475957
c-Myc Inhibitor II
The c-Myc Inhibitor II, also referenced under CAS 413611-93-5, controls the biological activity of c-Myc.
别名:
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
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
InChI key
KMJPYSQOCBYMCF-UHFFFAOYSA-N
assay
≥95% (HPLC)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze, protect from light
color
deep orange
solubility
DMSO: 50 mg/mL
shipped in
ambient
Quality Level
General description
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).
Packaging
Packaged under inert gas
Preparation Note
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
Other Notes
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.
Yin, X., et al. 2003. Oncogene22, 6151.
Sold under license of U.S. Patent 7,026,343.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Toxicity: Standard Handling (A)
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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
我们的科学家团队拥有各种研究领域经验，包括生命科学、材料科学、化学合成、色谱、分析及许多其他领域.
联系客户支持