866021-30-9Relevant articles and documents
Evaluation of 2-(piperidine-1-yl)-ethyl (PIP) as a protecting group for phenols: Stability to ortho-lithiation conditions and boiling concentrated hydrobromic acid, orthogonality with most common protecting group classes, and deprotection via Cope elimination or by mild Lewis acids
Norén, Rolf
, (2021/04/07)
A new protecting group, 2-(piperidine-1-yl)-ethyl (PIP), was evaluated as a protecting group for phenols. The PIP group was stable to ortho-lithiation conditions and refluxing with concentrated hydrobromic acid. Deprotection was accomplished by two routes, oxidation to N-oxides followed by Cope elimination (CE) and subsequent hydrolysis or ozonolysis of the vinyl ether or one-step deprotection by BBr3?Me2S. The PIP group is orthogonal to the O-benzyl, O-acetyl, O-t-butyldiphenylsilyl, O-methyl, O-p-methoxybenzyl, O-allyl, O-tetrahydropyranyl and N-t-butoxy carbonyl groups. The CE step was systematically studied and was found to give higher yields when the reaction was performed in the presence of silylating agents.
Differential response of estrogen receptor subtypes to 1,3-diarylindene and 2,3-diarylindene ligands
Clegg, Nicola J.,Paruthiyil, Sreenivasan,Leitman, Dale C.,Scanlan, Thomas S.
, p. 5989 - 6003 (2007/10/03)
Estrogen receptors (ERs) control transcription of genes important for normal human development and reproduction. The signaling networks are complex, and there is a need for a molecular level understanding of the roles of receptor subtypes ERα and ERβ in normal physiology and as therapeutic targets. We synthesized two series of ER ligands, based on a common indene scaffold, in an attempt to develop compounds that can selectively modulate ER-mediated transcription. The 3-ethyl-1,2-diarylindenes, utilizing an amide linker for the 1-aryl extension, bind weakly to the ERs. The 2,3-diarylindenes bind with high affinity to the ER subtypes and demonstrate a range of different biological activities, both in transcriptional reporter gene assays and inhibition of estradiol-stimulated proliferation of MCF-7 cells. Several ligands differentiate between ERα and ERβ subtypes at an estrogen response element (ERE), displaying various levels of partial to full agonist activity at ERα, while antagonizing estradiol action at ERβ.
