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Abstract
Tenidap is a novel, once-daily, cytokine modulating antirheumatic drug indicated for the treatment of rheumatoid arthritis (RA). In vitro, tenidap significantly inhibits the production of the pro-inflammatory cytokines, interleukin-1, interleukin-6 and tumour necrosis factor in human cell lines, and inhibits cytokine-mediated processes such as cartilage degradation, bone resorption, metalloprotease synthesis, endothelial cell adhesion and monocyte differentiation. Tenidap also inhibits cyclo-oxygenase. In RA patients, tenidap 120 mg/day is clinically equivalent to the combination of disease-modifying antirheumatic agents plus non-steroidal anti-inflammatory drugs (NSAIDs) and significantly more effective than NSAIDs. Tenidap also produces rapid, profound and sustained reductions in the serum levels of the acute phase proteins, C-reactive protein and serum amyloid A, an effect suggestive of disease modifying properties. In addition, tenidap reduces circulating levels of IL-6 in RA patients. Tenidap is well tolerated.