6524-81-8

Upstream product

• 92-66-0 4-bromo-1,1'-biphenyl 
• 103362-70-5 potassium ethyl methylmalonate 
• 609-08-5 Diethyl methylmalonate 
• 50712-64-6 ethyl 2-(4-nitrophenyl)propionate 
• 98-80-6 phenylboronic acid 
• 5459-35-8 2-bromo-acrylic acid ethyl ester 
• 5122-94-1 4-biphenylboronic acid 
• 5728-52-9 (4-biphenylyl)acetic acid 
• 14062-23-8 4-biphenylylacetic acid ethyl ester 
• 74-88-4 methyl iodide 
• 37940-57-1 1-biphenyl-4-yl-propan-1-one 
• 122-51-0 orthoformic acid triethyl ester 

Downstream Products

• 6341-72-6 2-(4-biphenylyl)propanoic acid 

Relevant academic research and scientific papers

Synthesis method of carbonyl alpha-position monomethyl substituted compound

The invention discloses a synthesis method of a carbonyl alpha-position monomethyl substituted compound, thesynthesis method comprises the following steps: taking substituted phenylboronic acid and ethyl 2-bromoacrylate as raw materials, taking THF and water as solvents, reacting K2CO3 and a catalyst Pd (OAc) 2 under the protection of nitrogen, purifying to obtain an intermediate product, dissolving the intermediate product in a methanol solvent, performing catalytic hydrogenation, reacting at room temperature, filtering, and spin-drying the solvent to obtain the carbonyl alpha-position monomethyl substituted compound. According to the synthesis method of the carbonyl alpha-position monomethyl substituted compound, the target compound can be conveniently obtained, the toxicity of reagents participating in the reaction is small, and the reaction conditions are mild. Post-treatment is simple and safe, the product quality is good, and the method is suitable for large-scale production.

The Suzuki-Miyaura Coupling of Nitroarenes

Synthesis of biaryls via the Suzuki-Miyaura coupling (SMC) reaction using nitroarenes as an electrophilic coupling partners is described. Mechanistic studies have revealed that the catalytic cycle of this reaction is initiated by the cleavage of the aryl-nitro (Ar-NO2) bond by palladium, which represents an unprecedented elemental reaction.

Pd-catalyzed decarboxylative cross-couplings of potassium malonate monoesters with aryl halides

An efficient catalytic protocol for Pd-catalyzed decarboxylative cross-coupling of potassium malonate monoesters and derivatives with aryl bromides and chlorides are described. Because of its broad applicability, this new catalytic system provides an alternative method for the preparation of diverse aryl acetic acids and derivatives.

Aryl acetylenes as mechanism-based inhibitors of cytochrome P450- dependent monooxygenase enzymes

Aryl acetylenes have been investigated as inhibitors of cytochrome P450 (P450)-dependent alkoxyresorufin dealkylation activities in liver microsomes prepared from rats exposed to β-naphthoflavone, isosafrole, or phenobarbital. Many of the acetylenes investigated produce pseudo-first- order time-dependent and NADPH-dependent losses of the dealkylation activities characteristic of mechanism-based irreversible inactivation (suicide inhibition). Replacing the terminal hydrogen of aryl acetylenes with a methyl group to convert ethynes into propynes enhances the inhibition of P450 1A enzymes; in some instances, this modification converts a reversible inhibitor of P450s into a suicide inhibitor. In contrast, ethynes are more effective suicide inhibitors of P450 2B-dependent dealkylations than the corresponding propynes. Aryl acetylenes with an ethynyl group on the 2 position of naphthalene or on the 9 position of phenanthrene and arylalkyl acetylenes with alkyl chains containing 2, 3, or 4 methylene groups are selective inhibitors of P450 2B1/2B2 in liver microsomes from rats. Aryl acetylenes also act as suicide inhibitors of P450 1A2 in human liver microsomes, of purified P450 1A2 from rabbit or rat liver in reconstituted systems, and of purified recombinant human P450 1A2 and 1A1 in reconstituted systems. 4-(1-Propynyl)biphenyl (4PBi) inactivated P450 1A2-dependent ethoxyresourfin deethylation (EROD) activity in human liver microsomes in an NADPH-dependent process (k(inactivation), 0.23 min-1; K1, 2.3 μM). 4PBi also inactivated purified recombinant human P450 1A2 (k(inactivation), 0.24 min-1; K(I), 4.3 μM). In agreement with previous reports [Yun, C.-H., Hammons, G. J., Jones, G., Martin, M. V., Hopkins, N. E., Alworth, W. L., and Guengerich, F. P. (1992) Biochemistry 31, 10556-10563], 2-ethyny]naphthalene (2EN) was not a suicide inhibitor of the P450 1A2 activity in human liver microsomes but did inactivate purified human P450 1A2. Neither 4PBi nor 2EN affected diagnostic activities of human microsomal P450 2E1, 2C9/10, 3A4, or 2C19. In the systems examined, the losses of P450-dependent activity produced by these aryl acetylenes were not accompanied by corresponding decreases in the measured P450 absorption spectra. Thus P450 inactivation by these aryl acetylenes does not involve labeling and destruction of the heme. Incubation of 4PBi with microsomal P450 1A1 or 1A2 from rat liver under conditions that lead to P450-dependent enzyme inactivations generates a 2-biphenylylpropionic acid product. This suggests that the suicide inhibition of P450s by propynylaryl acetylenes proceeds via a methylaryl ketene formed by a 1,2- methyl rearrangement, analogous to the mechanism of suicide inhibition by ethynyl acetylenes that proceed via ketene intermediates formed by 1,2- hydrogen shifts [Ortiz de Montellano, P. R., and Kunze, K. L. (1981) Arch. Biochem. Biophys. 209, 710-712].

Oxidative Rearrangement of Aryl Ethyl Ketones to Alkyl 2-Arylpropanoates by Lead(IV) Acetate

Treatment of the propiophenones p-R'C6H4COCH2Me (1; R' = H, Me, Bui, Ph, Br) with lead(IV) acetate in trialkyl orthoformate in the presence of acid catalyst is found to give alkyl esters of 2-arylpropanoic acids (2) in good to excellent yields via 1,2-aryl migration in (1).Hydrolysis of (2) leads to the corresponding acids, some of which are important pharmaceutical compounds.The rate of aryl migration increases when the substituent R' is an electron-releasing group such as methyl, isobutyl, or phenyl.The rate of rearrangement of the dimethyl acetals of (1); R' = H, Bui, Ph) is nearly the same as that of (1).Such rearrangement hardly occurs in the absence of acid catalyst.A reaction pathway involving the formation of a monoalkoxylead(IV) compound, and its decomposition accompanied with aryl migration is discussed.