Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Benzomorphans”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1993

[Benzomorphan analogs with doxpicomine partial structure: synthesis andpsychopharmacologic investigations of 5-aminomethyl- and 5-(alpha-aminobenzyl)- substituted 2,6-epoxy-3-benzoxocines].

Addition of the beta-alanine derivative 6 to the homophthalaldehyde monoacetal 5 and subsequent LiAlH4-reduction led to the dihydroxy acetal 8, which was cyclized with acid to give the 5-aminomethyl-2,6-epoxy-3-benzoxocines 2a and 2b. The reaction of 5 with the anion of the beta-lactam 9 yielded two separable diastereomers: 10a with u,l-configuration and 10b with 1,1-configuration. Via the 2-benzopyran 11a (11b), the aminoalcohol 12a (12b), and the secondary amine 13a (13b), the beta-lactam adduct 10a (10b) was transformed to give the 5-(alpha-dimethylaminobenzyl)-2,6-epoxy-3-benzoxocine 3d (3b). The relative configurations of all these "beta-lactam route" products (10-13, 3d, and 3b) were established by their 1H-NMR-spectra. Attempts failed to get the missing diastereomers 3a and 3c by epimerization of the beta-lactams 11a and 11b or by reductive amination of the benzoyl derivatives 17a and 17b. Finally, 3a and 3c were obtained by phenylmagnesium bromide addition to the nitriles 21a and 21b, followed by LiAlH4-reduction, formaldehyde/NaBH3CN methylation and chromatographic separation. In the Irwin-screen (mouse) only 2a.HCl, 3b, and 3d (100 mg/kg body weight) caused weak central effects.

Animals↗
PubMed1988

Assessment of the kappa-opioid activity of a series of 6,7-benzomorphans in the rabbit vas deferens.

The purpose of this study was to re-assess the classification in vivo of a series of (-)-normetazocine derivatives as kappa-opioid agonists. From their ability to inhibit contractions of the electrically stimulated rabbit vas deferens, the (2"S)-N-(2"-methoxypropyl) and N-(2"-methoxyisobutyl) derivatives were identified as full agonists. Several partial agonists were discerned, including the (2"S)-N-tetrahydrofurfuryl derivative, Mr2034. (+)-tifluadom, (+/-)-bremazocine, (-)-ketazocine and (+/-)-U-50,488 were used as reference compounds. Structure-activity relationships are discussed.

Animals↗
PubMed1989

Opioid-like discriminative stimulus properties of benzomorphans in the pigeon: stereospecificity and differential substitution patterns.

Pigeons were trained to discriminate the kappa-opioid agonist bremazocine (BREM) or the mu-opioid agonist fentanyl (FENT) from water. During tests of stimulus substitution, FENT and BREM failed to substitute for each other. The (-)-isomers of cyclazocine, pentazocine and ketocyclazocine substituted for the FENT but not the BREM stimulus. The (+)-isomers of these compounds, as well as the isomers of nallylnormetazocine, failed to substitute for either the FENT or BREM stimulus. In FENT- and BREM-trained pigeons, the (-)-isomers of cyclazocine, pentazocine, nallylnormetazocine and ketocyclazocine were more potent than their respective(+)-isomers in decreasing rates of responding. These results indicate that in the pigeon there is an isomeric separation of the discriminative stimulus properties of cyclazocine, pentazocine and ketocyclazocine and that the FENT-like stimulus effects of these drugs reside in their (-)-isomers. In addition, the present findings establish further that the classification of the discriminative stimulus effects of mu and kappa opioid compounds in the pigeon differ from those in rat and monkey.

Analgesics↗
PubMed1999

Binding of [3H]desglycinyl remacemide to rat brain membranes: association with the benzomorphan attachment site of the N-methyl-D-aspartic acid receptor channel.

Desglycinyl remacemide (DGR), a biologically active metabolite of remacemide, was radiolabeled in an attempt to develop a ligand binding assay to identify its site of action. Incubation of the radioligand with membranes obtained from P2 fractions of whole rat brain revealed a single population of specific [3H]-DGR binding sites having a Kd of 290 nM and a Bmax of 1.3 pmole/mg protein. The specific binding of [3H]-DGR is most enriched in the P2 subcellular fraction and is heterogeneously distributed throughout the brain. The binding of [3H]-DGR to rat brain membranes was inhibited most potently by MK-801 and SKF-10,047. In contrast, haloperidol, and other sigma receptor-active agents, were relatively inactive at this site. These data suggest that DGR interacts with a channel blocking site on the NMDA receptor.

Animals↗