Proteinase inhibitors, also known as protease inhibitors, have been investigated as potential therapeutic agents in the treatment of Rheumatoid Arthritis (RA), though their clinical use is not widespread. The rationale stems from the role of proteases—enzymes that degrade proteins—in the pathogenesis of RA. In RA, excessive activity of proteinases such as matrix metalloproteinases (MMPs) and serine proteases contributes to joint tissue destruction, cartilage degradation, and inflammation. Proteinase inhibitors can theoretically mitigate this process by blocking these enzymes, thereby protecting joint structures.

Scientifically, some endogenous proteinase inhibitors (e.g., alpha-1-antitrypsin, tissue inhibitors of metalloproteinases) have been found at altered levels in patients with RA, and animal studies have shown that pharmacological inhibition of certain proteinases can reduce joint damage. However, clinical trial evidence for the use of exogenous proteinase inhibitors as a treatment for RA in humans remains limited and inconclusive. Some small-scale studies and experimental drugs have demonstrated modest benefits, but large-scale, robust clinical trials are lacking, and no proteinase inhibitor is currently approved specifically for RA treatment.

In summary, while there is a scientific rationale and some preclinical evidence for the use of proteinase inhibitors in RA, the clinical evidence supporting their efficacy is weak, and their use is not a standard or well-validated treatment for RA at this time.