Anti-Human CD3 (Teplizumab)
Anti-Human CD3 (Teplizumab)
Product No.: LT2100
Product No.LT2100 Clone PRV-031 Target CD3 Product Type Biosimilar Recombinant Human Monoclonal Antibody Alternate Names Teplizumab, CD3ε, 876387-05-2 Isotype Human IgG1κ Applications ELISA , FA , FC , IP , WB |
Antibody DetailsProduct DetailsReactive Species Human Host Species Human Expression Host HEK-293 Cells FC Effector Activity Active Immunogen Human CD3 Product Concentration ≥ 5.0 mg/ml Endotoxin Level < 1.0 EU/mg as determined by the LAL method Purity ≥95% by SDS Page ⋅ ≥95% monomer by analytical SEC Formulation This biosimilar antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration. State of Matter Liquid Product Preparation Recombinant biosimilar antibodies are manufactured in an animal free facility using only in vitro protein free cell culture techniques and are purified by a multi-step process including the use of protein A or G to assure extremely low levels of endotoxins, leachable protein A or aggregates. Pathogen Testing To protect mouse colonies from infection by pathogens and to assure that experimental preclinical data is not affected by such pathogens, all of Leinco’s recombinant biosimilar antibodies are tested and guaranteed to be negative for all pathogens in the IDEXX IMPACT I Mouse Profile. Storage and Handling Functional grade preclinical antibodies may be stored sterile as received at 2-8°C for up to one month. For longer term storage, aseptically aliquot in working volumes without diluting and store at ≤ -70°C. Avoid Repeated Freeze Thaw Cycles. Regulatory Status Research Use Only (RUO). Non-Therapeutic. Country of Origin USA Shipping 2 -8°C Wet Ice Additional Applications Reported In Literature ? ELISA, WB, IP, FA, FC Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change. DescriptionDescriptionSpecificity This non-therapeutic biosimilar antibody uses the same variable region sequence as the therapeutic antibody Teplizumab. This product is for research use only. Teplizumab activity is directed against CD3 expressed on mature T cells. Background Type I diabetes is a chronic autoimmune disease that destroys insulin-producing beta-cells in the islets of Langerhans, leading to a dependence on exogenous insulin for survival1. Teplizumab (TZIELD) is a humanized, anti-CD3ε IgG1κ monoclonal therapeutic that delays the onset of Stage 3 Type 1 diabetes1, 2. CD3ε plays an essential role in T cell development and is part of the T cell-receptor CD3-complex, which acts as an external signal transducer3. Defects in CD3ε cause immunodeficiency and have been linked to susceptibility to type I diabetes in women.
Teplizumab is an Fc receptor-nonbinding anti-CD3 antibody4 whose Fc region is mutated (L234A; L235A) to reduce effector functions2. When Teplizumab is administered by intravenous infusion once daily for 14 consecutive days, it reduces the loss of beta-cell function1. Teplizumab treatment modifies CD8+ T lymphocytes, which are thought to kill beta-cells, to display a partially exhausted phenotype associated with delayed disease progression1, 5. Teplizumab delays the median onset of Stage 3 Type 1 diabetes by 2 years compared to placebo1, 2. Additionally, the effects of treatment persist over time. The median years to diabetes diagnosis after Teplizumab treatment is ~ 5 years compared to ~ 2 years in the placebo-treated group6. In November 2022, the United States Food and Drug Administration approved Teplizumab injection to delay the onset of Stage 3 Type 1 diabetes in adults and pediatric patients aged 8 years and older who have Stage 2 Type 1 diabetes7. Antigen Distribution CD3 is found on the surface of mature T cells. Ligand/Receptor Peptide antigen bound to MHC NCBI Gene Bank ID UniProt.org Research Area Biosimilars . Immunology Leinco Antibody AdvisorPowered by AI: AI is experimental and still learning how to provide the best assistance. It may occasionally generate incorrect or incomplete responses. Please do not rely solely on its recommendations when making purchasing decisions or designing experiments. Research-grade Teplizumab biosimilars are used as calibration standards or reference controls in PK bridging ELISA by preparing a quantitative standard curve with known concentrations of the biosimilar, enabling accurate measurement of Teplizumab concentration in serum samples. In a PK bridging ELISA for measuring Teplizumab in serum, the process involves the following steps:
Key Technical Notes:
This approach is consistent with industry best practices and regulatory guidance for ligand binding assays used in biosimilar PK bridging studies. The primary preclinical models where a research-grade anti-CD3 antibody is administered in vivo to study tumor growth inhibition and characterize tumor-infiltrating lymphocytes (TILs) are syngeneic mouse models and humanized mouse models. Key details:
Model Comparison Table
Summary of applications:
Both platforms are foundational for evaluating T cell-focused therapies, profiling TIL phenotypes, and characterizing tumor growth inhibition in vivo. Currently, there is no specific information available about researchers using Teplizumab biosimilars in conjunction with other checkpoint inhibitors, such as anti-CTLA-4 or anti-LAG-3 biosimilars, to study synergistic effects in complex immune-oncology models. Teplizumab is primarily used in the context of type 1 diabetes prevention and involves modulating immune responses, particularly CD8+ T cell exhaustion and modulation of other immune cell subsets. However, the concept of combining different immunotherapies, including checkpoint inhibitors like anti-CTLA-4 and anti-PD-1, is well-established in cancer research. These combinations aim to enhance antitumor responses by targeting multiple checkpoints involved in immune regulation. For example, combining anti-CTLA-4 and anti-PD-1 therapies has shown synergistic effects in advanced melanoma by targeting different aspects of T cell activation and suppression. To study synergistic effects in complex immune-oncology models, researchers typically employ a combination of in vitro and in vivo studies:
If a Teplizumab biosimilar were to be used in immune-oncology research, the approach would likely involve similar methodologies to explore its potential synergistic effects with other checkpoint inhibitors. This would require adapting Teplizumab's mechanism of modulating immune responses in diabetes to oncology contexts, where immune suppression involves different pathways. Potential Research Directions1. Mechanistic Understanding
2. Synergistic Effects
3. Clinical Relevance
By following these approaches, researchers can explore the potential of combining Teplizumab biosimilars with other checkpoint inhibitors in immune-oncology, although such specific studies are not currently documented. A Teplizumab biosimilar can be used as both the capture and detection reagent in a bridging anti-drug antibody (ADA) ELISA to monitor a patient's immune response to the therapeutic drug by detecting ADAs that bind to Teplizumab. In this bridging ELISA format:
Key steps in the assay:
Why use a biosimilar?
Clinical significance:
In summary, using a Teplizumab biosimilar as both capture and detection reagent in a bridging ADA ELISA enables sensitive and specific quantification of anti-Teplizumab antibodies in patient sera, thereby helping assess the immune response against the therapeutic drug. References & Citations1. Herold KC, Bundy BN, Long SA, et al. N Engl J Med. 381(7):603-613. 2019.
2. Kaplon H, Crescioli S, Chenoweth A, et al. MAbs. 15(1):2153410. 2023. 3. https://www.ncbi.nlm.nih.gov/gene/916 4. Herold KC, Hagopian W, Auger JA, et al. N Engl J Med. 346(22):1692-1698. 2002. 5. Long SA, Thorpe J, DeBerg HA, et al. Sci Immunol. 1(5):eaai7793. 2016. 6. Sims EK, Bundy BN, Stier K, et al. Sci Transl Med. 13(583):eabc8980. 2021. 7. https://www.fda.gov/news-events/press-announcements/fda-approves-first-drug-can-delay-onset-type-1-diabetes 8. Herold KC, Bluestone JA, Montag AG, et al. Diabetes. 41(3):385-391. 1992. 9. Herold KC, Gitelman SE, Ehlers MR, et al. Diabetes. 62(11):3766-3774. 2013. Technical ProtocolsCertificate of Analysis |
Formats Available
Prod No. | Description |
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LT2100 | |
LT2105 |
