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About This Item
Empirical Formula (Hill Notation):
C11H9NO5S
CAS Number:
Molecular Weight:
267.26
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
Assay:
≥98% (HPLC)
Form:
powder
Quality level:
Storage condition:
OK to freeze, protect from light
InChI
1S/C11H9NO5S/c1-8-2-4-9(5-3-8)18(15,16)11-7-6-10(17-11)12(13)14/h2-7H,1H3
SMILES string
O=S(C1=CC=C(O1)[N+]([O-])=O)(C2=CC=C(C)C=C2)=O
InChI key
GAUHIPWCDXOLCZ-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze, protect from light
color
off-white
solubility
DMSO: 100 mg/mL
shipped in
ambient
storage temp.
2-8°C
Quality Level
Related Categories
General description
A cell-permeable nitrofuran compound that selectively inhibits the E2 Ubiquitin-conjugating enzyme Ubc13- (Cat. No. 438075), but not UbcH5c-, catalyzed K63-linked polyUb chain formation by preventing Ubc13-Ub thioester bond formation. Effectively inhibits Ubc13-Uev1A (UBE2V1) E2 complex-mediated NF-κB activation, Ubc13-Mms2 (UBEV2) E2 complex-mediated DNA DSB (double-strand break) repair activation, as well as Ubc13-dependent p53 nuclear export in cultures (1 to 2 µM). The combined NF-κB inhibition and p53 activation via Ubc13 inhibition is shown to be particularly effective against the proliferation of ABC (Activated B-cell-like) and GCB (Germinal center B-cell-like) DLBCL (Diffuse Large B-Cell Lymphoma) cell lines and primary DLBCL cultures via apoptosis induction (1 to 2 µM).
Biochem/physiol Actions
Cell permeable: yes
Primary Target
Ubc13
Ubc13
Packaging
Packaged under inert gas
Preparation Note
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
Other Notes
Pulvino, M., et al. 2012. Blood 1668.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Toxicity: Standard Handling (A)
Storage Class
11 - Combustible Solids
wgk
WGK 3
Certificates of Analysis (COA)
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Juana Serrano-Lopez et al.
eLife, 10 (2021-04-09)
Innate immune cellular effectors are actively consumed during systemic inflammation, but the systemic traffic and the mechanisms that support their replenishment remain unknown. Here, we demonstrate that acute systemic inflammation induces the emergent activation of a previously unrecognized system of
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