In Vivo Star Anti-Mouse CD279 (PD1) / VEGFR-2 Bispecific Antibody

Cat # Size Price Quantity
5150011 mg$1750
5150025 mg$5950
51500325 mg$17850

Product Details


Clone29F.1A12 / DC101
ApplicationFunctional assay, animal model study
Host SpeciesCHO cells
ReactivityMouse
FormatLiquid
Target NamePD1, PD-1, PDCD1, CD279, SLEB2, VEGFR2, VEGF-R2, KDR, Tyrosin kinase growth factor receptor, homolog of FLK1 (FLK1), VEGFR
Product DescriptionIn Vivo Grade Recombinant Anti-mouse PD-1 / VEGFR-2 Bispecific Antibody
IsotypeMouse IgG2c LALAPG Kappa
Antibody TypeRecombinant
Regulatory StatusRUO
Purity>95% by reducing SDS-PAGE
Endotoxin< 1 EU per 1 mg of the protein by the LAL method.
Storage Conditions4ºC
GradeIn vivo
Recommended UsageThis product is suitable for in vivo animal use. Optimal amounts need to be determined empirically for each experiment.
RRIDAB_3739426
Research AreasImmune Checkpoints, Activated T cells, Cancer Immunology, Tregs, Tfh cells, Activated B cells
See All FormatsClone 29F.1A12 / DC101

Background Information


Programmed cell death protein 1 (PD-1) is an immune checkpoint receptor expressed primarily on activated T cells, B cells, and some myeloid cells. It plays a crucial role in regulating immune responses by maintaining peripheral tolerance and preventing autoimmunity. When PD-1 binds to its ligands PD-L1 or PD-L2 on antigen-presenting or tumor cells, it recruits SHP-2 phosphatase, which dephosphorylates key signaling molecules in the T cell receptor (TCR) pathway. This suppresses T cell proliferation, cytokine secretion, and cytotoxic activity. In cancer, chronic PD-1 engagement results in “T cell exhaustion,” allowing tumor cells to evade immune destruction. Therapeutic blockade of PD-1 with monoclonal antibodies such as nivolumab or pembrolizumab reactivates these T cells, enabling potent anti-tumor immune responses.

Vascular Endothelial Growth Factor Receptor 2 (VEGFR2), also known as KDR (kinase insert domain receptor) or Flk-1, is the principal receptor mediating the angiogenic effects of VEGF-A. VEGFR2 is expressed mainly on endothelial cells and functions as a receptor tyrosine kinase. Upon VEGF-A binding, VEGFR2 dimerizes and becomes autophosphorylated, initiating downstream signaling pathways such as MAPK, PI3K-Akt, and PLCγ, which drive endothelial cell proliferation, migration, and new vessel formation. In tumors, overactivation of VEGFR2 results in aberrant angiogenesis, leading to structurally and functionally abnormal vasculature that not only sustains tumor growth and metastasis but also creates an immunosuppressive microenvironment by limiting immune cell infiltration and promoting hypoxia.

A bispecific antibody targeting PD-1 and VEGFR2 would provide a synergistic approach to enhancing anti-tumor immunity. By simultaneously blocking PD-1, the antibody would reinvigorate exhausted cytotoxic T cells, restoring their ability to recognize and kill tumor cells. Concurrent inhibition of VEGFR2 signaling would normalize the tumor vasculature, reduce hypoxia, and improve the trafficking of activated T cells into the tumor microenvironment. Moreover, suppressing VEGF/VEGFR2-mediated immunosuppression would shift the tumor milieu toward a more pro-inflammatory and immune-permissive state. This dual mechanism could overcome resistance observed with single-agent checkpoint inhibitors or anti-angiogenic therapies alone. Additionally, combining checkpoint modulation and vascular normalization into a single molecule may optimize pharmacokinetics, enhance co-localization within the tumor, and reduce toxicity relative to combination regimens. Thus, a PD-1 × VEGFR2 bispecific antibody represents a promising next-generation immunotherapy platform capable of simultaneously activating immune effector cells and dismantling the physical and molecular barriers that protect tumors from immune attack.

Data Sheets


In Vivo Star Anti-Mouse CD279 (PD1) / VEGFR-2 Bispecific Antibody TDS

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Frequently Asked Questions


What are In Vivo Star Biofunctional Antibodies?
In Vivo Star antibodies are premium-grade monoclonal antibodies purified and formulated specifically for use in animal studies. Each lot is manufactured under stringent quality controls to ensure the low endotoxin levels, high purity, and functional activity required for reliable in vivo results.

How are these antibodies different from standard research antibodies (e.g., for Western blot or flow cytometry)?
Standard research antibodies are optimized for in vitro detection assays and may contain preservatives, carrier proteins (like BSA), or higher endotoxin levels unsuitable for injection. In Vivo Star antibodies are formulated in injectable-grade, azide-free, low-endotoxin buffers and validated for functional bioactivity in living systems rather than just antigen binding.

What endotoxin and purity specifications do these antibodies meet?
All In Vivo Star antibodies are tested and certified to meet low-endotoxin thresholds (typically <1 EU/mg, lot-dependent) using the LAL (Limulus Amebocyte Lysate) assay, and are purified to ≥95% purity by SEC-HPLC or SDS-PAGE. Exact specifications are provided on the Certificate of Analysis (CoA) for each lot.

Are these antibodies azide-free and carrier-free?
All In Vivo Star antibodies are formulated without sodium azide and without carrier proteins such as BSA or gelatin, since both can interfere with animal physiology or immune readouts during in vivo studies.

Do you provide isotype controls?
Matched isotype control antibodies (same host species, isotype, and formulation) are available upon request for most clones to support proper experimental controls.

How should In Vivo Star antibodies be stored and handled?
Store at 4°C for short-term use and avoid repeated freeze-thaw cycles, which can reduce bioactivity; aliquoting is recommended for long-term storage per the product-specific storage instructions on the Certificate of Analysis. Always confirm storage conditions and expiration on the CoA that accompanies each lot, as these can vary slightly by antibody.

Have a product or application question? Consult our FAQs or contact us.