SML0031
DBeQ
≥98% (HPLC)
Synonym(s):
JRF 12, N2,N4-dibenzylquinazoline-2,4-diamine
Sign In to View Organizational & Contract Pricing.
Select a Size
About This Item
Empirical Formula (Hill Notation):
C22H20N4
CAS Number:
Molecular Weight:
340.42
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
InChI
1S/C22H20N4/c1-3-9-17(10-4-1)15-23-21-19-13-7-8-14-20(19)25-22(26-21)24-16-18-11-5-2-6-12-18/h1-14H,15-16H2,(H2,23,24,25,26)
SMILES string
C(Nc1nc(NCc2ccccc2)c3ccccc3n1)c4ccccc4
InChI key
QAIMUUJJAJBPCL-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: ≥20 mg/mL
storage temp.
room temp
Quality Level
Related Categories
Application
HeLa cells were treated with DBeQ and the effects on in vivo ubiquitination and protein dislocation were studied by live cell imaging.
Biochem/physiol Actions
ATPase p97 inhibitor.
DBeQ is a potent and specific inhibitor of ATPase p97, an integral component of the ubiquitin-fusion degradation (UFD) pathway. DBeQ inhibits the degradation of ubiquitinated proteins, the endoplasmic reticulum-associated degradation pathway, and autophagosome maturation. The compound also potently inhibits cellular proliferation and induces caspase 3/7 activity and apoptosis.
Storage Class
11 - Combustible Solids
wgk
WGK 3
Choose from one of the most recent versions:
Already Own This Product?
Find documentation for the products that you have recently purchased in the Document Library.
Ainoa Figuerola-Conchas et al.
ACS chemical biology, 15(1), 243-253 (2019-12-04)
VCP/p97 belongs to the AAA+ ATPase family and has an essential role in several cellular processes ranging from cell division to protein homeostasis. Compounds targeting p97 inhibit the main ATPase domain and cause cell death. Here, using PNA-encoded chemical libraries
Holger W Auner et al.
PloS one, 8(9), e74415-e74415 (2013-09-27)
Inhibition of the proteasome is a widely used strategy for treating multiple myeloma that takes advantage of the heavy secretory load that multiple myeloma cells (MMCs) have to deal with. Resistance of MMCs to proteasome inhibition has been linked to
Ajit Tiwari et al.
Scientific reports, 6, 38681-38681 (2016-12-09)
Caveolin-1 (Cav1) drives the formation of flask-shaped membrane invaginations known as caveolae that participate in signaling, clathrin-independent endocytosis and mechanotransduction. Overexpression or mutations of Cav1 can lead to its mistrafficking, including its accumulation in a perinuclear compartment previously identified as
Stephanie L Moon et al.
The Journal of cell biology, 219(8) (2020-06-11)
Stress granules are dynamic assemblies of proteins and nontranslating RNAs that form when translation is inhibited in response to diverse stresses. Defects in ubiquitin-proteasome system factors including valosin-containing protein (VCP) and the proteasome impact the kinetics of stress granule induction
Aparna Shinde et al.
Cancer research, 79(8), 1831-1843 (2019-02-09)
The ability of breast cancer cells to transiently transition between epithelial and mesenchymal states contributes to their metastatic potential. Therefore, driving tumor cells into a stable mesenchymal state, as opposed to complete tumor cell eradication, presents an opportunity to pharmacologically
Articles
We presents an article on Autophagy in Cancer Promotes Therapeutic Resistance
Related Content
Autophagy in Cancer
Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.
Contact Technical Service