Humanized IgG1 anti‑CD117/c‑Kit monoclonal antibody that depletes endogenous hematopoietic stem cells to open marrow niches.
Humanized IgG1 monoclonal antibody targeting CD117 (c-Kit) on hematopoietic stem cells; blocks stem cell factor (SCF) binding and SCF–c-Kit signaling, depleting endogenous HSCs and opening marrow niches for transplantation conditioning.
YES
INDIRECT
Blocks SCF–c-Kit survival signaling on CD117+ hematopoietic stem cells, leading to loss of pro‑survival signals and apoptosis/depletion rather than direct immune cell–mediated killing.
Autologous, non–genetically engineered, ex vivo–expanded polyclonal multi–tumor-associated antigen (multiTAA)–specific T-cell therapy that recognizes multiple shared TAAs on pancreatic adenocarcinoma via native, MHC-restricted TCRs to mediate cytotoxic killing and cytokine-driven immune activation.
Autologous, ex vivo-expanded polyclonal CD4+/CD8+ T cells with native, MHC-restricted TCRs specific for multiple shared tumor-associated antigens on pancreatic adenocarcinoma. After infusion, these T cells recognize antigen-MHC complexes on tumor cells and mediate cytotoxic killing (perforin/granzyme) and cytokine-driven immune activation; multi-antigen targeting reduces antigen-loss escape and may improve durability.
YES
DIRECT
Autologous multiTAA-specific T cells recognize WT1-derived peptides presented on MHC via native TCRs and directly kill target cells through perforin/granzyme-mediated cytotoxicity (with cytokine-driven activation).
Biosimilar of infliximab (Remsima/CT-P13), a chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α to block TNFR1/2 signaling and downstream NF-κB activation, reducing proinflammatory cytokines, adhesion molecules, leukocyte recruitment, and keratinocyte hyperproliferation; may mediate Fc-dependent lysis/apoptosis of TNF-α–expressing cells.
IgG1 monoclonal antibody biosimilar to infliximab that binds soluble and transmembrane TNF-alpha, neutralizing TNF and blocking TNFR1/2 signaling and downstream NF-kB activation; decreases proinflammatory cytokines and adhesion molecules, limits leukocyte recruitment and keratinocyte hyperproliferation; may induce Fc-mediated lysis/apoptosis of TNF-alpha-expressing cells.
NO
INDIRECT
Neutralizes soluble TNF-alpha and blocks TNFR signaling; does not directly kill cells (Fc-mediated cytotoxicity applies only to transmembrane TNF).
Biosimilar of infliximab (Remsima/CT-P13), a chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α to block TNFR1/2 signaling and downstream NF-κB activation, reducing proinflammatory cytokines, adhesion molecules, leukocyte recruitment, and keratinocyte hyperproliferation; may mediate Fc-dependent lysis/apoptosis of TNF-α–expressing cells.
IgG1 monoclonal antibody biosimilar to infliximab that binds soluble and transmembrane TNF-alpha, neutralizing TNF and blocking TNFR1/2 signaling and downstream NF-kB activation; decreases proinflammatory cytokines and adhesion molecules, limits leukocyte recruitment and keratinocyte hyperproliferation; may induce Fc-mediated lysis/apoptosis of TNF-alpha-expressing cells.
YES
DIRECT
IgG1 binds transmembrane TNF-α on cells and, via its Fc, triggers ADCC by FcγR+ effector cells and complement-dependent cytotoxicity; ligation of tmTNF can also induce reverse-signaling apoptosis in the target cell.
Autologous, gene-modified TCR-T cell product. Patient T cells are engineered ex vivo to express a personalized T-cell receptor matched to the patient’s HLA class I type that recognizes tumor-specific peptides; cells are expanded and reinfused to mediate cytotoxic killing via TCR/CD3 activation, perforin/granzyme release, and cytokine secretion.
Autologous T cells are genetically engineered ex vivo to express a personalized T-cell receptor matched to the patient’s HLA class I that recognizes tumor-specific peptides. Upon peptide–HLA engagement, TCR/CD3 signaling activates the transferred T cells to kill tumor cells via perforin/granzyme release and cytokine secretion.
YES
DIRECT
Engineered TCR-T cells recognize the tumor peptide–HLA class I complex via the introduced TCR, activate through TCR/CD3, form an immunologic synapse, and induce target-cell death by perforin/granzyme–mediated apoptosis (with cytokine-mediated support).