Antibody–drug conjugate of farletuzumab linked to eribulin; targets FRα on tumor cells to deliver eribulin intracellularly, disrupting microtubules and inducing apoptosis.
FRα-targeted ADC: farletuzumab binds folate receptor‑α on tumor cells and is internalized; a cathepsin B–cleavable linker releases eribulin intracellularly, which binds the vinca domain of tubulin to inhibit microtubule polymerization, causing G2/M mitotic arrest and apoptosis (with potential bystander effect).
Farletuzumab binds FRα on tumor cells, the ADC is internalized, cathepsin B cleaves the linker to release eribulin, which inhibits microtubule polymerization (vinca domain), causing G2/M arrest and apoptosis (with potential bystander effect).
Anti–folate receptor alpha (FRα) IgG monoclonal antibody serving as the targeting moiety of MORAb-202 to bind FRα and enable receptor-mediated endocytosis.
Humanized IgG1 monoclonal antibody targeting folate receptor alpha (FR-alpha) overexpressed on epithelial cancers; binding elicits Fc-mediated ADCC and CDC to kill FR-alpha–positive cells and facilitates receptor-mediated internalization (serving as the targeting moiety for ADCs such as MORAb-202).
Farletuzumab binds FRα on target cells and engages effector functions via its Fc, inducing antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), leading to lysis of FRα-positive cells; it also undergoes receptor-mediated internalization (used for ADC delivery).
Fully human anti-CD20 monoclonal antibody (Kesimpta) administered subcutaneously; depletes CD20+ B cells via complement-dependent cytotoxicity and Fc-mediated antibody-dependent cytotoxicity/phagocytosis, reducing pathogenic B-cell activity in relapsing multiple sclerosis.
Fully human IgG1 anti-CD20 monoclonal antibody that binds CD20 on mature B cells and depletes them via complement-dependent cytotoxicity and Fc-mediated antibody-dependent cellular cytotoxicity/phagocytosis, reducing pathogenic B-cell antigen presentation and cytokine production (sparing stem cells and plasma cells).
Ofatumumab binds CD20 on B cells and induces complement-dependent cytotoxicity (MAC-mediated lysis) and Fc-mediated ADCC/antibody-dependent phagocytosis by NK cells and macrophages, directly depleting CD20+ cells.
Microtubule dynamics inhibitor payload released from MORAb-202 inside FRα-expressing cells, causing G2/M arrest and apoptosis.
Eribulin is a halichondrin B analogue that binds to the vinca domain of tubulin and inhibits microtubule polymerization, disrupting mitotic spindle formation and causing G2/M cell-cycle arrest and apoptosis. In MORAb-202, eribulin is the cytotoxic payload released intracellularly after FRα-mediated endocytosis.
Eribulin binds the vinca domain of beta‑tubulin, blocking microtubule polymerization and causing G2/M arrest and apoptosis (after intracellular delivery/release).
Gene-modified natural killer cells engineered with a chimeric antigen receptor targeting CLL1 (CLEC12A) to recognize and kill CLL1+ AML cells.
Allogeneic iPSC-derived natural killer cells engineered with a chimeric antigen receptor targeting CLL1 (CLEC12A) bind CLL1 on AML blasts. CAR engagement activates NK effector functions, inducing targeted cytotoxicity (perforin/granzyme) and cytokine release to eliminate CLL1+ leukemic cells while sparing CLL1-negative hematopoietic stem cells.
CAR-engineered NK cells bind CLL1 on targets, triggering NK activation and degranulation to kill CLL1+ cells via perforin/granzyme-mediated cytolysis (and death-receptor pathways).