14000-67-0

Basic information

• Product Name: benzyl 4-(2-hydroxyethyl)piperazine-1-carboxylate
• Synonyms: benzyl 4-(2-hydroxyethyl)piperazine-1-carboxylate;2-(N-Cbz-piperazin-1-yl)ethanol
• CAS NO: 14000-67-0
• Molecular Formula: C₁₄H₂₀N₂O₃
• Molecular Weight: 264.3202
• Mol File: 14000-67-0.mol

Chemical Properties

• Boiling Point: 286-288 °C(Press: 1 Torr)
• Appearance: /
• Density: 1.190±0.06 g/cm3(Predicted)
• PKA: 14.96±0.10(Predicted)
• CAS DataBase Reference: benzyl 4-(2-hydroxyethyl)piperazine-1-carboxylate(CAS DataBase Reference)
• NIST Chemistry Reference: benzyl 4-(2-hydroxyethyl)piperazine-1-carboxylate(14000-67-0)
• EPA Substance Registry System: benzyl 4-(2-hydroxyethyl)piperazine-1-carboxylate(14000-67-0)

Safety Data

• Hazardous Substances Data: 14000-67-0(Hazardous Substances Data)

Upstream product

• 103-76-4 1-(2-hydroxyethyl)piperazine 
• 96452-48-1 benzyl pyridin-2-yl carbonate 
• 68160-42-9 benzyl piperazine-1-carboxylate hydrochloride 
• 540-51-2 2-bromoethanol 
• 13139-17-8 N-(Benzyloxycarbonyloxy)succinimide 
• 501-53-1 benzyl chloroformate 
• 1417816-42-2 benzyl 4-pyridyl carbonate 

Downstream Products

• 500013-41-2 benzyl 4-(2-bromoethyl)piperazine-1-carboxylate 
• 108845-79-0 benzyl 4-(2-chloro-ethyl)piperazine-1-carboxylate hydrochloride 
• 934536-31-9 4-(2-Methanesulfonyloxy-ethyl)-piperazine-1-carboxylic acid benzyl ester 

Relevant articles and documents

BIFUNCTIONAL COMPOUNDS FOR THE TREATMENT OF CANCER

The invention provides bifunctional compounds of formula (I) or a pharmaceutically acceptable salt thereof. Formula (I). The compounds cause the degradation of SMARCA2 via the targeted ubiquination of SMARCA2 protein and subsequent proteasomal degradation and are thus useful for the treatment of cancer. The targeting ligand is of formula (TL).

BIFUNCTIONAL COMPOUNDS

The invention provides a bifunctional compound of formula (I), or a pharmaceutically acceptable salt thereof, wherein said Targeting Ligand, Linker and Degron are as described herein.

From PARP1 to TNKS2 inhibition: A structure-based approach

Tankyrases (TNKSs) have recently gained great consideration as potential targets in Wnt/β-catenin pathway-dependent solid tumors. Previously, we reported the 2-mercaptoquinazolin-4-one MC2050 as a micromolar PARP1 inhibitor. Here we show how the resolution of the X-ray structure of PARP1 in complex with MC2050, combined with the computational investigation of the structural differences between TNKSs and PARP1/2 active sites, provided the rationale for a structure-based drug design campaign that with a limited synthetic effort led to the discovery of the bis-quinazolinone 5 as a picomolar and selective TNKS2 inhibitor, endowed with antiproliferative effects in a colorectal cancer cell line (DLD-1) where the Wnt pathway is constitutively activated.

C40-, C28-, AND C-32-LINKED RAPAMYCIN ANALOGS AS MTOR INHIBITORS

The present disclosure relates to mTOR inhibitors. Specifically, the embodiments are directed to compounds and compositions inhibiting mTOR, methods of treating diseases mediated by mTOR, and methods of synthesizing these compounds.

C26-LINKED RAPAMYCIN ANALOGS AS MTOR INHIBITORS

The present disclosure relates to mTOR inhibitors. Specifically, the embodiments are directed to compounds and compositions inhibiting mTOR, methods of treating diseases mediated by mTOR, and methods of synthesizing these compounds.

BRM TARGETING COMPOUNDS AND ASSOCIATED METHODS OF USE

The present disclosure relates to bifunctional compounds, which find utility as modulators of SMARCA2 or BRM (target protein). In particular, the present disclosure is directed to bifunctional compounds, which contain on one end a ligand that binds to the Von Hippel-Lindau E3 ubiquitin ligase, and on the other end a moiety which binds the target protein, such that the target protein is placed in proximity to the ubiquitin ligase to effect degradation (and inhibition) of target protein. The present disclosure exhibits a broad range of pharmacological activities associated with degradation/inhibition of target protein. Diseases or disorders that result from aggregation or accumulation of the target protein are treated or prevented with compounds and compositions of the present disclosure.

N,N′-diarylurea compounds and N,N′-diarylthiourea compounds as inhibitors of translation initiation

Compositions and methods for inhibiting translation initiation are provided. Compositions, methods and kits for treating (1) cellular proliferative disorders, (2) non-proliferative, degenerative disorders, (3) viral infections, and/or (4) disorders associated with viral infections, using N,N′-diarylureas and/or N,N′-diarylthiourea compounds are described.

3-3-DI-SUBSTITUTED-OXINDOLES AS INHIBITORS OF TRANSLATION INITIATION

Compositions and methods for inhibiting translation are provided. Compositions, methods and kits for treating (1) cellular proliferative disorders, (2) non-proliferative, degenerative disorders, (3) viral infections, and/or (4) disorders associated with viral infections, using diaryloxindole compounds are described.

Aminolysis of benzyl 2-pyridyl thionocarbonate and t-butyl 2-pyridyl thionocarbonate: Effects of nonleaving groups on reactivity and reaction mechanism

A kinetic study is reported for nucleophilic substitution reactions of benzyl 2-pyridyl thionocarbonate (5b) and t-butyl 2-pyridyl thionocarbonate (6b) with a series of alicyclic secondary amines in H2O at 25.0 °C. Generalbase catalysis, which has often been reported to occur for aminolysis of esters possessing a C=S electrophilic center, is absent for the reactions of 5b and 6b. The Bronsted-type plots for the reactions of 5b and 6b are linear with ssnuc = 0.29 and 0.43, respectively, indicating that the reactions of 5b proceed through a stepwise mechanism with formation of a zwitterionic tetrahedral intermediate (T±) being the rate-determining step while those of 6b proceed through a concerted mechanism. The reactivity of 5b and 6b is similar to that of their oxygen analogues (i.e., benzyl 2-pyridyl carbonate 5a and t-butyl 2-pyridyl carbonate 6a, respectively), indicating that the effect of modification of the electrophilic center from C=O to C=S (i.e., from 5a to 5b and from 6a to 6b) on reactivity is insignificant. In contrast, 6b is much less reactive than 5b, indicating that the replacement of the PhCH2 in 5b by the t-Bu in 6b results in a significant decrease in reactivity as well as a change in the reaction mechanism (i.e., from a stepwise mechanism to a concerted pathway). It has been concluded that the contrasting reactivity and reaction mechanism for the reactions of 5b and 6b are not due to the electronic effects of PhCH2 and t-Bu but are caused by the large steric hindrance exerted by the bulky t-Bu in 6b.

Synthesis and SAR study of novel 3,3-diphenyl-1,3-dihydroindol-2-one derivatives as potent eIF2·GTP·Met-tRNAiMet ternary complex inhibitors

The growing recognition of inhibition of translation initiation as a new and promising paradigm for mechanism-based anti-cancer therapeutics is driving the development of potent, specific, and druggable inhibitors. The 3,3-diaryloxindoles were recently reported as potential inhibitors of the eIF2·GTP·Met-tRNAiMet ternary complex assembly and 3-{5-tert-butyl-2-hydroxyphenyl}-3-phenyl-1,3-dihydro-2H-indol-2- one #1181 was identified as the prototypic agent of this chemotype. Herein, we report our continuous effort to further develop this chemotype by exploring the structural latitude toward different polar and hydrophobic substitutions. Many of the novel compounds are more potent than the parent compound in the dual luciferase ternary complex reporter assay, activate downstream effectors of reduced ternary complex abundance, and inhibit cancer cell proliferation in the low μM range. Moreover, some of these compounds are decorated with substituents that are known to endow favorable physicochemical properties and as such are good candidates for evaluation in animal models of human cancer.