A HER2-targeted bispecific antibody–drug conjugate (ADC) administered IV every 3 weeks; binds two HER2 epitopes to enhance internalization and delivers an intracellular cytotoxic payload while also inhibiting HER2 signaling and potentially mediating ADCC.
TQB2102 is a bispecific anti‑HER2 antibody–drug conjugate that binds two distinct HER2 epitopes to enhance receptor engagement and internalization. After HER2-mediated uptake, it releases an intracellular cytotoxic payload to kill tumor cells. The antibody component can also inhibit HER2 signaling and may trigger Fc‑mediated effector functions such as ADCC.
YES
DIRECT
The HER2-targeted ADC binds HER2, is internalized, and releases an intracellular cytotoxic payload that kills the HER2-expressing cell; Fc functions may also trigger ADCC.
A single-dose allogeneic anti-CD19 chimeric antigen receptor T-cell (CAR-T) therapy using donor-derived T cells engineered to target CD19 on B cells, inducing profound B-cell depletion to suppress autoantibody production and reset humoral immunity in refractory SLE; administered after lymphodepleting chemotherapy.
Allogeneic donor-derived T cells engineered with an anti-CD19 chimeric antigen receptor recognize and kill CD19+ B cells/plasmablasts, causing profound B-cell depletion, suppression of autoantibody production, and reset of humoral immunity; administered after lymphodepleting chemotherapy.
YES
DIRECT
Anti-CD19 CAR-T cells recognize CD19 on B cells and directly induce killing via immune synapse formation with perforin/granzyme-mediated apoptosis (and Fas–FasL pathways).
An autologous, ex vivo–expanded T‑cell therapy composed of cytotoxic T lymphocytes engineered/selected to recognize personalized tumor‑specific antigens (neoantigens) via native TCRs; administered intraventricularly to target pediatric embryonal brain tumors.
Autologous, ex vivo–expanded cytotoxic T cells selected for reactivity to patient-specific tumor antigens/neoantigens via native TCRs. After intraventricular administration, TCR recognition of peptide–MHC on tumor cells activates CTLs to kill targets through perforin/granzyme release and cytokine-mediated immune responses in the CNS.
YES
DIRECT
TSA-T cells recognize the patient-specific neoantigen peptide–HLA-I complex via their TCRs and directly kill target cells by perforin/granzyme-mediated apoptosis (and possibly Fas/FasL).
An autologous, ex vivo–expanded T‑cell therapy composed of cytotoxic T lymphocytes engineered/selected to recognize personalized tumor‑specific antigens (neoantigens) via native TCRs; administered intraventricularly to target pediatric embryonal brain tumors.
Autologous, ex vivo–expanded cytotoxic T cells selected for reactivity to patient-specific tumor antigens/neoantigens via native TCRs. After intraventricular administration, TCR recognition of peptide–MHC on tumor cells activates CTLs to kill targets through perforin/granzyme release and cytokine-mediated immune responses in the CNS.
YES
DIRECT
TCR recognition of the neoantigen peptide–HLA-II complex on tumor cells activates the infused CTLs to kill the presenting cells via perforin/granzyme-mediated cytotoxicity.
TIGIT-targeting IgG1 monoclonal antibody with intact Fc; blocks TIGIT binding to CD155 (PVR) and CD112 (Nectin-2) to relieve TIGIT-mediated suppression, enhance CD8+ T-cell activity, and leverage Fc effector function for NK cell-mediated depletion of TIGIT-high intratumoral Tregs.
Humanized IgG1 anti-TIGIT immune checkpoint antibody that blocks TIGIT interaction with CD155 (PVR) and CD112 (Nectin-2), restoring CD226 co-stimulatory signaling and enhancing CD8+ T-cell and NK-cell activity; intact Fc enables ADCC/ADCP to deplete TIGIT-high intratumoral Tregs.
YES
DIRECT
Anti-TIGIT IgG1 binds TIGIT on target cells and engages Fcγ receptors on NK cells/macrophages, inducing ADCC/ADCP that depletes TIGIT-high cells (e.g., intratumoral Tregs).