| Bioactivity | CI-988 (PD134308) is a potent, selective and orally active CCK2R (cholecystokinin 2 receptor) antagonist with an IC50 of 1.7 nM for mouse cortex CCK2. CI-988 shows >1600-fold selectivity for CCK2 over CCK1 receptor. CI-988 has anxiolytic and anti-tumor effects[1][2][3]. |
| Target | IC50: 1.7 nM (Mouse cortex CCK2); 2717 nM (Rat pancreas CCK1) |
| Invitro | CI-988 inhibits specific 125I-BH-CCK-8 binding to NCI-H727 cells with high affinity (Ki of 4.5 nM). The increase in ROS caused by CCK-8 addition to NCI-727 cells is blocked significantly by CI-988. CI-988 (3 µM) inhibits the basal growth of NCI-H727 cells or that stimulated by CCK-8. CI-988 inhibits the ability of CCK-8 to cause ERK phosphorylation and elevate cytosolic Ca2+[1]. CI-988 inhibits in a dose-dependent manner the ability of CCK-8 to cause EGFR transactivation in NCI-H727 cells. CI-988 at doses of 1 and 10 µM weakly and strongly, respectively, inhibits the ability of 0.1µM CCK-8 to increase EGFR tyrosine phosphorylation. CI-988 antagonizes the ability of CCK-8 to cause lung cancer EGFR or ERK tyrosine phosphorylation[1]. |
| In Vivo | CI-988 (10 mg/kg; p.o.; daily; for 20 days) inhibits the growth of colorectal cancer in xenografts model mice[3]. Animal Model: |
| Name | CI-988 |
| CAS | 130332-27-3 |
| Formula | C35H42N4O6 |
| Molar Mass | 614.73 |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
| Reference | [1]. Terry W Moody, et al. CI-988 Inhibits EGFR Transactivation and Proliferation Caused by Addition of CCK/Gastrin to Lung Cancer Cells. J Mol Neurosci. 2015 Jul;56(3):663-72. [2]. J Hughes, et al. Development of a class of selective cholecystokinin type B receptor antagonists having potent anxiolytic activity. Proc Natl Acad Sci U S A. 1990 Sep;87(17):6728-32. [3]. R Romani, et al. Gastrin receptor antagonist CI-988 inhibits growth of human colon cancer in vivo and in vitro. Aust N Z J Surg. 1996 Apr;66(4):235-7. |