Table 3.
The mechanism of pharmaceutical action on the NLRP3 inflammasome with deterioration factors.
| Mechanism of action | Specificity | Applicable | ||
|---|---|---|---|---|
| Ageing | A deterioration of mitochondrial performance, diminished metabolism, increased oxidative stress, higher levels of mtROS production, the release of mtDNA | mtDNA | NLRP3 | Deterioration factor |
| Smoking | increases the expression of ACE2 receptor | ACE2 | ACE2 | Deterioration factor |
| Canakinumab | Inhibited the expression of IL-1 associated genes; targeted for IL-1β anti-inflammatory therapy | Heart | an IL-1β neutralizing antibod | X |
| Colchicine | Reduced acute inflammation in infarct areas, improved survival, inhibited heart failure, reduced ventricular remodelling and maintaining stability in cardiac function; colchicine reduces cytokine levels as well as the activation of macrophages, neutrophils, and the inflammasome. | Heart | caspase-1, NLRP3 | X |
| CY-09 | Binds to the NACHT domain, which limits NLRPS oligomerization and assembly of the inflammasome; inhibited NLRP3-mediated activation of ATPase selectively | ATP | NLRP3 | ?a |
| Dapansutrile (OLT1177) | A selective inhibitor of the NLRP3 inflammasome, with unique properties to reverse the metabolic costs of inflammation and to treat IL-1β– and IL-18–mediated diseases | Joint, Heart | NLRP3 | ? |
| Dapsone (Dapsone) | Reducing the inflammatory response of cells by binding myeloperoxidase. Dapsone compete with Ub and NLRP3. | Brain Heart | Inflammasome | Oa |
| MCC950 | Inhibited the NLRP3 inflammasome selectively. The diarylsulfonylurea compound MCC950 (originally reported as CRID3/CP-456773) | Heart | NLRP3 | ? |
| PEDF | Inhibited mitochondrial division through PEDFR/IPLA2 & mitochondrial fission-induced NLRP3inflammasome activation. | Heart | NLRP3 | ? |
| Statin | Reduced the expression if IL-1 associated genes; targeted for IL-1β and IL-18 | Heart | NLRP3 | O |
| TA (total flavones) | Inhibited cell death and reduced oxidative stress and inflammation | Heart | NLRP3 | ? |
| Tocilizumab | Decreased PAI-1 production and alleviated clinical manifestations in severe Covid-19patients | Heart | NLRP3 | X |
| TP (triptolide) | Inhibited the expression of NLRP3 and ASC as well as inflammasome assembly and blocked the NLRP3-TGFβ1-Smad pathway | Heart | NLRP3 | ? |
| Tranilast | Reduced cardiomyopathy in patients with muscular dystrophy. Acting as direct NLRP3 inhibitors | Heart | NLRP3 | ? |
| Thiolutin | Thiolutin nhibited the activation of multiple NLRP3 mutants linked with cryopyrin-associated periodic syndromes | Heart | NLRP3 | ? |
a
X: Clinically vague or negated, ?: No clinical study reports, O: Reported to be clinically applicable