CBP-501 acetate, a cell-permeable calmodulin -binding peptide and a G2-abrogating drug candidate, inhibits the activity of multiple Ser 216 -specific kinases, such as MAPKAP-K2, C-Tak1, CHK1 and CHK2, with IC50 values of 0.9 μM, 1.4 μM 3.4 μM and 6.5 μM, respectively. CBP-501 acetate is used for various types of cancer [1] [2].
In Vitro, CBP501 acetate enhances cytotoxicity of CDDP and Bleomycin against cancer cells both in vitro and in vivo[2].
References:
[1]. Enzler T, et al. A multicenter, randomized phase 2 study to establish combinations of CBP501, cisplatin and nivolumab for ≥3rd-line treatment of patients with advanced pancreatic adenocarcinoma. Eur J Cancer. 2024 Apr;201:113950.
[2]. Shi-Ken Sha, et al. Cell cycle phenotype-based optimization of G2-abrogating peptides yields CBP501 with a unique mechanism of action at the G2 checkpoint. Mol Cancer Ther. 2007 Jan;6(1):147-53.
In Vitro, CBP501 acetate enhances cytotoxicity of CDDP and Bleomycin against cancer cells both in vitro and in vivo[2].
References:
[1]. Enzler T, et al. A multicenter, randomized phase 2 study to establish combinations of CBP501, cisplatin and nivolumab for ≥3rd-line treatment of patients with advanced pancreatic adenocarcinoma. Eur J Cancer. 2024 Apr;201:113950.
[2]. Shi-Ken Sha, et al. Cell cycle phenotype-based optimization of G2-abrogating peptides yields CBP501 with a unique mechanism of action at the G2 checkpoint. Mol Cancer Ther. 2007 Jan;6(1):147-53.