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G3798

Sigma-Aldrich

10074-G5

≥98% (HPLC)

Sinónimos:

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

Fórmula empírica (notación de Hill):
C18H12N4O3
Número de CAS:
413611-93-5
Peso molecular:
332.31
Número MDL:
MFCD00576774
Código UNSPSC:
12352200
ID de la sustancia en PubChem:
329799918
NACRES:
NA.77

Nivel de calidad

100

Análisis

≥98% (HPLC)

formulario

powder

color

red

solubilidad

DMSO: >10 mg/mL

temp. de almacenamiento

room temp

cadena 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

Clave InChI

KMJPYSQOCBYMCF-UHFFFAOYSA-N

Acciones bioquímicas o fisiológicas

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.

Código de clase de almacenamiento

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

Clase de riesgo para el agua (WGK)

WGK 3

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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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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