p53 (17-26) acetate is a peptide derived from the P53 MDM2 binding domain, with a K d of 50 nM for MDM2. p53 (17-26) acetate causes cell lysis by damaging cancer cells and nuclear membranes, and induces cancer cell necrosis. p53 (17-26) acetate exhibits antitumor activity and is applicable to research related to pancreatic cancer [1] [2].
In Vivo, p53 (17-26) (2 mg; subcutaneous osmotic pump; 14 days) acetate eliminates intraperitoneal xenografted pancreatic cancer cells in nude mice[2]. p53 (17-26) (1-20 mg; subcutaneous osmotic pump; 14 days) acetate dose-dependently inhibits the growth of established subcutaneous xenograft pancreatic cancer in nude mice[2].
In Vitro, p53 (17-26) acetate binds tightly to the N-terminal domain of MDM2 (Kd = 50 nM) and induces global conformational changes in the MDM2 domain[1].
References:
[1]. Michl J, et al. PNC-28, a p53-derived peptide that is cytotoxic to cancer cells, blocks pancreatic cancer cell growth in vivo. Int J Cancer. 2006 Oct 1;119(7):1577-85.
In Vivo, p53 (17-26) (2 mg; subcutaneous osmotic pump; 14 days) acetate eliminates intraperitoneal xenografted pancreatic cancer cells in nude mice[2]. p53 (17-26) (1-20 mg; subcutaneous osmotic pump; 14 days) acetate dose-dependently inhibits the growth of established subcutaneous xenograft pancreatic cancer in nude mice[2].
In Vitro, p53 (17-26) acetate binds tightly to the N-terminal domain of MDM2 (Kd = 50 nM) and induces global conformational changes in the MDM2 domain[1].
References:
[1]. Michl J, et al. PNC-28, a p53-derived peptide that is cytotoxic to cancer cells, blocks pancreatic cancer cell growth in vivo. Int J Cancer. 2006 Oct 1;119(7):1577-85.