Fig. 3: Systemic administration of AC484 induces immune-dependent tumour regression in various syngeneic and metastatic mouse models.
From: The PTPN2/PTPN1 inhibitor ABBV-CLS-484 unleashes potent anti-tumour immunity
a, Tumour growth over time of B16 melanoma, KPC pancreatic cancer, and 4T1 and EMT-6 breast cancer tumours in AC484-treated (red), anti-PD-1-treated (blue) or control animals (black) (n = 5–10 animals per group, data are the mean ± s.e.m.). b, Tumour growth over time of CT26 colon cancer tumours in AC484-treated (red), anti-PD-1-treated (blue) AC484-treated and anti-PD-1-treated (purple) or control animals (black) (n = 10 animals per group, data are the mean ± s.e.m., statistics calculated as per cent tumour growth inhibition) c, Representative luciferase imaging at day 17 after challenge (left), tumour growth over time (middle) and survival analysis (right) of B16 metastasis model mice in AC484-treated (red), anti-PD-1-treated (blue) or control animals (black) (n = 10 per group). d, Tumour growth over time for KPC tumours in WT mice with or without AC484 (n = 10, n = 5, respectively), and for NSG mice with or without AC484 (n = 10, n = 5, respectively). e, Tumour growth over time for control of Ptpn2/n1-null B16 tumours treated with GVAX with or without AC484 (n = 5 animals per group, data are the mean ± s.e.m.). f, Tumour growth over time for KPC tumours treated with an isotype antibody (n = 10), anti-CD8b (n = 10) or an anti-NK1.1 depleting antibody (n = 10) and treated with AC484 (red) compared with an untreated control group (n = 10; black). g, Tumour growth over time for Jak1-null KPC tumours treated with isotype antibody (n = 5), anti-CD8b (n = 10) or anti-NK1.1 depleting antibody (n = 10) and treated with AC484 (red) compared with an untreated control group (n = 10; black).
