InVivoSIM anti-human IFNAR1 (Anifrolumab Biosimilar)
Product Details
This non-therapeutic biosimilar antibody uses the same variable regions from the therapeutic antibody Anifrolumab making it ideal for research use. This Anifrolumab biosimilar reacts with human IFNAR1 (IFN alpha/beta receptor subunit 1). IFNAR-1 is coexpressed with IFNAR-2 on nearly all cell types and together these two subunits make up the heterodimeric Type I IFN Receptor complex. Type I IFNs (IFN-α/β) bind to the Type I IFN Receptor complex to induce cellular responses including induction of anti-viral, anti-microbial, anti-tumor, and autoimmune responses as well as to regulate the activation, proliferation, and differentiation of many cell types. Anifrolumab is used to treat systemic lupus erythematosus (SLE) in adults.Specifications
Isotype | Human IgG1, Īŗ |
---|---|
Recommended Isotype Control(s) | RecombiMAb human IgG1 (K214R/L234F/L235E/P331S) isotype control, anti-hen egg lysozyme |
Recommended Dilution Buffer | InVivoPure pH 7.0 Dilution Buffer |
Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
Immunogen | Human IFNAR1 |
Reported Applications |
Functional assays Western blot ELISA |
Formulation |
PBS, pH 7.0 Contains no stabilizers or preservatives |
Endotoxin |
<0.5EU/mg (<0.0005EU/μg) Determined by LAL gel clotting assay |
Aggregation |
<5% Determined by SEC |
Purity |
>95% Determined by SDS-PAGE |
Sterility | 0.2 µm filtration |
Production | Purified from cell culture supernatant in an animal-free facility |
Purification | Protein A |
Molecular Weight | 150 kDa |
Murine Pathogen Tests |
Ectromelia/Mousepox Virus: Negative Hantavirus: Negative K Virus: Negative Lactate Dehydrogenase-Elevating Virus: Negative Lymphocytic Choriomeningitis virus: Negative Mouse Adenovirus: Negative Mouse Cytomegalovirus: Negative Mouse Hepatitis Virus: Negative Mouse Minute Virus: Negative Mouse Norovirus: Negative Mouse Parvovirus: Negative Mouse Rotavirus: Negative Mycoplasma Pulmonis: Negative Pneumonia Virus of Mice: Negative Polyoma Virus: Negative Reovirus Screen: Negative Sendai Virus: Negative Theilerās Murine Encephalomyelitis: Negative |
Storage | The antibody solution should be stored at the stock concentration at 4°C. Do not freeze. |
Recommended Products
- Cancer Research,
Enhancing the Anticancer Activity of a Carcinoma-Directed Peptide-HLA-I Fusion Protein by Armoring with Mutein IFNα.
In International Journal of Molecular Sciences on 29 March 2025 by Samplonius, D. F., van Wijngarden, A. P., et al.
Previously, we reported on the peptide-HLA-I fusion protein EpCAM-ReTARGTPR, which allows us to redirect the cytotoxic activity of pre-existing anti-CMV CD8pos T cell immunity to selectively eliminate EpCAMpos cancer cells. EpCAM-ReTARGTPR consists of the CMV pp65-derived peptide TPRVTGGGAM (TPR) fused in tandem with a soluble HLA-B*07:02/β2-microglobulin (β2M) molecule and an EpCAM-directed Fab antibody fragment. To further enhance its anticancer activity, we equipped EpCAM-ReTARGTPR with the immune-potentiating cytokine muteins IL2(H16A,F42A) and IFNαR149A, respectively. Both cytokines are engineered to have attenuated affinity for their respective cytokine receptors. Compared to EpCAM-ReTARGTPR, in vitro treatment of EpCAMpos carcinoma cell lines with EpCAM-ReTARGTPRvIL2 for 24 h increased the cytotoxic activity of PBMCs containing low levels of TPR-specific CD8pos T cells by ~15%, whereas EpCAM-ReTARGTPRIFNαR149A induced an increase of ~50%. Moreover, treatment for 120 h with EpCAM-ReTARGTPRIFNαR149A inhibited the proliferative capacity of the cancer cell lines OvCAR3 and PC3M by ~91% without compromising the viability of the TPR-specific CD8pos T cells and increased their capacity for IFNγ secretion. Importantly, EpCAM-ReTARGTPRIFNαR149A potently induced the elimination of primary EpCAMpos refractory carcinoma cells from a Merkel cell carcinoma (MCC) patient. Taken together, the armoring of the carcinoma-directed peptide-HLA-I fusion protein EpCAM-ReTARGTPR with IFNαR149A potently enhanced the efficacy of pre-existing anti-CMV CD8pos T cell immunity to selectively eliminate EpCAMpos cancer cells.