G3798
10074-G5
≥98% (HPLC)
別名:
N-2-ビフェニリル-7-ニトロ-2,1,3-ベンゾオキサジアゾール-4-アミン, N-[1,1′-ビフェニル-2-イル]-7-ニトロ-2,1,3-ベンゾオキサジアゾール-4-アミン, ビフェニル-2-イル-(7-ニトロベンゾ[1,2,5]オキサジアゾール-4-イル)アミン
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この商品について
実験式（ヒル表記法）:
C18H12N4O3
CAS番号:
分子量:
332.31
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
製品名
10074-G5, ≥98% (HPLC)
InChI key
KMJPYSQOCBYMCF-UHFFFAOYSA-N
SMILES string
[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
assay
≥98% (HPLC)
form
powder
color
red
solubility
DMSO: >10 mg/mL
storage temp.
room temp
Quality Level
Biochem/physiol Actions
10074-G5 is a c-Myc/Max interaction inhibitor.
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.
保管分類
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
wgk
WGK 3
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
ライフサイエンス、有機合成、材料科学、クロマトグラフィー、分析など、あらゆる分野の研究に経験のあるメンバーがおります。.
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