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Merck

382111

Histone Acetyltransferase Inhibitor IV, CPTH2

Sinónimos:

Histone Acetyltransferase Inhibitor IV, CPTH2, HAT Inhibitor IV, Cyclopentylidene-(4-(4ʹ-chlorophenyl)thiazol-2-yl)hydrazone, GCN5 Inhibitor II, N-acetyltransferase 10 Inhibitor I, NAT10 Inhibitor I

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Fórmula empírica (notación de Hill):
C14H14ClN3S
Número CAS:
357649-93-5
Peso molecular:
291.80
Número MDL:
MFCD02307488
Código UNSPSC:
12352200
NACRES:
NA.54

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Ensayo

≥95% (HPLC)

Nivel de calidad

100

Formulario

solid

fabricante / nombre comercial

Calbiochem®

condiciones de almacenamiento

OK to freeze
protect from light

color

brown

solubilidad

DMSO: 50 mg/mL

Condiciones de envío

ambient

temp. de almacenamiento

2-8°C

InChI

1S/C14H14ClN3S/c15-11-7-5-10(6-8-11)13-9-19-14(16-13)18-17-12-3-1-2-4-12/h5-9H,1-4H2,(H,16,18)

Clave InChI

YYTHPXHGWSAKIZ-UHFFFAOYSA-N

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Este artículo
382110540211528111
Histone Acetyltransferase Inhibitor IV, CPTH2

Sigma-Aldrich

382111

Histone Acetyltransferase Inhibitor IV, CPTH2

Histone Acetyltransferase Inhibitor II The Histone Acetyltransferase Inhibitor II, also referenced under CAS 932749-62-7, controls the biological activity of Histone Acetyltransferase. This small molecule/inhibitor is primarily used for Cell Structure applications.

Sigma-Aldrich

382110

Histone Acetyltransferase Inhibitor II

PTP Inhibitor IV The PTP Inhibitor IV, also referenced under CAS 329317-98-8, controls the biological activity of PTP. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

Sigma-Aldrich

540211

PTP Inhibitor IV

PI 3-Kα Inhibitor IV The PI 3-Kα Inhibitor IV, also referenced under CAS 1188890-32-5, controls the biological activity of PI 3-Kα. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

Sigma-Aldrich

528111

PI 3-Kα Inhibitor IV

assay

≥95% (HPLC)

assay

≥97% (HPLC)

assay

≥95% (HPLC)

assay

≥95% (HPLC)

form

solid

form

solid

form

solid

form

solid

Quality Level

100

Quality Level

100

Quality Level

100

Quality Level

100

manufacturer/tradename

Calbiochem®

manufacturer/tradename

Calbiochem®

manufacturer/tradename

Calbiochem®

manufacturer/tradename

Calbiochem®

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

2-8°C

storage condition

OK to freeze, protect from light

storage condition

OK to freeze, protect from light

storage condition

OK to freeze, protect from light

storage condition

OK to freeze, desiccated (hygroscopic), protect from light

Descripción general

A cell-permeable thiazolyl-hydrazone compound that inhibits the acetylation of histone H3 by recombinant human Gcn5 in a substrate-competive manner, while exhibiting little activity against rhGcn5 autoacetylation. Although functional knockout of Gcn5 in Saccharomyces cerevisiae by genetic deletion or by CPTH2 treatment is not detrimental to the survival of the budding yeast, CPTH2 treatment is shown to inhibit the growth of yeast strain genetically deleted of Gcn5, but not strains deleted of Elp3 or Sas2.

Envase

Packaged under inert gas

Nota de preparación

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.

Otras notas

Larrieu, D., et al. 2014. Science, 344, 527.
Chimenti, F., et al. 2009. J. Med. Chem.52, 530.

Información legal

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

Cláusula de descargo de responsabilidad

Toxicity: Standard Handling (A)

Código de clase de almacenamiento

11 - Combustible Solids

Clase de riesgo para el agua (WGK)

nwg

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Cancer research communications, 2(6), 402-416 (2023-01-24)
The emergence of treatment resistance significantly reduces the clinical utility of many effective targeted therapies. Although both genetic and epigenetic mechanisms of drug resistance have been reported, whether these mechanisms are stochastically selected in individual tumors or governed by a

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White Paper - The Message in the Marks: Deciphering Cancer Epigenetics

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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