Probing Adenosine and P2 Receptors: Design of Novel Purines and Nonpurines as Selective Ligands

探索腺苷和P2受体:设计新型嘌呤和非嘌呤类选择性配体

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Abstract

Recent approaches to the design of selective agonists and antagonists at adenosine (AR) and P2 receptors include both modifying known receptor ligands and searching for structurally diverse antagonists. The ribose-like moiety of nucleoside/nucleotide derivatives was rigidified with a methanocarba (mc) modification, to constrain the ring in a conformation that was favored in binding to ARs or P2Y receptors. (N)-mc analogs of various N(6)-substituted adenosine derivatives, including cyclopentyl and 3-iodobenzyl, in which the parent compounds are potent agonists at either A(1) or A(3)ARs, respectively, retained high receptor affinity and selectivity. For nucleotides acting as P2Y(1) receptor antagonists, the (N)-mc analog MRS 2279 ((1R,2S,4S,5S)-1-[(phosphato)methyl]-4-(2-chloro-6-methylaminopurin-9-yl) bicyclo [3.1.0]-hexane-2-phosphate) proved to be a selective antagonist, with an IC(50) of 52 nM. Other ribose substitutions possible in P2Y(1) receptor antagonists were 4- and 6-membered rings and acyclic derivatives. High affinity for the A(2B)AR was achieved through the formation of anilides and benzylamides of XCC (8-[4-[[[carboxy]methyl]oxy]phenyl]-1,3-dipropylxanthine). A p-cyanoaniline derivative (MRS 1754, K(i) value 1.97 nM) was 205-, 255-, and 289-fold selective for the human A(2B)ARs vs. human A(1)/A(2A)/A(3) ARs, respectively. A template approach based on the pyridine family, i.e., 1,4-dihydropyridine nucleus and the corresponding 3,5-diacylpyridines, was used for the design of novel adenosine antagonists. The pyridine derivative MRS 1523 (5-propyl-2-ethyl-4-propyl-3-(ethylsulfanylcarbonyl)-6-phenylpyridine-5-carboxylate) was shown to be a selective antagonist at the rat A(3)AR as well as the human A(3)AR. Chemical libraries were screened computationally and using binding assays to identify novel AR antagonists. Molecular modeling of ARs and P2Y receptors provided hypotheses for ligand docking. Drug Dev. Res. 52:178-186, 2001.

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