A humanized, afucosylated IgG1 monoclonal antibody (brand: Fasenra) that targets IL-5 receptor alpha (IL-5Rα) on eosinophils and basophils, blocks IL-5 signaling, and engages FcγRIIIa on NK cells to drive ADCC-mediated depletion of these cells; administered subcutaneously (e.g., 30 mg/10 mg) for eosinophilic asthma.
Benralizumab is an afucosylated humanized IgG1 monoclonal antibody that binds IL-5 receptor alpha on eosinophils and basophils, blocks IL-5 signaling, and engages FcγRIIIa on NK cells to trigger ADCC-mediated depletion of these cells, reducing eosinophilic inflammation.
YES
DIRECT
Benralizumab binds IL-5Rα on eosinophils/basophils and its afucosylated IgG1 Fc engages FcγRIIIa on NK cells to induce antibody-dependent cellular cytotoxicity (ADCC), leading to apoptosis and depletion of the target cells.
A humanized, afucosylated IgG1 monoclonal antibody (brand: Fasenra) that targets IL-5 receptor alpha (IL-5Rα) on eosinophils and basophils, blocks IL-5 signaling, and engages FcγRIIIa on NK cells to drive ADCC-mediated depletion of these cells; administered subcutaneously (e.g., 30 mg/10 mg) for eosinophilic asthma.
Benralizumab is an afucosylated humanized IgG1 monoclonal antibody that binds IL-5 receptor alpha on eosinophils and basophils, blocks IL-5 signaling, and engages FcγRIIIa on NK cells to trigger ADCC-mediated depletion of these cells, reducing eosinophilic inflammation.
NO
INDIRECT
Benralizumab binds IL-5Rα on eosinophils/basophils and uses its Fc to engage FcγRIIIa (CD16a) on NK cells, triggering ADCC to kill the IL-5Rα+ cells; CD16a+ NK cells are effectors, not targets.
Autologous anti-CD7 chimeric antigen receptor T-cell (CAR-T) therapy; patient T cells are engineered to express a CAR targeting CD7, and upon engagement they activate cytotoxic pathways to eliminate CD7+ malignant T cells.
Autologous T cells are engineered to express a chimeric antigen receptor that binds CD7 on T-lineage cells. Upon CD7 engagement, CAR signaling (CD3ζ with costimulatory domains) activates T‑cell cytotoxicity and cytokine release, leading to perforin/granzyme-mediated lysis of CD7+ malignant T-ALL/LL cells, with on‑target depletion of normal CD7+ T (and some NK) cells.
YES
DIRECT
Anti-CD7 CAR-T cells recognize CD7 on target cells; CAR signaling activates T-cell effector functions, releasing perforin and granzymes (and Fas–FasL signaling), leading to lysis/apoptosis of CD7+ cells.
Intravenous T-cell–engaging bispecific antibody (CD20×CD3; 2:1 format) that redirects patient T cells via CD3 to kill CD20-positive malignant B cells.
Glofitamab is an intravenous CD20×CD3 bispecific antibody (2:1 format, two CD20 arms and one CD3 arm) that simultaneously binds CD20 on B cells and CD3 on T cells, cross-linking them to form an immune synapse. This redirects and activates patient T cells to kill CD20-positive malignant B cells via perforin/granzyme-mediated cytotoxicity and apoptosis, independent of MHC presentation.
YES
DIRECT
The CD20×CD3 bispecific links T cells to CD20+ cells, forming an immune synapse and activating T cells to release perforin and granzymes, causing lysis/apoptosis of the CD20-expressing cells (MHC-independent).
Intravenous T-cell–engaging bispecific antibody (CD20×CD3; 2:1 format) that redirects patient T cells via CD3 to kill CD20-positive malignant B cells.
Glofitamab is an intravenous CD20×CD3 bispecific antibody (2:1 format, two CD20 arms and one CD3 arm) that simultaneously binds CD20 on B cells and CD3 on T cells, cross-linking them to form an immune synapse. This redirects and activates patient T cells to kill CD20-positive malignant B cells via perforin/granzyme-mediated cytotoxicity and apoptosis, independent of MHC presentation.
NO
INDIRECT
Glofitamab binds CD3 epsilon on T cells to recruit and activate them to kill CD20-positive B cells via perforin/granzyme; CD3-expressing T cells are not targeted for killing.