Anti-Human IL-12/23 (Ustekinumab) (I-1250-25mg)

IL-12 and IL-23 play a role in the differentiation and proliferation of type 1 T-helper cells (Th1)1. IL-12 stimulates IFN-γ and TNF-α production via Th1 differentiation, whereas IL-23 causes activation of IL-17-producing T cells2. IL-12 and IL-23 are members of the IL-12 cytokine family3. Members of the IL-12 family form soluble heterodimers consisting of α and β subunits. IL-12 and IL-23 both have a p40 subunit, and either p40 can bind to the IL-12 β1 receptor1,2,4. IL-23 consists of IL-12p40 and IL-23p193. IL-12 consists of IL-12p40 and IL-12p35. IL-23 is associated with various autoimmune inflammatory diseases and is particularly highly expressed in psoriasis skin lesions1,2. Furthermore, IL-23 is suspected to play a role in tumorigenesis3. Anti-IL12/23 p40 antibodies antagonize key pathways in inflammatory autoimmune diseases, such as arthritis and colitis1,2. Ustekinumab was developed from transgenic mice as an antibody against the p40 subunits of IL- 12/231,2. Ustekinumab binds with high affinity and specificity to p40, preventing interaction with the IL-12 β1 receptor found on natural killer cells or T cells and blocking downstream signaling, differentiation, and cytokine production1,2,4. Additionally, ustekinumab inhibits up-regulation of cutaneous lymphocyte antigen, IL-2, IL-2Rα, and IL-12R as well as secretion of IFN-γ, TNF-α, and IL-17A. Ustekinumab is used in clinical settings to treat plaque psoriasis, Crohn’s disease, and ulcerative colitis.