117997-80-5

Upstream product

• 35793-73-8 N-(tert-butyloxycarbonyl)-γ-benzyl-D-glutamic acid 
• 142-84-7 di-n-propylamine 
• 100-51-6 benzyl alcohol 
• 2578-33-8 D-glutamic acid-5-benzyl ester 
• 6893-26-1 D-Glutamic acid 

Downstream Products

• 117997-59-8 (R)-5-(dipropylamino)-4-<(1H-indol-2-ylcarbonyl)amino>-5-oxo-1-(phenylmethoxy)pentanoic acid 
• 117997-76-9 ε-benzyl-D-glutamic acid dipropylamide hydrochloride 
• 120452-48-4 (S)-3-{(S)-2-[(S)-2-((R)-4-Amino-4-dipropylcarbamoyl-butyrylamino)-3-(1H-indol-3-yl)-propionylamino]-4-methylsulfanyl-butyrylamino}-N-((S)-1-carbamoyl-2-phenyl-ethyl)-succinamic acid; compound with trifluoro-acetic acid 
• 120452-46-2 (S)-3-[(S)-2-((R)-4-Amino-4-dipropylcarbamoyl-butyrylamino)-4-methylsulfanyl-butyrylamino]-N-((S)-1-carbamoyl-2-phenyl-ethyl)-succinamic acid; compound with trifluoro-acetic acid 
• 109736-35-8 (S)-3-[(S)-2-((R)-4-tert-Butoxycarbonylamino-4-dipropylcarbamoyl-butyrylamino)-4-methylsulfanyl-butyrylamino]-N-((S)-1-carbamoyl-2-phenyl-ethyl)-succinamic acid 

Relevant academic research and scientific papers

Synthesis of a radoilabeled type A cholecystokinin receptor antagonist, (R)-N-pentyl-N-(4,5-di[3H]pentyl)N(α)-(3-quinolinoyl)glutamic acid amide

A method for the preparation of a radiolabeled CCK(A)-specific antagonist, (R)-N-pentyl-N-(4,5-di[3H]pentyl)N(α)-(3-quinolinoyl)glutamic acid amide, [3H]-A-65186, is described. (R)-γ-Benzyl-N-BOC-glutamic acid was coupled with N-(4-pentenyl)-N-pentylamine using BOPCl and TEA in dichloromethane to provide the corresponding amide. Deprotection of the α-amino moiety followed by coupling with 3-quinolinecarboxylic acid in the presence of EDCI, TEA, and HOBt in dichloromethane resulted in (R)-N-(4-pentenyl)-N-pentyl γ-benzyl-N(α)-(3-quinolinoyl)glutamic acid amide. Tritiation with concomitant hydrogenolysis of the benzyl ester proceeds smoothly to provide [3H]-A-65186.

Novel glutamic acid derived cholecystokinin receptor ligands

Novel aryl amide analogues of glutamic acid dialkylamide have been synthesized to test for a possible structural analogy between glutamic acid and benzodiazepine CCK antagonists such as compounds 2 and 24 (lorglumide and MK-329, respectively). In support of the structural model, certain of these hybrid compounds are more potent in pancreas CCK radioligand binding assays than corresponding lorglumide-type reference compounds. Modifications previously found in the benzodiazepine antagonists to result in brain CCK/gastrin receptor selectivity were also incorporated to produce an aryl urea series of glutamic acid analogues. None of these compounds were brain CCK/gastrin selective; however, one was potent and selective in the pancreas binding assay. The model appears to be most useful in the design of selective ligands for the pancreas type CCK receptor.