Ixekizumab (LY2439821) is a humanized IgG4 monoclonal antibody that selectively binds and neutralizes interleukin IL-17A with a Kd value of <3 pM. It blocks the binding of IL-17A to IL-17RA but not to other IL-17 family members. Ixekizumab is used for the treatment of moderate to severe plaque psoriasis, psoriasis, arthritis, and psoriasis.

Ixekizumab (0.1-10000 pM) dose-dependently inhibits the secretion of growth-regulated oncogene (GRO)α induced by human IL-17A or human IL-17A/F heterodimers from HT-29 cells. Similarly, Ixekizumab demonstrates dose-dependent inhibition of GROα secretion from HT-29 cells induced by cynomolgus monkey IL-17A.[1]
The equilibrium KD values of Ixekizumab for IL-17A in humans and cynomolgus monkeys were 1.8 pM and 0.8 pM, respectively. Ixekizumab exhibited binding to rabbit IL-17A as well, although with a lower affinity and heterogeneous binding (with KD values of 1.3 nM and 14 nM, respectively). Notably, Ixekizumab did not demonstrate any binding to IL-17A in either mice or rats.[1]

Ixekizumab (0.001-1 mg/kg; i.v.; C57BL/6 mice) exhibits a dose-dependent reduction in the secretion of keratinocyte chemoattractant (KC) induced by human IL-17A in the plasma of C57BL/6 mice. In male cynomolgus monkeys, intravenous (IV) administration of 1 mg/kg results in a mean elimination half-life of 6.5 days. Subcutaneous (SC) administration of 1 mg/kg yields a maximum plasma concentration of approximately 11.1 µg/mL around 72 hours post-dose, with a mean elimination half-life of about 10.3 days.[1]