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Merck
CN

382190

Histone Lysine Methyltransferase Inhibitor

The Histone Lysine Methyltransferase Inhibitor, also referenced under CAS 935693-62-2, controls the biological activity of Histone Lysine Methyltransferase. This small molecule/inhibitor is primarily used for Cancer applications.

Synonym(s):

Histone Lysine Methyltransferase Inhibitor, 2-(Hexahydro-4-methyl-1H-1,4-diazepin-1-yl)-6,7-dimethoxy-N-(1-(phenylmethyl)-4-piperidinyl)-4-quinazolinamine, BIX-01294, HMTase Inhibitor, EHMT2/G9a Inhibitor I, EHMT2/G9a Inhibitor I, HMTase Inhibitor, 2-(Hexahydro-4-methyl-1H-1,4-diazepin-1-yl)-6,7-dimethoxy-N-(1-(phenylmethyl)-4-piperidinyl)-4-quinazolinamine, BIX-01294

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About This Item

Empirical Formula (Hill Notation):
C28H38N6O2
CAS Number:
Molecular Weight:
490.64
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77
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Product Name

Histone Lysine Methyltransferase Inhibitor, The Histone Lysine Methyltransferase Inhibitor, also referenced under CAS 935693-62-2, controls the biological activity of Histone Lysine Methyltransferase. This small molecule/inhibitor is primarily used for Cancer applications.

SMILES string

N2(CCC(CC2)Nc3nc(nc5c3cc(c(c5)OC)OC)N4CCN(CCC4)C)Cc1ccccc1

InChI

1S/C28H38N6O2/c1-32-12-7-13-34(17-16-32)28-30-24-19-26(36-3)25(35-2)18-23(24)27(31-28)29-22-10-14-33(15-11-22)20-21-8-5-4-6-9-21/h4-6,8-9,18-19,22H,7,10-17,20H2,1-3H3,(H,29,30,31)

InChI key

OSXFATOLZGZLSK-UHFFFAOYSA-N

assay

≥97% (HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
protect from light

color

off-white

solubility

DMSO: 10 mg/mL
ethanol: 10 mg/mL

shipped in

ambient

storage temp.

−20°C

Quality Level

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Toxicity: Standard Handling (A)

General description

A cell-permeable diazepinyl-quinazolinamine, non-SAM (S-adenosylmethionine) analog-based HMTase (histone methyltransferase) inhibitor that selectively interferes with the G9a-catalyzed H3K9me2 (histone H3 Lys9 dimethylation) modification (IC50 = 1.7 µM) in a reversible manner. It inhibits the GLP-catalyzed H3K9me3 only at much higher concentrartions (IC50 = 38 µM) and exhibits little activity against H3 methylations catalyzed by other HMTases (PRMT1, SET7/9, ESET, SUV39H1). Shown to effectively synergize with Oct3/4 and Klf4 in inducing reprogramming of primary murine fetal NPCs (Neural Progenitor Cells) into iPS (induced Pluripotent Stem) cells without additional viral transduction of Sox2 and c-Myc.

Other Notes

Shi, Y., et al. 2008. Cell Stem Cell2, 525.
Kubicek, S., et al. 2007. Mol. Cell25, 473.

Packaging

Packaged under inert gas

Storage Class

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

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Cancer is a complex disease manifestation. At its core, it remains a disease of abnormal cellular proliferation and inappropriate gene expression. In the early days, carcinogenesis was viewed simply as resulting from a collection of genetic mutations that altered the gene expression of key oncogenic genes or tumor suppressor genes leading to uncontrolled growth and disease (Virani, S et al 2012). Today, however, research is showing that carcinogenesis results from the successive accumulation of heritable genetic and epigenetic changes. Moreover, the success in how we predict, treat and overcome cancer will likely involve not only understanding the consequences of direct genetic changes that can cause cancer, but also how the epigenetic and environmental changes cause cancer (Johnson C et al 2015; Waldmann T et al 2013). Epigenetics is the study of heritable gene expression as it relates to changes in DNA structure that are not tied to changes in DNA sequence but, instead, are tied to how the nucleic acid material is read or processed via the myriad of protein-protein, protein-nucleic acid, and nucleic acid-nucleic acid interactions that ultimately manifest themselves into a specific expression phenotype (Ngai SC et al 2012, Johnson C et al 2015). This review will discuss some of the principal aspects of epigenetic research and how they relate to our current understanding of carcinogenesis. Because epigenetics affects phenotype and changes in epigenetics are thought to be key to environmental adaptability and thus may in fact be reversed or manipulated, understanding the integration of experimental and epidemiologic science surrounding cancer and its many manifestations should lead to more effective cancer prognostics as well as treatments (Virani S et al 2012).

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