Anti-Human CD3 (Teplizumab) - Fc Muted™

Leinco Technologies
Product Code: LEI-LT2105
Product Group: Primary Antibodies
CodeSizePrice
LEI-LT2105-customCustomEnquire
Quantity:
LEI-LT2105-500ug500 ug£408.00
Quantity:
LEI-LT2105-1.0mg1.0mg£693.00
Quantity:
Prices exclude any Taxes / VAT

Overview

Host Type: Human
Antibody Isotype: Human IgG1κ
Antibody Clonality: Monoclonal
Antibody Clone: PRV-031
Regulatory Status: RUO
Target Species: Human
Applications:
  • Enzyme-Linked Immunosorbent Assay (ELISA)
  • Flow Cytometry
  • Functional Study
  • Immunoprecipitation (IP)
  • Western Blot (WB)
Shipping:
2 - 8°C Wet Ice
Storage:
Functional grade biosimilar 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 -80°C.?Avoid Repeated Freeze Thaw Cycles.

Further Information

Antigen Distribution:
CD3 is found on the surface of mature T cells.
Concentration:
? 5.0 mg/ml
Conjugate/Tag/Label:
Purified No Carrier Protein
Format:
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.
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.
Immunogen:
Human CD3
Long Description:
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.
NCBI Gene:
915
Purity:
?95% by SDS Page, ?95% monomer by analytical SEC
Target:
CD3

References

1. 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.