Colchicine is effective in an acute attack and can have a prophylactic action suppressing the number of acute attacks, but it will not prevent gout from progressing to gouty arthritis. Colchicine does not target uric acid metabolism, but works by blocking the inflammatory response via various mechanisms including:[16,17]

• inhibiting granulocytes from moving into the inflamed area,
• stopping microtubules (structural elements within cells) from aggregating, disrupting inflammasome activation, impairing transportation within cells and blocking cell division or mitosis;
• reducing lactic acid production by leukocytes which reduces uric acid deposition;
• interfering with kinin (peptide hormones) formation;
• reducing phagocytosis, in part by suppressing glucose oxidation.

Canakinumab, an interleukin-1 beta (IL-1 beta) antibody, counters the effects of overproduction of IL-1 beta released by macrophage inflammasomes triggered by urate crystals.[16]