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Interferon alpha 2 (IFNα2) Masked ImmunoCytokine (MIC) fused to antibody targeting CD138

IFNα2 ImmunoCytokine

Fused to anti-CD138 IgG1

Peptide Mask

  • Why Interferon Alpha 2? Interferons have direct anti-tumor activity as well as being master regulators of both innate and adaptive immune responses. IFNα induces tumor cell-specific cell death as tumor cells are more susceptible to IFNα induced apoptosis. IFNα also causes activation of NK cells and induces synergy of anti-tumor antigen antibody-dependent cell-mediated cytotoxicity. 

  • Why target CD138? Multiple Myeloma and many solid tumors express a CD138 receptor.  Tumor antigen targeting enhances tumor retention and localizes the fused cytokine to the target cell surface.  By fusing an anti-CD138 antibody to the MIC, the antibody binds to its antigen on the tumor cell surface (where the proteases are located) providing an enhanced opportunity for cleavage.  Thus, Nammi’s MICs retain full potency vs non-masked controls in preclinical studies.

  • Mask rationale: The mask prevents systemic IFN receptor binding while maintaining anti-tumor activity. The masks are attached through a peptide sequence that is sensitive to cleavage by tumor-selective proteases; thereby allowing activation of the IFN selectively within the tumor environment.

  • Target Indication:  Multiple Myeloma and solid tumors expressing a CD138 receptor include Hepatocellular, ovarian, breast, prostate, bladder, Gastrointestinal and head and neck carcinomas.  QXL138AM was granted FDA Orphan Drug Designation for the treatment of Multiple Myeloma and Pancreatic Cancer. 

QXL138AM Mechanism of Action
QXL138AM MOA.png
Anti-Tumor Efficacy in Vivo*

Demonstrated Tumor Growth Inhibition Vs. Wide Range of Tumor Indications

QXL138 TGI -2.1.png

*An unmasked murine surrogate version of QXL138AM was used in this study

Demonstrated Tumor Growth Inhibition in U266 and H929 Multiple Myeloma human Models

U266 vs QXL138AM.png
H929 vs QXL138AM.png



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