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SML1652

Sigma-Aldrich

RGFP966

≥98% (HPLC)

Synonym(s):

(2E)-N-(2-Amino-4-fluorophenyl)-3-[(2E)-1-(3-phenyl-2-propen-1-yl)-1H-pyrazol-4-yl]-2-propenamide, (E)-N-(2-amino-4-fluorophenyl)-3-(1-cinnamyl-1H-pyrazol-4-yl)acrylamide, RGFP 966

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About This Item

Empirical Formula (Hill Notation):
C21H19FN4O
CAS Number:
1396841-57-8
Molecular Weight:
362.40
MDL number:
MFCD26960954
UNSPSC Code:
12352200
PubChem Substance ID:
329825992
NACRES:
NA.77

Quality Level

100

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 20 mg/mL, clear

storage temp.

2-8°C

SMILES string

NC1=CC(F)=CC=C1NC(/C=C/C(C=N2)=CN2C/C=C/C3=CC=CC=C3)=O

InChI

1S/C21H19FN4O/c22-18-9-10-20(19(23)13-18)25-21(27)11-8-17-14-24-26(15-17)12-4-7-16-5-2-1-3-6-16/h1-11,13-15H,12,23H2,(H,25,27)/b7-4+,11-8+

InChI key

BLVQHYHDYFTPDV-VCABWLAWSA-N

Biochem/physiol Actions

RGFP966 changes signal-specific primary auditory cortical plasticity. It is highly effective in cardiomyopathy-associated pathologies.
RGFP966 is a selective inhibitor of histone deacetylase 3 (HDAC3) with an IC50 value of 80 nM and no inhibition of any other HDACs at concentrations up to 15 μM. In mouse studies, RGFP966 facilitated extinction of cocaine-seeking behavior and enhanced long-term object memory acquisition and consolidation. In a rat study, RGFP966 ameliorated amyloid-β oligomer-induced synaptic plasticity impairment. RGFP966 was also found to reduce proliferation and inducd differentiation in mouse lymphoid and myeloid malignancies.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Certificates of Analysis (COA)

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Tunicamycin enhances the antitumor activity of trastuzumab on breast cancer in vitro and in vivo.
Bieszczad KM, et al.
The Journal of Neuroscience, 35(38), 13124-13132 (2015)
Anto Sam Crosslee Louis Sam Titus et al.
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Histone deacetylase-3 (HDAC3) promotes neurodegeneration in various cell culture and in vivo models of neurodegeneration but the mechanism by which HDAC3 exerts neurotoxicity is not known. HDAC3 is known to be a transcriptional co-repressor. The goal of this study was
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To separate causal effects of histone acetylation on chromatin accessibility and transcriptional output, we used integrated epigenomic and transcriptomic analyses following acute inhibition of major cellular lysine acetyltransferases P300 and CBP in hematological malignancies. We found that catalytic P300/CBP inhibition
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eLife, 9 (2020-05-08)
The Xist lncRNA mediates X chromosome inactivation (XCI). Here we show that Spen, an Xist-binding repressor protein essential for XCI , binds to ancient retroviral RNA, performing a surveillance role to recruit chromatin silencing machinery to these parasitic loci. Spen
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