A broadly neutralizing monoclonal antibody targeting the CD4 binding site on HIV‑1 Env (synonyms: 3BNC117‑LS, teropavimab); neutralizes virus and mediates Fc‑dependent effector functions (e.g., ADCC/ADCP).
Broadly neutralizing monoclonal antibody (3BNC117-LS/teropavimab) that binds the CD4-binding site on HIV-1 Env gp120, preventing attachment to CD4 and viral entry; its Fc domain mediates effector functions (e.g., ADCC and ADCP, and potentially CDC) to promote clearance of virions and infected cells.
NO
INDIRECT
GS-5423 binds HIV-1 Env on infected cells; its Fc engages CD16a on NK cells/macrophages to trigger ADCC/ADCP against Env+ cells. CD16a+ effector cells are not targeted or killed.
A broadly neutralizing monoclonal antibody targeting the CD4 binding site on HIV‑1 Env (synonyms: 3BNC117‑LS, teropavimab); neutralizes virus and mediates Fc‑dependent effector functions (e.g., ADCC/ADCP).
Broadly neutralizing monoclonal antibody (3BNC117-LS/teropavimab) that binds the CD4-binding site on HIV-1 Env gp120, preventing attachment to CD4 and viral entry; its Fc domain mediates effector functions (e.g., ADCC and ADCP, and potentially CDC) to promote clearance of virions and infected cells.
NO
INDIRECT
GS-5423 binds HIV-1 Env on infected cells; its Fc engages FcγRIIa (CD32a) on myeloid effector cells to trigger ADCP/ADCC (±CDC) that kills Env+ targets, not the CD32a-expressing cells.
A broadly neutralizing monoclonal antibody targeting the V3‑glycan epitope on HIV‑1 Env (synonyms: 10‑1074‑LS, zinlirvimab); neutralizes virus and mediates Fc‑dependent effector functions (e.g., ADCC/ADCP).
Broadly neutralizing IgG1 monoclonal antibody (10-1074-LS/zinlirvimab) that binds the V3-glycan (N332) epitope on HIV-1 Env gp120, neutralizing virus by blocking Env-mediated entry; Fc domain engagement mediates effector functions (ADCC/ADCP). LS mutations extend serum half-life.
YES
DIRECT
Antibody binds Env gp120 on infected cell surfaces; its IgG1 Fc engages Fcγ receptors on NK cells/macrophages to trigger ADCC/ADCP (and potentially complement), killing the Env-expressing cells.
Autologous T lymphocytes genetically modified to express a PSCA-targeted chimeric antigen receptor with 4-1BB co-stimulation and CD3ζ signaling, including a truncated CD19 tag for selection/tracking; administered intravenously after lymphodepletion.
Autologous T lymphocytes engineered to express a PSCA-specific chimeric antigen receptor (scFv-4-1BB-CD3zeta). CAR binding to PSCA on tumor cells delivers CD3zeta activation and 4-1BB co-stimulation, promoting T-cell proliferation, cytokine release, and perforin/granzyme-mediated killing of PSCA-positive cells. A truncated CD19 tag enables selection/tracking; given after lymphodepletion to support CAR-T expansion.
YES
DIRECT
CAR-T cells bind PSCA on target cells and, via CD3ζ activation with 4-1BB co-stimulation, directly kill PSCA-positive cells through perforin/granzyme (and Fas–FasL) cytotoxicity.
An intravenous biological immunotherapy in first-in-human monotherapy dose-escalation/expansion, likely targeting the CD47–SIRPα innate immune checkpoint (antibody or fusion protein) to block the “don’t-eat-me” signal and enhance macrophage-mediated phagocytosis and antitumor immunity, with focus on HER2-positive tumors.
Bispecific anti-CD47/anti-HER2 monoclonal antibody that targets HER2-positive tumor cells and blocks the CD47–SIRPα checkpoint to abrogate the tumor 'don't-eat-me' signal, enhancing macrophage-mediated phagocytosis and antigen presentation, with secondary activation of antitumor T-cell responses.
NO
INDIRECT
The drug targets HER2 on tumor cells and blocks CD47–SIRPα to permit macrophage-mediated phagocytosis and downstream T-cell responses. CD47 expression alone is not sufficient; HER2+ cells are eliminated via immune-mediated killing, not by direct cytotoxic action on CD47.