InVivoSIM anti-human PD-L1 (Atezolizumab Biosimilar)
Product Details
This non-therapeutic biosimilar antibody uses the same variable regions from the therapeutic antibody Atezolizumab making it ideal for research use. This Atezolizumab biosimilar reacts with human PD-L1 (programmed death ligand 1) also known as B7-H1 or CD274. PD-L1 is a 40 kDa type I transmembrane protein that belongs to the B7 family of the Ig superfamily. PD-L1 is expressed on T lymphocytes, B lymphocytes, NK cells, dendritic cells, as well as IFNĪ³ stimulated monocytes, epithelial cells and endothelial cells. PD-L1 binds to its receptor, PD-1, found on CD4 and CD8 thymocytes as well as activated T and B lymphocytes and myeloid cells. Engagement of PD-L1 with PD-1 leads to inhibition of TCR-mediated T cell proliferation and cytokine production. PD-L1 is thought to play an important role in tumor immune evasion. Induced PD-L1 expression is common in many tumors and results in increased resistance of tumor cells to CD8 T cell mediated lysis. Atezolizumab blocks the interaction of PD-L1 with PD-1 and CD80.Specifications
| Isotype | Human IgG1 |
|---|---|
| Recommended Isotype Control(s) | RecombiMAb human IgG1 isotype control, anti-hen egg lysozyme |
| Recommended Dilution Buffer | InVivoPure pH 7.0 Dilution Buffer |
| Immunogen | Not available or unknown |
| Reported Applications |
Flow Cytometry Western Blot |
| Formulation |
PBS, pH 7.0 Contains no stabilizers or preservatives |
| Endotoxin |
<1EU/mg (<0.001EU/Ī¼g) Determined by LAL gel clotting assay |
| Aggregation |
<5% Determined by SEC |
| Purity |
>95% Determined by SDS-PAGE |
| Sterility | 0.2 Āµm filtration |
| Production | Purified from cell culture supernatant |
| Purification | Protein A |
| RRID | AB_2894730 |
| 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 4Ā°C. Do not freeze. |
Recommended Products
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Recommended Isotype Control(s)
RecombiMAb human IgG1 isotype control, anti-hen egg lysozyme
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Recommended Dilution Buffer
InVivoPure pH 7.0 Dilution Buffer
in vitro PD-L1 blockade
Sun R, Meng Z, Lee H, Offringa R, Niehrs C. (2023). "ROTACs leverage signaling-incompetent R-spondin for targeted protein degradation" Cell Chem Biol 30(7):739-752.e8. PubMed
Proteolysis-targeting chimeras (PROTACs) are an emerging technology for therapeutic intervention, but options to target cell surface proteins and receptors remain limited. Here we introduce ROTACs, bispecific WNT- and BMP-signaling-disabled R-spondin (RSPO) chimeras, which leverage the specificity of these stem cell growth factors for ZNRF3/RNF43 E3 transmembrane ligases, to target degradation of transmembrane proteins. As a proof-of-concept, we targeted the immune checkpoint protein, programmed death ligand 1 (PD-L1), a prominent cancer therapeutic target, with a bispecific RSPO2 chimera, R2PD1. The R2PD1 chimeric protein binds to PD-L1 and at picomolar concentration induces its lysosomal degradation. In three melanoma cell lines, R2PD1 induced between 50 and 90% PD-L1 protein degradation. PD-L1 degradation was strictly dependent on ZNRF3/RNF43. Moreover, R2PD1 reactivates cytotoxic T cells and inhibits tumor cell proliferation more potently than Atezolizumab. We suggest that signaling-disabled ROTACs represent a paradigm to target cell surface proteins for degradation in a range of applications.
in vitro PD-L1 blockade
Zhao Y, Caron C, Chan YY, Lee CK, Xu X, Zhang J, Masubuchi T, Wu C, Bui JD, Hui E. (2023). "cis-B7:CD28 interactions at invaginated synaptic membranes provide CD28 co-stimulation and promote CD8+ T cell function and anti-tumor immunity" Immunity 56(6):1187-1203.e12. PubMed
B7 ligands (CD80 and CD86), expressed by professional antigen-presenting cells (APCs), activate the main co-stimulatory receptor CD28 on T cells in trans. However, in peripheral tissues, APCs expressing B7 ligands are relatively scarce. This raises the questions of whether and how CD28 co-stimulation occurs in peripheral tissues. Here, we report that CD8+ T cells displayed B7 ligands that interacted with CD28 in cis at membrane invaginations of the immunological synapse as a result of membrane remodeling driven by phosphoinositide-3-kinase (PI3K) and sorting-nexin-9 (SNX9). cis-B7:CD28 interactions triggered CD28 signaling through protein kinase C theta (PKCĪø) and promoted CD8+ T cell survival, migration, and cytokine production. In mouse tumor models, loss of T cell-intrinsic cis-B7:CD28 interactions decreased intratumoral T cells and accelerated tumor growth. Thus, B7 ligands on CD8+ T cells can evoke cell-autonomous CD28 co-stimulation in cis in peripheral tissues, suggesting cis-signaling as a general mechanism for boosting T cell functionality.
