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Merck

SML1652

RGFP966

≥98% (HPLC), Thyroid hormone, powder

동의어(들):

(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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제품정보 (DICE 배송 시 비용 별도)

실험식(Hill 표기법):
C21H19FN4O
CAS 번호:
Molecular Weight:
362.40
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
Assay:
≥98% (HPLC)
Form:
powder
Quality level:
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제품 이름

RGFP966, ≥98% (HPLC)

Quality Level

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 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.
RGFP966 is a selective inhibitor of histone deacetylase 3 (HDAC3).
RGFP966 changes signal-specific primary auditory cortical plasticity. It is highly effective in cardiomyopathy-associated pathologies.


저장 등급

11 - Combustible Solids

wgk

WGK 3



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문서 라이브러리에서 최근에 구매한 제품에 대한 문서를 찾아보세요.

문서 라이브러리 방문



Epigenetics in Human Disease, 1110-1110 (2018)
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.
BMC neuroscience, 20(1), 65-65 (2019-12-31)
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