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About This Item
Empirical Formula (Hill Notation):
C20H17FN2O4S
CAS Number:
Molecular Weight:
400.42
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
InChI
1S/C20H17FN2O4S/c1-13-10-15(14-6-3-2-4-7-14)11-18(19(13)21)20(25)22-23-28(26,27)17-9-5-8-16(24)12-17/h2-12,23-24H,1H3,(H,22,25)
InChI key
KVJFJJXCBRSCDY-UHFFFAOYSA-N
SMILES string
OC1=CC(S(NNC(C2=CC(C3=CC=CC=C3)=CC(C)=C2F)=O)(=O)=O)=CC=C1
assay
≥98% (HPLC)
form
powder
storage condition
protect from light
color
white to beige
solubility
DMSO: soluble
storage temp.
−20°C
Quality Level
Related Categories
Biochem/physiol Actions
Cell-permeable, potent, selective, Ac-CoA competitive and reversible inhibitor of HBO1, KAT6A, and TIP60 acetyltransferases
WM-3835is a cell-permeable hydroxybenzenesulfonohydrazide compound that acts as a potent, selective, Ac-CoA competitive and reversible inhibitor of HBO1, KAT6A, and TIP60 acetyltransferases (IC50 = 0.030, 0.017 and 0.312 µM, respectively). WM-3835 is non-cytotoxic, dose-dependently, and rapidly decreases H3K14Ac levels (IC50 = 0.341 µM) and inhibits AML cells growth (IC50 = 0.297 µM in Molm13). Induces apoptosis, downregulates HOXA and IL-6 expression and up-regulates ALB secretion and delays hepatocyte and hMPC senescence. WM-1385 potently inhibits POS-1 xenograft growth in SCID mice (10 mg/kg, i.p.).
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Regulatory Information
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Yan-Yang Gao et al.
Theranostics, 11(10), 4599-4615 (2021-03-24)
HBO1 (KAT7 or MYST2) is a histone acetyltransferase that acetylates H3 and H4 histones. Methods: HBO1 expression was tested in human OS tissues and cells. Genetic strategies, including shRNA, CRISPR/Cas9 and overexpression constructs, were applied to exogenously alter HBO1 expression
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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