Tremelimumab Biosimilar, Human CTLA-4 monoclonal antibody
Specificité
The in vivo grade tremelimumab biosimilar specifically binds to the human protein receptor CD152 / CTLA4.
Attributs du produit
Recombinant Chimeric IgG2 Monoclonal Antibody.
Purification
Protein A affinity column
Pureté
> 95% by SDS-PAGE under reducing conditions and HPLC.
Stérilité
0.2 μm filtered
niveau d'endotoxine
< 1 EU per 1 mg of the protein by the LAL method.
Immunogène
The anti-human CTLA-4 monoclonal antibody tremelimumab biosimilar (research grade) was produced in mammalian cells.
Isotype
IgG2, kappa
Indications d'application
ELISA, neutralization, in vivo functional assays such as bioanalytical PK and ADA assays, and those in vitro and in vivo assays for studying biological pathways affected by tremelimumab.
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
PBS, pH 7.4, no stabilizers or preservatives.
Agent conservateur
Without preservative
Conseil sur la manipulation
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
Stock
-20 °C
Stockage commentaire
12 months from date of receipt, -20 to -70°C as supplied. 1 month from date of receipt, 2 to 8°C as supplied.
Date de péremption
12 months
Antigène
CTLA-4 (Tremelimumab Biosimilar)
Classe de substances
Biosimilar
Sujet
What is Tremelimumab biosimilar research grade? Tremelimumab (formerly ticilimumab) is a fully human monoclonal antibody against CTLA-4 / CD152. It is an immune checkpoint blocker. Unlike Ipilimumab (another fully human anti-CTLA-4 / CD152 monoclonal antibody), which is an IgG1 isotype, tremelimumab is an IgG2 isotype.Tremelimumab Biosimilar uses the same protein sequences as the therapeutic antibody tremelimumab.
Tremelimumab aims to stimulate an immune system attack on tumors. Cytotoxic T lymphocytes (CTLs) can recognize and destroy cancer cells. However, there is also an inhibitory mechanism (immune checkpoint) that interrupts this destruction. Tremelimumab turns off this inhibitory mechanism and allows CTLs to continue to destroy the cancer cells. This is immune checkpoint blockade.
Tremelimumab binds to the protein CTLA-4 / CD152, which is expressed on the surface of activated T lymphocytes and inhibits the killing of cancer cells. Tremelimumab blocks the binding of the antigen-presenting cell ligands B7.1 and B7.2 to CTLA-4 / CD152, resulting in inhibition of B7-CTLA-4-mediated downregulation of T-cell activation; subsequently, B7.1 or B7.2 may interact with another T-cell surface receptor protein, CD28, resulting in a B7-CD28-mediated T-cell activation unopposed by B7-CTLA-4-mediated inhibition.