Table 3.
The application of drugs for NLRP3 inflammasome in kidney diseases.
| Drug | Target spot | Mechanism | Kidney diseases | Adverse effect | Clinical stage |
|---|---|---|---|---|---|
| MCC950 [[106], [107], [108], [109], [110], [111]] | NLRP3 | NLRP3 induced ASC oligomerization was blocked | Diabetic nephropathy, Hypertensive nephropathy, Contrast medium nephropathy,Kidney damage caused by cisplatin and sepsis | Liver toxicity | Preclinical study |
| Tranilast [[112], [113], [114]] | NLRP3 | Enhanced NLRP3 ubiquitination,Binding NACHT and inhibiting NLRP3-NLRP3 interaction | Diabetic nephropathy | NA | Clinical application |
| Β-hydroxybuty -rate [115,116] |
NLRP3 | Inhibited K+ efflux and reduced ASC oligomerization and speckle formation | Hyperoxalate renal tubular injury | NA | Preclinical study |
| CY-09 [117,118] | NLRP3 | Bind to ATP binding motif of NACHT domain and inhibit NLRP3 ATP activity | Ischemia-reperfusion nephropathy | NA | Preclinical study |
| VX-740/765 [119] | Caspase-1 | Selective inhibition of caspase-1 | NA | Liver toxicity | Preclinical study |
| AZD9056 [120] | P2X7 | P2X7 Antagonistic P2X7 | NA | NA | Phase II clinical study |
| Brilliant blue G [121,122] | P2X7 | Selective antagonism of P2X7 | Hypertensive nephropathy, Lupus nephritis | NA | Preclinical study |
| Glibenclamide [[123], [124], [125]] | K+ channel | ATP sensitive K+ channel inhibitors | Chronic kidney disease | Abnormal glucose metabolism | Clinical application |