2,2- bis(hydroxymethyl)- 1- azabicyclo(2,2,2,)octan- 3- one

01/01/2011 - "In contrast, combined treatment with PRIMA-1 and 2aG4 was extremely effective in suppressing tumor growth in both models and completely eradicated approximately 30% of tumors in the BT-474 model. "
01/01/2017 - "In this study, we investigated the anti-cancer activity of PRIMA-1 and PRIMA-1MET (APR-246), two compounds which were previously reported to reactivate mutant p53 and convert it to a form with wild-type (WT) properties. "
08/01/2013 - "In this study, we investigated the ability of PRIMA-1 to induce autophagy in cancer cells. "
03/27/2013 - "Importantly, nutlin and PRIMA-1 have successfully reached the stage of phase I/II clinical trials in at least one type of hematological cancer. "
01/01/2011 - "Mechanistic studies determined that PRIMA-1 reactivated mtp53 and also exposed AP on the surface of tumor cells as determined by enhanced 2aG4 binding. "

11/01/2009 - "Mechanistic studies showed that PRIMA-1 induced the mitochondrial-dependent apoptotic pathway in mtp53-expressing breast cancer cells. "
01/01/2019 - "Size-exclusion chromatography of the lysates from mutant p53-containing breast cancer and ovarian cell lines confirmed that PRIMA-1 substantially decreases p53 aggregates. "
01/01/2017 - "Using a panel of 18 breast cancer cell lines and 2 immortalized breast cell lines, inhibition of proliferation by PRIMA-1 and PRIMA-1MET was found to be cell-line dependent, but independent of cell line molecular subtype. "
12/15/2012 - "Under normoxia, PRIMA-1 was active against breast cancer cells harboring mutant p53. "
11/12/2010 - "PRIMA-1 cytotoxicity correlates with nucleolar localization and degradation of mutant p53 in breast cancer cells."

06/01/2005 - "In this study, we examined toxicity of PRIMA-1 to three premalignant human colorectal adenoma cell lines (RG/C2, BR/C1, and AA/C1) and four colorectal carcinoma cell lines (DLD-1, SW480, LOVO, and HCT116) and its mechanism of action. "
09/01/2013 - "Seven-week-old mice were treated with a single dose of NNK (10 µmol/mouse) by intraperitoneal injection and, 3 weeks later, were randomized to mice fed a control diet or experimental diets containing 50 or 100 ppm CP-31398 or 150 or 300 ppm Prima-1 for either 17 weeks (10 mice/group) or 34 weeks (15 mice/group) to assess the efficacy against lung adenoma and adenocarcinoma. "
09/01/2013 - "We studied chemopreventive effects of p53-modulating agents, namely, CP-31398 and Prima-1, on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung adenoma and adenocarcinoma formation in female A/J mice. "

12/15/2012 - "Our results suggest that PRIMA-1 may help to prevent hypoxia-mediated tumor chemoresistance."
11/18/2016 - "Since hypoxia increases the toxicity of the p53 activator, Prima-1 against breast cancer cells irrespective of their p53 status, we also investigated whether Prima-1 reversed hypoxic resistance to 3-BrPA. "
12/15/2012 - "This report shows for the first time that hypoxia increases PRIMA-1 toxicity in human breast cancer cells, partly by modulating p53 conformation and by inducing superoxide turnover. "
12/15/2012 - "However, hypoxia further increased the susceptibility of mutant p53 breast cancer SKBR3 cells to lower PRIMA-1 levels, possibly through oxidative stress since this was counteracted by N-acetylcysteine. "
12/15/2012 - "Hypoxia, Mn-SOD and H(2)O(2) regulate p53 reactivation and PRIMA-1 toxicity irrespective of p53 status in human breast cancer cells."

09/01/2013 - "Seven-week-old mice were treated with a single dose of NNK (10 µmol/mouse) by intraperitoneal injection and, 3 weeks later, were randomized to mice fed a control diet or experimental diets containing 50 or 100 ppm CP-31398 or 150 or 300 ppm Prima-1 for either 17 weeks (10 mice/group) or 34 weeks (15 mice/group) to assess the efficacy against lung adenoma and adenocarcinoma. "
09/01/2013 - "We studied chemopreventive effects of p53-modulating agents, namely, CP-31398 and Prima-1, on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung adenoma and adenocarcinoma formation in female A/J mice. "