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MC1742 Sale

目录号 : GC45906

An inhibitor of class I and class IIb HDACs

MC1742 Chemical Structure

Cas No.:1776116-74-5

规格 价格 库存 购买数量
1mg
¥340.00
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5mg
¥1,191.00
现货
10mg
¥2,039.00
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产品描述

MC1742 is an inhibitor of class I histone deacetylases (HDACs; IC50s = 0.1, 0.11, 0.02, and 0.61 μM for HDAC1, -2, -3, and -8, respectively) and class IIb HDACs (IC50s = 7 and 40 nM for HDAC6 and HDAC10, respectively).1 It is selective for class I and class IIb over class IIa HDACs (IC50s = >50 μM for HDAC4, -5, -7, and -9). MC1742 reduces proliferation of HOS, MG-63, RD, A204, SK-ES-1, and A673 sarcoma cancer stem cells (CSCs). It increases levels of acetylated histone H3 and acetylated tubulin and induces apoptosis in MG-63 CSCs when used at a concentration of 2 μM. MC1742 also reactivates HIV-1 in JLAT 10.6 latently infected cells (EC50 = 350 nM).2

|1. Di Pompo, G., Salerno, M., Rotili, D., et al. Novel histone deacetylase inhibitors induce growth arrest, apoptosis, and differentiation in sarcoma cancer stem cells. J. Med. Chem. 58(9), 4073-4079 (2015).|2. Heffern, E.F.W., Ramani, R., Marshall, G., et al. Identification of isoform-selective hydroxamic acid derivatives that potently reactivate HIV from latency. J. Virus Erad. 5(2), 84-91 (2019).

Chemical Properties

Cas No. 1776116-74-5 SDF
Canonical SMILES O=C1N=C(SCCCCC(NO)=O)NC(C(C=C2)=CC=C2C3=CC=CC=C3)=C1
分子式 C21H21N3O3S 分子量 395.5
溶解度 DMSO: 100 mM 储存条件 Store at -20°C
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1 mM 2.5284 mL 12.6422 mL 25.2845 mL
5 mM 0.5057 mL 2.5284 mL 5.0569 mL
10 mM 0.2528 mL 1.2642 mL 2.5284 mL
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Research Update

Identification of isoform-selective hydroxamic acid derivatives that potently reactivate HIV from latency

J Virus Erad 2019 Apr 1;5(2):84-91.PMID:31191911doi

Objectives: Current antiretroviral therapy can suppress HIV replication, increase CD4 count and result in increased lifespan. However, it cannot eradicate the virus due to the presence of latent provirus in cellular reservoirs, such as resting CD4+ T cells. Using combination latency-reversing agents to shock the virus out of latency for elimination through immune clearance or viral cytopathic effect is one of the most promising strategies for HIV eradication. Specifically, recent evidence shows that isoform-selective histone deacetylase inhibitors may be more effective than their non-selective counterparts. Therefore, identification and characterisation of new isoform-selective compounds are of prime importance. Here, we sought to determine the ability of two new isoform-targeted hydroxamic acid derivatives to reactivate HIV from latency. Methods: We used cell lines and infected primary resting CD4+ T cells. These were treated with these compounds with HIV reactivation measured using fluorescence-activated cell sorting, Western blots and luciferase luminescence. Isoform selectivity and acetylation of the HIV promoter were measured by Western blotting and chromatic immunoprecipitation. Results and conclusions: The two new hydroxamic acid derivatives, MC2625 and MC1742, potently reactivate HIV from latency. These compounds are isoform-selective histone deacetylate inhibitors that increase the levels of histone acetylation at the HIV promoter. In addition, they synergise effectively with the protein kinase C modulators bryostatin-1 and INDY, an inhibitor of the dual-specificity tyrosine phosphorylation regulated kinase 1A. We conclude that the combinations of new hydroxamic acid derivatives and bryostatin-1 or INDY could be a new tool for HIV reactivation in the cure efforts.

A potent HDAC inhibitor blocks Toxoplasma gondii tachyzoite growth and profoundly disrupts parasite gene expression

Int J Antimicrob Agents 2022 Mar;59(3):106526.PMID:35041939DOI:10.1016/j.ijantimicag.2022.106526.

Introduction: Toxoplasmosis is a major health issue worldwide, especially for immune-deficient individuals and the offspring of newly infected mothers. It is caused by a unicellular intracellular parasite called Toxoplasma gondii. Although the drugs commonly used to treat toxoplasmosis are efficient, they present serious side effects and adverse events are common. Therefore, there is a need for the discovery of new compounds with potent anti-Toxoplasma gondii activity. Methods: This study tested compounds designed to target enzymes that are involved in the epigenetic regulation of gene expression. Results: Among the most active compounds, an HDAC inhibitor showing an IC50 of 30 nM with a selectivity index above 100 was identified. MC1742 was active at inhibiting the growth of the parasite in vitro but also at preventing the consequences of the acute disease in vivo. This compound induced hyper-acetylation of histones, while the acetylated tubulin level remained unchanged. After MC1742 treatment, the parasite expression profile was profoundly changed with the activation of genes preferentially expressed in the sexual stages that are normally repressed in the tachyzoite stage. Conclusions: These findings suggest that this compound disturbs the Toxoplasma gondii gene expression program, inducing parasite death.

Novel histone deacetylase inhibitors induce growth arrest, apoptosis, and differentiation in sarcoma cancer stem cells

J Med Chem 2015 May 14;58(9):4073-9.PMID:25905694DOI:10.1021/acs.jmedchem.5b00126.

Musculoskeletal sarcomas are aggressive malignancies of bone and soft tissues often affecting children and adolescents. Histone deacetylase inhibitors (HDACi) have been proposed to counteract cancer stem cells (CSCs) in solid neoplasms. When tested in human osteosarcoma, rhabdomyosarcoma, and Ewing's sarcoma stem cells, the new HDACi MC1742 (1) and MC2625 (2) increased acetyl-H3 and acetyl-tubulin levels and inhibited CSC growth by apoptosis induction. At nontoxic doses, 1 promoted osteogenic differentiation. Further investigation with 1 will be done in preclinical sarcoma models.