M344 - CAS 251456-60-7
Catalog number: 251456-60-7
Category: Inhibitor
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Molecular Formula:
C16H25N3O3
Molecular Weight:
307.39
COA:
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Targets:
HDAC
Description:
M344 is a potent HDAC inhibitor, which can also induced expression of the pro-apoptotic genes, Puma and Bax, together with the morphological features of apoptosis, in MCF-7 cells.
Purity:
>98%
Synonyms:
M344; M 344; M-344
MSDS:
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InChIKey:
MXWDSZWTBOCWBK-UHFFFAOYSA-N
InChI:
InChI=1S/C16H25N3O3/c1-19(2)14-10-8-13(9-11-14)16(21)17-12-6-4-3-5-7-15(20)18-22/h8-11,22H,3-7,12H2,1-2H3,(H,17,21)(H,18,20)
Canonical SMILES:
CN(C)C1=CC=C(C=C1)C(=O)NCCCCCCC(=O)NO
1.Rapid Identification of Potential Drugs for Diabetic Nephropathy Using Whole-Genome Expression Profiles of Glomeruli.
Shi J1, Jiang S1, Qiu D1, Le W1, Wang X1, Lu Y1, Liu Z1. Biomed Res Int. 2016;2016:1634730. doi: 10.1155/2016/1634730. Epub 2016 Mar 16.
Objective. To investigate potential drugs for diabetic nephropathy (DN) using whole-genome expression profiles and the Connectivity Map (CMAP). Methodology. Eighteen Chinese Han DN patients and six normal controls were included in this study. Whole-genome expression profiles of microdissected glomeruli were measured using the Affymetrix human U133 plus 2.0 chip. Differentially expressed genes (DEGs) between late stage and early stage DN samples and the CMAP database were used to identify potential drugs for DN using bioinformatics methods. Results. (1) A total of 1065 DEGs (FDR < 0.05 and fold change > 1.5) were found in late stage DN patients compared with early stage DN patients. (2) Piperlongumine, 15d-PGJ2 (15-delta prostaglandin J2), vorinostat, and trichostatin A were predicted to be the most promising potential drugs for DN, acting as NF-κB inhibitors, histone deacetylase inhibitors (HDACIs), PI3K pathway inhibitors, or PPARγ agonists, respectively.
2.Histone deacetylase inhibitor-induced cell death in bladder cancer is associated with chromatin modification and modifying protein expression: A proteomic approach.
Li QQ1, Hao JJ2, Zhang Z2, Hsu I1, Liu Y2, Tao Z2, Lewi K1, Metwalli AR1, Agarwal PK1. Int J Oncol. 2016 Apr 7. doi: 10.3892/ijo.2016.3478. [Epub ahead of print]
The Cancer Genome Atlas (TCGA) project recently identified the importance of mutations in chromatin remodeling genes in human carcinomas. These findings imply that epigenetic modulators might have a therapeutic role in urothelial cancers. To exploit histone deacetylases (HDACs) as targets for cancer therapy, we investigated the HDAC inhibitors (HDACIs) romidepsin, trichostatin A, and vorinostat as potential chemotherapeutic agents for bladder cancer. We demonstrate that the three HDACIs suppressed cell growth and induced cell death in the bladder cancer cell line 5637. To identify potential mechanisms associated with the anti-proliferative and cytotoxic effects of the HDACIs, we used quantitative proteomics to determine the proteins potentially involved in these processes. Our proteome studies identified a total of 6003 unique proteins. Of these, 2472 proteins were upregulated and 2049 proteins were downregulated in response to HDACI exposure compared to the untreated controls (P<0.
3.Photoorganocatalytic One-Pot Synthesis of Hydroxamic Acids from Aldehydes.
Papadopoulos GN1, Kokotos CG2. Chemistry. 2016 Apr 1. doi: 10.1002/chem.201600333. [Epub ahead of print]
An efficient one-pot synthesis of hydroxamic acids from aldehydes and hydroxylamine is described. A fast, visible-light-mediated metal-free hydroacylation of dialkyl azodicarboxylates was used to develop the subsequent addition of hydroxylamine hydrochloride. A range of aliphatic and aromatic aldehydes were employed in this reaction to give hydroxamic acids in high to excellent yields. Application of the current methodology was demonstrated in the synthesis of the anticancer medicine vorinostat.
4.Molecular profiling of a case of advanced pancreatic cancer identifies an active and tolerable combination of targeted therapy with backbone chemotherapy.
Johnson B1, Vanderwalde A1, Javadi N1, Feldman R1, Reddy SB1. J Gastrointest Oncol. 2016 Apr;7(2):E6-E12. doi: 10.3978/j.issn.2078-6891.2015.091.
Typical survival with common 1(st)-line regimens for pancreatic cancer range from 6-11 months. We report a case of a patient with stage IVB pancreatic adenocarcinoma treated with gemcitabine and erlotinib who stopped therapy after 3 months without achieving a response due to intolerance. To decide upon additional treatment options, molecular analysis was performed on liver metastasis which revealed KRAS, FBXW7, APC, and ATM mutations, with thymidylate synthase (TS) negativity and PD-1 positivity. Based on this profile of TS negativity and ATM mutation, a combination strategy was devised consisting of capecitabine, oxaliplatin, bevacizumab and vorinostat. The patient had a near complete response to therapy with this regimen. In refractory metastatic pancreatic cancer, responses of this magnitude are rarely seen. To our knowledge, this represents the first demonstrated activity of this combination in the metastatic setting which could prompt further investigation of its use in large scale clinical trials.
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CAS 251456-60-7 M344

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