Ixekizumab 是一种人源化 IgG4 单克隆抗体，可选择性结合和中和白细胞介素 IL-17A (KD<3 pm)。ixekizumab 直接阻断 il-17a 与 il-17ra 的结合，但不与其他 il-17 家族成员结合。ixekizumab 用于中重度斑块型银屑病的研究。
货号:ajcx33300
CAS:1143503-69-8
分子式:N/A
分子量：N/A
溶解度:N/A
纯度：98%
存储：Store at -20°C
库存：现货

Background:

Ixekizumab (LY2439821) is a humanized IgG4 monoclonal antibody that selectively binds and neutralizes interleukin IL-17A (KD<3 pM). Ixekizumab directly blocks IL-17A binding to IL-17RA (IL-17A receptor) but does not bind to other IL-17 family members. Ixekizumab is used for the research of moderate-to-severe plaque psoriasis[1][2].

The equilibrium KD of Ixekizumab for human and cynomolgus monkey IL-17A were 1.8 pM and 0.8 pM, respectively. Ixekizumab also bound to rabbit IL-17A, but the affinity was lower, and the binding was heterogeneous (KD of 1.3 nM and 14 nM). Ixekizumab shows no binding to either mouse or rat IL-17A[1].Ixekizumab (0.1-10000 pM) inhibits human IL-17A- or human IL-17A/F heterodimer-induced growth-regulated oncogene (GRO)α secretion from HT-29 cells in a dose-dependent fashion. Ixekizumab inhibits cynomolgus monkey IL-17A-induced GROα secretion from HT-29 cells in a dose-dependent fashion[1].

Ixekizumab (0.001-1 mg/kg; i.v.) is able to decrease human IL-17A-induced keratinocyte chemoattractant (KC) secretion in the plasma of the C57BL/6 mice in a dose-dependent manner[1].In male cynomolgus monkeys, following IV administration of 1 mg/kg, Ixekizumab is eliminated with a mean half-life of 6.5 days. After SC administration of 1 mg/kg, Ixekizumab reaches an average maximal plasma concentration of 11.1 µg/mL ~72 hours postdose. The mean elimination half-life following the SC injection was 10.3 days[1].

[1]. Liu L, et al. Generation and characterization of ixekizumab, a humanized monoclonal antibody that neutralizes interleukin-17A. J Inflamm Res. 2016;9:39-50. Published 2016 Apr 19.
[2]. Griffiths CE, et al. Comparison of ixekizumab with etanercept or placebo in moderate-to-severe psoriasis (UNCOVER-2 and UNCOVER-3): results from two phase 3 randomised trials. Lancet. 2015;386(9993):541-551.