Disease relevance of Reduced haloperidol

• In agreement with our previous reports, adenosine antagonists reduced haloperidol-induced c-fos and neurotensin gene expression as well as catalepsy [1].
• The sigma receptor ligand, reduced haloperidol, induces apoptosis and increases intracellular-free calcium levels [Ca2+]i in colon and mammary adenocarcinoma cells [2].
• The subjects were 101 Japanese schizophrenic inpatients receiving oral haloperidol 12 mg/d. The Css of haloperidol and reduced haloperidol were measured in duplicate by high performance liquid chromatographic method, and were corrected to the mean body weight [3].
• These results clearly demonstrate that amantadine greatly reduced haloperidol-induced striatal dopamine receptor hypersensitivity and support the hypothesis that amantadine given concurrently with neuroleptic agents might serve to prevent the development of human tardive dyskinesia [4].

Psychiatry related information on Reduced haloperidol

• Plasma concentrations of haloperidol and reduced haloperidol were measured by high-performance liquid chromatography together with clinical assessment by the Brief Psychiatric Rating Scale (BPRS) and the Udvalg for Kliniske Undersogelser side effect rating scale just before and during itraconazole treatment and 1 week after its discontinuation [5].
• Haloperidol and reduced haloperidol serum levels: correlation with psychopathology in acute schizophrenia [6].
• A chemometric procedure is described to optimize the separation of some drugs used in the treatment of psychotic disorders: haloperidol, levomepromazine, risperidone, venlafaxine, carbamazepine and their main metabolites: reduced haloperidol, 9-hydroxy risperidone, desmethyl levomepromazine, desmethyl venlafaxine [7].

High impact information on Reduced haloperidol

• Plasma concentrations of haloperidol and reduced haloperidol were measured by HPLC [8].
• The effects of acute administration of reduced haloperidol (RHAL) on homovanillic acid (HVA) in the caudate and prefrontal cortex were examined in rats [9].
• Reduced haloperidol is also a substrate of CYP3A4 and inhibitor of CYP2D6 [10].
• In-vitro studies were performed using human liver microsomes and c-DNA-expressed human P450 isoforms to identify the cytochrome P450 isoenzyme(s) involved in the back oxidation and N-dealkylation of reduced haloperidol [11].
• In-vitro characterization of the cytochrome P450 isoenzymes involved in the back oxidation and N-dealkylation of reduced haloperidol [11].

Biological context of Reduced haloperidol

• Effects of the CYP2D6 genotype on the steady-state plasma concentrations of haloperidol and reduced haloperidol in Japanese schizophrenic patients [12].
• Pharmacokinetics of haloperidol and reduced haloperidol in Chinese schizophrenic patients after intravenous and oral administration of haloperidol [13].
• Back conversion from the reduced metabolite to the parent drug through oxidation contributes even less to the total biotransformation of reduced haloperidol [14].
• Since both anticholinergic agents reduced haloperidol-induced defecation it is suggested that their effectiveness is mediated through peripheral mechanisms [15].
• Of all the ligands tested, rimcazole and reduced haloperidol were the most potent inhibitors of cell proliferation [16].

Anatomical context of Reduced haloperidol

• There was a trend in this cohort for negative symptom improvement to be associated with the ratio of haloperidol to reduced haloperidol in red blood cells [17].
• The data suggest that the metabolite, reduced haloperidol, is not an effective neuroleptic drug in the central nervous system [18].
• Guinea pig microsomes efficiently reduced haloperidol molecules in a fashion not dependent on nicotinamide cofactors and not inhibited by carbon monoxide [19].
• Reduced haloperidol (100 microM) increased the intracellular free calcium levels [Ca2+]i in both cell lines, which was independent of extracellular calcium, suggesting that the rise in [Ca2+]i was from intracellular stores and that an increase in [Ca2+]i may act as a "trigger" for apoptosis in these cell lines [2].

Associations of Reduced haloperidol with other chemical compounds

• Red blood cell (RBC) and plasma concentrations of haloperidol (H) and reduced haloperidol (RH) were determined in nine patients (five men, four women) who had been receiving monthly injections of haloperidol decanoate (HD) for at least 3 months [20].
• In 39 patients who received haloperidol regularly we measured plasma concentrations of haloperidol glucuronide (HAL-GL), reduced haloperidol glucuronide (RHAL-GL), haloperidol (HAL), reduced haloperidol (RHAL), and HAL reductase activity in red blood cells [21].
• 5. The present results provide in vitro functional evidence for a sigma receptor type preferentially sensitive to BD-737, reduced haloperidol, BD-1008 and also to NE-100, that differs from the already identified sigma(1), sigma(2) and sigma(3) sites [22].
• The steady-state plasma concentrations of risperidone, 9-hydroxyrisperidone, haloperidol, and reduced haloperidol were measured after the subjects had been on the treatment for at least 2 weeks, and CYP2D6 genotypes were identified in all subjects [23].
• Quinidine, the most specific inhibitor for this cytochrome P450 potently inhibited the oxidative conversion of reduced haloperidol to haloperidol [24].

Gene context of Reduced haloperidol

• These results strongly suggest that back oxidation and N-dealkylation of reduced haloperidol in human liver microsomal preparations are mediated by CYP3A4 [11].
• Carteolol 8-hydroxylase activity, which is a selective reaction probe for CYP2D6 activity, was inhibited by reduced haloperidol with a k(i) value of 4.3 micromol x l(-1) [25].
• The effect of a genetic polymorphism of inducibility of cytochrome P450 (CYP) 1A2 on the steady state plasma concentrations (Css) of haloperidol and reduced haloperidol was studied to clarify if these Css are dependent on the CYP1A2 activity [3].
• Effect of a genetic polymorphism of CYP1A2 inducibility on the steady state plasma concentrations of haloperidol and reduced haloperidol in Japanese patients with schizophrenia [3].
• In this study, the hypothesis was partially investigated by determining the potencies of haloperidol and reduced haloperidol and the corresponding pyridinium and tetrahydropyridine metabolites, compared with MPP+ and MPTP, as inhibitors of the noradrenaline transporter (NAT), dopamine transporter (DAT) and 5-HT transporter (SERT) [26].

Analytical, diagnostic and therapeutic context of Reduced haloperidol

• Serum concentrations of haloperidol and is metabolite, reduced haloperidol, were measured by high performance liquid chromatography [27].
• Plasma concentrations of haloperidol (HAL) and reduced haloperidol (RHAL) were measured in 8 schizophrenic patients, neuroleptic-free for at least 4 weeks, after repeated oral administrations of 10 mg HAL and RHAL [28].
• It is concluded that serum concentrations of reduced haloperidol are of minor value for the interpretation of data of therapeutic drug monitoring of haloperidol in patients with acute schizophrenia [29].
• 3. Haloperidol and reduced haloperidol plasma levels were assayed by radioimmunoassay and liquid chromatography [30].

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