Fig. 1
Pep R potentiates the anti-PD-1 antitumor efficacy in murine MC38 colon cancer and B16-human-CXCR4 mice models. a. MC38 colon cancer. Mice were subcutaneously inoculated with 1 × 106 MC38 colon cancer cells. When tumors reached 250 mm3 volume (day 20) mice were randomized and treated for 2 weeks according to treatment schedule (Peptide R 2 mg/kg ip, 5 day/week; anti–PD-1 5 mg/kg i.p. twice weekly). Relative Tumor Volume (RTV) (mean ± SEM, n = 4 per group), untreated (n = 4), anti-mouse PD-1 (n = 4), Pep R (n = 4), anti-PD-1 + Pep R combination (n = 4). RTV: Untreated 14.75 ± 3.07; anti-PD-1 11.91 ± 4.60, Pep R 20.0 ± 2.95; anti-PD-1 + Pep R 5.52 ± 3.22. b. B16 melanoma-human-CXCR4. Mice were subcutaneously inoculated with 5 × 105 B16-human-CXCR4 cells and treated as above. Mean tumor volumes (MTV) ± SEM. Untreated mice (n = 12), anti-PD-1 (n = 10), Pep R (n = 8), anti-PD-1 + Pep R combination (n = 10). Response time trends recorded for different treatment was analyzed by comparing means at each time point using repeated measures analysis of variance (RMANOVA with Tukey HSD post hoc-test);* p < 0.05