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Merck
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주요 문서

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M5820

Sigma-Aldrich

M344

≥98% (HPLC), powder

동의어(들):

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

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About This Item

실험식(Hill 표기법):
C16H25N3O3
CAS Number:
251456-60-7
Molecular Weight:
307.39
MDL number:
MFCD03453554
UNSPSC 코드:
12352200
PubChem Substance ID:
329818022
NACRES:
NA.77

Quality Level

100

분석

≥98% (HPLC)

양식

powder

저장 조건

protect from light

색상

white to beige

solubility

DMSO: 10 mg/mL, clear

저장 온도

2-8°C

SMILES string

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)

InChI key

MXWDSZWTBOCWBK-UHFFFAOYSA-N

생화학적/생리학적 작용

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.

특징 및 장점

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.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable

가장 최신 버전 중 하나를 선택하세요:

시험 성적서(COA)

Lot/Batch Number
0000394760
0000394759
0000390803
0000390803
0000394760

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문서 라이브러리 방문

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
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
Jalila Chagraoui et al.
Cell stem cell, 28(1), 48-62 (2021-01-09)
Human hematopoietic stem cells (HSCs) exhibit attrition of their self-renewal capacity when cultured ex vivo, a process that is partially reversed upon treatment with epigenetic modifiers, most notably inhibitors of histone deacetylases (HDACs) or lysine-specific demethylase LSD1. A recent study showed
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
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
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Discover Bioactive Small Molecules for Gene Regulation

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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