Fully human IgG1 anti-CD20 monoclonal antibody (Kesimpta) administered subcutaneously; depletes B cells via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity to reduce neuroinflammation in relapsing multiple sclerosis.
Fully human IgG1 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ B cells via complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC), thereby reducing B‑cell antigen presentation, cytokine/autoantibody production, and neuroinflammation in relapsing multiple sclerosis; spares stem cells and plasma cells.
Ofatumumab binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated antibody‑dependent cellular cytotoxicity, leading to lysis of CD20+ cells.
First-generation BCR-ABL tyrosine kinase inhibitor used to suppress leukemic proliferation in CML.
ATP-competitive tyrosine kinase inhibitor targeting BCR-ABL (and also PDGFR and KIT), blocking downstream phosphorylation signaling to suppress proliferation and induce apoptosis of malignant cells (e.g., CML; GIST via KIT).
Imatinib directly inhibits PDGFRB tyrosine kinase activity, suppressing downstream survival/proliferation signaling and inducing apoptosis in PDGFRB‑dependent cells (non–immune-mediated).
Autologous genetically engineered T cells expressing a chimeric antigen receptor targeting GUCY2C; infused once after lymphodepletion to mediate HLA-independent cytotoxicity and cytokine release against GUCY2C-positive colorectal cancer cells.
Autologous T cells genetically engineered to express a chimeric antigen receptor that binds GUCY2C on colorectal cancer cells, triggering HLA-independent T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity to kill GUCY2C-positive tumor cells; given after lymphodepletion to enhance expansion and persistence.
CAR-T cells recognize GUCY2C on target cells and, upon activation, kill them via perforin/granzyme-mediated cytotoxicity (HLA-independent).
Autologous ex vivo–expanded tumor-infiltrating lymphocytes (TIL) used for adoptive cell therapy; mediate antigen-specific tumor killing via TCR recognition and cytotoxic effector functions.
Autologous ex vivo–expanded tumor-infiltrating lymphocytes that recognize tumor antigens via their endogenous T-cell receptors engaging peptide–MHC on tumor cells, mediating antigen-specific cytotoxicity through perforin/granzyme release and cytokine secretion, leading to targeted tumor cell killing and immune amplification within the tumor microenvironment.
TIL recognize tumor peptide–HLA class I complexes via their endogenous TCRs and directly kill target cells through perforin/granzyme-mediated apoptosis (with possible Fas–FasL and cytokine contributions).
Autologous ex vivo–expanded tumor-infiltrating lymphocytes (TIL) used for adoptive cell therapy; mediate antigen-specific tumor killing via TCR recognition and cytotoxic effector functions.
Autologous ex vivo–expanded tumor-infiltrating lymphocytes that recognize tumor antigens via their endogenous T-cell receptors engaging peptide–MHC on tumor cells, mediating antigen-specific cytotoxicity through perforin/granzyme release and cytokine secretion, leading to targeted tumor cell killing and immune amplification within the tumor microenvironment.
Endogenous TCRs on the infused TILs recognize the tumor antigen peptide presented on HLA class II, triggering cytotoxic effector functions (perforin/granzyme release and Fas–FasL/TNF signaling) that induce apoptosis of peptide–HLA-II–positive cells.