Anti-Human EGFL7 Recombinant Antibody (TAB-902) (CAT#: TAB-902)

Bill, Marius, et al. "EGFL7 antagonizes NOTCH signaling and represents a novel therapeutic target in acute myeloid leukemia." Clinical Cancer Research 26.3 (2020): 669-678. https://doi.org/10.1158/1078-0432.CCR-19-2479

This study investigated the role of EGF-like domain 7 (EGFL7) in acute myeloid leukemia (AML) and its potential as a therapeutic target. The researchers found that EGFL7 is upregulated in AML and contributes to leukemogenesis by antagonizing NOTCH signaling. Through various in vitro and in vivo experiments, the study demonstrated that blocking EGFL7 with an anti-EGFL7 antibody (parsatuzumab) reactivated NOTCH signaling, leading to increased differentiation and apoptosis of leukemic cells. Additionally, anti-EGFL7 treatment prolonged the survival of AML mouse models, indicating the potential of EGFL7 as a novel therapeutic target for AML.
Creative Biolabs provided the anti-EGFL7 therapeutic antibody, parsatuzumab (Cat#: TAB-902), which was critical for the experiments that demonstrated the reactivation of NOTCH signaling and the resulting differentiation and apoptosis of AML cells. The use of parsatuzumab allowed the researchers to validate the therapeutic potential of targeting EGFL7 in AML and provided significant insights into the molecular mechanisms by which EGFL7 influences leukemogenesis. This contribution was essential for establishing EGFL7 as a viable target for AML treatment.

Papaioannou, Dimitrios, et al. "Prognostic and biological significance of the proangiogenic factor EGFL7 in acute myeloid leukemia." Proceedings of the National Academy of Sciences 114.23 (2017): E4641-E4647. https://doi.org/10.1073/pnas.1703142114

This research investigates the prognostic and biological significance of Epithelial Growth Factor-Like 7 (EGFL7) in acute myeloid leukemia (AML). The study demonstrates that EGFL7 mRNA and protein expression levels are significantly increased in AML blasts compared to normal bone marrow cells. High EGFL7 expression was associated with lower complete remission rates and shorter event-free and overall survival in both younger and older patients with cytogenetically normal AML. Importantly, the research reveals that AML blasts secrete EGFL7 protein, with higher levels detected in sera from AML patients compared to healthy controls. Treatment of AML blasts with recombinant EGFL7 in vitro resulted in increased leukemic blast cell growth and phosphorylated AKT levels, while EGFL7 blockade with an anti-EGFL7 antibody reduced growth potential and viability of AML cells.
Creative Biolabs provided humanized murine monoclonal antibody that binds to the EGFL7 protein and inhibits its function (parsatuzumab) for the study. The antibody would be crucial for the experiments demonstrating EGFL7's role in AML blast proliferation and for the therapeutic blockade studies. The availability of high-quality, validated reagents targeting EGFL7 would enable researchers to effectively investigate the autocrine mechanism by which EGFL7 supports leukemic blast growth and evaluate the potential of EGFL7-targeted therapy in AML treatment.