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178276

Apicidin, Fusarium sp.

A potent, cell-permeable inhibitor of histone deacetylase (IC50= 700 pM for parasitic histone deactetylase) that also exibits antiprotozoal and potential anti-malarial properties.

Synonym(e):

Apicidin, Fusarium sp., cyclo-[L-(2-Amino-8-oxodecanoyl)-L-(N-methoxytryptophan)-L-isoleucyl-D-pipecolinyl], HDAC Inhibitor XI

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PackungsgrößeSKUVerfügbarkeitPreis
1 mg
Warenkorb auf Verfügbarkeit prüfen
€ 175,00
5 mg
Warenkorb auf Verfügbarkeit prüfen
€ 411,00

Über diesen Artikel

Empirische Formel (Hill-System):
C34H49N5O6
Molekulargewicht:
623.78
NACRES:
NA.77
UNSPSC Code:
12352200
Assay:
≥95% (HPLC)
Form:
solid
Quality level:
Storage condition:
OK to freeze, protect from light

€ 175,00


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Quality Level

assay

≥95% (HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze, protect from light

color

white

solubility

DMSO: 50 mg/mL, ethanol: soluble

shipped in

ambient

storage temp.

−20°C

Biochem/physiol Actions

Cell permeable: yes
Product does not compete with ATP.
Reversible: no

Packaging

Packaged under inert gas

Other Notes

Due to the nature of the Hazardous Materials in this shipment, additional shipping charges may be applied to your order. Certain sizes may be exempt from the additional hazardous materials shipping charges. Please contact your local sales office for more information regarding these charges.

Legal Information

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

Disclaimer

Toxicity: Highly Toxic (H)

Lagerklasse

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Verwandter Inhalt

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).

Global Trade Item Number

SKUGTIN
178276-5MG04055977222418
178276-1MG04055977222401

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