HER2-targeted antibody–drug conjugate; an anti-HER2 monoclonal antibody linked to MMAE (microtubule inhibitor) that is released after internalization to induce mitotic arrest and apoptosis, with potential ADCC/bystander effects.
HER2‑targeted antibody–drug conjugate: the anti‑HER2 mAb binds HER2 on tumor cells, is internalized, and releases the cytotoxic payload MMAE (microtubule inhibitor) after linker cleavage, disrupting tubulin polymerization to induce mitotic arrest and apoptosis; may also mediate ADCC and bystander killing.
YES
DIRECT
Anti-HER2 ADC binds HER2 on tumor cells, is internalized, and releases MMAE after linker cleavage, disrupting microtubules to cause mitotic arrest and apoptosis; Fc-mediated ADCC and bystander killing can also contribute.
Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
YES
DIRECT
ULBP3 engages NKG2D on allogeneic Vγ9Vδ2 T cells, activating them to kill target cells via perforin/granzyme-mediated cytotoxicity.
HER2-targeted antibody–drug conjugate; an anti-HER2 monoclonal antibody linked to MMAE (microtubule inhibitor) that is released after internalization to induce mitotic arrest and apoptosis, with potential ADCC/bystander effects.
HER2‑targeted antibody–drug conjugate: the anti‑HER2 mAb binds HER2 on tumor cells, is internalized, and releases the cytotoxic payload MMAE (microtubule inhibitor) after linker cleavage, disrupting tubulin polymerization to induce mitotic arrest and apoptosis; may also mediate ADCC and bystander killing.
NO
INDIRECT
RC48 binds HER2 on tumor cells, is internalized, and releases MMAE, which then binds β‑tubulin to disrupt microtubules and cause mitotic arrest/apoptosis. β‑tubulin expression alone does not make cells targeted by the drug.
Recombinant SIRPα–IgG4 Fc fusion protein that binds CD47 to block the "don’t‑eat‑me" signal and enhance macrophage/monocyte phagocytosis.
Recombinant SIRPα–IgG4 Fc fusion protein that binds CD47 on tumor cells, blocking the CD47–SIRPα “don’t‑eat‑me” signal and thereby promoting macrophage/monocyte phagocytosis and innate anti-tumor activity.
YES
DIRECT
Blocking CD47–SIRPα removes the ‘don’t‑eat‑me’ signal and, via the IgG4 Fc engaging Fcγ receptors, directly promotes macrophage/monocyte antibody‑dependent cellular phagocytosis of CD47+ cells.
SIRPα–Fc fusion protein that binds CD47 to inhibit the "don’t‑eat‑me" signal and promote macrophage-mediated phagocytosis.
Recombinant SIRPα–Fc fusion protein that binds and blocks CD47 on tumor cells, interrupting the CD47–SIRPα inhibitory checkpoint (“don’t‑eat‑me” signal) to promote macrophage/monocyte-mediated phagocytosis, aided by Fc engagement of Fcγ receptors.
YES
DIRECT
Blocks the CD47–SIRPα “don’t‑eat‑me” signal and engages Fcγ receptors, enabling macrophage/monocyte antibody‑dependent cellular phagocytosis of CD47+ cells, leading to their killing.