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Sigma-Aldrich

Ubiquitin E1 Inhibitor, PYR-41

The Ubiquitin E1 Inhibitor, PYR-41 controls the biological activity of Ubiquitin E1. This small molecule/inhibitor is primarily used for Protease Inhibitors applications.

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Synonym(s):
Ubiquitin E1 Inhibitor, PYR-41, 4-(4-(5-Nitro-furan-2-ylmethylene)-3,5-dioxo-pyrazolidin-1-yl)-benzoic acid ethyl ester, trihydrate, Ubiquitin-Activating Enzyme E1 Inhibitor, PYR-41
Empirical Formula (Hill Notation):
C17H13N3O7 · 3H2O
Molecular Weight:
425.35
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

Assay

≥90% (sum of two isomers, HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
protect from light

color

dark purple

solubility

DMSO: 10 mg/mL

shipped in

wet ice

storage temp.

−20°C

General description

A cell-permeable pyrazone compound that irreversibly (presumably via covalent modification) inhibits ubiquitin-activating enzyme E1 activity (IC50<10 µM in cell-free E1 ubiquitination reactions), while exhibiting little or no activity against E3, E2, or caspase enzymatic activity. Blocks ubiquitination-dependent protein degradation and other ubiquitination-mediated cellular activities. E1 inactivation by PYR-41 or other means has been shown to result in an overall elevation of sumoylation.

Packaging

Packaged under inert gas

Warning

Toxicity: Irritant (B)

Reconstitution

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 1 month at -20°C. At room temperature, compound will undergo ~1% decomposition per day.

Other Notes

Yang, Y., et al. 2007. Cancer Res.67, 9472.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Subhash Mehto et al.
The EMBO journal, 41(23), e111289-e111289 (2022-10-13)
The NOD1/2-RIPK2 is a key cytosolic signaling complex that activates NF-κB pro-inflammatory response against invading pathogens. However, uncontrolled NF-κB signaling can cause tissue damage leading to chronic diseases. The mechanisms by which the NODs-RIPK2-NF-κB innate immune axis is activated and

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