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SML3067

Sigma-Aldrich

WM-1119

≥98% (HPLC)

Sinónimos:

2-Fluoro-N′-(3-fluoro-5-(pyridin-2-yl)benzoyl)benzenesulfonohydrazide, 3-Fluoro-N′-(2-fluorophenyl)sulfonyl-5-(2-pyridyl)benzohydrazide, WM 1119, WM1119

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About This Item

Fórmula empírica (notación de Hill):
C18H13F2N3O3S
Número de CAS:
2055397-28-7
Peso molecular:
389.38
MDL number:
MFCD31690337
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

100

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

2-8°C

SMILES string

FC1=CC(C2=NC=CC=C2)=CC(C(NNS(C3=CC=CC=C3F)(=O)=O)=O)=C1

Biochem/physiol Actions

WM-1119 is a potent and selective, acetyl coenzyme A (Acetyl-CoA)-competitive inhibitor against MYST family histone acetyltransferases KAT6A and KAT6B (KAT6B Kd = 2.1 nM by SPR, IC50 = 37 nM by activity assay; KAT7/5 Kd = 0.53/2.2 μM; no affinity toward 159 diverse biological targets). WM-1119 induces MEF G1 cell cycle arrest (1-10 μM), inhibits EMRK1184 lymphoma growth in cultures (IC50 = 250 nM) and in mice in vivo (50 mg/kg 3x or 4x i.p. per day).

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Jonathan B Baell et al.
Nature, 560(7717), 253-257 (2018-08-03)
Acetylation of histones by lysine acetyltransferases (KATs) is essential for chromatin organization and function1. Among the genes coding for the MYST family of KATs (KAT5-KAT8) are the oncogenes KAT6A (also known as MOZ) and KAT6B (also known as MORF and
Daniel L Priebbenow et al.
Journal of medicinal chemistry, 63(9), 4655-4684 (2020-03-03)
A high-throughput screen designed to discover new inhibitors of histone acetyltransferase KAT6A uncovered CTX-0124143 (1), a unique aryl acylsulfonohydrazide with an IC50 of 1.0 μM. Using this acylsulfonohydrazide as a template, we herein disclose the results of our extensive structure-activity
Laura MacPherson et al.
Nature, 577(7789), 266-270 (2019-12-13)
Acute myeloid leukaemia (AML) is a heterogeneous disease characterized by transcriptional dysregulation that results in a block in differentiation and increased malignant self-renewal. Various epigenetic therapies aimed at reversing these hallmarks of AML have progressed into clinical trials, but most
Rodrigo A Gier et al.
Nature communications, 11(1), 3455-3455 (2020-07-15)
CRISPR-based genetic screening has revolutionized cancer drug target discovery, yet reliable, multiplex gene editing to reveal synergies between gene targets remains a major challenge. Here, we present a simple and robust CRISPR-Cas12a-based approach for combinatorial genetic screening in cancer cells.

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