A masked immunocytokine comprising an anti‑CD138 human IgG1 antibody fused to human interferon‑α2a, administered IV every 2 weeks to target CD138+ tumor cells and concentrate IFN‑α signaling (IFNAR–JAK/STAT), enhancing antiproliferative/apoptotic effects and immune activation; Fc may mediate ADCC/CDC.
Masked immunocytokine: an anti‑CD138 IgG1 fused to IFN‑α2a via a protease‑cleavable, peptide mask. After binding CD138 on tumor cells, tumor proteases unmask IFN‑α, enabling local IFNAR engagement and JAK/STAT signaling to induce antiproliferative/apoptotic effects and enhance innate/adaptive immunity; the IgG1 Fc may also mediate ADCC/CDC against CD138+ cells.
YES
DIRECT
After QXL138AM binds CD138 and is proteolytically unmasked, the released IFN-alpha engages IFNAR2 (with IFNAR1) on nearby cells, activating JAK/STAT and interferon-stimulated genes that induce antiproliferative and pro-apoptotic signaling, leading to cell death.
A masked immunocytokine comprising an anti‑CD138 human IgG1 antibody fused to human interferon‑α2a, administered IV every 2 weeks to target CD138+ tumor cells and concentrate IFN‑α signaling (IFNAR–JAK/STAT), enhancing antiproliferative/apoptotic effects and immune activation; Fc may mediate ADCC/CDC.
Masked immunocytokine: an anti‑CD138 IgG1 fused to IFN‑α2a via a protease‑cleavable, peptide mask. After binding CD138 on tumor cells, tumor proteases unmask IFN‑α, enabling local IFNAR engagement and JAK/STAT signaling to induce antiproliferative/apoptotic effects and enhance innate/adaptive immunity; the IgG1 Fc may also mediate ADCC/CDC against CD138+ cells.
NO
INDIRECT
The drug binds CD138 on tumor cells. Its IgG1 Fc engages CD16a on NK cells to drive ADCC against CD138+ cells, and unmasked IFN-α signals via IFNAR to induce tumor cell apoptosis. CD16a-expressing cells (NK cells) are engaged as effectors, not killed.
A masked immunocytokine comprising an anti‑CD138 human IgG1 antibody fused to human interferon‑α2a, administered IV every 2 weeks to target CD138+ tumor cells and concentrate IFN‑α signaling (IFNAR–JAK/STAT), enhancing antiproliferative/apoptotic effects and immune activation; Fc may mediate ADCC/CDC.
Masked immunocytokine: an anti‑CD138 IgG1 fused to IFN‑α2a via a protease‑cleavable, peptide mask. After binding CD138 on tumor cells, tumor proteases unmask IFN‑α, enabling local IFNAR engagement and JAK/STAT signaling to induce antiproliferative/apoptotic effects and enhance innate/adaptive immunity; the IgG1 Fc may also mediate ADCC/CDC against CD138+ cells.
NO
INDIRECT
QXL138AM targets CD138 on tumor cells; protease unmasking enables IFN-α to trigger IFNAR–JAK/STAT apoptosis/antiproliferation in CD138+ cells, and the IgG1 Fc engages Fcγ receptors (including CD32a) on immune effectors to mediate ADCC/ADCP/CDC against CD138+ targets. CD32a+ cells are effectors, not killed by the drug.
A masked immunocytokine comprising an anti‑CD138 human IgG1 antibody fused to human interferon‑α2a, administered IV every 2 weeks to target CD138+ tumor cells and concentrate IFN‑α signaling (IFNAR–JAK/STAT), enhancing antiproliferative/apoptotic effects and immune activation; Fc may mediate ADCC/CDC.
Masked immunocytokine: an anti‑CD138 IgG1 fused to IFN‑α2a via a protease‑cleavable, peptide mask. After binding CD138 on tumor cells, tumor proteases unmask IFN‑α, enabling local IFNAR engagement and JAK/STAT signaling to induce antiproliferative/apoptotic effects and enhance innate/adaptive immunity; the IgG1 Fc may also mediate ADCC/CDC against CD138+ cells.
NO
INDIRECT
QXL138AM binds CD138, not CD64. After CD138 binding, tumor proteases unmask IFN-α to induce apoptosis/antiproliferative signaling in CD138+ tumor cells and activate immunity. The IgG1 Fc engages Fcγ receptors (including CD64) on immune cells to mediate ADCC/CDC against CD138+ targets. CD64+ cells serve as effectors and are not directly targeted or killed.
A masked immunocytokine comprising an anti‑CD138 human IgG1 antibody fused to human interferon‑α2a, administered IV every 2 weeks to target CD138+ tumor cells and concentrate IFN‑α signaling (IFNAR–JAK/STAT), enhancing antiproliferative/apoptotic effects and immune activation; Fc may mediate ADCC/CDC.
Masked immunocytokine: an anti‑CD138 IgG1 fused to IFN‑α2a via a protease‑cleavable, peptide mask. After binding CD138 on tumor cells, tumor proteases unmask IFN‑α, enabling local IFNAR engagement and JAK/STAT signaling to induce antiproliferative/apoptotic effects and enhance innate/adaptive immunity; the IgG1 Fc may also mediate ADCC/CDC against CD138+ cells.
NO
INDIRECT
QXL138AM targets CD138, not C1q. After binding CD138, tumor proteases unmask IFN-α, which signals via IFNAR to induce apoptosis and growth arrest; the IgG1 Fc can recruit ADCC/CDC (via C1q) against CD138+ cells. Cells expressing C1q are not targeted or killed.