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NCDM-32B Sale

(Synonyms: N-(9-二甲基氨基-1-氧代壬基)-N-羟基-Β-丙氨酸甲酯) 目录号 : GC65138

NCDM-32B 是一种有效的选择性 KDM4 抑制剂,可抑制乳腺癌的生存能力和转化表型。

NCDM-32B Chemical Structure

Cas No.:1239468-48-4

规格 价格 库存 购买数量
5mg
¥2,340.00
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产品描述

NCDM-32B is a potent and selective KDM4 inhibitor that impaires viability and transforming phenotypes of breast cancer[1].

[1]. Ye Q, et al. Genetic alterations of KDM4 subfamily and therapeutic effect of novel demethylase inhibitor in breast cancer. Am J Cancer Res. 2015 Mar 15;5(4):1519-30.

Chemical Properties

Cas No. 1239468-48-4 SDF Download SDF
别名 N-(9-二甲基氨基-1-氧代壬基)-N-羟基-Β-丙氨酸甲酯
分子式 C15H30N2O4 分子量 302.41
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1 mM 3.3068 mL 16.5338 mL 33.0677 mL
5 mM 0.6614 mL 3.3068 mL 6.6135 mL
10 mM 0.3307 mL 1.6534 mL 3.3068 mL
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Research Update

Genetic alterations of KDM4 subfamily and therapeutic effect of novel demethylase inhibitor in breast cancer

Am J Cancer Res 2015 Mar 15;5(4):1519-30.PMID:26101715doi

The histone lysine demethylase KDM4 subfamily, comprised of four members (A, B, C, and D), play critical roles in controlling transcription, chromatin architecture and cellular differentiation. We previously demonstrated that KDM4C is significantly amplified and overexpressed in aggressive basal-like breast cancers and functions as a transforming oncogene. However, information regarding the genomic and transcriptomic alterations of the KDM4 subfamily in different subtypes of breast cancer remains largely incomplete. Here, we conducted a meta-analysis of KDM4A, B, C and D in breast cancer and identified associations among recurrent copy number alterations, gene expression and breast cancer subtypes. We demonstrated that KDM4A and D are also significantly overexpressed in basal-like breast cancer, whereas KDM4B overexpression is more dominant in estrogen-receptor-positive, luminal breast cancer. Next, we investigated the therapeutic potential of a novel histone demethylase inhibitor, NCDM-32B, in breast cancer. The treatment of basal breast cancer cell lines with NCDM-32B resulted in the decrease of cell viability and anchorage independent growth in soft agar. Furthermore, we found that NCDM-32B impaired several critical pathways that drive cellular proliferation and transformation in breast cancer. Our findings demonstrate genetic amplification and overexpression of the KDM4 demethylases in different subtypes of breast cancer. Furthermore, histone methylation is reversible and KDM4 demethylases are druggable targets. Thus, KDM4 inhibitors may serve as a novel therapeutic approach for a subset of aggressive breast cancer.

New BRAF knockin mice provide a pathogenetic mechanism of developmental defects and a therapeutic approach in cardio-facio-cutaneous syndrome

Hum Mol Genet 2014 Dec 15;23(24):6553-66.PMID:25035421DOI:10.1093/hmg/ddu376.

Cardio-facio-cutaneous (CFC) syndrome is one of the 'RASopathies', a group of phenotypically overlapping syndromes caused by germline mutations that encode components of the RAS-MAPK pathway. Germline mutations in BRAF cause CFC syndrome, which is characterized by heart defects, distinctive facial features and ectodermal abnormalities. To define the pathogenesis and to develop a potential therapeutic approach in CFC syndrome, we here generated new knockin mice (here Braf(Q241R/+)) expressing the Braf Q241R mutation, which corresponds to the most frequent mutation in CFC syndrome, Q257R. Braf(Q241R/+) mice manifested embryonic/neonatal lethality, showing liver necrosis, edema and craniofacial abnormalities. Histological analysis revealed multiple heart defects, including cardiomegaly, enlarged cardiac valves, ventricular noncompaction and ventricular septal defects. Braf(Q241R/+) embryos also showed massively distended jugular lymphatic sacs and subcutaneous lymphatic vessels, demonstrating lymphatic defects in RASopathy knockin mice for the first time. Prenatal treatment with a MEK inhibitor, PD0325901, rescued the embryonic lethality with amelioration of craniofacial abnormalities and edema in Braf(Q241R/+) embryos. Unexpectedly, one surviving pup was obtained after treatment with a histone 3 demethylase inhibitor, GSK-J4, or NCDM-32B. Combination treatment with PD0325901 and GSK-J4 further increased the rescue from embryonic lethality, ameliorating enlarged cardiac valves. These results suggest that our new Braf knockin mice recapitulate major features of RASopathies and that epigenetic modulation as well as the inhibition of the ERK pathway will be a potential therapeutic strategy for the treatment of CFC syndrome.