Allogeneic T cells from the patient's prior HSCT donor engineered to express an anti-CD7 chimeric antigen receptor; upon CD7 binding, initiates cytotoxic killing of CD7+ malignant T cells via TCR-like signaling, perforin/granzyme pathways, and cytokine release. Expected on-target depletion of normal CD7+ T cells and some NK cells, causing T-cell aplasia.
Allogeneic T cells from the prior HSCT donor are engineered to express an anti‑CD7 chimeric antigen receptor. CAR engagement with CD7 on malignant T cells triggers TCR-like signaling that activates cytotoxic effector functions, leading to perforin/granzyme-mediated lysis and cytokine release. On‑target effects include depletion of normal CD7+ T cells (and some NK cells), causing T‑cell aplasia.
YES
DIRECT
Anti-CD7 CAR T cells bind CD7 on target cells and, upon CAR engagement, activate T-cell cytotoxic programs leading to perforin/granzyme-mediated lysis (and potentially Fas/FasL), directly killing CD7+ cells.
Allogeneic, off-the-shelf T cells engineered with an anti-CD19 chimeric antigen receptor to target and eliminate CD19-expressing B-lineage cells, inducing transient B-cell aplasia to reduce autoantibody production and reset humoral immunity in refractory SLE.
Allogeneic T cells engineered with an anti-CD19 chimeric antigen receptor recognize and kill CD19-expressing B-lineage cells. CAR engagement triggers T-cell cytotoxicity (perforin/granzyme) leading to depletion of CD19+ B cells and plasmablasts, inducing transient B-cell aplasia, reducing autoantibody production, and resetting humoral immunity in refractory SLE.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells and trigger T-cell cytotoxicity, lysing targets via perforin/granzyme-mediated apoptosis (and death receptor pathways).
A biological monoclonal antibody targeting the KIT (CD117) receptor; blocks KIT/stem cell factor signaling to suppress and deplete mast cells, aiming to reduce mast cell–driven inflammation in eosinophilic esophagitis.
Monoclonal antibody targeting KIT (CD117) that blocks stem cell factor (SCF)–KIT signaling, suppressing and depleting mast cells and thereby reducing mast cell–driven inflammation (e.g., in eosinophilic esophagitis).
YES
DIRECT
Blocks SCF–KIT survival signaling on KIT+ mast cells, leading to apoptosis and depletion; Fc effector functions may also contribute via ADCC/ADCP against KIT-expressing cells.
Intravenous human polyclonal anti-HBs IgG (brand: Hepatect CP) used as passive immunotherapy before liver resection or transplant; neutralizes HBV virions and HBsAg subviral particles to lower HBsAg, can be internalized by hepatocytes to inhibit HBsAg/virion secretion, and mediates Fc-dependent ADCC against HBV-infected hepatocytes; preclinical data suggest direct anti-tumor effects on HBV-related HCC tumor-initiating cells.
Human polyclonal anti-HBs IgG that passively neutralizes HBV virions and HBsAg subviral particles to lower circulating HBsAg; can be internalized by hepatocytes to inhibit HBsAg and virion secretion; Fc region engages Fc-gamma receptors to mediate ADCC against HBV-infected hepatocytes, with preclinical evidence of direct anti-tumor effects on HBV-related HCC tumor-initiating cells.
YES
DIRECT
Anti-HBs IgG binds HBsAg on infected hepatocytes; Fc engages FcγR+ effector cells to mediate ADCC (and can activate complement/CDC), leading to lysis of HBsAg-expressing cells.
Intravenous human polyclonal anti-HBs IgG (brand: Hepatect CP) used as passive immunotherapy before liver resection or transplant; neutralizes HBV virions and HBsAg subviral particles to lower HBsAg, can be internalized by hepatocytes to inhibit HBsAg/virion secretion, and mediates Fc-dependent ADCC against HBV-infected hepatocytes; preclinical data suggest direct anti-tumor effects on HBV-related HCC tumor-initiating cells.
Human polyclonal anti-HBs IgG that passively neutralizes HBV virions and HBsAg subviral particles to lower circulating HBsAg; can be internalized by hepatocytes to inhibit HBsAg and virion secretion; Fc region engages Fc-gamma receptors to mediate ADCC against HBV-infected hepatocytes, with preclinical evidence of direct anti-tumor effects on HBV-related HCC tumor-initiating cells.
NO
INDIRECT
HBIG binds HBsAg on infected hepatocytes; its Fc engages CD16A (FCGR3A) on NK cells to trigger ADCC that kills HBsAg+ hepatocytes. CD16A-expressing cells act as effectors and are not killed.