Extended Data Fig. 8: RIPR-PD1 reduces MC38 colon carcinoma tumour growth.
From: Immune receptor inhibition through enforced phosphatase recruitment
a, b, Analysis of the RIPR-PD1(F2) binding affinity to mouse PD-1 by SPR. c, d, Analysis of RIPR-PD1(RMP) binding affinity to mouse PD-1 by SPR. In a–d, data are representative of 2 independent experiments. CD8+ mouse T cells were stimulated with plate-bound 2C11 overnight. e, f, Quantification of CD69 upregulation for cells treated with RIPR-PD1(F2) (e) or RIPR-PD1(RMP) (f). g, Proliferation (CellTiter-Glo) analysis of anti-CD3 treated CD4+ mouse T cells in the presence of F2 or RMP RIPR-PD1. In e–g, data are mean ± s.d. from n = 2 biological replicates from 1 representative of 3 independent experiments. h, MC38 tumour growth for mice treated with PBS, anti-PD1 (clone RMP1-14, 200 μg every 3 days) or RIPR-PD1(RMP) (200 μg daily). Data are mean ± s.e.m. from n = 10 mice. i, Representative images of the mice 24 days after inoculation with MC38 cells for the indicated treatments. Data shown are representative of 2 independent experiments, n = 10 mice per group. j, Individual tumour volume measurements for the data shown in Fig. 4f. The n values stated are the number of tumour-free mice. k, Percent survival for mice treated as described in h–j. In h–j, data shown are representative of 2 independent experiments, n = 10 mice per group.
