Axial spondyloarthritis is a rheumatic disease characterized by inflammation and bone formation causing impaired function of the spine and affected joints. Basic research has highlighted the key role of dysregulation of tumor necrosis factor α, interleukin- 23 and interleukin-17 cytokine production in the etiology of axial spondyloarthritis. Tumor necrosis factor α and interleukin-17 inhibitors have been shown to be effective in clinical trials and are currently approved biological disease-modifying drugs for all disease subgroups. The presumed efficacy of IL-23 blockade has not been confirmed in two clinical trials with anti-IL-23 monoclonal antibodies. Janus kinase inhibitors appear to be a new treatment option.