| 包装 | 价格(元) |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
Preparation Method | For inhibitor compound testing,Specifically, 5 μL of 5 nM HDAC9 in assay buffer was added to the plates with 100 nL of compounds at various concentration predispensed in 100% DMSO.The final concentrations of HDAC9 and class IIa HDAC substrate in the plate were 2.5 nM and 4.5 μM, respectively. After incubation for 45 min at room temperature, 10 mL of 2 developer solution was added per well. |
Reaction Conditions | 10 mM TMP195 ( final concentration)for 45min |
Applications | TMP195 is a selective class IIa histone deacetylase (HDAC) inhibitor with Kis of 59, 60, 26, 15 nM for HDAC4, HDAC5, HDAC7 and HDAC9, respectively. |
Cell lines | Human monocytes |
Preparation Method | Monocytes were differentiated into antigen presenting cells in medium with penicillin and streptomycin in the presence of 0.1% (v/v) DMSO or 300 nM TMP195 for 5 days. |
Reaction Conditions | 300 nM TMP195 for 5 days |
Applications | TMP195 promotes the differentiation of human monocytes into antigen presenting cells with IL-4 and GM-CSF in vitro.· |
Animal models | Mmtv-pymt transgenic mice |
Preparation Method | Mice were treated with intraperitoneal (i.p.) injections of 50 μl of the vehicle dimethyl sulfoxide (DMSO) or 50 μl of TMP195 dissolved in 100% DMSO at a final concentration of 50 mg per kg daily. |
Dosage form | 50 mg /kg TMP195 for two weeks（Intraperitoneal injection＿/p> |
Applications | TMP195 reduces tumor burden and lung metastasis in vivo by regulating macrophage phenotype, changing tumor microenvironment. TMP195 induces recruitment and differentiation of highly phagocytic and stimulating macrophages within tumors. TMP195 significantly reduces proliferating tumor cells, especially in the leading edge of tumor. Induction of antitumor macrophages by TMP195 has been shown to enhance the efficacy and persistence of standard chemotherapy regimens and checkpoint blockade immunotherapy in a murine model of breast cancer |
| 产品描述 | TMP195 is a potent and selective class IIa HDAC inhibitor with IC50s of 59 nM, 60 nM, 26 nM and 15 nM for HDAC4, HDAC5, HDAC7 and HDAC9, respectively[1]. TMP195 promotes the differentiation of human monocytes into antigen presenting cells with IL-4 and GM-CSF in vitro[2]. In renal tubular cell,TMP195 inhibited LPS-induced upregulation of multiple proinflammatory cytokines/chemokines, including intercellular adhesion molecule-1, monocyte chemoattractant protein-1, tumor necrosis factor-α, and interleukin-1β, and accumulation of inflammatory cells in the injured kidney[3]. As a potent and selective inhibitor of class IIa histone deacetylase, In vitro TMP195 treatment significantly enhances drug-induced apoptosis and sensitizes multidrug-resistant cancer cells overexpressing ABCB1 or ABCG2 to anticancer drugs[5].TMP195 enhances phagocytic responses to antibody-opsonised CLL cells and E. coli within 30 min of treatment. The enhanced response is phenocopied by knockdown of the Class IIa HDAC, HDAC7, or by low concentrations of the pan-HDAC inhibitor, vorinostat[6]. TMP195 reduces tumor burden and lung metastasis in vivo by regulating macrophage phenotype, changing tumor microenvironment. TMP195 induces recruitment and differentiation of highly phagocytic and stimulating macrophages within tumors. TMP195 significantly reduces proliferating tumor cells, especially in the leading edge of tumor[2].In mice,Pharmacological inhibition of HDAC9 with the class IIa HDAC inhibitor TMP195 attenuates lesion formation by reducing endothelial activation and leukocyte recruitment along with limiting proinflammatory responses in macrophages[4].In C57BL/6J mice, Treatment of L6 myotubes with HDAC inhibitors TMP195 or skeletal muscle with a combination of HDAC and sirtuin inhibitors increased tubulin and pan-protein acetylation, demonstrating effective impairment of HDAC and sirtuin deacetylase activities[7]. References: |
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