|Nigericin||Unit size||Cat. code||Docs||Qty||Price|
Nigericin sodium salt; Potassium ionophore
NLRP3 Inflammasome Inducer - Nigericin sodium salt
Nigericin sodium salt is a microbial toxin derived from the gram-positive bacteria Streptomyces hygroscopicus. It triggers the NLRP3 inflammasome-dependent induction of interleukin-1β (IL-1β) and IL-18 .
- Inducer of the NLRP3 inflammasome
- Potassium ionophore
- Each lot is functionally tested
InvivoGen also offers:
Read our review on the NLRP3 inflammasome.
Download our Practical guide on Inflammasomes.
1. Mariathasan S. et al., 2006. Cryopyrin activates the inflammasome and ATP. Nature 440;228-32.
IL-1β production in THP1-Null2 cells. Human THP-1 monocytes were primed with LPS-EK (1 µg/ml) prior to incubation with increasing concentrations of Nigericin. After 6h and 24h activation, IL-1β secretion was assessed in the culture supernatant using HEK-Blue™ IL-1β sensor cells and the SEAP detection reagent QUANTI-Blue™ Solution. The optical density (OD) was read at 630 nm.
Working concentration: 1-10 µM
CAS number: 28643-80-3
Synonym: Antibiotic K178, Polyetherin A
Molecular weight: 746.94 g/mol
Solubility: 5 mg/ml in ethanol
- The biological activity has been validated using cellular assays.
- The absence of bacterial contamination (e.g. lipoproteins and endotoxins) has been confirmed using HEK-Blue™ TLR2 and HEK-Blue™ TLR4 cells.
Nigericin is provided as a sodium salt and is available in two quantities:
- tlrl-nig: 10 mg
- tlrl-nig-5: 50 mg
Nigericin is shipped at room temperature.
Store at -20 °CBack to the top
Nigericin sodium salt acts as a potassium ionophore. It probably activates NLRP3 through the intracellular potassium (K+) efflux across the membrane . Whether the formation of non‑selective pannexin-1 pores also contributes to NLRP3 activation upon Nigericin treatment remains unclear .
The NLRP3 inflammasome is an intracellular multi-protein complex that plays a central role in innate immunity. It is activated by a two-step process. A first signal (‘priming’) is provided by pathogen-associated molecular patterns (PAMPs) or cytokines. It allows the transcriptional upregulation of key inflammasome actors and the post-translational modification of NLRP3 . The second signal (‘activation’) is provided by a wide array of stimuli including microbial toxins, endogenous molecules or crystalline substances. The current paradigm is that NLRP3 does not bind directly to these molecules. Rather it senses downstream cytosolic stress signals such as K+ efflux. This triggers inflammasome multimerization and pro-caspase-1 maturation. Proximity-induced autolytic activation of caspase-1 leads to the formation of gasdermin D (GSDMD) pores at the cell surface, allowing IL-1β/IL-18 and alarmin secretion, and ultimately, pyroptosis [3,4].
1. Muñoz-Planillo R. et al., 2013.K+ efflux is the common trigger of NLRP3 inflammasome activation by bacterial toxins and particulate matter. Immunity. 38(6):1142-53..
2. Pelegrin P, & Surprenant A., 2007. Pannexin-1 couples to maitotoxin- and nigericin-induced interleukin-1beta release through a dye uptake-independent pathway. J Biol Chem. 282(4):2386-94.
3. Swanson K.V. et al., 2019. The NLRP3 inflammasome: molecular activation and regulation to therapeutics. Nat. Rev. Immunol. 19:477.
4. Groslambert M. & Py B. 2018. Spotlight on the NLRP3 inflammasome pathway. J. Inflamm. Res. 11:359.
Chemical structure of nigericin:
Back to the top