Butaclamol

Buprenorphine 2, 321 Bupropion l 4 Buquinolate U 346 Burimamide 251 Buspirone 300 Butabarbital 1, 268 Butacaine J, T2 Butacetin 2 95 Butaclamol 2, 226 Butalbital 1, 268 Butami rate 7, 76 Butamisole 226 Butaperazine 381... 

Aboul-Enein, H.Y. and Hefnawy, M.M., Chiral analysis of butaclamol enantiomers in human plasma by HPLC using a macrocychc antibiotic (vancomycin) chiral stationary phase and sohd phase extraction. Chirality, 16, 147, 2004. 

Fig. 7.6 Nonbound SCH 23390 in a competitive MS binding assay for dopamine Di receptors monitored at a transition from 288.1 91.2 m/z from binding samples without or with (+)-butaclamol. Intensity (/) is shown (a) without (+)-butaclamol, (b) with 30 nM (+)-butaclamol, (c) with 10 pM (+)-butaclamol. (a-c) Representative chromatograms after HPLC separation (RP8 column solvent CH3CN/0.1% HCOOH in H2O 1 1 300 pL min ).

Figure 7.6 exemplifies the results for the dopamine antagonist (+)-butaclamol (Fig. 7.4). 

Fig. 7.7 Representative binding curve obtained by nonlinear regression from a competitive MS binding assay for dopamine Di receptors, in which (+)-butaclamol competes with SCH 23390 as marker. The points describe nonbound SCH 23390 quantified by LC-ESI-MS/MS. Data reflect means (+s) from binding samples, each performed in quadruplicate.

In this way, the affinities of (+)-butaclamol, chlorpromazine and (S)-sulpiride (Fig. 7.4) for the D2 receptor were characterized. The competition curves obtained [e.g. for (+)-butaclamol. Fig. 7.10] were as expected, but showed an unusually... 

Bucainide, 125 Bucloxic acid, 126 Buformin, 21 Bufuralol, 110 Burnetanide, 87 Bunaftine, 211 Bunamidine, 212 Bunitridine, 215 Bunitrolol, 106, 110 Bunolol, 110, 215 Bupicomide, 280 Buprenorphine, 321 Bupropion, 124 Burimamide, 251 Buspirone, 300 Butacetin, 95 Butamirate, 76 Butaclamol, 226 Butorphanol, 325 Butropium bromide, 308... 

The stereospecific dopaminergic antagonists (-) and (+) butaclamol and cis- and trans-flupenthixol were of equal potency in their effects on calmodulin-dependent phosphodiesterase activity. This contrasts with the marked difference in the potency of each pair of stereoisomers as dopamine antagonists. It appears unlikely that the calmodulin-dependent phosphodiesterase activity (and by inference calmodulin) plays any role in the actions of dopaminergic antagonists upon the bovine parathyroid gland. 

Die specificity of the dopamine receptor was further studied with a series of dopaminergic antagonists of well known pharmacological activity. The 30-40% inhibitory effect of 10 nM dopamine was completely reversed by the addition of increasing concentrations of the potent neuroleptics (+)butaclamol (Kp = 1.5 nM) and (-)sulpiride (Kp = 0.5 nM) while their pharmacologically weak enantiomers (-)butaclamol and (+)sulpiride were 86 and 167 times less potent, respectively. The neuroleptics spiroperidol, thioproperazine, domperidone, haloperidol, fluphenazine and pimozide completely reversed the inhibitory effect of dopamine at low Kp values ranging from 0.02 to 0.8 nM (41). 

Porcine anterior pituitary membranes were incubated with increasing concentrations (10 pM-900 pM) of [sHjn-propylapomorphine in the presence of 10 / M and 1 mM GTP and in the absence of GTP as the control. Nonspecific binding was determined in the presence of 1 mM (+)butaclamol and was the same with or without the addition of GTP. Data were analyzed as described in Figure 1. The number of sites labelled by [3H]n-propylapomorphine was 26.7 pM (absence), 19.6 pM in the presence of 10 / M GTP and 6.0 pM in the presence of 1 mM GTP and dissociation constants for the ligand were 280 and 210 pM. The experiment was performed in duplicate and is representative of three such experiments. 

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