27773-03-1

Basic information

• Product Name: 2-Phenyl-1,3-dioxolane-2-acetic acid ethyl ester
• Synonyms: 2-Phenyl-1,3-dioxolane-2-acetic acid ethyl ester
• CAS NO: 27773-03-1
• Molecular Formula: C₁₃H₁₆O₄
• Molecular Weight: 236.26
• Mol File: 27773-03-1.mol
• Article Data: 8

Chemical Properties

• Appearance: /
• CAS DataBase Reference: 2-Phenyl-1,3-dioxolane-2-acetic acid ethyl ester(CAS DataBase Reference)
• NIST Chemistry Reference: 2-Phenyl-1,3-dioxolane-2-acetic acid ethyl ester(27773-03-1)
• EPA Substance Registry System: 2-Phenyl-1,3-dioxolane-2-acetic acid ethyl ester(27773-03-1)

Safety Data

• Hazardous Substances Data: 27773-03-1(Hazardous Substances Data)

Upstream product

• 5764-85-2 Ethyl 3-hydroxy-3-phenylpropanoate 
• 94-02-0 ethyl 3-oxo-3-phenylpropionate 
• 107-21-1 ethylene glycol 

Downstream Products

• 74949-66-9 (2-phenyl-[1,3]dioxolan-2-yl)-acetic acid hydrazide 
• 50337-24-1 2-(2-hydroxyethyl)-2-phenyl-1,3-dioxolane 
• 125261-01-0 2-(2-phenyl-1,3-dioxolan-2-yl)acetaldehyde 
• 10229-22-8 N-benzyl-3-oxo-3-phenylpropionamide 
• 1430751-40-8 1-benzyl-4-iodo-5-phenyl-1H-pyrazole 

Relevant articles and documents

Design, Synthesis, and Biochemical Characterization of Non-Native Antagonists of the Pseudomonas aeruginosa Quorum Sensing Receptor LasR with Nanomolar IC50 Values

Quorum sensing (QS), a bacterial cell-to-cell communication system mediated by small molecules and peptides, has received significant interest as a potential target to block infection. The common pathogen Pseudomonas aeruginosa uses QS to regulate many of its virulence phenotypes at high cell densities, and the LasR QS receptor plays a critical role in this process. Small molecule tools that inhibit LasR activity would serve to illuminate its role in P. aeruginosa virulence, but we currently lack highly potent and selective LasR antagonists, despite considerable research in this area. V-06-018, an abiotic small molecule discovered in a high-throughput screen, represents one of the most potent known LasR antagonists but has seen little study since its initial report. Herein, we report a systematic study of the structure-activity relationships (SARs) that govern LasR antagonism by V-06-018. We synthesized a focused library of V-06-018 derivatives and evaluated the library for bioactivity using a variety of cell-based LasR reporter systems. The SAR trends revealed by these experiments allowed us to design probes with 10-fold greater potency than that of V-06-018 and 100-fold greater potency than other commonly used N-acyl-l-homoserine lactone (AHL)-based LasR antagonists, along with high selectivities for LasR. Biochemical experiments to probe the mechanism of antagonism by V-06-018 and its analogues support these compounds interacting with the native ligand-binding site in LasR and, at least in part, stabilizing an inactive form of the protein. The compounds described herein are the most potent and efficacious antagonists of LasR known and represent robust probes both for characterizing the mechanisms of LuxR-type QS and for chemical biology research in general in the growing QS field.

APOPTOSIS-INDUCING AGENTS FOR THE TREATMENT OF CANCER AND IMMUNE AND AUTOIMMUNE DISEASES

Disclosed are compounds which inhibit the activity of anti-apoptotic Bc1-xL proteins, compositions containing the compounds and methods of treating diseases during which is expressed anti-apoptotic Bc1-xL protein.

Titanocene-catalyzed asymmetric ketone hydrosilylation: The effect of catalyst activation protocol and additives on the reaction rate and enantioselectivity

The efficient asymmetric hydrosilylation of ketones with a chiral titanocene catalyst has been realized. In this procedure, (R,R)-ethylenebis(tetrahydroindenyl) titanium difluoride (1) was used as the precatalyst, and alcohol additives were employed. Arom