Target Validation Information | |||||
---|---|---|---|---|---|
Target ID | T29500 | ||||
Target Name | Alpha-1B adrenergic receptor | ||||
Target Type | Successful |
||||
Drug Potency against Target | Imidazolidin-2-ylidene-quinoxalin-6-yl-amine | Drug Info | Ki = 11000 nM | ||
Imidazolidin-2-ylidene-o-tolyl-amine | Drug Info | Ki = 2500 nM | |||
4-(3-Hydroxy-piperidin-3-yl)-benzene-1,2-diol | Drug Info | Ki = 15000 nM | [526729] | ||
BMY-7378 | Drug Info | Ki = 191 nM | [527512] | ||
MAZAPERTINE | Drug Info | Ki = 47 nM | [533800] | ||
AGN-192172 | Drug Info | Ki = 8900 nM | |||
RWJ-68157 | Drug Info | Ki = 3536 nM | [525785] | ||
4-(3,4-Dihydro-1H-isoquinolin-2-yl)-quinoline | Drug Info | Ki = 3200 nM | [526618] | ||
Methamphetamine | Drug Info | EC50 = 12.3 nM | [552643] | ||
ISOCLOZAPINE | Drug Info | IC50 = 64 nM | [534532] | ||
SK&F-86466 | Drug Info | Ki = 485 nM | [533638] | ||
4-((Z)-1-Naphthalen-1-yl-propenyl)-1H-imidazole | Drug Info | Ki = 57 nM | [534160] | ||
4-(4-Isopropyl-morpholin-2-yl)-benzene-1,2-diol | Drug Info | Ki = 6700 nM | [526729] | ||
4-(4-Methyl-indan-1-yl)-1H-imidazole | Drug Info | Ki = 73 nM | [534467] | ||
RX-821002 | Drug Info | Ki = 27 nM | [533375] | ||
UH-301 | Drug Info | Ki = 6080 nM | [534363] | ||
4-(1-Naphthalen-1-yl-vinyl)-1H-imidazole | Drug Info | Ki = 1734 nM | [534160] | ||
NIGULDIPINE | Drug Info | Ki = 85 nM | [533638] | ||
6-fluoronorepinehprine | Drug Info | Ki = 4000 nM | [530478] | ||
(+/-)-nantenine | Drug Info | Ki = 1191 nM | [530558] | ||
WB-4101 | Drug Info | Ki = 9.9 nM | [533682] | ||
MEDETOMIDINE | Drug Info | Ki = 1102 nM | [533805] | ||
FLUANISONE | Drug Info | Ki = 0.87 nM | [533378] | ||
Methoxamine | Drug Info | EC50 = 65000 nM | [553243] | ||
SK&F-105854 | Drug Info | Ki = 783 nM | [533638] | ||
4-Benzo[b]thiophen-4-yl-1H-imidazole | Drug Info | Ki = 343 nM | [525720] | ||
4-Morpholin-2-yl-benzene-1,2-diol | Drug Info | Ki = 7400 nM | [526729] | ||
4-(1-Naphthalen-1-yl-propyl)-1H-imidazole | Drug Info | Ki = 574 nM | [534160] | ||
AGN-193080 | Drug Info | Ki = 470 nM | |||
Phendimetrazine | Drug Info | EC50 = 8300 nM | [552643] | ||
4-((E)-1-Naphthalen-1-yl-propenyl)-1H-imidazole | Drug Info | Ki = 387 nM | [534160] | ||
4-(1-Naphthalen-1-yl-ethyl)-1H-imidazole | Drug Info | Ki = 536 nM | [533805] | ||
SK&F-106686 | Drug Info | Ki = 15 nM | [533638] | ||
(2-Bromo-phenyl)-(1H-imidazol-2-yl)-amine | Drug Info | Ki = 11000 nM | [534315] | ||
TIOSPIRONE | Drug Info | Ki = 1.5 nM | [534093] | ||
2-Pyridin-4-yl-1,2,3,4-tetrahydro-isoquinoline | Drug Info | Ki = 5800 nM | [526618] | ||
A-123189 | Drug Info | Ki = 9.09 nM | [526051] | ||
A-119637 | Drug Info | Ki = 4.66 nM | [526051] | ||
Sunepitron | Drug Info | Ki = 35 nM | [528210] | ||
OCTOCLOTHEPIN | Drug Info | Ki = 0.56 nM | [531171] | ||
SK&F-104856 | Drug Info | Ki = 23 nM | [533638] | ||
SNAP-8719 | Drug Info | Ki = 165 nM | [527512] | ||
SK&F-104078 | Drug Info | Ki = 87 nM | [533638] | ||
RWJ-25730 | Drug Info | Ki = 8.2 nM | [533800] | ||
N-(5-Bromo-quinoxalin-6-yl)-guanidine | Drug Info | Ki = 17000 nM | |||
4-(4-butylpiperidin-1-yl)-1-o-tolylbutan-1-one | Drug Info | Ki = 65 nM | [531079] | ||
RWJ-69736 | Drug Info | Ki = 10000 nM | [525785] | ||
CORYNANTHEINE | Drug Info | Ki = 517 nM | [533638] | ||
SNAP-5089 | Drug Info | Ki = 269 nM | [533638] | ||
LEVONORDEFRIN | Drug Info | Ki = 9221 nM | [534160] | ||
(2,6-Dichloro-phenyl)-(1H-imidazol-2-yl)-amine | Drug Info | Ki = 6000 nM | [534315] | ||
4-(2,3-Dihydro-1H-phenalen-1-yl)-1H-imidazole | Drug Info | Ki = 55 nM | [534160] | ||
Dextroamphetamine | Drug Info | EC50 = 7.07 nM | [552643] | ||
Siramesine | Drug Info | IC50 = 330 nM | [533739] | ||
Action against Disease Model | Methoxamine | alpha-Adrenergic receptor stimulation regulates the activity of a n uMber of different cardiac ion channels, including those underlying one or more distinct Cl- conductances. The whole-cell patch-clamp technique was used in the present study to investigate the effects of alpha-adrenergic stimulation on the beta-adrenergically regulated Cl- current in guinea pig ventricular myocytes. Neither alpha 1-adrenergic receptor stimulation with methoxamine (25 to 500 m uMol/L) nor direct activation of endogenous protein kinase C (PKC) with phorbol 12,13-dibutyrate (PDBu, 100 nmol/L) evoked a Cl- current. On the contrary, the Cl- current activated by 30 nmol/L isoproterenol was inhibited by methoxamine, with an EC50 of 6.7 +/- 2.6 m uMol/L, and this response was blocked by prazosin, an alpha 1-adrenergic receptor antagonist. Prazosin also decreased the EC50 for current activation by norepinephrine from 53 +/- 7.1 to 18 +/- 3.8 nmol/L, demonstrating that the ability of this endogenous neurotransmitter to activate the Cl- current through beta-adrenergic receptor stimulation is limited by its intrinsic ability to also activate alpha-adrenergic receptors. Methoxamine did not inhibit the Cl- current evoked by either direct activation of adenylate cyclase with forskolin or inhibition of phosphodiesterase activity with 3-isobutyl-1-methylxanthine, indicating that alpha-adrenergic stimulation inhibits beta-adrenergic responses at a point upstream of adenylate cyclase activation. Methoxamine also did not inhibit the Cl- current activated by histamine, suggesting that alpha-adrenergic stimulation specifically inhibits beta-adrenergic receptor-mediated responses. The inhibitory effect of methoxamine was not mimicked by PDBu, and it persisted in the presence of bisindolylmaleimide, a selective PKC inhibitor. However, methoxamine inhibition of the isoproterenol-activated Cl- current was sensitive to pertussis toxin. These results suggest that alpha-adrenergic receptor stimulation inhibits the beta-adrenergically activated Cl- current, demonstrating a novel mechanism by which alpha-adrenergic receptors may regulate ion channel activity in the heart. | [553228] | Drug Info | |
Dextroamphetamine | Probing mesocorticolimbic dopamine function in severe depression using dextroamphetamine revealed an altered behavioural response and a disrupted mesocorticolimbic circuitry in behavioural and functional magnetic resonance imaging (fMRI) studies. The purpose of this study was to use a similar approach in alcohol dependence. Behavioural Study: to assess dextroamphetamine subjective effects in alcohol-dependent and depressed alcohol-dependent participants. fMRI Study: to assess how the mesocorticolimbic circuitry would respond to a dextroamphetamine challenge in alcohol-dependent participants exposed to alcohol cues. Methods. In both studies, a single oral 30 mg dose of dextroamphetamine was the pharmacological intervention. Behavioural Study: randomized, double-blind,placebo-controlled, between-subject study. Eighteen alcohol-dependent and 22 depressed alcohol-dependent participants were compared using validated self-report drug effect tools (e.g. Addiction Research Center Inventory). fMRI Study: single-blind, between-subject study. fMRI blood oxygen level-dependent (BOLD) activation was measured in 14 alcohol-dependent and 9 healthy control participants during an alcohol-cue exposure task pre- and post-drug. Results. Behavioural Study: DRUG (F 1,40 =18.6; p <0.001) and GROUP (F 1,40 =16.6; p <0.001) main effects but no GROUP?DRUG interaction effects (F1,40 =0.02; p =0.88) were detected, even when only severely depressed alcohol-dependent individuals were included (F1,30 =0.04; p =0.84). fMRI Study: Alcohol-dependent participants exhibited greater ventral striatal activation compared to controls pre-drug and post-drug effect (F 1,40 =20.1; z =3.8; p <0.001; k >10; (x =10; y =-2; z =-14)). A GROUP?DRUG interaction effect was detected in the medial orbitofrontal cortex (mOFC) (F1,40 =21.5; z =4.0; p <0.001; k >10; (x =-12; y =28; z =-20). The alcohol-dependent group exhibited a negligible mOFC response across both pre- and post-drug scanning sessions. In contrast, controls exhibited attenuation of mOFC response post-drug. Conclusion. The lack of significant GROUP?DRUG interaction effects in the Behavioural Study may suggest different neurobiological mechanisms underlying alcohol dependence and depression mesocorticolimbic dysfunction. Alcohol dependence appeared to mitigate the impact of depression severity on participants' behavioural responses to dextroamphetamine. The fMRI Study data suggest there may be ventral striatal and mOFC disruption in alcohol-dependent participants. We suggest the mOFC may be involved in the reported lossof prefrontal modulation of dopamine cell activity in alcohol dependence. This supports a key role for the mOFC in mesocorticolimbic dysfunction in alcohol dependence. | Drug Info | |||
Lisdexamfetamine | These studies investigated the absorption and metabolic conversion of lisdexamfetamine dimesylate (LDX), a prodrug stimulant that requires conversion to d-amphetamine for activity. Oral absorption of LDX was assessed in rat portal and jugular blood, and perfusion of LDX into isolated intestinal segments of anesthetized rats was used to assess regional absorption. Carrier-mediated transport of LDX was investigated in Caco-2 cells and Chinese hamster ovary (CHO) cells expressing h uMan peptide transporter-1 (PEPT1). LDX metabolism was studied in rat and h uMan tissue homogenates and h uMan blood fractions. LDX was approximately10-fold higher in portal blood versus systemic blood. LDX and d-amphetamine were detected in blood following perfusion of the rat small intestine but not the colon. Transport of LDX in Caco-2 cells had permeability apparently similar to cephalexin and was reduced with concurrent PEPT1 inhibitor. Affinity for PEPT1 was also demonstrated in PEPT1-transfected CHO cells. LDX metabolism occurred primarily in whole blood (rat and h uMan), only with red blood cells. Slow hydrolysis in liver and kidney homogenates was probably due to residual blood. The carrier-mediated absorption of intact LDX, likely by the high-capacity PEPT1 transporter, and subsequent metabolism to d-amphetamine in a high-capacity system in blood (ie, red blood cells) may contribute to the consistent, reproducible pharmacokinetic profile of LDX. | [553060] | Drug Info | ||
Propericiazine | 2-Chloro-11-(2-dimethyl-aminoethoxy) dibenzo [b, f] thiepin (zotepine) is a new neuroleptic drug which is structurally different from known neuroleptics. Zotepine, chlorpromazine, propericiazine, and cyproheptadine inhibited hyperthermia induced by dosing with fenfluramine in rats in a warm environment (26-28 degrees C). Fenfluramine is known to induce hyperthermia by mediation of central serotonin. Zotepine had a 10 times or greater potency than chlorpromazine, propericiazine and cyproheptadine in inhibiting the hyperthermia. Thioridazine did not inhibit the hyperthermia, whereas haloperidol accelerated the hyperthermia. Zotepine was also the most potent inhibitor of 3H-serotonin binding to rat cortical synaptosomes in vitro. However, cyproheptadine had the strongest anti-serotonin activity in rat fundus preparations, while zotepine and other neuroleptics showed the same order of potency. These results showed that zotepine is a unique neuroleptic with potent central anti-serotonin activity. The central anti-serotonin activity of zotepine is discussed in connection with its lesser extrapyramidal side effects in h uMans. | [553159] | Drug Info | ||
References | |||||
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Ref 526051 | Bioorg Med Chem Lett. 2001 May 7;11(9):1119-21.Two novel and potent 3-[(o-methoxyphenyl)piperazinylethyl]-5-phenylthien. | ||||
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Ref 531171 | J Med Chem. 2010 Oct 14;53(19):7021-34.Exploring the neuroleptic substituent in octoclothepin: potential ligands for positron emission tomography with subnanomolar affinity for |A(1)-adrenoceptors. | ||||
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Ref 531079 | J Med Chem. 2010 Sep 9;53(17):6386-97.Discovery of N-{1-[3-(3-oxo-2,3-dihydrobenzo[1,4]oxazin-4-yl)propyl]piperidin-4-yl}-2-phenylacetamide (Lu AE51090): an allosteric muscarinic M1 receptor agonist with unprecedented selectivity and procognitive potential. | ||||
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