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Merck

G3798

10074-G5

≥98% (HPLC)

Synonym(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

Empirical Formula (Hill Notation):
C18H12N4O3
CAS Number:
413611-93-5
Molecular Weight:
332.31
NACRES:
NA.77
PubChem Substance ID:
329799918
UNSPSC Code:
12352200
MDL number:
MFCD00576774
Assay:
≥98% (HPLC)
Form:
powder
Quality level:
100

Key Documents

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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

100

Related Categories

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.

Storage Class

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

wgk

WGK 3

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Certificates of Analysis (COA)

Lot/Batch Number
0000124785
0000124786
0000078958
0000078959
0000036685

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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
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
Gabriella T Heller et al.
Science advances, 6(45) (2020-11-06)
Disordered proteins are challenging therapeutic targets, and no drug is currently in clinical use that modifies the properties of their monomeric states. Here, we identify a small molecule (10074-G5) capable of binding and sequestering the intrinsically disordered amyloid-β (Aβ) peptide
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
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
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