Experimental AA-amyloidosis in mice is inhibited by treatment with the anti-rheumatic drug tenidap.

In a mouse model for induction of experimental AA-amyloidosis, treatment with tenidap was shown to inhibit the development of amyloidosis. Studies have shown that the drug inhibits the cytokines interleukin (IL)-6, IL-1 and tumour necrosis factor alpha (TNF-alpha) which are known to stimulate hepatocytes to synthesize acute phase proteins (APPs). The APP serum amyloid protein (SAA) is the precursor for amyloid protein AA and tenidap treatment reduces the serum levels of SAA in mouse and humans. It is suggested that reduction of SAA levels reduces the risk of AA fibril formation and thus the development of amyloidosis.