SML3159
WM-2474
≥98% (HPLC)
同義詞:
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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About This Item
推薦產品
品質等級
化驗
≥98% (HPLC)
形狀
powder
顏色
white to beige
溶解度
DMSO: 2 mg/mL, clear
儲存溫度
2-8°C
SMILES 字串
O=C(C1=C(F)C=CC(C2=CC=NN=C2)=C1)NNS(=O)(C3=CC=CC=C3)=O
InChI
1S/C17H13FN4O3S/c18-16-7-6-12(13-8-9-19-20-11-13)10-15(16)17(23)21-22-26(24,25)14-4-2-1-3-5-14/h1-11,22H,(H,21,23)
InChI 密鑰
WYMCVPPNOFFNGE-UHFFFAOYSA-N
生化／生理作用
Inactive analog of and negative control for the potent and selective, MYST family histone acetyltransferases KAT6A and KAT6B inhibitor WM-1119.
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.
訊號詞
Warning
危險聲明
危險分類
Eye Irrit. 2 - Skin Irrit. 2
儲存類別代碼
11 - Combustible Solids
水污染物質分類（WGK）
WGK 3
閃點（°F）
Not applicable
閃點（°C）
Not applicable
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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