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CRID3 sodium salt
Biological Activity for CRID3 sodium salt
CRID3 sodium salt is a potent NLRP3 inflammasome inhibitor; closes the active conformation of NLRP3 to the inactive state. Directly interacts with the Walker B motif within the NLRP3 NACHT domain. Inhibits IL-1β, IL-18 and IL-1α production (IC50 values are 7.2, 10.3 and 12-18 nM, respectively). Selective for NLRP3 over NLRC4 inflammasome and Toll-like receptor signaling. Reduces severity of experimental autoimmune encephalomyelitis, skin inflammation and airway inflammation in mice. Also glutathione S-transferase omega 1 inhibitor. Orally bioavailable.
Sold for research purposes under agreement from Pfizer Inc
Technical Data for CRID3 sodium salt
|Storage||Store at +4°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solubility Data for CRID3 sodium salt
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for CRID3 sodium salt
The following data is based on the product molecular weight 426.46. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.34 mL||11.72 mL||23.45 mL|
|5 mM||0.47 mL||2.34 mL||4.69 mL|
|10 mM||0.23 mL||1.17 mL||2.34 mL|
|50 mM||0.05 mL||0.23 mL||0.47 mL|
Product Datasheets for CRID3 sodium salt
References for CRID3 sodium salt
References are publications that support the biological activity of the product.
Laliberte et al (2003) Glutathione S-transferase omega 1-1 is a target of cytokine release inhibitory drugs and may be responsible for their effect on interleukin-1β posttranslational processing. J.Biol.Chem. 278 16567 PMID: 12624100
Coll et al (2015) A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases. Nat.Med. 21 248 PMID: 25686105
Gordon et al (2018) Inflammasome inhibition prevents a-synuclein pathology and dopaminergic neurodegeneration in mice. Sci.Transl.Med. 10 eaah4066 PMID: 30381407
Tapia-Abellán et al (2019) MCC950 closes the active conformation of NLRP3 to an inactive state. Nat.Chem.Biol. 15 560 PMID: 31086329
Coll et al (2019) MCC950 directly targets the NLRP3 ATP-hydrolysis motif for inflammasome inhibition. Nat.Chem.Biol. 15 556 PMID: 31086327
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Keywords: CRID3 sodium salt, CRID3 sodium salt supplier, CP456773, cytokine, release, inhibitory, drug, CRID3, Glutathione, S-transferase, omega, 1, GSTO1, inhibitors, inhibits, MCC950, nod-like, receptors, NLRP3, inflammasome, CP-456773, MCC, 950, Other, Transferases, Cytokines, Inflammasomes, 5479, Tocris Bioscience
2 Citations for CRID3 sodium salt
Citations are publications that use Tocris products. Selected citations for CRID3 sodium salt include:
Goddard et al (2019) Enteropathogenic Escherichia coli Stimulates Effector-Driven Rapid Caspase-4 Activation in Human Macrophages. Cell Rep 27 1008 PMID: 31018119
Chauhan et al (2018) BAX/BAK-Induced Apoptosis Results in Caspase-8-Dependent IL-1β Maturation in Macrophages. Cell Rep 25 2354 PMID: 30485805
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.
Rheumatoid Arthritis Poster
Rheumatoid arthritis (RA) is a chronic destructive inflammatory autoimmune disease that results from a breakdown in immune tolerance, for reasons that are as yet unknown. This poster summarizes the pathology of RA and the inflammatory processes involved, as well as describing some of the epigenetic modifications associated with the disease and the potential for targeting these changes in the discovery of new treatments.