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. Author manuscript; available in PMC: 2013 Dec 13.
Published in final edited form as: J Med Chem. 2012 Nov 27;55(23):10729–10734. doi: 10.1021/jm301468k

Figure 3.

Figure 3

Biological characterization of MCo-CVX cyclotides. A. Competitive inhibition of SDF1α-mediated CXCR4 activation by different cyclotides. The peptide CVX15 Gln6Cit and the small molecule CXCR4 antagonist AMD3100 were used as controls. The assay was performed using CXCR4-bla U2OS cells. B. Inhibition of Erk phosphorylation (residues Thr202 and Tyr204) by cyclotide MCo-CVX-5c. Cyclotide MCoTI-I and peptide CVX15 Gln6Cit were used as negative and positive controls, respectively. Erk phosphorylation was visualized by Western blot using CaOV3 cells treated with increasing amounts of CXCR4 inhibitor in the presence of SDF1α. C. Dose response inhibition of HIV-1 replication in MT-4 cells by cyclotides MCoTI-I and MCo-CVX-5c. The peptide CVX15 Gln6Cit and the small molecule HIV-1 integrase inhibitor, Raltegravir, were used as positive controls. Cyclotide MCoTI-I was used as negative control. The average of standard deviation of three experiments is shown. NB and ND stand for not bound and not determined, respectively.