5001-96-7

Basic information

• Product Name: (2-FLUORO-4-BIPHENYL)ACETIC ACID
• Synonyms: (2-FLUORO-4-BIPHENYL)ACETIC ACID;2-Fluoro-[1,1'-Biphenyl]-4-acetic Acid;2-Fluoro-4-biphenylylacetic Acid;2-(2-Fluoro-[1,1'-biphenyl]-4-yl)acetic acid;[1,1'-Biphenyl]-4-acetic acid, 2-fluoro-
• CAS NO: 5001-96-7
• Molecular Formula: C14H11FO2
• Molecular Weight: 230.23
• Product Categories: Aromatics Compounds;Aromatics;Intermediates;Intermediates & Fine Chemicals;Pharmaceuticals
• Mol File: 5001-96-7.mol
• Article Data: 8

Chemical Properties

• Melting Point: 140-142°C
• Boiling Point: 375.695°C at 760 mmHg
• Flash Point: 181.014°C
• Appearance: /
• Density: 1.235g/cm³
• Vapor Pressure: 0mmHg at 25°C
• Refractive Index: 1.579
• Storage Temp.: -20°C Freezer
• CAS DataBase Reference: (2-FLUORO-4-BIPHENYL)ACETIC ACID(CAS DataBase Reference)
• NIST Chemistry Reference: (2-FLUORO-4-BIPHENYL)ACETIC ACID(5001-96-7)
• EPA Substance Registry System: (2-FLUORO-4-BIPHENYL)ACETIC ACID(5001-96-7)

Safety Data

• Hazardous Substances Data: 5001-96-7(Hazardous Substances Data)

Usage

Description

(2-FLUORO-4-BIPHENYL)ACETIC ACID, also known as (2-Fluoro-4-biphenyl)acetic Acid, is an organic compound that serves as an intermediate in the synthesis of various pharmaceuticals. It is characterized by its slightly yellow solid appearance and plays a crucial role in the development of anti-inflammatory medications.

Uses

Used in Pharmaceutical Industry:
(2-FLUORO-4-BIPHENYL)ACETIC ACID is used as an intermediate compound for the synthesis of Flurbiprofen (F598700), an anti-inflammatory drug. It is utilized for its analgesic properties, helping to alleviate pain and reduce inflammation in various conditions.
Additionally, as an intermediate, (2-FLUORO-4-BIPHENYL)ACETIC ACID may be involved in the production of other pharmaceuticals with different applications, although the provided materials do not specify these other uses.

InChI:InChI=1/C14H11FO2/c15-13-8-10(9-14(16)17)6-7-12(13)11-4-2-1-3-5-11/h1-8H,9H2,(H,16,17)

Upstream product

• 108-86-1 bromobenzene 
• 352-70-5 m-Fluorotoluene 
• 127425-73-4 1-bromo-4-(bromomethyl)-2-fluorobenzene 
• 499983-13-0 2-( 4-bromo-3-fluorophenyl)acetonitrile 
• 452-74-4 4-bromo-3-fluorotoluene 
• 1393566-55-6 2--(2--fluoro--[1,1'--biphenyl]--4--yl)acetaldehyde 
• 57592-43-5 2-fluoro-1,1'-biphenyl-4-carbaldehyde 
• 216701-21-2 (2-fluoro-[1,1’-biphenyl]-4-yl)methanol 
• 124-38-9 carbon dioxide 
• 69168-29-2 2-fluoro-4-methyl-1,1'-biphenyl 

Downstream Products

• 5104-49-4 fluorobiprofen 
• 866235-92-9 C₁₈H₁₉FO₂ 
• 1279100-88-7 2-fluoro-2-(2-fluorobiphenyl-4-yl)acetic acid 
• 1279100-90-1 C₂₆H₃₉FO₂Si₂ 
• 5104-49-4 (S)-(+)-flurbiprofen 
• 5104-49-4 (R)-flurbiprofen 
• 1264273-70-2 n-butyl 2-(2-fluorobiphenyl-4-yl)acetate 
• 147964-44-1 desmethylflurbiprofen 

Relevant articles and documents

Oxidation of Alkynyl Boronates to Carboxylic Acids, Esters, and Amides

A general efficient protocol was developed for the synthesis of carboxylic acids, esters, and amides through oxidation of alkynyl boronates, generated directly from terminal alkynes. This protocol represents the first example of C(sp)?B bond oxidation. This approach displays a broad substrate scope, including aryl and alkyl alkynes, and exhibits excellent functional group tolerance. Water, primary and secondary alcohols, and amines are suitable nucleophiles for this transformation. Notably, amino acids and peptides can be used as nucleophiles, providing an efficient method for the synthesis and modification of peptides. The practicability of this methodology was further highlighted by the preparation of pharmaceutical molecules.

New flurbiprofen derivatives: Synthesis, membrane affinity and evaluation of in vitro effect on β-amyloid levels

Alzheimer′s disease (AD) is characterized by irreversible and progressive loss of memory and cognition and profound neuronal loss. Current therapeutic strategies for the treatment of AD have been directed to a variety of targets with the aim of reversing or preventing the disease but, unfortunately, the available treatments often produce no significant clinical benefits. During the last decades compounds that inhibit or modulate γ-secretase, reducing β amyloid (Aβ) levels, have been considered as potential therapeutics for AD. Among these the (R)-enantiomer of flurbiprofen (FLU) seems to be very promising, but it shows low brain penetration. In this study, in order to improve the properties of FLU against Alzheimer′s pathogenesis we synthesized some novel FLU lipophilic analogues. Lipophilicity of the new molecules has been characterized in terms of clogP, log KC18/W and log K IAM/W values. Permeability has been determined in both gastrointestinal PAMPA (PAMPA-GI) at different pH values and in brain blood barrier PAMPA (PAMPA-BBB) models. They were also tested for their ability to inhibit in vitro γ-secretase activity using rat CTXTNA2 astrocytes. Interestingly, the investigated molecules demonstrated to reduce Aβ 42 levels without affecting the amyloid precursor protein APP level in a clear concentrations-dependent manner.

Inhibition of amyloidogenesis by nonsteroidal anti-inflammatory drugs and their hybrid nitrates

Poor blood-brain barrier penetration of nonsteroidal anti-inflammatory drugs (NSAIDs) has been blamed for the failure of the selective amyloid lowering agent (SALA) R-flurbiprofen in phase 3 clinical trials for Alzheimer's disease (AD). NO-donor NSAIDs (NO-NSAIDs) provide an alternative, gastric-sparing approach to NSAID SALAs, which may improve bioavailability. NSAID analogues were studied for anti-inflammatory activity and for SALA activity in N2a neuronal cells transfected with human amyloid precursor protein (APP). Flurbiprofen (1) analogues were obtained with enhanced anti-inflammatory and antiamyloidogenic properties compared to 1, however, esterification led to elevated A 1-42 levels. Hybrid nitrate prodrugs possessed superior anti-inflammatory activity and reduced toxicity relative to the parent NSAIDs, including clinical candidate CHF5074. Although hybrid nitrates elevated A 1-42 at higher concentration, SALA activity was observed at low concentrations (1 μM): both A1-42 and the ratio of A 42/A1-40 were lowered. This biphasic SALA activity was attributed to the intact nitrate drug. For several compounds, the selective modulation of amyloidogenesis was tested using an immunoprecipitation MALDI-TOF approach. These data support the development of NO-NSAIDs as an alternative approach toward a clinically useful SALA.