Figure 6.

Enhanced antitumor immunity by CompK treatment in a mouse syngeneic tumor model. (A) Inhibition of pSLP76 by CompK in MC38 OVA tumor-bearing mouse model. CompK was administrated to mice bearing MC38 OVA tumor at 100 mpk, two times per day for five consecutive days. Blood samples were collected to analyze pSLP76 in T cells by FACS. (B) Increased tumor antigen-specific CD8+ T cells by CompK. OVA+CD8+ T cells in the blood were measured by OVA tetramer staining followed by FACS analysis. (C) Promoted tumor regression by treatment with combination of CompK and anti-PD1. C57BL/6 mice were implanted with MC38 tumor cells followed by treatment with isotype control antibody, anti-PD1, and combination of CompK plus anti-PD1. All groups contain the same amount of vehicle used to formulate CompK. Tumor volumes were monitored up to 58 days. Compound dosing was discontinued on day 28. (D) No significant difference of body weights among study groups. Body weights were monitored during the time period of compound administration. (E) Improved priming of immune cells by CompK plus anti-PD1. Draining lymph nodes were collected at the end of study. Quantitative PCR analysis was conducted to investigate proinflammatory markers. Comparison was made between groups of anti-PD1 alone and anti-PD1 plus CompK. Statistical analysis was conducted using Student t-test. *P≤0.05, **P<0.01, ***P<0.001, ****P<0.0001. Data are presented as mean±SEM. CompK, compound K; GZMB, Granzyme B; IL, interleukin; OVA, ovalbumin; PFN, perforin; TDLN, tumor-draining lymph node.