CAP-100 is a monoclonal antibody targeting CCR7. It neutralizes the ligand binding site and signaling of CCR7. This compound effectively inhibits migration, extravasation, homing, and survival in chronic lymphocytic leukemia (CLL) samples induced by CCR7. CAP-100 can mediate potent tumor cell killing through host immune mechanisms and exhibits favorable toxicity profiles in related hematopoietic cell subsets. It is involved in research on antitumor activity and diseases like chronic lymphocytic leukemia (CLL).

CAP-100 demonstrates a high affinity for the immunogen CCR7 SYM1899 (100 ng) with an EC50 value of 1.78 ng/mL when present at 0.1-10 ng/μL. It exhibits dose-dependent inhibition of ligand-induced activation in CCL19-stimulated CCR7+ CHO-K1 cells, achieving nearly full suppression at concentrations of 0.01-100 μg/mL. At higher concentrations (0.1-100 μg/mL), CAP-100 binds to CCR7+ non-tumor cells from healthy donors. Furthermore, CAP-100 (1-100 μg/mL) inhibits the increase of D-actin following CCL19/CCL21 stimulation in chronic lymphocytic leukemia (CLL) cells. Over a period of four hours, CAP-100 (0.1-100 μg/mL) demonstrates a strong dose-dependent inhibition, blocking the migration of CCR7-driven T-PLL cells towards 1 μg/mL CCL19 or CCL21. Although CAP-100 (10-100 μg/mL, 24 hours) does not directly induce specific cell death, it reduces CCR7-mediated cell viability, crucial for CLL cell protection. At 10 μg/mL, CAP-100 activates human NK-92-CD16+ cells, leading to potent ADCC against target CLL cells.

CAP-100 administered intravenously at a dose of 10 μg/mL as a single injection reduces the homing of CCR7-expressing cells to lymph nodes in NSG mice. A single intravenous dose of CAP-100 ranging from 25 to 200 μg extends the median overall survival and diminishes tumor burden and lymph node infiltration in mice with Granta-519-luc+. Compared with Trastuzumab (200 μg), single-dose intravenous CAP-100 (10-200 μg) significantly prolongs the lifespan of JVM-3-bearing SCID mice.