Daclizumab

Daclizumab (Ro 24-7375) is a humanized, monoclonal antibody that blocks CD25 (α-subunit of the high-affinity interleukin-2 receptor (IL-2R-HA)). Daclizumab inhibits effector T cell activation, regulatory T cell (Treg) expansion and survival, and activation-induced T-cell apoptosis. Daclizumab increases IL-2 bioavailability to bind to the intermediate-affinity IL-2R (IL-2R-IA), driving the expansion of anti-inflammatory CD56bright natural killer (NK) cells. Daclizumab can be used for multiple sclerosis and cancer research^[1]. IC50 & Target:IL-2Ra/CD25 In Vitro:Daclizumab (10 μg/mL) significantly inhibits late-phase CD40L expression on activated human CD4⁺T cells (both naive CD45RA⁺CD45RO^- and memory CD45RA^-CD45RO⁺ subsets) in PBMC cultures stimulated with anti-CD3/anti-CD28^[2].
Daclizumab (10 μg/mL) abolishes the restoration of CD40L expression by recombinant IL-2 (rIL-2), confirming that CD28-dependent CD40L expression is mediated via IL-2R signaling^[2].
Daclizumab (10 μg/mL) inhibits CD40L expression on Th1-polarized (cultured with rIL-12, rIL-2, anti-IL-4) and Th2-polarized (cultured with rIL-4, low-dose rIL-2) human CD4⁺ T cells after restimulation^[2].
Daclizumab (10 μg/mL, 48 h) inhibits CD40L expression on cells that divided once and reduces expression on non-dividing cells^[2].
Daclizumab (10 μg/mL, 48-72 h) markedly inhibits rIL-12-enhanced CD40L expression in PBMC cultures^[2].
In Vivo:Daclizumab (100 μg/mouse, i.v., once weekly for 4 weeks on days 0, 7, 14, 21) exhibits significant anti-tumor efficacy in NOD/SCID mice bearing MET-1 human T-cell leukemia cells^[3].