CAP-100

CAP-100 (0.1-10 ng/μL) demonstrates the most potent binding to CCR7 immunogen SYM1899 (100 ng) with a EC₅₀ of 1.78 ng/mL^[1].
CAP-100 (0.01-100 μg/mL) shows dose-dependent inhibition of ligand-induced activation, reaching maximal inhibitions close to 100% in CCR7⁺ CHO-K1 cells stimulated with CCL19^[1].
CAP-100 (0.1-100 μg/mL) binds to CCR7⁺ non-tumor PB or BM cells from healthy donors at high experimental concentrations^[1].
CAP-100 (1-100 μg/mL) impairs the increase of D-actin upon CCL19/CCL21 stimulation in CLL cells^[1].
CAP-100 (0.1-100 μg/mL, 4 h) demonstrates a strong dose-related inhibitory activity against CCR7-driven T-PLL cells migration towards 1 μg/mL of CCL19 or CCL21^[1].
CAP-100 (10 μg/mL) impairs CCR7-induced migration of CCL cells in trans-endothelial migration (TEM) assays^[1].
CAP-100 (10-100 μg/mL, 24 h) does not mediate direct specific-induced cell death but impairs the viability of CCR7-mediated cells which is the protective function in CLL^[1].
CAP-100 (10 μg/mL) activated human NK-92-CD16⁺ cells to induce a strong ADCC on target CLL cells^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.