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M5820

Sigma-Aldrich

M344

≥98% (HPLC), powder

Sinônimo(s):

4-(Dimethylamino)-N-[7-(hydroxyamino)-7-oxoheptyl]-benzamide, MS 344, D237, N-Hydroxy-7-(4-dimethylaminobenzoyl)-aminoheptanamide

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About This Item

Fórmula empírica (Notação de Hill):
C16H25N3O3
Número CAS:
251456-60-7
Peso molecular:
307.39
Número MDL:
MFCD03453554
Código UNSPSC:
12352200
ID de substância PubChem:
329818022
NACRES:
NA.77

Ensaio

≥98% (HPLC)

Formulário

powder

condição de armazenamento

protect from light

cor

white to beige

solubilidade

DMSO: 10 mg/mL, clear

temperatura de armazenamento

2-8°C

cadeia de caracteres SMILES

CN(C)c1ccc(cc1)C(=O)NCCCCCCC(=O)NO

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)

chave InChI

MXWDSZWTBOCWBK-UHFFFAOYSA-N

Categorias relacionadas

Ações bioquímicas/fisiológicas

M344 is a HDAC inhibitor and subtype selective for HDAC6 over HDAC1.
M344 is a HDAC inhibitor; subtype selective for HDAC6 over HDAC1. M344 inhibits HDAC (IC50 = 100 nM) and also inhibits hyperacetylation of histone H4, terminal cell differentiation, transcription (γ-globin), and tumor cell death.

Características e benefícios

This compound is a featured product for Gene Regulation research. Click here to discover more featured Gene Regulation products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

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Certificados de análise (COA)

Lot/Batch Number
023M4732V
072M4713V
071M4773V
071M4727V
070M4718

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Yezhong Wang et al.
International journal of cancer, 145(9), 2496-2508 (2019-04-10)
JNK activity has been implicated in the malignant proliferation, invasion and drug-resistance of glioma cells (GCs), but the molecular mechanisms underlying JNK activation are currently unknown. Here, we reported that MKK7, not MKK4, directly activates JNK in GCs and exerts
R Pérez-Carro et al.
Clinical genetics, 86(2), 167-171 (2013-07-31)
Hereditary tyrosinemia type I (HT1) is a rare disease caused by a deficiency of fumarylacetoacetate hydrolase (FAH) in the tyrosine catabolic pathway, resulting mainly in hepatic alterations due to accumulation of the toxic metabolites fumarylacetoacetate, maleylacetoacetate and succinylacetone. We have
Weiwen He et al.
Oncotarget, 7(6), 6727-6747 (2016-01-07)
Activator protein 1 (AP-1) is a transcriptional factor composed of the dimeric members of bZIP proteins, which are frequently deregulated in human cancer cells. In this study, we aimed to identify an oncogenic AP-1 dimer critical for the proliferation of
Pakavarin Louphrasitthiphol et al.
Molecular cell, 79(3), 472-487 (2020-06-13)
It is widely assumed that decreasing transcription factor DNA-binding affinity reduces transcription initiation by diminishing occupancy of sequence-specific regulatory elements. However, in vivo transcription factors find their binding sites while confronted with a large excess of low-affinity degenerate motifs. Here, using
Christophe Decroos et al.
Biochemistry, 54(42), 6501-6513 (2015-10-16)
Cornelia de Lange Syndrome (CdLS) spectrum disorders are characterized by multiple organ system congenital anomalies that result from mutations in genes encoding core cohesin proteins SMC1A, SMC3, and RAD21, or proteins that regulate cohesin function such as NIPBL and HDAC8.
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Histone Modification and Chromatin Remodeling | Epigenetics

Epigenetic modifications are thought to occur through two key interconnected processes—DNA methylation and the covalent modification of histones.

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We offer a variety of small molecule research tools, such as transcription factor modulators, inhibitors of chromatin modifying enzymes, and agonists/antagonists for target identification and validation in gene regulation research; a selection of these research tools is shown below.

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