Anti-CD30 IgG1 antibody–drug conjugate (ADC) linked to monomethyl auristatin E (MMAE), a microtubule inhibitor. After binding CD30 and internalization, MMAE is released to disrupt microtubules and induce apoptosis. Used in this trial both unlabeled (predose) and as a radiolabeled PET tracer.
Anti-CD30 IgG1 antibody–drug conjugate linked via a valine–citrulline cleavable linker to monomethyl auristatin E (MMAE). After binding CD30 and internalization into CD30-positive cells, the linker is proteolytically cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis.
YES
DIRECT
Anti-CD30 ADC binds CD30 on target cells, is internalized, the valine–citrulline linker is cleaved to release MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis.
Anti-CD30 IgG1 antibody–drug conjugate (ADC) linked to monomethyl auristatin E (MMAE), a microtubule inhibitor. After binding CD30 and internalization, MMAE is released to disrupt microtubules and induce apoptosis. Used in this trial both unlabeled (predose) and as a radiolabeled PET tracer.
Anti-CD30 IgG1 antibody–drug conjugate linked via a valine–citrulline cleavable linker to monomethyl auristatin E (MMAE). After binding CD30 and internalization into CD30-positive cells, the linker is proteolytically cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis.
NO
INDIRECT
Brentuximab vedotin binds CD30 (not beta-tubulin); after internalization into CD30+ cells, MMAE is released and binds beta-tubulin to block microtubule polymerization, causing G2/M arrest and apoptosis. Beta-tubulin expression alone does not make cells targets.
Anti-HER2 antibody–drug conjugate (RC48) that binds HER2, is internalized, and releases the microtubule inhibitor MMAE to induce cell-cycle arrest/apoptosis; may also mediate ADCC.
An anti-HER2 IgG1 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE to block tubulin polymerization, causing G2/M arrest and apoptosis; the antibody component may also mediate ADCC.
YES
DIRECT
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE, which inhibits microtubule polymerization causing G2/M arrest and apoptosis; the IgG1 Fc can also mediate ADCC against HER2+ cells.
Anti-HER2 antibody–drug conjugate (RC48) that binds HER2, is internalized, and releases the microtubule inhibitor MMAE to induce cell-cycle arrest/apoptosis; may also mediate ADCC.
An anti-HER2 IgG1 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE to block tubulin polymerization, causing G2/M arrest and apoptosis; the antibody component may also mediate ADCC.
NO
INDIRECT
The ADC targets HER2, not beta-tubulin. After HER2 binding and internalization, MMAE is released and binds beta-tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC may also contribute.