M5820

M344

Name: M344
Brand: SIGMA

≥98% (HPLC), HDAC inhibitor, powder

Synonym(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

Empirical Formula (Hill Notation):

C₁₆H₂₅N₃O₃

CAS Number:

251456-60-7

Molecular Weight:

307.39

UNSPSC Code:

12352200

PubChem Substance ID:

329818022

NACRES:

NA.77

MDL number:

MFCD03453554

Product Name

M344, ≥98% (HPLC), powder

SMILES string

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

InChI key

MXWDSZWTBOCWBK-UHFFFAOYSA-N

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)

assay

≥98% (HPLC)

form

powder

storage condition

protect from light

color

white to beige

solubility

DMSO: 10 mg/mL, clear

storage temp.

2-8°C

Quality Level

100

Related Categories

Bioactive Small Molecule Inhibitors

Bioactive Small Molecules

Biochem/physiol Actions

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.

Features and Benefits

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

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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MKK7 transcription positively or negatively regulated by SP1 and KLF5 depends on HDAC4 activity in glioma.

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

UM171 Preserves Epigenetic Marks that Are Reduced in Ex Vivo Culture of Human HSCs via Potentiation of the CLR3-KBTBD4 Complex.

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

Tuning Transcription Factor Availability through Acetylation-Mediated Genomic Redistribution.

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

Functional analysis and in vitro correction of splicing FAH mutations causing tyrosinemia type I.

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

HDAC inhibitors suppress c-Jun/Fra-1-mediated proliferation through transcriptionally downregulating MKK7 and Raf1 in neuroblastoma cells.

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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