所有图片(1)
别名:
(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
经验公式（希尔记法）:
C21H19FN4O
推荐产品
质量水平
检测方案
≥98% (HPLC)
形式
powder
颜色
white to beige
溶解性
DMSO: 20 mg/mL, clear
储存温度
2-8°C
SMILES字符串
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
生化/生理作用
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.
WGK
WGK 3
Epigenetics in Human Disease, 1110-1110 (2018)
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
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)
Targeting histone acetylation dynamics and oncogenic transcription by catalytic P300/CBP inhibition.
Simon J Hogg et al.
Molecular cell, 81(10), 2183-2200 (2021-05-22)
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
Ava C Carter et al.
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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