Table 2.
Inhibitors of NLRP3 pathways as well as their effects in cell cultures, animal models, or patients of inflammatory diseases.
Inhibitors | Molecular mechanism | Cell/animal model/patients | Ref |
---|---|---|---|
MCC950 | Block the ATPase domain of NLRP3 and inhibit the activation of typical and atypical NLRP3 inflammasome | Autoimmune encephalomyelitis Cryopyrin-associated periodic syndrome Muckle-Wells syndrome |
[124] |
| |||
MNS | Bind to the LRR and NACHT domains and suppress ATPase activity of NLRP3 | Bone marrow-derived macrophages | [91] |
| |||
CY-09 | Inhibit NLRP3 ATPase activity | Cryopyrin-associated autoinflammatory syndrome Type 2 diabetes Synovial fluid cells from gout patients |
[137] |
| |||
OLT1177 | Inhibit NLRP3 ATPase activity and block canonical and noncanonical activation of NLRP3 inflammasome | Human blood-derived macrophages Human blood neutrophils Monocytes isolated from patients with cryopyrin-associated periodic syndrome Spleen cells from mice |
[128] |
| |||
Glyburide | Inhibit ATP-sensitive K+ channels, act as downstream of the P2X7 receptor, and inhibit ASC aggregation | Bone marrow-derived macrophages Familial cold-associated autoinflammatory syndrome patients |
[129] |
| |||
16673-34-0 | Interfere the downstream of NLRP3 conformational changes and bind to ASC | Acute myocardial infarction | [138] |
| |||
JC124 | Block ASC aggregation, caspase-1 activation, and IL-1β secretion | Acute myocardial infarction Alzheimer's disease |
[139] [140] |
| |||
BHB | Inhibit K+ efflux and block ASC aggregation | Muckle-Wells syndrome Familial cold autoinflammatory syndrome Urate crystal-induced peritonitis |
[70] |
| |||
Parthenolide | Inhibit caspase-1 activation and NLRP3 ATPase activity | Bone marrow-derived macrophages Cystic fibrosis |
[131] [141] |
| |||
Bay 11-7082 | Alkylation of cysteine residues of the NLRP3 ATPase region | Psoriasis-like dermatitis Diabetic nephropathy |
[142] [143] |