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Principaux documents

475957

Sigma-Aldrich

c-Myc Inhibitor II

The c-Myc Inhibitor II, also referenced under CAS 413611-93-5, controls the biological activity of c-Myc.

Synonyme(s) :

c-Myc Inhibitor II, 7-Nitro-N-(2-phenylphenyl)-2,1,3-benzoxadiazol-4-amine, Biphenyl-2-yl-(7-nitrobenzo[1,2,5]oxadiazol-4-ylamine, 10074-G5

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About This Item

Formule empirique (notation de Hill):
C18H12N4O3
Numéro CAS:
Poids moléculaire :
332.31
Numéro MDL:
Code UNSPSC :
12352200

Niveau de qualité

Essai

≥95% (HPLC)

Forme

solid

Fabricant/nom de marque

Calbiochem®

Conditions de stockage

OK to freeze
protect from light

Couleur

deep orange

Solubilité

DMSO: 50 mg/mL

Conditions d'expédition

ambient

Température de stockage

2-8°C

InChI

1S/C18H12N4O3/c23-22(24)16-11-10-15(17-18(16)21-25-20-17)19-14-9-5-4-8-13(14)12-6-2-1-3-7-12/h1-11,19H

Clé InChI

KMJPYSQOCBYMCF-UHFFFAOYSA-N

Description générale

A cell-permeable benzoxadiazole compound that is shown to preferentially disrupt the interactions of c-Myc-Max, Mad1-Max, and Myf5-HEB, over those of 31 other pairs of HLH-, ZIP-, and HLH-ZIP-containing proteins. Similarly to 10058-F4 (Cat. No. 475956), 10074-G5 is shown to selectively inhibit the c-Myc-dependent growth of rat fibroblast cell line TGR1 and effectively suppress c-Myc-dependent transcription activity. Binding studies using various mutated and truncated c-Myc constructs reveal that 10074-G5 targets c-Myc helix-1 region between aa residues 363 and 381 (KD = 4.4 µM), while 10058-F4 interaction site is located within aa residues 402 through 412 (KD = 13 µM).
A cell-permeable benzoxadiazole compound that is shown to preferentially disrupt the interactions of c-Myc-Max, Mad1-Max, and Myf5-HEB, over those of 31 other pairs of HLH-, ZIP-, and HLH-ZIP-containing proteins. Similarly to 10058-F4 (Cat. No. 475956), 10074-G5 is shown to selectively inhibit the c-Myc-dependent growth of rat fibroblast cell line TGR1 and effectively suppress c-Myc-dependent transcription activity. Binding studies using various mutated and truncated c-Myc constructs reveal that 10074-G5 targets c-Myc helix-1 region between aa 363 and 381 (KD = 4.4 µM), while 10058-F4 interaction site is located within aa residues 402 through 412 (KD = 13 µM).

Conditionnement

Packaged under inert gas

Avertissement

Toxicity: Standard Handling (A)

Reconstitution

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Autres remarques

Follis, A.V., et al. 2008. Chem. Biol.15, 1149.
Yin, X., et al. 2003. Oncogene22, 6151.

Sold under license of U.S. Patent 7,026,343.

Informations légales

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

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Consulter la Bibliothèque de documents

Yue-Zhi Lee et al.
Pharmacological research, 152, 104581-104581 (2019-12-04)
Interruption of the Warburg effect - the observation that un-stimulated macrophages reprogram their core metabolism from oxidative phosphorylation toward aerobic glycolysis to become pro-inflammatory M1 macrophages upon stimulation - is an emerging strategy for the treatment of cancer and anti-inflammatory
Batuhan Mert Kalkan et al.
Microvascular research, 130, 104001-104001 (2020-03-22)
Endothelial dysfunction is prominent in atherosclerosis, hypertension, diabetes, peripheral and cardiovascular diseases, and stroke. Novel therapeutic approaches to these conditions often involve development of tissue-engineered veins with ex vivo expanded endothelial cells. However, high cell number requirements limit these approaches
Ashutosh Singh et al.
The Journal of biological chemistry, 297(1), 100903-100903 (2021-06-23)
c-Myc is a transcription factor that plays a crucial role in cellular homeostasis, and its deregulation is associated with highly aggressive and chemotherapy-resistant cancers. After binding with partner MAX, the c-Myc-MAX heterodimer regulates the expression of several genes, leading to

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