Ilumya (tildrakizumab) affects the immune system by blocking the inflammatory response which changes how your body responds to autoimmune conditions, such as psoriasis, but also to an infection. This may increase your risk of infection or cause reactivation of some infections, such as tuberculosis.

Ilumya blocks the inflammatory response by binding selectively to interleukin-23 (IL-23) which is a naturally occurring cytokine. Cytokines are substances released by cells of the immune system that influence other cells. IL-23 plays a key role in promoting inflammation and regulating other cytokines (such as IL-17) and inflammatory substances, such as TNF-α3-7. IL-23 is thought to be crucial in regulating inflammation that stems from infection or chronic autoimmune conditions, such as psoriasis, inflammatory bowel disease, rheumatoid arthritis, and multiple sclerosis. In these conditions, IL-23 maintains immune cells in an inflammatory state.

By blocking the effects of IL-23, Ilumya helps control the release of IL-17 and TNF-α, which reduces inflammation. It also decreases how many inflammatory cells are present within psoriatic lesions and helps prevent plaque formation and resolves tissue damage. Because it precisely targets the inflammatory pathway at IL-23, it does not modify the effects of another cytokine, IL-12 which helps to protect against infection and cancer. Ilumya can still increase a person’s risk of infection or cause reactivation of tuberculosis; however, the risk for serious infection is low (0.3%) and similar to placebo (a medicine with no active ingredient in it).

Ilumya is approved for the treatment of moderate-to-severe plaque psoriasis in adults who are candidates for systemic therapy or phototherapy. It is given by subcutaneous (under the skin) injection every 12 weeks following an initial dosing of two injections four weeks apart.