PPT

• CAT Number: I010412
• CAS Number: 263717-53-9
• Molecular Formula: C24H22N2O3
• Molecular Weight: 386.451
• Purity: ≥95%
• Synonyms: Propylpyrazole triol; PPT; 4,4/’,4/’/’-(4-Propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol
• Target: Estrogen Receptor/ERR
• Solubility: Soluble to 5 mM in ethanol and to 100 mM in DMSO
• Storage: Store at +4°C
• IUPAC Name: 4-[2,3-bis(4-hydroxyphenyl)-4-propyl-1H-pyrazol-5-ylidene]cyclohexa-2,5-dien-1-one
• InChI: InChI=1S/C24H22N2O3/c1-2-3-22-23(16-4-10-19(27)11-5-16)25-26(18-8-14-21(29)15-9-18)24(22)17-6-12-20(28)13-7-17/h4-15,25,28-29H,2-3H2,1H3
• InChIKey: UOSWGERPQQOSHS-UHFFFAOYSA-N
• SMILES: CCCC1=C(N(NC1=C2C=CC(=O)C=C2)C3=CC=C(C=C3)O)C4=CC=C(C=C4)O

PPT (CAT: I010412) is a selective agonist for the estrogen receptor beta (ERβ). It is a synthetic compound designed to specifically activate ERβ while having a minimal affinity for the estrogen receptor alpha (ERα). PPT has been extensively studied for its pharmacological effects and potential applications. It has shown promise in various areas, including neuroprotection, cardiovascular protection, and anticancer activities. PPT’s selectivity for ERβ activation makes it a valuable tool for understanding the distinct functions and signaling pathways mediated by ERβ. Furthermore, its potential therapeutic applications span from neurodegenerative disorders to hormone-related cancers, warranting further exploration and research.

Reference

1. J Steroid Biochem Mol Biol. 2012 May;130(1-2):26-35. doi:
10.1016/j.jsbmb.2011.12.018. Epub 2012 Jan 14.

Estrogen receptor-beta agonist diarylpropionitrile counteracts the estrogenic
activity of estrogen receptor-alpha agonist propylpyrazole-triol in the mammary
gland of ovariectomized Sprague Dawley rats.

Song X(1), Pan ZZ.

Author information:
(1)Department of Animal Science, Vermont Cancer Center, University of Vermont,
Burlington, VT 05405, USA.

Although estrogen can bind both types of estrogen receptors, estrogen
receptor-alpha (ERα) is dominant in mediating estrogenic activity in the mammary
gland and uterus. Excessive estrogenic activity such as estrogen-based
postmenopausal hormone replacement therapy increases the risk for breast and
endometrial cancers. The adverse effect of estrogen on uterine endometrium can be
opposed by progestins; however, estrogen-plus-progestin regimen imposes
substantially greater risk for breast cancer than estrogen alone. In this study,
we used ERα-selective agonist propylpyrazole-triol (PPT) and ERβ-selective
agonist diarylpropionitrile (DPN) to activate ERα and estrogen receptor-beta
(ERβ) separately in an ovariectomized rat model and determined whether
PPT-activated ERα function in the mammary gland can be suppressed by DPN
activated ERβ. Ovariectomized rats were randomly divided into six groups and
treated with DMSO (control), DPN, PPT, PPT/DPN, PPT/Progesterone, and
PPT/Progesterone/DPN, respectively. In the mammary gland, PPT but not DPN
increased cell proliferation and amphiregulin gene expression; importantly, the
stimulatory effect of PPT on mammary cell proliferation and amphiregulin gene
expression can be suppressed by DPN. In the uterus, the effect of PPT on uterine
weight and endometrial cell proliferation was not inhibited by DPN but can be
inhibited by progesterone. These data provide in vivo evidence that PPT activated
ERα activity in the mammary gland can be opposed by ERβ-selective agonist DPN,
which may be explored for the development of better hormone replacement therapy
regimen with less risk for breast cancer.