| 包装 | 价格(元) |
| 1mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
Preparation Method | For ATPase activity assay, purified recombinant human proteins (1.4 ng/uL) were incubated at 37℃ with indicated concentrations of CY-09 for 15 min in the reaction buffer. ATP (25 um, Ultra-Pure ATP) was then added, and the mixture was further incubated at 37 ℃ for another 40 min. |
Reaction Conditions | 0.1-1uM CY-09 with protein incubate for 15 minutes |
Applications | Cy-09 inhibited the ATPase activity of purified NLRP3 at a dose of 0.1 - 1 uM. The inhibitory effect of CY-09 on NLRP3 ATPase activity was specific because it had no effect on the ATPase activity of purified NLRC4 NLRP1 NOD2 or RIG-I. |
Cell lines | MDM cells(BMDM and PMDM) |
Preparation Method | To induce NLRP3 inflammasome activation, MDM cells were stimulated with LPS for 3 h. CY-09 or other inhibitors were added into the culture for 30 min, and then the cells were stimulated for 4 h with MSU, Salmonella typhimurium or for 30 min with ATP or nigericin. |
Reaction Conditions | 1-10 μM Cy-09 for 30 min |
Applications | Cy-09 specifically blocks NLRP3 activation in macrophages. |
Animal models | C57BL/6J mice |
Preparation Method | C57BL/6J mice were injected with 40 mg/kg CY-09 or vehicle 30 min before injection of MSU. After 6 h, mice were killed, and peritoneal cavities underwent lavage with 10 ml ice-cold PBS. |
Dosage form | 40 mg/kg CY-09 (intraperitoneal injection) |
Applications | Cy-09 inhibited NLRP3 activation in vivo and prevented neonatal mortality in CAPS mouse model. |
| 产品描述 | CY-09, a specific inhibitor of the NLRP3 inflammasome, directly targets NLRP3 and has an IC50 value of 18.9, 8.18, >50, >50 and 26.0 uM for each of the five major cytochrome P450 enzymes. CY-09 directly binds to the ATP-binding motif of NLRP3 NACHT domain and inhibits NLRP3 ATPase activity, resulting in the suppression of NLRP3 inflammasome assembly and activation[1]. CY-09 exhibited a dose-dependent inhibitory effect on monosodium urate (MSU), nigericin, and ATP-induced caspase-1 activation and IL-1β secretion at the doses of 1-10 uM in LPS-primed BMDMs. Cytosolic LPS induced noncanonical NLRP3 activation in BMDMs could also be blocked by CY-09 treatment[1]. CY-09 can maintain extracellular matrix (ECM) homeostasis and regulate inflammation in TNF-α treated chondrocytes via inhibition of NLRP3 inflammasome-mediated pyroptosis[2].CY-09 reduced the production of inflammatory cytokines, intracellular Ca2+ levels, and the activation of TRPA1 by inhibiting the activation of inflammasomes, thereby reducing the proinflammatory polarization of macrophages and alleviating animal pain and injury[3]. M1-polarized macrophage infiltration and NLRP3 inflammasome activation increased in the cardiac ventricle after diabetic stroke. CY-09 restored cardiac function, The M1-polarized macrophage-NLRP3 inflammasome activation is a pathway underlying the brain-heart interaction after diabetic stroke[7]. CY-09 was tested against the five major cytochrome P450 enzymes 1A2, 2C9, 2C19, 2D6, and 3A4 with half maximal inhibitory concentration (IC50) values of 18.9, 8.18, >50, >50, and 26.0 uM, respectively, which exhibited low risk of drug drug interactions. CY-09 treatment in vivo efficiently suppressed MSU injection induced IL-1β production and neutrophil influx, suggesting that CY-09 can block MSU-induced NLRP3 inflammasome activation in vivo[1]. When investigate whether CY-09 is effective for the treatment of NAFLD in a high-fat diet (HFD)-induced mouse model.CY-09 reduces hepatic steatosis in experimental NAFLD mice and CY-09 may be a potential therapeutic drug of NAFLD in clinical practice[4]. Compared with surgery alone, sleeve gastroplasty mimicking ESG combined with CY-09 resulted in weight loss, significantly improved insulin resistance, and better remission of NAS[5]. In db/db mice, inflammation, oxidative stress, apoptosis and fibrosis increased, while CY-09 exerted renoprotection by inhibiting NLRP3 inflammasome activation[6]. References: |
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