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.
YES
DIRECT
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.
YES
DIRECT
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).
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.
NO
INDIRECT
PHN-010 binds an undisclosed tumor cell surface antigen (not topoisomerase I), is internalized, and releases a payload that inhibits topoisomerase I to induce DNA damage and apoptosis; topoisomerase I is the intracellular payload target, not the directly targeted antigen.
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.
YES
DIRECT
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.
A recombinant human broadly neutralizing monoclonal antibody that targets the HIV-1 gp120 V3-glycan (N332) supersite to inhibit viral entry; neutralizes diverse HIV-1 strains and can mediate Fc-dependent effector functions (ADCC/ADCP). The LS Fc mutations enhance FcRn binding and extend serum half-life.
10-1074-LS is a broadly neutralizing human monoclonal antibody that binds the HIV-1 Env gp120 V3-glycan (N332) supersite, blocking Env–CD4 interactions and viral attachment/entry to neutralize diverse HIV-1 strains. Its Fc region can engage Fcγ receptors to mediate effector functions such as ADCC and ADCP, aiding clearance of virions/infected cells. LS Fc mutations (M428L/N434S) enhance FcRn binding, extending serum half-life.
YES
INDIRECT
The antibody binds Env on infected cell surfaces and recruits FcγR-expressing effector cells to mediate ADCC/ADCP, leading to clearance of infected cells; it also neutralizes virions by blocking Env–CD4 interaction.