52516-30-0

Usage

Chemical Properties

Clear colorless to pale yellow liquid

InChI:InChI=1/C9H10F3N/c10-9(11,12)8-3-1-2-7(6-8)4-5-13/h1-3,6H,4-5,13H2/p+1

Upstream product

• 2338-76-3 3-trifluoromethylphenylacetonitrile 
• 75-52-5 nitromethane 
• 454-89-7 3-Trifluoromethylbenzaldehyde 
• 60-29-7 diethyl ether 
• 368-77-4 3-trifluoromethylbenzonitrile 
• 1997-80-4 2-(3-trifluoromethylphenyl)-ethyl bromide 
• 402-24-4 3-(trifluoromethyl)styrene 
• 1336-21-6 ammonium hydroxide 
• 705-29-3 3-Trifluoromethylbenzyl chloride 

Downstream Products

• 79988-70-8 5,5-methylenebis-2,4,6-triaminopyrimidine 
• 79988-67-3 6-[2-(3-Trifluoromethyl-phenyl)-ethyl]-5,6,7,8-tetrahydro-pyrimido[4,5-d]pyrimidine-2,4-diamine 
• 875305-17-2 (4-tert-butyl-benzyl)-[2-(3-trifluoromethyl-phenyl)-ethyl]-amine 
• 248930-57-6 (2RS,3R)-3-amino-4-cyclohexyl-2-hydroxy-N-(3-(trifluoromethyl)phenethyl)butanamide Hydrochloride 
• 1219623-52-5 2-(2-oxo-3,3-diphenylpyrrolidin-1-yl)-N-{2-[3-(trifluoromethyl)phenyl]ethyl}acetamide 

Relevant academic research and scientific papers

Molecular determinants for the interaction of the valvulopathic anorexigen norfenfluramine with the 5-HT2B receptor

S-(+)-Norfenfluramine (SNF)-an active metabolite of the now-banned anorexigen fenfluramine-has been implicated in the drug's appetite-suppressing actions and its life-threatening cardiovascular side effects. SNF reduces appetite through serotonin 5-HT2C receptor activation; it causes cardiopulmonary side effects through 5-HT2B receptor activation. Thus, we attempted to identify molecular determinants of SNF binding to 5-HT2B receptors distinct from those underlying SNF-5-HT 2C/2A receptor interactions. Mutagenesis implicated Val2.53 in SNF binding to 5-HT2B receptors. Ligand docking simulations suggested both Val2.53 γ-methyl groups form stabilizing van der Waals' (vdW) interactions with the α-methyl group of SNF. A V2.53L mutation induced a 17-fold decrease in affinity; molecular dynamics (MD) simulations suggested that this decrease resulted from the loss of one 2.53-α-methyl group vdW interaction. Supporting this, 1) the binding of norfenfluramine (NF) analogs lacking an S-(+) α-methyl group (RNF and α-desmethyl-NF) was less sensitive to the V2.53L mutation, and 2) a V2.53A mutation decreased SNF affinity 190-fold, but decreased RNF and α-desmethyl-NF affinities only 16- and 45-fold, respectively. We next addressed whether the α-methyl group of SNF contributes to 5-HT2C/2A receptor affinity. Removal of the α-methyl group (RNF and α-desmethyl-NF), which reduced 5-HT 2B receptor binding 3-fold, did not affect 5-HT2C/2A receptor binding. An α-ethyl substituent (α-ethyl-NF), which decreased 5-HT2B receptor affinity 46-fold, reduced 5-HT2C and 5-HT2A receptor binding by 14- and 5-fold, respectively. Finally, we determined that residue 2.53 affects SNF potency and efficacy at 5-HT2B receptors but not at 5-HT2C and 5-HT2A receptors. In conclusion, vdW interactions between residue 2.53 and the α-methyl group of SNF contribute to the ligand's 5-HT2 receptor subtype-selective pharmacology. Copyright

Direct Primary Amination of Alkylmetals with NH-Oxaziridine

A method for the primary electrophilic amination of primary, secondary, and tertiary organometallic substrates from a bench-stable NH-oxaziridine reagent is described. This facile and highly chemoselective transformation occurs at ambient temperature and without transition metal catalysts or purification by column chromatography to provide alkylamine products in a single step. Density functional theory (DFT) calculations revealed that, despite the basicity of alkylmetals, the direct NH-transfer pathway is favored over proton and O-transfer.

17a-HYDROXYLASE/C17,20-LYASE INHIBITORS

The present invention provides compounds of Formula (I), or a pharmaceutically acceptable salt thereof, where R1, R2, R3, R4, R5, R6, A and n are as defined herein. A deuteriated derivative of the compound of Formula (I) is also provided.

17α-HYDROXYLASE/C17,20-LYASE INHIBITORS

The present invention provides compounds of Formula (I), or a pharmaceutically acceptable salt thereof, where R1, R2, R3, R4, R5, R6, A and n are as defined herein. A deuteriated derivative of the compound of Formula (I) is also provided.

Regioselective hydroboration-oxidation and -amination of fluoro-substituted styrenes

Hydroboration of fluorinated styrenes with common hydroborating agents results in polymerization. However, regioselective hydroboration has been achieved by utilizing iodoborane-dimethyl sulfide. A series of fluorinated β-phenethyl alcohols and amines were synthesized via this methodology.

Process for preparing fluorine-containing phenethylamines and novel fluorine-containing β-iminovinyl-and β-iminoethylbenzenes

The present invention relates to a process for preparing fluorine-containing phenethylamines which is characterized in that, in a first step, a substituted bromobenzene is reacted with an N-vinylimide in the presence of a palladium catalyst, in a second step, the resulting substituted β-iminovinylbenzene is hydrogenated catalytically and in a third step, the substituted β-iminovinylbenzene obtained in the second step is cleaved. This process also provides access to novel β-iminovinyl- and β-iminoethylbenzenes.

2-guanidino-4-arylthiazoles for treatment of peptic ulcers

2-Guanidino-4-arylthiazole compounds of the formula STR1 a pharmaceutically acceptable cationic or acid addition salt thereof wherein R1 is hydrogen, (C1 -C10)alkyl, optionally substituted phenyl or certain optionally substituted aralkyl groups; R2 is hydrogen or (C1 -C4)alkyl, and Ar is certain optionally substituted pyrrolyl or indolyl groups; method for their use in treatment of gastric ulcers, by inhibition of parietal cell H+ /K+ ATPase, and antiinflammatory conditions in combination with piroxicam, for use in mammals, and pharmaceutical compositions containing said compounds.

N-phenylalkylbenzamide fungicides

Compounds of the formula (I): STR1 wherein: X=O, S, or NOH; R1 is H or CH3 ; n=1, 2, or 3; R2, R3, and R4 are as defined in one of the following paragraphs (a) R2 and R3 are independently Cl or Br, and R4 is H; (b) R2, R3 and R4 are independently Cl or Br; (c) R2 is F, R3 is Cl, and R4 is H; or (d) R2 and R3 are CH3 or C2 H5, and R4 is H; R5, R6 and R7 are as defined in one of the following paragraphs (a) one of R6 and R7 is CF3, R5 and the other of R6 and R7 is H; (b) R5 and R6 are H; and R7 is F, Cl, or Br; (c) R5 and R7 are independently F, Cl or Br and R6 is H; (d) R5 and R6 are independently F, Cl, or Br, and R7 is H; (e) R6 and R7 are independently F, Cl, or Br, and R5 is H; or (f) R6 is phenoxy and R5 and R7 are H are plant fungicides. Combinations, compositions, and fungicidal methods employing the compounds of formula (I) are also provided.

Inactivation of Leukocyte Elastase by Aryl Azolides and Sulfonate Salts. Structure-Activity Relationship Studies

The inhibitory activity of a series of aryl azolides and sulfonate salts toward human leukocyte elastase is reported.Several of the compounds were found to be potent inhibitors of the enzyme.Active compounds were obtained only when the specificity group and the reactive moiety were separated by a two-carbon chain.The introduction of hydrophobic groups enhanced the inhibitory activity of these compounds, with the exception of the sulfonate salts.The nature of the leaving group had had a profound effect on inhibitory activity, with compounds 23 and 26 being the most active (kobsd/ = 11722 and 13500 M-1 s-1, respectively).