)

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-

InChI key

GPURHDUTZUYAFI-GHXNOFRVSA-N

SMILES string

OC1=CC=C(/C=C2SC(N(CC(C)C)C\2=O)=S)C=C1

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 20 mg/mL, clear

storage temp.

2-8°C

Quality Level

Catégories apparentées

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.
PFM01 is a cell-permeable N-alkylated Mirin derivative that selectively inhibits against MRE11 endo-, but not exo-, nuclease activity.

pictograms

Exclamation mark

signalword

Warning

Hazard Classifications

Acute Tox. 4 Oral - Eye Irrit. 2 - Skin Irrit. 2

Classe de stockage

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Consulter la Bibliothèque de documents

Sarah R Hengel et al.
Cell chemical biology, 24(9), 1101-1119 (2017-09-25)
To maintain stable genomes and to avoid cancer and aging, cells need to repair a multitude of deleterious DNA lesions, which arise constantly in every cell. Processes that support genome integrity in normal cells, however, allow cancer cells to develop
Lea Völkening et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 34(2), 2812-2820 (2020-01-08)
The Mre11A/RAD50/NBN complex (MRN) is an essential regulator of the cellular damage response after DNA double-strand breaks (DSBs). More recent work has indicated that MRN may also impact on the duration of mitosis. We show here that RAD50-deficient fibroblasts exhibit
Donna R Whelan et al.
Proceedings of the National Academy of Sciences of the United States of America, 118(11) (2021-03-13)
Homologous recombination (HR) is a major pathway for repair of DNA double-strand breaks (DSBs). The initial step that drives the HR process is resection of DNA at the DSB, during which a multitude of nucleases, mediators, and signaling proteins accumulates

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