A subcutaneous human afucosylated IgG1 monoclonal antibody (also known as AMG 451/KHK4083) targeting OX40 (TNFRSF4). It blocks OX40–OX40L costimulatory signaling and depletes OX40-expressing activated effector/memory T cells via enhanced ADCC, reducing pathogenic T-cell activation, survival, and cytokine production in atopic dermatitis.
Afucosylated human IgG1 monoclonal antibody against OX40 (TNFRSF4) that blocks OX40–OX40L costimulatory signaling and depletes OX40-expressing activated effector/memory T cells via enhanced ADCC, thereby reducing T‑cell activation, survival, and inflammatory cytokine production in atopic dermatitis.
YES
DIRECT
Afucosylated IgG1 binds OX40 on activated T cells and engages Fcγ receptors on effector cells (e.g., NK cells), triggering enhanced ADCC (and phagocytosis) to deplete OX40+ cells.
HER2-targeted antibody–drug conjugate (anti-HER2 mAb linked to MMAE) that binds HER2, is internalized, and releases MMAE to inhibit microtubules, causing mitotic arrest and apoptosis (with possible bystander effect).
HER2-targeted antibody–drug conjugate in which disitamab (anti-HER2 mAb) delivers the microtubule inhibitor MMAE. After HER2 binding and internalization, linker cleavage releases MMAE to block tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander killing.
YES
DIRECT
Anti-HER2 ADC binds HER2, is internalized, and releases MMAE that inhibits tubulin polymerization, causing G2/M arrest and apoptosis (with possible bystander killing).
HER2-targeted antibody–drug conjugate (anti-HER2 mAb linked to MMAE) that binds HER2, is internalized, and releases MMAE to inhibit microtubules, causing mitotic arrest and apoptosis (with possible bystander effect).
HER2-targeted antibody–drug conjugate in which disitamab (anti-HER2 mAb) delivers the microtubule inhibitor MMAE. After HER2 binding and internalization, linker cleavage releases MMAE to block tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander killing.
NO
INDIRECT
The ADC binds HER2 on tumor cells and is internalized; linker cleavage releases MMAE, which binds β‑tubulin to disrupt microtubules, causing G2/M arrest and apoptosis. Killing is directed by HER2 targeting (with possible bystander effect), not by β‑tubulin expression itself.
Genetically engineered autologous T cells expressing a chimeric antigen receptor targeting CD70 for MHC-independent recognition and killing of CD70-positive tumor cells; administered after lymphodepletion.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that specifically binds CD70 on tumor cells, enabling MHC-independent recognition. CAR signaling (CD3ζ with costimulation) activates the T cells to proliferate, release cytokines, and deliver cytotoxic killing of CD70-positive tumor cells. Lymphodepletion prior to infusion enhances CAR-T expansion and persistence.
YES
DIRECT
CD70 CAR-T cells bind CD70 on target cells and, upon CAR activation, kill via perforin/granzyme-mediated apoptosis (and Fas–FasL), lysing CD70-positive cells.
An autologous, genetically modified BCMA-targeting chimeric antigen receptor (CAR) T-cell therapy engineered to express a high-affinity BCMA-directed CAR with CD3ζ signaling and costimulation; administered as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells are genetically modified to express a high‑affinity BCMA‑directed chimeric antigen receptor with CD3ζ signaling and costimulatory domains. Upon binding BCMA on malignant plasma/B‑lineage cells, the CAR activates T‑cell effector functions, leading to proliferation, cytokine release, and cytotoxic killing of BCMA‑expressing tumor cells. Administered after lymphodepleting chemotherapy to promote in vivo expansion and persistence.
YES
DIRECT
BCMA-directed CAR T cells bind BCMA on target cells and kill them via T-cell effector functions, primarily perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, after CAR signaling (CD3ζ with costimulation).