401-25-2

Upstream product

• 452-71-1 4-fluor-2-methylaniline 
• 98-88-4 benzoyl chloride 
• 446-33-3 5-Fluoro-2-nitrotoluene 
• 13939-06-5 molybdenum hexacarbonyl 
• 98-80-6 phenylboronic acid 

Downstream Products

• 59541-83-2 5-fluoro-2-phenyl-1H-indole 
• 1027369-63-6 4-(5-fluoro-2-phenyl-1H-indol-3-yl)-3,6-dihydro-2H-pyridine-1-carboxylic acid benzyl ester 
• 1026390-87-3 (3S,4S)-4-(5-Fluoro-2-phenyl-1H-indol-3-yl)-3-hydroxy-piperidine-1-carboxylic acid benzyl ester 

Relevant academic research and scientific papers

Iron-catalysed radical cyclization to synthesize germanium-substituted indolo[2,1-a]isoquinolin-6(5H)-ones and indolin-2-ones

A simple and efficient strategy for iron-catalysed cascade radical cyclization was developed, by which an array of germanium-substituted indolo[2,1-a]isoquinolin-6(5H)-ones and indolin-2-ones were obtained in one pot with germanium hydrides as radical precursors. A rapid intramolecular radical trapping mode enabled the selective arylgermylation of alkenes over the prevalent hydrogermylation reaction.

Palladium-Catalyzed Amide Synthesis via Aminocarbonylation of Arylboronic Acids with Nitroarenes

A palladium-catalyzed aminocarbonylation of aryl boronic acids with nitroarenes for the synthesis of amides has been developed. A wide range of substrates were well-tolerated and gave the corresponding amides in moderate to good yields. No external oxidant or reductant was needed in this procedure. This procedure provides a redox-economical process for the synthesis of amides.

Anxiolytic-like effects of N,N-dialkyl-2-phenylindol-3-ylglyoxylamides by modulation of translocator protein promoting neurosteroid biosynthesis

Novel N,N-disubstituted indol-3-ylglyoxylamides (1-56), bearing different combinations of substituents R1-R5, were synthesized and evaluated as ligands of the translocator protein (TSPO), the 18 kDa protein representing the minimal f

AMIDE DERIVATIVES AND DRUGS

The present invention provides an amide derivative represented by the following formula [1]: wherein n represents 0 or 1; X represents CR4 or N; Y represents CR6 or N; Z represents CR7 or N; R1 and R2 may be the same or different and each represents hydrogen, optionally substituted alkyl, acyl, optionally substituted aryl, or an optionally substituted aromatic heterocyclic group; R4, R5, R6 and R7 may be the same or different and each represents hydrogen, halogen, hydroxy, amino, alkyl, haloalkyl, alkoxy, monoalkylamino, dialkylamino, arylalkyl, cyano, or nitro; and R3 represents optionally substituted alkylamino, optionally substituted arylamino, or optionally substituted cyclic amino, or a pharmaceutically acceptable salt thereof, and a pharmaceutical composition comprising them as an active ingredient. The compound of the present invention is useful as a TGF-β inhibitor.

3-(4-Fluoropiperidin-3-yl)-2-phenylindoles as high affinity, selective, and orally bioavailable h5-HT2A receptor antagonists

The development of very high affinity, selective, and bioavailable h5-HT2A receptor antagonists is described. By investigation of the optimal position for the basic nitrogen in a series of 2-phenyl-3-piperidylindoles, it was found that with the basic nitrogen at the 3-position of the piperidine it was not necessary to further substitute the piperidine in order to obtain good binding at h5-HT2A receptors. This meant the compounds no longer had high affinity at the IKr potassium channel, an issue with previous series of 2-aryl-3-(4-piperidyl)indoles. Improvements could be made to oral bioavailability in this series by reduction of the pKa of the basic nitrogen, by adding a fluorine atom to the piperidine ring, leading to 3-(4-fluoropiperidin-3-yl)-2-phenyl-1H-indole (17). Metabolic studies with this compound identified oxidation at the 6-position of the indole as a major route in vitro and in vivo in rats. Blocking this position with a fluorine atom led to 6-fluoro-3-(4-fluoropiperidin-3-yl)-2-phenyl-1H-indole (22), an antagonist with 0.06 nM affinity for h5-HT2A receptors, with bioavailability of 80% and half-life of 12 h in rats.