貨號	規(guī)格	價格	上海	北京	武漢	南京
S82976-5mg	98.0%	￥456.00 S82976-5mg ￥456.00 現(xiàn)貨	1 1	-	-	-
S82976-10mg	98.0%	￥696.00 S82976-10mg ￥696.00 現(xiàn)貨	5 5	-	-	-
S82976-25mg	98.0%	￥1280.00 S82976-25mg ￥1280.00 現(xiàn)貨	6 6	-	-	-
S82976-100mg	≥98%	￥3760.00 S82976-100mg ￥3760.00 2-3天	0 貨期：2-3天	-	-	-

產(chǎn)品介紹

RGFP966 is an HDAC3 inhibitor (IC50: 0.08 μM) and does not affect other HDACs at concentrations up to 15 μM.

產(chǎn)品描述：

RGFP966 is an HDAC3 inhibitor (IC50: 0.08 μM) and does not affect other HDACs at concentrations up to 15 μM.

靶點：

HDAC

體外研究：

RGFP966 is specific for HDAC3 (IC50: 0.08 μM) and no effective inhibition of any other HDAC at concentrations up to 15 μM. In LPS/IFNγ-stimulated RAW 264.7 macrophages treatment with RGFP966 did not change the expression of the genes TNFα, iNOS, and IL-10 but provided a significant downregulation of the expression of the pro-inflammatory genes IL-1β, IL-6 and IL-12b. RGFP966 resulted in decreased cell growth in CTCL cell lines due to increased apoptosis that was associated with DNA damage and impaired S phase progression

體內(nèi)研究：

All mice exhibited a robust preference for the cocaine-paired context after cocaine-conditioned place preference (CPP) training. Treatment with RGFP966 (3 or 10 mg/kg, s.c.)immediately after the drug-free preference tests resulted in significant extinction of CPP on posttest 2 and posttest 3. Treatment with 10 mg/kg, but not with 3 mg/kg, resulted in a significantly rapid reduction of CPP on the subsequent days. RGFP966 at doses of 10 and 25 mg/kg improves motor deficits on rotarod and in open field exploration, accompanied by neuroprotective effects on striatal volume

細胞實驗：

To investigate the influence of the HDAC 3-selective inhibitor RGFP966 on cell viability, RAW 264.7 macrophages, HBE cells and hASM cells were seeded in 96-well plates. To obtain identical cell density at the start of the experiments, RAW 264.7 macrophages were seeded at 25,000 cells/cm2, HBE cells and hASM cells were seeded at 70% confluency (based on surface area) and were serum-starved for 24 h prior incubation with RGFP966. Shortly before incubation with RGFP966, the medium was replaced by 100 μl fresh (if appropriate serum free) culture medium. Incubations with LPS and IFNγ were performed as described for HDAC 1–3 downregulation by siRNA. After 20 h of incubation with RGFP966, 20 μl of CellTiter 96 AQueous One Solution reagent was added to each well and incubated at 37 °C for 1 h in the dark. The absorbance at 490 nm was measured using a Synergy H1 plate reader. LPS/IFNγ-stimulated cells without addition of RGFP966 were considered 100%

動物實驗：

Subthreshold training and a 24-h retention test for location-dependent object recognition memory (OLM) and novel object recognition memory (ORM) were performed as described previously. Mice received an injection of RGFP966 (3, 10, or 30 mg/kg s.c) or vehicle alone either 1 h before or immediately after a 3-min training seeion

參考文獻：

1. Jia H, et al. The Effects of Pharmacological Inhibition of Histone Deacetylase 3 (HDAC3) in Huntington's Disease Mice. PLoS One. 2016 Mar 31;11(3):e0152498. 2. Leus NG, et al. HDAC 3-selective inhibitor RGFP966 demonstrates anti-inflammatory properties in RAW 264.7 macrophages and mouse precision-cut lung slices by attenuating NF-κB p65 transcriptional activity. Biochem Pharmacol. 2016 May 15;108:58-74. 3. Wells CE, et al. Inhibition of histone deacetylase 3 causes replication stress in cutaneous T cell lymphoma. PLoS One. 2013 Jul 22;8(7):e68915. 4. Malvaez M, et al. HDAC3-selective inhibitor enhances extinction of cocaine-seeking behavior in a persistent manner. Proc Natl Acad Sci U S A. 2013 Feb 12;110(7):2647-52.

溶解性：

Soluble in DMSO

保存條件：

-20℃

配置溶液濃度參考：

	1mg	5mg	10mg
1 mM	2.759 ml	13.797 ml	27.594 ml
5 mM	0.552 ml	2.759 ml	5.519 ml
10 mM	0.276 ml	1.38 ml	2.759 ml
50 mM	0.055 ml	0.276 ml	0.552 ml

注意：

部分產(chǎn)品我司僅能提供部分信息，我司不保證所提供信息的權(quán)威性，僅供客戶參考交流研究之用。

參考文獻(1篇)

1. [IF=5.486] Hao Zhang et al."Acetylation stabilizes the signaling protein WISP2 by preventing its degradation to suppress the progression of acute myeloid leukemia."JOURNAL OF BIOLOGICAL CHEMISTRY.2023 Feb;:102971

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