SML3159
WM-2474
≥98% (HPLC)
동의어(들):
WM-2474, MOZ-IN-2, N′-(2-Fluoro-5-(pyridazin-4-yl)benzoyl)benzenesulfonohydrazide, N′-(Benzenesulfonyl)-2-fluoro-5-pyridazin-4-yl-benzohydrazide, WM 1119 inactive control, WM 1119 negative control, WM 2474, WM-1119 inactive control, WM-1119 negative control, WM1119 inactive control, WM1119 negative control, WM2474
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모든 사진(1)
About This Item
실험식(Hill 표기법):
C17H13FN4O3S
CAS Number:
Molecular Weight:
372.37
MDL number:
UNSPSC 코드:
12352200
NACRES:
NA.77
Quality Level
분석
≥98% (HPLC)
형태
powder
색상
white to beige
solubility
DMSO: 2 mg/mL, clear
저장 온도
2-8°C
SMILES string
O=C(C1=C(F)C=CC(C2=CC=NN=C2)=C1)NNS(=O)(C3=CC=CC=C3)=O
생화학적/생리학적 작용
WM-2474 is an inactive analog of and negative control (KAT6B IC50 >125 μM) for the potent and selective, MYST family histone acetyltransferases KAT6A and KAT6B inhibitor WM-1119.
신호어
Warning
유해 및 위험 성명서
Hazard Classifications
Eye Irrit. 2 - Skin Irrit. 2
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
시험 성적서(COA)
제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.
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
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