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Dokumente

SML1652

Sigma-Aldrich

RGFP966

≥98% (HPLC)

Synonym(e):

(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

Empirische Formel (Hill-System):
C21H19FN4O
CAS-Nummer:
1396841-57-8
Molekulargewicht:
362.40
MDL-Nummer:
MFCD26960954
UNSPSC-Code:
12352200
PubChem Substanz-ID:
329825992
NACRES:
NA.77

Qualitätsniveau

100

Assay

≥98% (HPLC)

Form

powder

Farbe

white to beige

Löslichkeit

DMSO: 20 mg/mL, clear

Lagertemp.

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+

InChIKey

BLVQHYHDYFTPDV-VCABWLAWSA-N

Biochem./physiol. Wirkung

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.

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Analysenzertifikate (COA)

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Sigma-Aldrich

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5-Aza-2′-Desoxycytidin

Trichostatin A ≥98% (HPLC), from Streptomyces sp.

Sigma-Aldrich

T8552

Trichostatin A

Quercetin ≥95% (HPLC), solid

Sigma-Aldrich

Q4951

Quercetin

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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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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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