DC101 (ATCC® HB-11534)

Organism: Rattus norvegicus (B cell); Mus musculus (myeloma), rat (B cell); mouse (myeloma)  /  Cell Type: hybridoma  /  Tissue: Spleen  / 

Organism Rattus norvegicus (B cell); Mus musculus (myeloma), rat (B cell); mouse (myeloma)
Tissue
Spleen
Cell Type hybridoma
Product Format frozen
Morphology lymphoblast
Culture Properties suspension
Biosafety Level 1
Strain Lewis (B cell); BALB/c (myeloma)
Applications
DC101 was found to be specific for the murine tyrosine kinase receptor FLK-1. ELISA data showed that the antibody bound to purified FLK-1:SEAP but not alkaline phosphatase or other receptor tyrosine kinases such as FLK-2.
Treatment with DC101 antibody completely inhibits the growth of established epidermoid, glioblastoma, pancreatic, and renal human tumor xenografts by suppression of tumor-induced neovascularization
Storage Conditions liquid nitrogen vapor phase
Derivation
Animals were hyperimmunized with an immune complex consisting of the mouse FLK-1:SEAPs soluble receptor, a rabbit anti-alkaline phosphatase polyclonal antibody and Protein-G sepharose beads.
Spleen cells were fused with NS-1 mouse myeloma cells.
Genes Expressed
immunoglobulin; monoclonal antibody; against murine vascular endothelial growth factor (VEGF) receptor-2 (Flk-1/KDR)
Cellular Products
immunoglobulin; monoclonal antibody; against murine vascular endothelial growth factor (VEGF) receptor-2 (Flk-1/KDR)
Comments
DC101 was found to be specific for the murine tyrosine kinase receptor FLK-1. ELISA data showed that the antibody bound to purified FLK-1:SEAP but not alkaline phosphatase or other receptor tyrosine kinases such as FLK-2.
DC101 does not cross-react with the human VEGFR2/KDR.
Treatment with DC101 antibody completely inhibits the growth of established epidermoid, glioblastoma, pancreatic, and renal human tumor xenografts by suppression of tumor-induced neovascularization
Complete Growth Medium The base medium for this cell line is ATCC-formulated Dulbecco's Modified Eagle's Medium, Catalog No. 30-2002. To make the complete growth medium, add the following components to the base medium: fetal bovine serum to a final concentration of 10%.
Subculturing
Protocol: Cultures can be maintained by the addition of fresh medium or replacement of medium. Alternatively, cultures can be established by centrifugation with subsequent resuspension at 2 X 10 exp5 viable cells/ml. Maintain cell density between 1 X 10 exp5 and 1 X 10 exp6 viable cells/ml.
Medium Renewal: Every 2 to 3 days
Cryopreservation
Freeze medium: Complete growth medium 92.5%; DMSO, 7.5%
Storage temperature: liquid nitrogen vapor phase
Culture Conditions
Temperature: 37.0°C
Isotype IgG1; kappa light chain
Name of Depositor ImClone Systems Inc.
References

Rockwell P, Goldstein NI. Monoclonal antibodies specific to VEGF receptors and uses thereof. US Patent 5,955,311 dated Sep 21 1999

Witte L, et al. Monoclonal antibodies targeting the VEGF receptor-2 (Flk1/KDR) as an anti-angiogenic therapeutic strategy. Cancer Metastasis Rev. 17: 155-161, 1998. PubMed: 9770111

Prewett M, et al. Antivascular endothelial growth factor receptor (fetal liver kinase 1) monoclonal antibody inhibits tumor angiogenesis and growth of several mouse and human tumors. Cancer Res. 59: 5209-5218, 1999. PubMed: 10537299

Shaheen RM, et al. Effects of an antibody to vascular endothelial growth factor receptor-2 on survival, tumor vascularity, and apoptosis in a murine model of colon carcinomatosis. Int. J. Oncol. 18: 221-226, 2001. PubMed: 11172585

Kadambi A, et al. Vascular endothelial growth factor (VEGF)-C differentially affects tumor vascular function and leukocyte recruitment: role of VEGF-receptor 2 and host VEGF-A. Cancer Res. 61: 2404-2408, 2001. PubMed: 11289105

Kozin SV, et al. Vascular endothelial growth factor receptor-2-blocking antibody potentiates radiation-induced long-term control of human tumor xenografts. Cancer Res. 61: 39-44, 2001. PubMed: 11196192

Zimmermann RC, et al. Preovulatory treatment of mice with anti-VEGF receptor 2 antibody inhibits angiogenesis in corpora lutea. Microvasc. Res. 62: 15-25, 2001. PubMed: 11421657

Klement G, et al. Continuous low-dose therapy with vinblastine and VEGF receptor-2 antibody induces sustained tumor regression without overt toxicity. J. Clin. Invest. 105: R15-R24, 2000. PubMed: 10772661

Stoelcker B, et al. VEGF/Flk-1 interaction, a requirement for malignant ascites recurrence. J. Inferon Cytokine Res. 20: 511-517, 2000. PubMed: 10841080

Basic Documentation
References

Rockwell P, Goldstein NI. Monoclonal antibodies specific to VEGF receptors and uses thereof. US Patent 5,955,311 dated Sep 21 1999

Witte L, et al. Monoclonal antibodies targeting the VEGF receptor-2 (Flk1/KDR) as an anti-angiogenic therapeutic strategy. Cancer Metastasis Rev. 17: 155-161, 1998. PubMed: 9770111

Prewett M, et al. Antivascular endothelial growth factor receptor (fetal liver kinase 1) monoclonal antibody inhibits tumor angiogenesis and growth of several mouse and human tumors. Cancer Res. 59: 5209-5218, 1999. PubMed: 10537299

Shaheen RM, et al. Effects of an antibody to vascular endothelial growth factor receptor-2 on survival, tumor vascularity, and apoptosis in a murine model of colon carcinomatosis. Int. J. Oncol. 18: 221-226, 2001. PubMed: 11172585

Kadambi A, et al. Vascular endothelial growth factor (VEGF)-C differentially affects tumor vascular function and leukocyte recruitment: role of VEGF-receptor 2 and host VEGF-A. Cancer Res. 61: 2404-2408, 2001. PubMed: 11289105

Kozin SV, et al. Vascular endothelial growth factor receptor-2-blocking antibody potentiates radiation-induced long-term control of human tumor xenografts. Cancer Res. 61: 39-44, 2001. PubMed: 11196192

Zimmermann RC, et al. Preovulatory treatment of mice with anti-VEGF receptor 2 antibody inhibits angiogenesis in corpora lutea. Microvasc. Res. 62: 15-25, 2001. PubMed: 11421657

Klement G, et al. Continuous low-dose therapy with vinblastine and VEGF receptor-2 antibody induces sustained tumor regression without overt toxicity. J. Clin. Invest. 105: R15-R24, 2000. PubMed: 10772661

Stoelcker B, et al. VEGF/Flk-1 interaction, a requirement for malignant ascites recurrence. J. Inferon Cytokine Res. 20: 511-517, 2000. PubMed: 10841080