目录号 | 产品详情 | 靶点 | |
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T79689 | Sirtuin | ||
SIRT6-IN-3 (compound 8a) 作为SIRT6的选择性抑制剂,其IC50值为7.49 μM。该化合物能有效抑制胰腺导管腺癌 (PDAC) 细胞的增殖,并诱导细胞凋亡。SIRT6-IN-3 通过抑制 DNA 损伤的修复作用,增强了吉西他滨对癌细胞的敏感性,常用于胰腺癌相关研究。 | |||
T12455 | PI3K | ||
PI3K/HDAC-IN-1 is a potent PI3K and HDAC dual inhibitor(IC50s of 8.1 nM and 1.4 nM, respectively). | |||
T74783 | HDAC | ||
HDAC-IN-53是一种口服活性的选择性HDAC1-3抑制剂,其IC50分别为47 nM、125 nM和450 nM。该化合物不针对II类HDAC(HDAC4、5、6、7、9;IC50>10 μM)展现抑制作用。HDAC-IN-53能够诱导caspase依赖的细胞凋亡并在裸鼠中显著抑制人肿瘤异种移植物生长,同时抑制携带MC38结肠癌的免疫活性小鼠的肿瘤发展。 | |||
T36629 | |||
Givinostat (ITF-2357) is a HDAC inhibitor with an IC50 of 198 and 157 nM for HDAC1 and HDAC3, respectively. Givinostat (ITF2357) suppresses total LPS-induced IL-1β production robustly compared with the reduction by ITF3056. At 25, 50, and 100 nM, Givinostat reduced IL-1β secretion more than 70%. Givinostat (ITF-2357) suppresses the production of IL-6 in PBMCs stimulated with TLR agonists as well as the combination of IL-12 plus IL-18. IL-6 secretion decreases to 50% at 50 nM Givinostat, but at 100 and 200 nM, there is no reduction[1]. As shown by the CCK-8 assay, Givinostat (ITF-2357) inhibits JS-1 cell proliferation in a concentration-dependent manner. Treatment with Givinostat ≥500 nM is associated with significant inhibition of JS-1 cell proliferation (P<0.01). Also, the cell inhibition rate significantly differs between the group cotreated with Givinostat ≥250 nM plus LPS and the group without LPS treatment (same Givinostat concentration) (P<0.05)[2]. Givinostat (ITF2357) at 10 mg/kg is used as a positive control and, as expected, reduced serum TNFα by 60%. Strikingly, pretreatment of ITF3056 starting at 0.1 mg/kg significantly reduces the circulating TNFα by nearly 90%. To achieve a significant increase in serum IL-1β production, a higher dose of LPS is injected (10 mg/kg), and blood is collected after 4 h. Similarly, when pretreated with lower doses of Givinostat (ITF-2357) (1 or 5 mg/kg), there is a 22% reduction for 1 mg/kg and 40% for 5 mg/kg[1]. [1]. Li S, et al. Specific inhibition of histone deacetylase 8 reduces gene expression and production of proinflammatory cytokines in vitro and in vivo. J Biol Chem. 2015 Jan 23;290(4):2368-78. [2]. Wang YG, et al. Givinostat inhibition of hepatic stellate cell proliferation and protein acetylation. World J Gastroenterol. 2015 Jul 21;21(27):8326-39. [3]. Leoni F, et al. The histone deacetylase inhibitor ITF2357 reduces production of pro-inflammatory cytokines in vitro and systemic inflammation in vivo. Mol Med. 2005 Jan-Dec;11(1-12):1-15. |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-02317 | HDAC8 Protein, Mouse, Recombinant (His) | Mouse | Baculovirus-Insect Cells | ||
Histone deacetylase 8, also known as HDAC8 and HDACL1, is a nucleus and cytoplasm protein that belongs to the histone deacetylase family and HD type 1 subfamily. Histone deacetylases (HDACs) are a growing family of enzymes implicated in transcriptional regulation by affecting the acetylation state of core histones in the nucleus of cells. HDAC8 / HDACL1 is weakly expressed in most tissues. It is expressed at a higher level in the heart, brain, kidney, and pancreas and also in the liver, lung, placenta, prostate, and kidney. HDAC8 / HDACL1 is responsible for the deacetylation of lysine residues on the N-terminal part of the core histones ( H2A, H2B, H3, and H4 ). Histone deacetylation gives a tag for epigenetic repression and plays an important role in transcriptional regulation, cell cycle progression, and developmental events. Histone deacetylases act via the formation of large multiprotein complexes. HDAC8 / HDACL1 may play a role in smooth muscle cell contractility. HDAC8 / HDACL1 may be a potential drug target for neuroblastoma differentiation therapy using selective inhibitors, avoiding unspecific side effects.
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TMPY-01333 | HDAC8 Protein, Human, Recombinant (GST) | Human | Baculovirus-Insect Cells | ||
Histone deacetylase 8, also known as HDAC8 and HDACL1, is a nucleus and cytoplasm protein that belongs to the histone deacetylase family and HD type 1 subfamily. Histone deacetylases (HDACs) are a growing family of enzymes implicated in transcriptional regulation by affecting the acetylation state of core histones in the nucleus of cells. HDAC8 / HDACL1 is weakly expressed in most tissues. It is expressed at a higher level in the heart, brain, kidney, and pancreas and also in the liver, lung, placenta, prostate, and kidney. HDAC8 / HDACL1 is responsible for the deacetylation of lysine residues on the N-terminal part of the core histones ( H2A, H2B, H3, and H4 ). Histone deacetylation gives a tag for epigenetic repression and plays an important role in transcriptional regulation, cell cycle progression, and developmental events. Histone deacetylases act via the formation of large multiprotein complexes. HDAC8 / HDACL1 may play a role in smooth muscle cell contractility. HDAC8 / HDACL1 may be a potential drug target for neuroblastoma differentiation therapy using selective inhibitors, avoiding unspecific side effects.
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