Anti-Mouse CD309 (VEGFR2) [Clone DC101] — Purified in vivo GOLD™ Functional Grade

Anti-Mouse CD309 (VEGFR2) [Clone DC101] — Purified in vivo GOLD™ Functional Grade

Product No.: V173

[product_table name="All Top" skus="V173"]

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Clone
DC101
Target
VEGFR2
Formats AvailableView All
Product Type
Hybridoma Monoclonal Antibody
Alternate Names
CD309, KDR, FLK-1, vascular endothelial growth factor receptor 2
Isotype
Rat IgG1 κ
Applications
FA
,
WB

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Antibody Details

Product Details

Reactive Species
Mouse
Host Species
Rat
Recommended Isotype Controls
Recommended Dilution Buffer
Immunogen
Recombinant full-length Mouse VEGFR2 protein
Product Concentration
≥ 5.0 mg/ml
Endotoxin Level
< 1.0 EU/mg as determined by the LAL method
Purity
≥95% monomer by analytical SEC
>95% by SDS Page
Formulation
This monoclonal 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
Functional grade preclinical antibodies are manufactured in an animal free facility using in vitro 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.
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
Country of Origin
USA
Shipping
2 - 8°C Wet Ice
Additional Applications Reported In Literature ?
FA,
WB
Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change.

Description

Description

Specificity
DC101 activity is directed against VEGFR-2.
Background
Vascular endothelial growth factors (VEGF) and VEGF receptors (VEGFR) play an essential role in angiogenesis1. There are three VEGFRs: VEGFR-1, VEGFR-2, and VEGFR-3. VEGFR-1 and VEGFR-2 are responsible for angiogenesis, and VEGFR-3 affects lymphogenesis. In the pathogenesis of diseases including diabetes mellitus, rheumatoid arthritis, and cancer, new blood vessel formation is highjacked. Changes at the VEGF/VEGFR-2 axis are particularly potent at allowing VEGF-induced proliferation, migration, and vascular endothelial cell differentiation during tumor angiogenesis. Additionally, VEGFR-2 is upregulated in tumor vascular endothelial cells, and VEGF levels are associated with poor prognosis and resistance to chemotherapy. Consequently, the VEGF/VEGFR axis is a prime anti-cancer target.

DC101 greatly reduces melanoma tumor growth and cell proliferation in murine mouse models without adverse effects as well as promotes tumor vessel normalization2. Additionally, DC101 therapy enhances immune cell penetration of melanoma cells by increasing the proportion of CD19+ B cells, CD11c+ dendritic cells, and CD3+ and CD8+ T cells. DC101 treatment also increases expression of PD-1 and PD-L1 in CD45+ immune cells and tumors. Additionally, DC101 directly inhibits angiogenesis in vivo, and, in tumors, reduces xenograft tumor growth, decreases endothelial cells and microvessel density, and increases tumor cell apoptosis3.

DC101 binds to an extracellular, ligand-binding domain on the amino-terminal of VEGFR-2, thereby blocking ligand binding and preventing VEGF165-induced receptor phosphorylation4. DC101 has been used in Cy5.5-, FITC, and HYNIC-labeled chitosan conjugates to study VEGFR-2 expression in ischemia5.
Antigen Distribution
VEGFR-2 is widely expressed by vascular endothelial cells, some vascular tumors, carcinomas, malignant melanomas, and lymphomas. Certain leukemia cells express functional VEGFR on the cell surface.
Ligand/Receptor
VEGF-A, VEGF-C, and VEGF-D splice isoforms
NCBI Gene Bank ID
UniProt.org
Research Area
Cell Biology
.
Immunology

Leinco Antibody Advisor

Powered 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.

DC101 is a rat monoclonal antibody clone that targets vascular endothelial growth factor receptor 2 (VEGFR-2) and is extensively used in mouse studies for cancer research and immunotherapy applications.

Direct Antibody Treatment

DC101 is administered directly to tumor-bearing mice as an antiangiogenic therapy. The antibody works by binding to VEGFR-2 on endothelial cells, directly inhibiting angiogenesis and reducing tumor growth. In experimental settings, DC101 treatment results in decreased endothelial cells and microvessel density in tumors, effectively starving tumors of their blood supply.

In immune-competent FVB mice, DC101 treatment alone leads to tumor regression through a T cell-dependent mechanism. The antibody induces significant expansion of tumor-specific CD8+ T cells and can result in durable tumor regression. Notably, tumors continue to regress both during and after DC101 treatment, indicating sustained therapeutic effects.

CAR-T Cell Therapy Applications

DC101 is also used to engineer chimeric antigen receptor (CAR) T cells that target VEGFR-2-expressing cells. In these studies, T cells are genetically modified to express DC101-based CARs, creating DC101-CAR T cells. These engineered T cells can specifically recognize and respond to VEGFR-2-expressing tumor cells and endothelial cells.

The DC101-CAR T cells demonstrate antigen-specific responses, including proliferation and IFN-? secretion when exposed to VEGFR-2-expressing targets. These modified T cells have shown effectiveness against multiple types of established syngeneic tumors in mouse models.

Immune Response Modulation

The effectiveness of DC101 varies significantly depending on the immune status of the mouse model. In FVB mice (which lack immune tolerance to tumor antigens), DC101 induces robust T cell-dependent tumor regression with enhanced tumor-specific immune responses. However, in neu-N mice (which have preexisting immune tolerance), DC101 only slows tumor growth without inducing frank regression.

To overcome immune tolerance in tolerant mouse models, DC101 can be combined with other treatments such as regulatory T cell depletion using cyclophosphamide, which enhances vaccine-induced tumor regression responses. This approach demonstrates how DC101 can be integrated into combination immunotherapy strategies.

DC101 treatment enhances the presentation of heterogeneous tumor epitopes, potentially expanding the repertoire of immune recognition beyond single immunodominant epitopes. This broad immune activation contributes to its therapeutic efficacy in immunocompetent mouse models.

The correct storage temperature for sterile packaged clone DC101 (anti-mouse VEGFR-2 monoclonal antibody) is -20°C to -70°C, using a manual defrost freezer and avoiding repeated freeze-thaw cycles.

This storage condition maintains antibody stability for up to 12 months from the date of receipt. For shorter-term storage (up to 1 month), 2°C to 8°C may be acceptable, but for long-term preservation, freezing at -20°C to -70°C is specifically recommended. Always follow these precautions:

  • Use a manual defrost freezer
  • Avoid repeated freeze-thaw cycles, as this can degrade antibody quality

There is no indication in authoritative sources that clone DC101 should be stored at standard refrigerator (2–8°C) or room temperature for long-term use.

The most commonly used antibodies or proteins combined with DC101 (an anti-VEGFR2 antibody) in the literature include:

  • Anti-VEGF-A antibody (e.g., 2G11-2A05): Frequently co-administered with DC101 to simultaneously block VEGF-A ligand and its receptor, enhancing anti-angiogenic effects in tumor models.
  • Cetuximab (anti-EGFR antibody): Used in combination with DC101 to concurrently inhibit EGFR and VEGFR2 signaling, particularly in models of squamous cell carcinoma and other epithelial tumors.
  • Chemotherapeutic agents (e.g., gemcitabine): DC101 is often paired with cytotoxic drugs to assess synergistic effects on inhibiting tumor growth, as noted in pancreatic cancer research.
  • Other VEGFR pathway-related antibodies (e.g., anti-FLK2 (2A13), anti-FLK2 (23H7)): Used for mechanistic studies or as controls in experiments examining VEGF pathway inhibition.
  • Secondary detection antibodies: Such as anti-rat IgG-biotin or rabbit polyclonal antibodies used in immunoprecipitation, immunoblotting, or detection assays alongside DC101.

Context and common combinations:

  • The dual blockade of VEGF ligand (e.g., VEGF-A) and its receptor (VEGFR2) is a prominent strategy to intensify inhibition of angiogenesis in oncology research.
  • EGFR inhibitors (like cetuximab) are often combined with DC101 to target both angiogenic and proliferative pathways, particularly in epithelial cancers.
  • Chemotherapy plus anti-VEGFR2 therapy: Combined regimens evaluate whether anti-angiogenic therapies sensitize tumors to standard cytotoxic agents or reduce resistance.

These patterns reflect a strategy aimed at disrupting multiple complementary pathways to enhance anti-tumor efficacy. DC101 is often used not in isolation, but as part of a combinatorial approach with other targeted or conventional therapies in preclinical models.

Clone DC101, a monoclonal antibody targeting VEGFR-2 (also known as Flk-1 or KDR), is widely cited in scientific literature for its role in inhibiting angiogenesis and tumor growth. Key findings from DC101-related studies include:

  • Inhibition of Tumor Angiogenesis and Growth: DC101 significantly reduces tumor vascularization and growth across diverse preclinical cancer models, including pulmonary metastases, mammary carcinoma (4T1), and melanoma (B16). Effects include substantial decreases in microvessel density (up to 90% reduction after 2 weeks), suppression of tumor cell proliferation, induction of tumor cell and endothelial cell apoptosis, and increased tumor necrosis.

  • Survival Benefits: In murine models, DC101 treatment not only diminishes tumor growth, but extends survival—treated mice outlive control mice with markedly reduced tumor burdens, and some demonstrate complete absence of macroscopic metastases.

  • Synergistic Effects in Combination Therapy: DC101 synergizes with other therapies, such as cetuximab (an anti-EGFR antibody), to further suppress tumor growth and metastasis, as demonstrated in squamous cell carcinoma of the tongue models. Combination therapies can significantly reduce regional lymph node metastasis rates compared to monotherapies.

  • Immunomodulatory Actions: Beyond antiangiogenic effects, DC101 has been shown to induce T cell–dependent antitumor immune responses. In immunocompetent mice bearing highly immunogenic tumors, DC101 leads to T cell–mediated tumor regression, requiring both CD4+ and CD8+ T cells. The antitumor effect is lost if T cells are depleted. Notably, DC101 can potentiate responses to tumor vaccines, with combined therapy yielding stronger immune activation than either agent alone.

  • Vascular and Stromal Remodeling: DC101 prompts rapid regression of preexisting blood vessels in tumors and reduces stromal protease expression, mechanisms thought to contribute to its anti-tumor action and potentially affect tumor microenvironment reorganization.

  • VEGF Pathway Specificity: DC101 specifically neutralizes mouse VEGFR-2 signaling, permitting distinction between paracrine and autocrine VEGF/VEGFR-2 activity in experimental models. This has enabled deeper investigation into VEGF-dependent tumor and endothelial biology.

In summary, scientific literature identifies DC101 as a critical research tool for dissecting VEGFR-2's role in tumor growth, angiogenesis, immune activation, and therapeutic combinations, substantiating its dual capacity for direct tumor suppression and indirect enhancement of antitumor immunity.

References & Citations

1. Spratlin J. Curr Oncol Rep. 13(2):97-102. 2011.
2. Wang Z, Shi X, Zhao Y, et al. Biochem Biophys Res Commun. 661:10-20. 2023.
3. Prewett M, Huber J, Li Y, et al. Cancer Res. 59(20):5209-5218. 1999.
4. Patent EP1602668A1: https://patentimages.storage.googleapis.com/10/da/cb/f945064c422659/EP1602668A1.pdf
5. Lee CM, Kim EM, Cheong SJ, et al. J Biomed Mater Res A. 92(4):1510-1517. 2010.
6. Rockwell P, Neufeld G, Glassman A, et al. Mol Cell Differ. 3(1): 91–109. 1995.
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Disclaimer AlertProducts are for research use only. Not for use in diagnostic or therapeutic procedures.