methyl 4-hydroxyphenyllactate

11/01/1989 - "MeHPLA binds to nuclear type II binding sites with a very high binding affinity (Kd approximately 4-5 nM), blocks uterine growth in vivo, and inhibits MCF-7 human breast cancer cell growth in vitro. "
10/01/2003 - "Methyl para-hydroxyphenyllactate (MeHPLA) was observed to suppress the cellular proliferation of estrogen-sensitive MCF-7 breast cancer cells in vitro and to suppress the growth of rat uteri in vivo. "
05/25/1988 - "Competition analysis revealed that MeHPLA binds to nuclear type II sites with a high binding affinity, while physiological levels of this compound blocked estradiol stimulation of uterine growth in vivo and inhibited the growth of MCF-7 human breast cancer cells in vitro. "
05/01/1992 - "These findings demonstrate that esterase-stable type II antagonists such as BDHPC and BMHPC inhibit mammary cancer cell proliferation in vitro and in vivo and support earlier studies demonstrating that MeHPLA and functionally related compounds may regulate malignant cell proliferation at the level of this binding site."
10/20/1997 - "2,6-bis((3, 4-dihydroxyphenyl)-methylene) cyclohexanone (BDHPC) is an esterase-resistant analogue of MeHPLA which binds irreversibly to EBS-II and inhibits growth of breast cancer cells. "

03/01/1990 - "The present studies were performed to examine the metabolic fate of [3H]MeHPLA in mouse mammary tumors. "
03/01/1990 - "Methyl p-hydroxyphenyllactate and nuclear type II binding sites in malignant cells: metabolic fate and mammary tumor growth."
03/01/1990 - "Taken together, these results suggest esterase hydrolysis of MeHPLA in mammary tumors may result in a deficiency in this compound which correlates with a loss of regulatory control."
03/01/1993 - "Therefore, combination therapy with MeHPLA agonists plus standard anti-neoplastic agents such as 5-Fluorouracil (FU) may result in tumor growth inhibition with minimal non-specific cytotoxicity. "
05/01/1992 - "This ligand is inactivated by MeHPLA esterase in mammary tumors, resulting in a deficiency in MeHPLA, high quantities of unoccupied type II sites, and uncontrolled cellular proliferation. "