| Bioactivity | CORM-3, a carbon monoxide-releasing molecule, attenuates NF-κB p65 nuclear translocation, reduces ROS generation and enhances intracellular glutathione and superoxide dismutase levels. CORM-3 reduces NLRP3 inflammasome activation[1][2][3]. | |||||||||
| Invitro | CORM-3 suppresses caspase-1 activation and the secretion of interleukin (IL)-1β and IL-18 in macrophages in response to lipopolysaccharide (LPS) and ATP. CORM-3 inhibits the oligomerization of the adaptor protein apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), which is required for NLRP3-dependent caspase-1 activation[2]. | |||||||||
| In Vivo | CORM-3 (4 mg/kg, ip) reduces NLRP3 inflammasome activation and inhibits hyperglycemia-induced inflammation in mice[2]. Animal Model: | |||||||||
| Name | CORM-3 | |||||||||
| CAS | 475473-26-8 | |||||||||
| Formula | C5H4ClNO5Ru | |||||||||
| Molar Mass | 294.61 | |||||||||
| Appearance | Solid | |||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | |||||||||
| Storage |
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| Reference | [1]. Foresti R, et al. Vasoactive properties of CORM-3, a novel water-soluble carbon monoxide-releasing molecule. Br J Pharmacol. 2004 Jun;142(3):453-60. [2]. Lee DW, et al. Carbon monoxide regulates glycolysis-dependent NLRP3 inflammasome activation in macrophages. Biochem Biophys Res Commun. 2017 Nov 18;493(2):957-963. [3]. Huang Y, et al. Carbon monoxide (CO) inhibits hydrogen peroxide (H2O2)-induced oxidative stress and the activation of NF-κB signaling in lens epithelial cells. Exp Eye Res. 2018 Jan;166:29-39. |