Glycoengineered chimeric IgG1 anti-CD20 monoclonal antibody (TG-1101/BRIUMVI). Afucosylation enhances FcγRIIIa binding and antibody-dependent cellular cytotoxicity; also induces complement-dependent cytotoxicity and apoptosis, leading to rapid, sustained depletion of CD20+ B cells in relapsing multiple sclerosis.
Glycoengineered, afucosylated chimeric IgG1 monoclonal antibody targeting CD20 on B cells; enhanced FcγRIIIa binding drives potent antibody-dependent cellular cytotoxicity (ADCC), also triggers complement-dependent cytotoxicity (CDC) and apoptosis, resulting in rapid and sustained depletion of CD20+ B cells.
YES
DIRECT
Binds CD20 on B cells and engages immune effectors via its Fc to induce ADCC (enhanced via FcγRIIIa), activates complement for CDC, and can trigger apoptosis, leading to depletion of CD20+ cells.
Glycoengineered chimeric IgG1 anti-CD20 monoclonal antibody (TG-1101/BRIUMVI). Afucosylation enhances FcγRIIIa binding and antibody-dependent cellular cytotoxicity; also induces complement-dependent cytotoxicity and apoptosis, leading to rapid, sustained depletion of CD20+ B cells in relapsing multiple sclerosis.
Glycoengineered, afucosylated chimeric IgG1 monoclonal antibody targeting CD20 on B cells; enhanced FcγRIIIa binding drives potent antibody-dependent cellular cytotoxicity (ADCC), also triggers complement-dependent cytotoxicity (CDC) and apoptosis, resulting in rapid and sustained depletion of CD20+ B cells.
NO
INDIRECT
CD16a (Fc gamma RIIIa) on NK cells is an effector receptor bound by the afucosylated Fc of ublituximab to drive ADCC against CD20+ B cells; CD16a-expressing cells are not targeted or killed by the drug.
Autologous, genetically engineered T cells expressing a CD7-specific chimeric antigen receptor to recognize and eliminate CD7-positive malignant T cells.
Autologous T cells are genetically engineered to express a CD7-specific chimeric antigen receptor; upon binding CD7 on malignant T cells, CAR signaling activates the T cells to proliferate, release cytotoxic mediators, and lyse CD7-positive tumor cells independently of the native TCR.
YES
DIRECT
CAR-T cells bind CD7 on target cells, become activated, and kill via perforin/granzyme release and death-receptor pathways, lysing CD7-positive cells.
Antibody-drug conjugate targeting MET (c-Met/HGFR); after internalization it releases a topoisomerase I inhibitor payload that causes DNA damage and tumor cell death.
Monoclonal antibody–drug conjugate targeting MET (c-Met/HGFR); after binding and internalization, it releases a topoisomerase I inhibitor payload that inhibits DNA replication, causing DNA damage and death of MET-expressing tumor cells.
YES
DIRECT
The ADC binds MET on target cells, is internalized, and releases a topoisomerase I inhibitor payload that blocks DNA replication and causes DNA damage, leading to cell death.
Long-acting LS-engineered human IgG1 broadly neutralizing monoclonal antibody targeting the HIV-1 gp120 CD4-binding site to block attachment/entry; extended half-life via enhanced FcRn binding and may mediate Fc-effector functions (e.g., ADCC/ADCP).
Long-acting LS-engineered human IgG1 broadly neutralizing monoclonal antibody that binds the HIV-1 gp120 CD4-binding site, blocking attachment to CD4 and preventing viral entry; LS Fc modifications enhance FcRn binding to extend half-life and may enable Fc-mediated effector functions (e.g., ADCC/ADCP) against Env-expressing cells.
NO
INDIRECT
VRC01.23LS binds HIV-1 gp120, not FcRn. LS mutations enhance FcRn-mediated recycling to extend half-life; they do not direct cytotoxicity toward FcRn-expressing cells. Any killing is of HIV Env–expressing infected cells via Fc-mediated ADCC/ADCP, not of FcRn+ cells.