CD30-directed antibody–drug conjugate; internalized into Hodgkin/Reed-Sternberg cells to release MMAE (a microtubule inhibitor), inducing apoptosis and potentially mediating ADCC.
CD30-directed antibody–drug conjugate that binds CD30 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE via proteolytic cleavage of a valine–citrulline linker, causing tubulin depolymerization, G2/M arrest, and apoptosis; may also mediate ADCC.
YES
DIRECT
Anti‑CD30 ADC binds CD30, is internalized, linker is cleaved to release MMAE, which inhibits tubulin, causing G2/M arrest and apoptosis; ADCC may also contribute.
An antibody–drug conjugate (ADC) consisting of a humanized anti–B7‑H3 (CD276) IgG1 linked via a protease‑cleavable linker to a duocarmycin DNA‑alkylating payload. After binding B7‑H3 on tumor cells and internalization, it releases the payload to cause DNA minor‑groove alkylation, DNA damage, and tumor cell death. Administered IV (2.7 mg/kg q28d).
Humanized anti-B7-H3 (CD276) IgG1 ADC with a protease-cleavable linker to a duocarmycin payload; after B7-H3 binding and internalization by tumor cells, linker cleavage releases duocarmycin, which binds the DNA minor groove and alkylates adenine (N3), causing DNA damage and tumor cell death.
YES
DIRECT
The ADC binds B7-H3 on target cells, is internalized, and a protease-cleavable linker releases a duocarmycin payload that alkylates DNA (minor groove, N3 adenine), causing DNA damage and cell death.
Autologous, gene-modified T cells expressing a cooperative/dual chimeric antigen receptor targeting ADGRE2 (EMR2) and CLEC12A (CLL-1) to mediate cytotoxic killing of AML blasts/LSCs while aiming to spare normal myeloid cells.
Autologous T cells engineered to express a cooperative dual chimeric antigen receptor targeting ADGRE2 (EMR2) and CLEC12A (CLL-1) on AML blasts and leukemic stem cells; antigen binding activates CAR signaling leading to T-cell activation and cytotoxic killing of malignant cells while aiming to spare normal myeloid cells.
YES
DIRECT
CAR T cells engage CLEC12A (in a cooperative dual-CAR with ADGRE2), triggering CAR signaling that activates T-cell cytotoxicity (perforin/granzyme release and death-receptor pathways) to lyse CLEC12A-positive cells.
Humanized IgG1 monoclonal antibody targeting CD117 (c-KIT) on hematopoietic stem and progenitor cells; blocks SCF-c-KIT signaling to deplete CD117+ cells. Administered IV on Day 1 of each 8-week cycle for up to 4 cycles.
Humanized IgG1 monoclonal antibody targeting CD117 (c-KIT) on hematopoietic stem and progenitor cells; blocks stem cell factor (SCF)–c-KIT signaling to suppress survival/maintenance and deplete CD117+ cells (including malignant clones), with depletion aided by Fc-mediated effector functions such as ADCC/phagocytosis.
YES
DIRECT
The anti-CD117 IgG1 binds c-KIT on CD117+ cells, blocks SCF–c-KIT survival signaling, and engages Fcγ receptor–bearing immune cells to mediate ADCC and antibody-dependent phagocytosis, depleting/killing CD117+ cells.
Chimeric anti‑CD20 IgG1 monoclonal antibody that induces B‑cell depletion via ADCC, CDC, and apoptosis.
Chimeric anti‑CD20 IgG1 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ cells via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Binds CD20 on B cells and induces Fc-mediated ADCC by NK/macrophages, complement-dependent cytotoxicity (MAC formation), and can trigger apoptosis via CD20 crosslinking.