Intravenous broadly neutralizing monoclonal antibody targeting conserved HIV-1 Env epitopes; blocks viral entry and enables Fc-mediated clearance of infected cells.
Broadly neutralizing monoclonal antibody that binds conserved epitopes on the HIV-1 envelope (Env) glycoprotein, neutralizing virus by blocking attachment/fusion and entry into CD4+ T cells; Fc region can mediate effector functions (e.g., ADCC/ADCP/complement) to promote clearance of infected cells and virions.
Antibody binds Env (V3 glycan supersite) on HIV‑infected cells and engages Fc receptors/complement to trigger ADCC, ADCP, and CDC, resulting in lysis or phagocytic clearance of Env-positive cells.
CD3/CD19 bispecific T-cell engager (BiTE) that redirects CD3+ T cells to kill CD19+ B-precursor leukemia cells.
A CD3/CD19 bispecific T‑cell engager (BiTE) that binds CD3 on T cells and CD19 on B‑lineage leukemia/lymphoma cells, forming an immunologic synapse that activates T cells to kill CD19+ targets via perforin/granzyme release and cytokine-mediated cytotoxicity, independent of MHC.
Blinatumomab bridges CD3+ T cells to CD19+ cells, forming an immunologic synapse that triggers T‑cell perforin/granzyme release and cytokine-mediated killing (MHC-independent).
Oral, selective BCL-2 inhibitor (BH3 mimetic) that induces apoptosis.
Selective BCL-2 inhibitor (BH3 mimetic) that binds and neutralizes anti-apoptotic BCL-2, displacing pro-apoptotic proteins to restore mitochondrial apoptosis and induce cancer cell death.
Selective BH3-mimetic inhibition of BCL-2 in target cells releases pro-apoptotic proteins, activates BAX/BAK, induces mitochondrial outer membrane permeabilization, caspase activation, and apoptotic cell death.
Autologous T cells genetically modified to express a chimeric antigen receptor targeting B-cell maturation antigen (BCMA/TNFRSF17) on multiple myeloma cells, enabling antigen-specific T-cell activation and cytotoxicity.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds BCMA (TNFRSF17) on multiple myeloma cells, leading to antigen-specific T‑cell activation, proliferation, cytokine release, and cytotoxic killing of BCMA‑expressing tumor cells.
BCMA-specific CAR-T cells bind BCMA on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis and apoptosis (including death-receptor pathways).
A subcutaneous, full-length bispecific T‑cell–engaging monoclonal antibody (CD3×CD20) that binds CD20 on malignant B cells and CD3 on T cells to form an immune synapse, activate T cells, and induce targeted cytotoxic killing of CD20+ follicular lymphoma cells.
A subcutaneous full-length bispecific anti-CD3×CD20 monoclonal antibody that simultaneously binds CD20 on malignant B cells and CD3 on T cells, forming an immune synapse to activate and redirect T-cell cytotoxicity for targeted killing of CD20-positive follicular lymphoma cells.
The CD3×CD20 bispecific antibody bridges CD20+ cells to T cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme–mediated lysis) to kill CD20-expressing cells.