A human IgG1 broadly neutralizing monoclonal antibody engineered with an LS Fc mutation for extended half-life; binds the HIV-1 Env gp120 V2 apex to block viral entry and can mediate Fc-dependent effector functions (ADCC/ADCP).
Human IgG1 broadly neutralizing monoclonal antibody with an LS Fc mutation for extended half-life (enhanced FcRn binding); binds the HIV-1 Env gp120 V2 apex to neutralize virions and block viral entry, and can engage Fc gamma receptors to mediate ADCC/ADCP against Env-expressing infected cells.
The IgG1 antibody binds the Env gp120 V2 apex on infected cells and engages Fcγ receptors to trigger NK-cell ADCC and macrophage ADCP (and potentially complement/CDC), killing Env-expressing cells.
Lentiviral CAR T cells targeting GPRC5D; IV dose-escalated infusion; mediates MHC-independent killing of GPRC5D+ myeloma cells/plasma cells.
Autologous/allogeneic T cells are lentivirally transduced to express a CAR specific for GPRC5D. Upon binding GPRC5D on malignant plasma cells, the CAR triggers MHC-independent T-cell activation, leading to cytotoxic killing via perforin/granzyme release and cytokine-mediated elimination of GPRC5D-positive myeloma cells.
GPRC5D-specific CAR T cells bind GPRC5D on target cells, become activated, and kill via T-cell cytotoxicity (perforin/granzyme–mediated lysis, with possible Fas/FasL and cytokine-mediated effects).
A human IgG1 broadly neutralizing monoclonal antibody with an LS Fc mutation for extended half-life; targets the HIV-1 Env gp120 CD4 binding site to prevent viral entry and can engage Fc-mediated effector functions.
Human IgG1 broadly neutralizing monoclonal antibody with an LS Fc mutation to extend half-life; binds the HIV-1 Env gp120 CD4 binding site to neutralize virions and block attachment/entry into CD4+ T cells. Its Fc region can engage Fc gamma receptors to mediate ADCC/ADCP, aiding clearance of Env-expressing infected cells.
The IgG1 bnAb binds gp120 on Env-expressing infected cells and engages Fcγ receptors on NK cells/monocytes to trigger ADCC/ADCP; it can also activate complement (CDC), leading to lysis of the target cell.
An anti‑HER2 antibody–drug conjugate consisting of a humanized anti‑HER2 monoclonal antibody linked to the microtubule inhibitor MMAE; kills HER2‑expressing tumor cells with a bystander effect.
Humanized anti-HER2 monoclonal antibody conjugated to the microtubule inhibitor MMAE. Binds HER2 on tumor cells, is internalized, and releases MMAE via a cleavable linker to disrupt microtubules, causing G2/M arrest and apoptosis; cytotoxic payload can diffuse for a bystander effect on neighboring cells with lower HER2 expression.
Anti-HER2 ADC binds HER2, is internalized, and releases MMAE via a cleavable linker; MMAE disrupts microtubules causing G2/M arrest and apoptosis (with possible bystander killing).
Engineered CAR T cells directed at CD38 using lentiviral transduction; IV infusion with dose escalation; targets CD38+ plasma cell/myeloma malignancies via CAR-mediated T-cell activation and cytotoxicity.
Gene-modified T cells transduced (lentiviral) to express a chimeric antigen receptor that binds CD38 on target cells. CAR engagement triggers T‑cell activation and proliferation with cytokine release and perforin/granzyme-mediated cytotoxicity, leading to MHC-independent killing of CD38-positive plasma cell/myeloma malignancies.
CAR T cells recognize CD38 on target cells, form an immune synapse, and kill via perforin/granzyme-mediated lysis and apoptosis (plus Fas/FasL and cytokine-mediated effects), independent of MHC.