Aselizumab (HuDreg-55) is an humanized IgG4 mAb against L-selectin. However, L-selectin (CD62L) is a cell adhesion molecule expressed on circulating neutrophils. It regulates migrating cells to chemotaxis towards the site of injury. Aselizumab may be account for a high rate of infections and leucopenia after truma.
Aselizumab can disulfide with human-mouse monoclonal HuDreg-55 light chain to form dimer[1].Aselizumab (5-500 ng/mL; 25 min) blocks L-selectin-dependent adhesion of human lymphocytes to high endothelial venules in frozen sections of lymph nodes[3].
Aselizumab (10 mg/kg; i.v.; single dose) shows terminal elimination half-lives at 12.0 days in rhesus monkeys[3].
References:
[1]. Seekamp A, et al. The effect of anti-L-selectin (aselizumab) in multiple traumatized patients--results of a phase II clinical trial. Crit Care Med. 2004 Oct;32(10):2021-8.
[2]. Rahman I, et al. L-selectin regulates human neutrophil transendothelial migration. J Cell Sci. 2021 Feb 8;134(3):jcs250340.
[3]. Co MS, et al. Properties and pharmacokinetics of two humanized antibodies specific for L-selectin. Immunotechnology. 1999 Mar;4(3-4):253-66.