Fig. 4: Anti-PD1-mIL12mut2 effectively suppresses tumor growth without toxicity.
a C57BL/6 mice were inoculated with 5 ×105 MC38 tumor cells. Tumor-bearing mice (n = 5/group) were intraperitoneally treated with PBS or different doses of αPD1-mIL12mut2 on days 14, 17 and 20. The tumor growth of mice was recorded. b MC38 tumor-bearing mice (n = 4/group) were intraperitoneally treated with PBS or equimolar αPD-1 or αEGFR-mIL12mut2 or the mixture of αPD-1 and αEGFR-mIL12mut2 or αPD1-mIL12mut2 on days 14, 17 and 20. The tumor growth of mice was measured. c C57BL/6 mice were inoculated with 5 ×105 MC38-EGFR5 tumor cells. Tumor-bearing mice (n = 4/group) were intraperitoneally treated with PBS or an equimolar mixture of αPD-1 and αEGFR-mIL12mut2 or αPD1-mIL12mut2 on days 14, 17, and 20. The tumor growth of mice was monitored. d Humanized mice were inoculated with 2 ×106 A549 tumor cells. Tumor-bearing mice (n = 4/group) were intraperitoneally treated with PBS or equimolar αhPD-1 or αhPD1-hIL12mut2 on days 12, 15, 18 and 21. The tumor growth of mice was measured. e–g MC38 tumor-bearing mice (n = 3/group) were intraperitoneally treated once with PBS or 5 μg αPD1-mIL12wt or 20 μg αPD1-mIL12wt or 20 μg αPD1-mIL12mut2. e The body weight change curve of mice. f IFN-γ and g ALT in serum were measured after treatment. All data are shown as mean ± SEM from two to three independent experiments. The P value was determined by two-way ANOVA (a–g).
