Presentation Title

Anti-Angiogenesis Effect Associated with Inhibition of VEGFR by F16 Treatment in U87 cell line and Glioblastoma Xenograft Tumors

Format

Poster

Abstract

Objective. This study was conducted to determine the effectiveness of the Anti-angiogenic Agent F16 treatment using glioblastoma cell line and xenograft tumor implanted in nude mice. Background. Glioblastoma multiforme (GBM) tumors are highly vascularized tumors, and their growth is angiogenesis-dependent; antagonizing tumor angiogenesis by using angiogenesis inhibitors is considered as one of the promising approaches. Methods. In this context, intensive pre-clinical evaluation of a novel small molecule named F16 has exhibited potent anti-angiogenic and anti-tumor activities by selectively antagonizing Vascular Endothelial Growth Factor Receptor (VEGFR) in the in vitro and in vivo models. Results. Our in vitro studies have clearly demonstrated the ability of F16 to inhibit U87MG cell survival, migration, and invasion. Furthermore, pharmacokinetic evaluation of F16 with tissue distribution analysis has shown that this molecule is transported across the blood-brain barrier and accumulates in the brain regions with no signs of neurotoxicity. Therefore, we conducted experiments to determine the efficacy of F16 in delaying glioblastoma progression via inhibiting tumor angiogenesis using the xenograft model. Our in vivo studies with the subcutaneously implanted tumors indicated that F16 is efficacious in delaying tumor growth by blocking tumor angiogenesis. Conclusion. Our in vitro and in vivo results strongly demonstrated that F16 has significant cytotoxic effects on U87MG cells and the host mice also showed a good level of tolerability for F16 treatments. Further studies are underway to complete the pre-clinical testing of F16. Grants. This research was supported by the Royal Dames of Cancer Research Inc. Ft. Lauderdale, FL

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Anti-Angiogenesis Effect Associated with Inhibition of VEGFR by F16 Treatment in U87 cell line and Glioblastoma Xenograft Tumors

Objective. This study was conducted to determine the effectiveness of the Anti-angiogenic Agent F16 treatment using glioblastoma cell line and xenograft tumor implanted in nude mice. Background. Glioblastoma multiforme (GBM) tumors are highly vascularized tumors, and their growth is angiogenesis-dependent; antagonizing tumor angiogenesis by using angiogenesis inhibitors is considered as one of the promising approaches. Methods. In this context, intensive pre-clinical evaluation of a novel small molecule named F16 has exhibited potent anti-angiogenic and anti-tumor activities by selectively antagonizing Vascular Endothelial Growth Factor Receptor (VEGFR) in the in vitro and in vivo models. Results. Our in vitro studies have clearly demonstrated the ability of F16 to inhibit U87MG cell survival, migration, and invasion. Furthermore, pharmacokinetic evaluation of F16 with tissue distribution analysis has shown that this molecule is transported across the blood-brain barrier and accumulates in the brain regions with no signs of neurotoxicity. Therefore, we conducted experiments to determine the efficacy of F16 in delaying glioblastoma progression via inhibiting tumor angiogenesis using the xenograft model. Our in vivo studies with the subcutaneously implanted tumors indicated that F16 is efficacious in delaying tumor growth by blocking tumor angiogenesis. Conclusion. Our in vitro and in vivo results strongly demonstrated that F16 has significant cytotoxic effects on U87MG cells and the host mice also showed a good level of tolerability for F16 treatments. Further studies are underway to complete the pre-clinical testing of F16. Grants. This research was supported by the Royal Dames of Cancer Research Inc. Ft. Lauderdale, FL