MEDI-3622

MEDI-3622 specifically recognizes ADAM17 on human peripheral blood leukocytes, including both CD56_bright CD3⁻ and CD56_dim CD3⁻ human NK cell subsets^[1].
MEDI-3622 (1 µg/mL; 2 h) blocks ADAM17-mediated shedding of CD16A and CD62L by enriched human peripheral blood NK cells activated by trastuzumab-bound SKOV-3 ovarian cancer cells, without inhibiting NK cell activation (CD107a upregulation)^[1].
MEDI-3622 (1 µg/mL; 4 h) significantly enhances IFNγ secretion by enriched human peripheral blood NK cells stimulated by trastuzumab-bound SKOV-3 or MA-148 ovarian cancer cells, and rituximab-bound Raji Burkitt's lymphoma cells, across all tested effector:target ratios (10:1 to 1:10), but does not affect granzyme A or granzyme B secretion^[1].
MEDI-3622 (1 µg/mL; 4 h) enhancement of IFNγ secretion by enriched human peripheral blood NK cells stimulated with trastuzumab-bound SKOV-3 ovarian cancer cells is dependent on CD16A activity^[1].
MEDI-3622 (1 µg/mL; 4 h) enhances IFNγ secretion by NK92 human NK cells expressing wildtype CD16A (but not non-cleavable CD16A) stimulated by trastuzumab-bound SKOV-3 ovarian cancer cells, indicating the effect is mediated by blocking CD16A shedding^[1].

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