Autologous anti-BCMA CAR-T cell therapy (lentiviral-transduced T cells) that binds BCMA on malignant plasma cells/mature B cells and activates T-cell–mediated cytotoxicity.
Autologous T cells are lentiviral-transduced to express a chimeric antigen receptor that targets BCMA on malignant plasma cells/mature B cells; CAR engagement activates T‑cell signaling (CD3ζ with costimulation), leading to targeted cytotoxicity and elimination of BCMA-expressing cells.
Anti-BCMA CAR T cells bind BCMA on target cells; CAR signaling (CD3ζ with costimulation) activates T cells to kill BCMA+ cells via perforin/granzyme release and death-receptor pathways.
Anti-CD38 IgG1 monoclonal antibody that induces ADCC, CDC, ADCP, and direct apoptosis of CD38+ plasma cells and immunosuppressive subsets.
Human IgG1κ monoclonal antibody targeting CD38 on plasma cells and other immune cells; induces direct apoptosis and Fc-mediated effector functions—ADCC, CDC, and ADCP—leading to depletion of CD38+ malignant plasma cells and immunosuppressive Tregs, Bregs, and MDSCs, producing antitumor and immunomodulatory effects.
Daratumumab binds CD38 on target cells and triggers Fc-mediated ADCC (NK cells), CDC (complement), and ADCP (macrophages), and can induce direct apoptosis of CD38+ cells.
An intravenous antibody–drug conjugate (ADC) composed of a monoclonal antibody targeting an undisclosed tumor-associated surface antigen linked to a cytotoxic payload, likely a topoisomerase I inhibitor. Upon binding and internalization, it releases the payload to cause DNA damage and apoptosis, with potential bystander effect, in advanced solid tumors.
Intravenous monoclonal antibody–drug conjugate that binds a tumor-associated surface antigen, is internalized, and releases a cytotoxic payload—likely a topoisomerase I inhibitor—to induce DNA damage and apoptosis, with potential bystander effect, in antigen-expressing solid tumors.
ADC binds the tumor-associated surface antigen, is internalized, and releases a topoisomerase I inhibitor payload that causes DNA damage and apoptosis in antigen-expressing cells (with potential bystander effect).
Autologous, genetically modified TCR-T cell therapy engineered to express an affinity-enhanced T-cell receptor that recognizes MAGE-A4 peptide presented by HLA-A*02; administered as a single weight-based IV infusion to mediate antigen-specific cytotoxicity via TCR/CD3 signaling, perforin/granzyme release, and cytokine secretion.
Autologous T cells genetically modified to express an affinity-enhanced TCR that recognizes MAGE-A4 peptide presented by HLA-A*02 on tumor cells; TCR/CD3 engagement activates the T cells to mediate antigen-specific killing via perforin/granzyme release and cytokine secretion.
Affinity-enhanced TCR-T cells recognize the MAGE-A4 peptide presented by HLA-A*02 on target cells and kill them via TCR/CD3-triggered perforin/granzyme-mediated cytolysis and cytokine release.
Also known as JSP191; a subcutaneous monoclonal antibody targeting c-KIT (CD117) that blocks stem cell factor binding to inhibit SCF/c-KIT signaling, depleting or functionally inhibiting c-KIT–dependent cells (notably tissue mast cells) to reduce mast-cell activation and mediator release.
Humanized monoclonal antibody against CD117 (c-KIT) that blocks stem cell factor (SCF) binding, inhibiting SCF/c-KIT signaling and depleting or functionally inhibiting c-KIT–dependent cells (notably mast cells and hematopoietic stem/progenitor cells), thereby reducing mast-cell activation and mediator release.
By binding CD117 (c-KIT) and blocking SCF–c-KIT survival signaling, it depletes c-KIT–dependent cells (e.g., HSCs, mast cells), leading to apoptosis/loss of viability; Fc effector functions may also contribute to immune-mediated clearance.