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G3798

Sigma-Aldrich

10074-G5

≥98% (HPLC)

Synonyme(s) :

Biphenyl-2-yl-(7-nitrobenzo[1,2,5]oxadiazol-4-yl)amine, N-2-Biphenylyl-7-nitro-2,1,3-benzoxadiazol-4-amine, N-[1,1′-Biphenyl-2-yl]-7-nitro-2,1,3-Benzoxadiazol-4-amine

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About This Item

Formule empirique (notation de Hill):
C18H12N4O3
Numéro CAS:
413611-93-5
Poids moléculaire :
332.31
Numéro MDL:
MFCD00576774
Code UNSPSC :
12352200
ID de substance PubChem :
329799918
Nomenclature NACRES :
NA.77

Niveau de qualité

100

Pureté

≥98% (HPLC)

Forme

powder

Couleur

red

Solubilité

DMSO: >10 mg/mL

Température de stockage

room temp

Chaîne SMILES 

[O-][N+](=O)c1ccc(Nc2ccccc2-c3ccccc3)c4nonc14

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

Actions biochimiques/physiologiques

10074-G5 is a c-Myc/Max interaction inhibitor. The c-Myc oncoprotein and its partner Max are intrinsically disordered (ID) monomers that undergo coupled folding and binding upon heterodimerization. 10074-G5, similarly to 10058-F4 (#F3680), specifically inhibits this interaction by binding to c-Myc, thus preventing C-Myc specific DNA binding and target genes regulation. 10074-G5 (2.8 microM) is slightly more potent that 10058-F4 (5.2 microM). It was discovered that 10074-G5 binds to a different specific binding site (region) of C-Myc than 10054-F4. Thus, the compound may become desirable for probing different interactions.

Code de la classe de stockage

6.1C - Combustible, acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

Classe de danger pour l'eau (WGK)

WGK 3

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Chengsheng Wu et al.
BMC cancer, 18(1), 361-361 (2018-04-04)
The phenomenon that malignant cells can acquire stemness under specific stimuli, encompassed under the concept of cancer cell plasticity, has been well-described in epithelial malignancies. To our knowledge, cancer cell plasticity has not yet been described in hematopoietic cancers. To
Quan Yang et al.
Frontiers in immunology, 12, 627072-627072 (2021-03-13)
The accumulation of myeloid-derived suppressor cells (MDSCs) is one of the major obstacles to achieve an appropriate anti-tumor immune response and successful tumor immunotherapy. MDSCs in tumor-bearing hosts are primarily polymorphonuclear (PMN-MDSCs). However, the mechanisms regulating the development of MDSCs
Alina Castell et al.
Scientific reports, 8(1), 10064-10064 (2018-07-04)
MYC is a key player in tumor development, but unfortunately no specific MYC-targeting drugs are clinically available. MYC is strictly dependent on heterodimerization with MAX for transcription activation. Aiming at targeting this interaction, we identified MYCMI-6 in a cell-based protein
Udom Lao-On et al.
Biochimica et biophysica acta. Molecular basis of disease, 1866(3), 165656-165656 (2019-12-25)
Here we showed that the c-Myc oncogene is responsible for overexpression of pyruvate carboxylase (PC) in highly invasive MDA-MB-231 cells. Pharmacological inhibition of c-Myc activity with 10074-G5 compound, resulted in a marked reduction of PC mRNA and protein, concomitant with
Huabo Wang et al.
Oncotarget, 6(18), 15857-15870 (2015-06-04)
The c-Myc (Myc) oncoprotein is deregulated in a large proportion of diverse human cancers. Considerable effort has therefore been directed at identifying pharmacologic inhibitors as potential anti-neoplastic agents. Three such groups of small molecule inhibitors have been described. The first
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Oncogenes and Tumor Suppressors Reprogram Metabolism

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