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| Targets |
Anti-Mouse VEGFR-2 Antibody (DC101) targets the vascular endothelial growth factor receptor 2 (VEGFR-2), also known as KDR, Flk-1, or CD309. VEGFR-2 is a receptor tyrosine kinase that serves as the primary mediator of VEGF-induced angiogenesis, endothelial cell proliferation, migration, and survival. By binding to mouse VEGFR-2, DC101 blocks the interaction between VEGF and its receptor, thereby inhibiting downstream signaling pathways including PI3K/AKT, MAPK/ERK, and PLCγ/PKC. This blockade results in inhibition of endothelial cell function and tumor angiogenesis. The antibody is highly specific for mouse VEGFR-2 and does not cross-react with human VEGFR-2, making it suitable for studies in murine models. Its specificity profile enables researchers to study VEGFR-2 function in mouse systems without interference from other VEGF receptors.
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| ln Vitro |
In vitro, Anti-Mouse VEGFR-2 Antibody (DC101) blocks VEGFR signaling in endothelial cell-based assays. The antibody inhibits VEGF-induced endothelial cell proliferation, migration, and tube formation, which are key steps in angiogenesis. In studies using mouse endothelial cells, DC101 effectively neutralizes VEGFR-2 activity, leading to reduced downstream signaling as measured by phosphorylation of AKT and ERK. The antibody has been shown to induce tumor cell apoptosis indirectly through its anti-angiogenic effects. In functional assays, DC101 blocks VEGF binding to VEGFR-2 on the cell surface, preventing receptor activation and subsequent signaling cascades. The in vitro potency of DC101 is typically assessed using endothelial cell-based assays such as BrdU incorporation for proliferation, transwell migration assays, and Matrigel tube formation assays, with appropriate controls including isotype-matched antibodies.
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| ln Vivo |
In vivo, Anti-Mouse VEGFR-2 Antibody (DC101) has been extensively studied in various murine tumor models. In a study using female Balb/c mice bearing H22 tumors, DC101 was administered intraperitoneally at 10 mg/kg on days 2, 5, and 8. The treatment promoted tumor vascular normalization, improved tumor vascular perfusion, reduced hypoxic regions within tumors, and increased the number of CD8+ T cells infiltrating the tumor. DC101 greatly reduces melanoma tumor growth and cell proliferation in murine models without adverse effects. In several different animal models, DC101 has been shown to block VEGF binding to its receptor, inhibit VEGF-mediated signaling, and cause tumor regression believed to result from angiogenesis inhibition. The antibody is also used in studies of colorectal and gastric cancers, demonstrating broad utility in cancer research.
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| Enzyme Assay |
In vitro enzyme or receptor binding assay protocols for Anti-Mouse VEGFR-2 Antibody (DC101) typically involve binding and blocking assays to characterize its interaction with VEGFR-2. A standard receptor binding assay would use mouse VEGFR-2 extracellular domain protein immobilized on ELISA plates, followed by incubation with varying concentrations of DC101 and detection with an anti-rat IgG-HRP conjugate. Alternatively, flow cytometry can be used with mouse endothelial cells expressing surface VEGFR-2, where cells are incubated with DC101 and binding is detected with fluorescently labeled secondary antibodies. For blocking assays, VEGF binding to VEGFR-2 can be assessed by incubating cells or receptor protein with DC101 prior to addition of labeled VEGF, with competition measured by reduced VEGF binding. Surface plasmon resonance (SPR) can also be employed to measure binding kinetics (ka, kd, KD) between DC101 and VEGFR-2. These assays typically include appropriate controls such as isotype-matched antibodies and irrelevant target antibodies.
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| Cell Assay |
In vitro cell-based assay protocols for Anti-Mouse VEGFR-2 Antibody (DC101) typically use mouse endothelial cell lines (e.g., MS1, bEND.3) or primary mouse endothelial cells to assess the antibody's functional activity. A standard protocol for proliferation assays involves seeding cells in 96-well plates, serum-starving overnight, then treating with VEGF (e.g., 10-50 ng/mL) in the presence or absence of DC101 at various concentrations (e.g., 0.1-100 μg/mL) for 48-72 hours. Cell proliferation is measured using BrdU incorporation, MTT, or direct cell counting. Migration assays use transwell chambers with VEGF as a chemoattractant, and cells are allowed to migrate for 4-24 hours with or without DC101. Tube formation assays involve plating cells on Matrigel and quantifying capillary-like structure formation after 6-18 hours. Signaling assays assess VEGFR-2 phosphorylation by Western blot or ELISA following VEGF stimulation with or without DC101 pretreatment. These assays are typically performed in triplicate with appropriate isotype controls.
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| Animal Protocol |
In vivo animal experimental protocols for Anti-Mouse VEGFR-2 Antibody (DC101) typically involve administration to tumor-bearing mice via intraperitoneal (IP) injection. A standard protocol for studying the antibody's anti-tumor activity involves implanting tumor cells (e.g., H22, melanoma, or colorectal cancer cells) subcutaneously or orthotopically in immunocompetent mice. Once tumors reach a certain size (e.g., 50-100 mm3), mice are randomized into treatment groups and administered DC101 at doses ranging from 5 to 40 mg/kg, typically 2-3 times per week. Treatment duration may range from 2 to 6 weeks depending on the study design. Endpoints include tumor volume measurement (caliper measurement 2-3 times per week), tumor weight at necropsy, survival analysis, assessment of tumor vascular density (CD31 staining), hypoxia (pimonidazole staining), and immune cell infiltration (CD8+ T cell staining). Pharmacodynamic endpoints include assessment of VEGFR-2 phosphorylation and downstream signaling in tumor tissues. Appropriate controls include vehicle (PBS) and isotype-matched control antibody groups.
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| ADME/Pharmacokinetics |
Pharmacokinetic properties of Anti-Mouse VEGFR-2 Antibody (DC101) have been characterized to some extent in the context of its use in murine models. As a monoclonal antibody (rat IgG1, ~150 kDa), DC101 would be expected to have a relatively long half-life in mice, typically several days to weeks, due to FcRn-mediated recycling. Following intraperitoneal administration, the antibody is absorbed into the systemic circulation, with peak concentrations typically achieved within 1-3 days. The volume of distribution is generally limited to the plasma and interstitial spaces (~50-100 mL/kg). Clearance occurs through proteolytic degradation and, to a lesser extent, through target-mediated elimination due to binding to VEGFR-2. The antibody is supplied as a sterile solution and stored at low temperature (-20°C) with shipping on blue ice. Specific PK parameters such as half-life, Cmax, AUC, and bioavailability may vary depending on the mouse strain, dose, and administration route.
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| Toxicity/Toxicokinetics |
Anti-Mouse VEGFR-2 Antibody (DC101) has been evaluated in preclinical toxicology studies as part of its development for research applications. In murine models, DC101 has been shown to greatly reduce tumor growth without adverse effects. The antibody is well-tolerated at therapeutic doses (e.g., 10-40 mg/kg, 2-3 times per week) with no significant body weight loss or overt toxicity reported. Potential on-target toxicities related to VEGFR-2 inhibition, such as effects on normal angiogenesis (e.g., wound healing, reproductive function), may occur but are generally not assessed in short-term tumor studies. The antibody is not intended for human use and is supplied with endotoxin levels <1.0 EU/mg to minimize inflammatory responses in vivo. Researchers should follow standard safety precautions when handling the antibody, including use of appropriate personal protective equipment and adherence to institutional biosafety guidelines.
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| Additional Infomation |
Anti-Mouse VEGFR-2 Antibody (DC101) is a research-grade monoclonal antibody used as a tool for studying tumor angiogenesis and the role of VEGFR-2 in cancer. It is a rat-derived antibody against mouse VEGFR-2 that serves as a mouse analogue of the human therapeutic antibody ramucirumab. DC101 induces tumor cell apoptosis by blocking VEGF-VEGFR binding and inhibiting tumor angiogenesis. It has been used extensively in studies of colorectal cancer, gastric cancer, melanoma, and other tumor types. The antibody promotes tumor vascular normalization, improves tumor perfusion, reduces hypoxia, and increases CD8+ T cell infiltration. DC101 has not entered clinical trials (the human analogue ramucirumab is clinically approved), but it remains a valuable preclinical tool. Its mechanism involves competitive blocking of VEGF binding to VEGFR-2, thereby inhibiting angiogenesis and indirectly suppressing tumor growth. It is available exclusively for research purposes.
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| Appearance |
Liquid
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
Typically soluble in DMSO (e.g. 10 mM)
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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