About InVivoSIM anti-human EGFR (Cetuximab Biosimilar) This non-therapeutic biosimilar antibody uses the same variable regions from the therapeutic antibody Cetuximab making it ideal for research use. This Cetuximab biosimilar reacts with human EGFR (epidermal growth factor receptor) also known as ErbB-1. EGFR is a 170 kDa cell-surface receptor and belongs to the ErbB family of receptors. EGFR signaling is activated upon binding one of its ligands including epidermal growth factor (EGF), transforming growth factor α (TGF α), Amphiregulin, and heparin binding-EGF (HB-EGF). Upon activation, EGFR transitions from an inactive monomeric form to an active homodimer. This initiates several downstream signal transduction cascades including the MAPK, Akt and JNK pathways, leading to DNA synthesis and cell proliferation. EGFR overexpression or constitutive activation are associated with many cancers. For this reason, anti-EGFR monoclonal antibody mediated immunotherapies are currently being explored as cancer treatments. Cetuximab inhibits tumor cell proliferation by blocking the interaction of EGF with EGFR. InVivoSIM anti-human EGFR (Cetuximab Biosimilar) Specifications IsotypeHuman IgG1 Recommended Isotype Control(s)RecombiMAb human IgG1 isotype control, anti-hen egg lysozyme Recommended Dilution BufferInVivoPure pH 7.0 Dilution Buffer ImmunogenHuman EGFR (ErbB1) Reported ApplicationsEGFR blockade ELISA Flow Cytometry FormulationPBS, pH 7.0 Contains no stabilizers or preservatives Endotoxin<1EU/mg (<0.001EU/μg) Determined by LAL gel clotting assay Aggregation<5% Determined by SEC Purity>95% Determined by SDS-PAGE Sterility0.2 μm filtration ProductionPurified from cell culture supernatant in an animal-free facility PurificationProtein A RRIDAB_2894723 Molecular Weight150 kDa StorageThe antibody solution should be stored at the stock concentration at 4°C. Do not freeze. Application ReferencesInVivoSIM anti-human EGFR (Cetuximab Biosimilar) (CLONE: Cetuximab)Linde IL, Prestwood TR, Qiu J, Pilarowski G, Linde MH, Zhang X, Shen L, Reticker-Flynn NE, Chiu DK, Sheu LY, Van Deursen S, Tolentino LL, Song WC, Engleman EG (2023). "Neutrophil-activating therapy for the treatment of cancer" Cancer Cell 41(2):356-372.e10. PubMedDespite their cytotoxic capacity, neutrophils are often co-opted by cancers to promote immunosuppression, tumor growth, and metastasis. Consequently, these cells have received little attention as potential cancer immunotherapeutic agents. Here, we demonstrate in mouse models that neutrophils can be harnessed to induce eradication of tumors and reduce metastatic seeding through the combined actions of tumor necrosis factor, CD40 agonist, and tumor-binding antibody. The same combination activates human neutrophils in vitro, enabling their lysis of human tumor cells. Mechanistically, this therapy induces rapid mobilization and tumor infiltration of neutrophils along with complement activation in tumors. Complement component C5a activates neutrophils to produce leukotriene B4, which stimulates reactive oxygen species production via xanthine oxidase, resulting in oxidative damage and T cell-independent clearance of multiple tumor types. These data establish neutrophils as potent anti-tumor immune mediators and define an inflammatory pathway that can be harnessed to drive neutrophil-mediated eradication of cancer.
