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Poster lunch

1925 - Surface Engineered Nanocapsules of Crocetin as Novel inhibitor of VEGFR2 on Cancer induced Chick Embryo (18P)


18 Nov 2017


Poster lunch


Cancer Biology


Vikas Kumar


Annals of Oncology (2017) 28 (suppl_10): x1-x6. 10.1093/annonc/mdx652


V. Kumar, M. Rahman

Author affiliations

  • Pharmaceutical Sciences, Sam Higginbottom University of Agriculture, Technology & Sciences (SHUATS), 211007 - Allahabad/IN


Abstract 1925


Angiogenesis plays a fundamental and decisive role in the development of solid tumor growth and progression of chronic inflammation. Malignancies constantly generate certain mediators which are inducing proliferation, expression, angiogenesis and permitting tumor cells. Judah Folkman and colleagues suggested the concept of angiogenic inhibition of tumor growth. Vascular endothelial growth factor (VEGF) is a multifunctional protein, expressed and secreted during wound healing and tumor angiogenesis via pro-angiogenic factors. VGEF is a prime target for scrutinizing therapeutic agents because it is a validated significant pathway. Considering this we have fabricated the surface engineered nanocapsules of crocetin as a potential VEGFR2 kinase inhibitor for anticancer effect.


Emulsion solvent evaporation technique was used for the preparation of crocetin-loaded PLGA nanoparticles (CA-PLGA-NP) and poly-disparity, particle size, drug release potency and zeta potential were scrutinized, respectively. Further docking study was performed via using the docking server for scrutinized the cost effective drug. Flow cytometirc, MTT assay and confocal microscope analyses were performed on human hepatocellular carcinoma cell lines HepG2 and HuH-7, and further chick embryo was used for determination of in ovo angiogenic inhibition. The formulation was further labeled with technetium-99m to scrutinize the biodistribution, and scintigraphic study following intravenous administration in solid tumor bearing mice was also performed.


The prepared formulation of crocetin showed the smooth spherical small surface with relative narrow size distribution. In cell lines study, the formulation demonstrated higher cyto-toxicity compared with the free drug due to enhanced cellular uptake (in vitro). CA showed the potent protein inhibitor of VEGFR2 in docking study. IC50 value clearly showed that CA-PLGA-NP has significant anti-proliferative effect against HCC cell lines, and in ovo study clearly suggested that CA-PLGA-NP is nontoxic to normal cells. The scintigraphic image and radiolabeled CA-PLGA-NP showed slower blood clearance and higher uptake of formulation into the tumor site.


Collectively, we can conclude that we have developed a novel formulation for hepatic cancer.

Clinical trial identification


Legal entity responsible for the study

Sam Higginbottom University of Agriculture, Technology & Sciences (SHUATS)




All authors have declared no conflicts of interest.

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