Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Thioridazine metabolism

Thioridazine [NE] Decreased thioridazine metabolism additive prolongation of QTC interval. [Pg.1399]

Fluvoxamine, propranolol, and pindolol also inhibit thioridazine metabolism and can raise thioridazine to dangerous levels... [Pg.449]

If patient is taking drugs that inhibit thioridazine metabolism, including CYP450 inhibitors... [Pg.449]

Beta-blocking agents may inhibit thioridazine metabolism, increasing plasma levels and toxicity. [Pg.687]

Use of a hERG blocker in a patient also taking CYP3A4 inhibitors (e.g. antibacterial macrolides, azole antifungals, HIV protease inhibitors) or CYP2D6 inhibitors (quinidine, halofantrine, fluoxetine, paroxetine, thioridazine, terbinafine) the hERG blocker, if mostly metabolized by these CYP isoforms, may accumulate because... [Pg.62]

Phenothiazines The phenothiazines (PTZs) undergo extensive metabolism. Metabolic routes include S-oxidation, aromatic hydroxylation, N-dealkylation, N-oxidation, and a combination of these processes. Chlorpromazine, for example, possesses 168 possible metabolites, a large proportion of which are pharmacologically active compounds. The development of an HPLC assay capable of resolving a large number of these metabolites is virtually impossible and assays that permit the simultaneous determination of the parent compound and a selected number of active metabolites must suffice. The PTZ group of compounds includes chlorpromazine, thioridazine, fluphenazine, and perphenazine. [Pg.34]

Drugs that may be affected by duloxetine include drugs extensively metabolized by CYP2D6 (eg, flecainide, phenothiazines, propafenone, tricyclic antidepressants, thioridazine), alcohol, CNS-acting drugs, MAOIs, and drugs highly bound to plasma proteins (eg, warfarin). [Pg.1073]

Maynard, G.L. and Soni, P. (1996) Thioridazine interferences with imipramine metabolism and measurement. Ther Drug Monit 18 729-731. [Pg.66]

There are several antipsychotics that are substrates to CYP2D6 (von Bahr et ah, 1991 Jerling et ah, 1996 Ring et ah, 1996 (Fang and Gorrod, 1999 Flockhart and Oesterheld, 2000) (Table 26.3). Moreover, several antipsychotics may act as inhibitors of CYP2D6-mediated biotransformation. These include thioridazine, chlorpromazine, haloperidol, fluphenazine, and pimozide (Desta et ah, 1998 Shin et ah, 1999). Of particular salience is the fact that the serotonin selective reuptake inhibitors (SSRIs) fluoxetine and paroxetine are metabolized to a significant extent by this isoenzyme. [Pg.333]

Cardiovascular side effects. Ziprasidone produced a mean QTc prolongation of 21 ms at maximal blood levels achieved with typical therapeutic doses. However, in all clinical trials, the rate of QTc intervals greater than 500 ms (considered a threshold for arrhythmia risk) did not differ from the rate associated with placebo (<0.1%). The QTc effect of ziprasidone is larger than that of other atypical antipsychotics but smaller than that of thioridazine. Blood levels of ziprasidone increased about 40% when ketoconazole (a metabolic inhibitor) was coadministered, and no change in QTc duration was detected. [Pg.122]

Most antipsychotic drugs are readily but incompletely absorbed. Furthermore, many undergo significant first-pass metabolism. Thus, oral doses of chlorpromazine and thioridazine have systemic availability of 25-35%, whereas haloperidol, which has less first-pass metabolism, has an average systemic availability of about 65%. [Pg.629]

Chlorpromazine Blockade of D2 receptors >> 5 2 receptors .-Receptor blockade (fluphenazine least) muscarinic (M)-receptor blockade (especially chlorpromazine and thioridazine) Hx-receptor blockade (chlorpromazine, thiothixene) t central nervous system (CNS) depression (sedation) t decreased seizure threshold t QT prolongation (thioridazine) Psychiatric schizophrenia (alleviate positive symptoms), bipolar disorder (manic phase) nonpsychiatric antiemesis, preoperative sedation (promethazine) pruritus Oral and parenteral forms, long half-lives with metabolism-dependent elimination Toxicity Extensions of effects on a - and M- receptors blockade of dopamine receptors may result in akathisia, dystonia, parkinsonian symptoms, tardivedyskinesia, and hyperprolactinemia... [Pg.642]

Secondary> hyperparathyroidism 30 mg PO daily Parathyroid carcinoma 30 mg PO bid titrate q2—4wk based on Ca PTH levels swallow whole take w/ food Caution [C, /—] w/ Szs Disp Tabs SE N/V/D, myalgia, dizziness, 4- Ca2+ Interactions T Effects W/ CYP3A4 inhibitors such as ketoconazole, itraconazole, erythromycin T effects OF drugs metabolized at CYP2D6 such as TCA, thioridazine, flecainide, vinblastine EMS Monitor ECG for signs of hypocalcemia (T QT interval) OD May cause severe hypocalcemia calcium salts can be given... [Pg.112]

Various factors may account for the variability in response to neuroleptics. These include differences in the diagnostic criteria, concurrent administration of drugs which may affect the absorption and metabolism of the neuroleptics (e.g. tricyclic antidepressants), different times of blood sampling, and variations due to the different type of assay method used. In some cases, the failure to obtain consistent relationships between the plasma neuroleptic concentration and the clinical response may be explained by the contribution of active metabolites to the therapeutic effects. Thus chlorpromazine, thioridazine, levomepromazine (methotrime-prazine) and loxapine have active metabolites which reach peak plasma concentrations within the same range as those of the parent compounds. As these metabolites often have pharmacodynamic and pharmacokinetic activities which differ from those of the parent compound, it is essential to determine the plasma concentrations of both the parent compound and its metabolites in order to establish whether or not a relationship exists between the plasma concentration and the therapeutic outcome. [Pg.284]

Cyt 2D6 metabolizes haloperidol, risperidone, thioridazine, sertindole, olanzapine and clozapine common substrates - fluoxetine, paroxetine, sertraline, venlafaxine, amitriptyline, clomipramine, desipramine, imipramine, nortriptyline, propranolol, metoprolol, timolol, codeine, encainide, flecanide. Common inhibitors - paroxetine, sertraline, fluoxetine. [Pg.462]

H2-labelled thioridazine 56 (the phenothiazine-type antipsychotic agent) has been obtained recently39 for metabolic and pharmacokinetic studies by a new route (equation 16) from 2-(2-hydroxyethyl)piperidine 57. The key steps in this sequence of reactions involve ruthenium tetroxide oxidation of the 7V,0-diacetylated starting material 58 and subsequent lithium aluminium deuteride reduction of the 2-(2-acetoxyethyl)-6-piper-idinone (59, R = Ac). Treatment of 60 with thionyl chloride produced 2-(2-chloroethyl)-l-methyl[6,6-2H2]piperidine which, on N(10)-alkylation of 2-methylthio-10i/-phenothia-zine, yielded 56. For each of the seven steps in the conversion of 57 to 56 the yield has been at least 76%40. [Pg.1128]

Fluvoxamine increased thioridazine concentrations three-fold (45) in 10 patients with schizophrenia taking steady-state thioridazine who were given fluvoxamine (25 mg bd) for 1 week. Fluvoxamine interferes with the metabolism of thioridazine, probably via CYP2C19 and/ or CYP1A2. [Pg.66]

The effects of neuroleptic drugs on serum lipids in adults have been reviewed (439). Haloperidol and the atypical neuroleptic drugs ziprasidone, risperidone, and aripipra-zole, are associated with lower risks of hyperlipidemia, whereas chlorpromazine, thioridazine, and the atypical drugs quetiapine, olanzapine, and clozapine are associated with higher risks. Treatment of the metabolic disturbances caused by neuroleptic drugs has also been reviewed (440). [Pg.219]

Phenytoin induces hepatic microsomal drug-metabolizing enzymes and thus reduces concentrations of haloperidol (663,664), thioridazine (664), and tiotixene (665). In two patients phenytoin reduced plasma clozapine concentrations and worsened psychosis (666). [Pg.235]

Based on published data in humans, concomitant medications were classified as potential inhibitors (cimetidine, fluoxetine, levopromazine, paroxetine, and thioridazine) or inducers of haloperidol metabolism (carbamazepine, phenobarbital, and phenytoin). [Pg.297]

Nakagami T, Yasui-Furukori N, Saito M, Mihara K, De Vries R, Kondo T, Kaneko S. Thioridazine inhibits risperidone metabolism a clinically relevant drug interaction. J Clin Psychopharmacol 2005 25 89-91. [Pg.362]

Thioridazine 25 mg bd significantly increased the steady-state plasma concentration of risperidone (3 mg bd) and reduced 9-hydroxyrisperidone in 12 patients with schizophrenia (38). Since risperidone mainly undergoes 9-hydroxylation yielding an active metabolite, 9-hydroxyrisperidone, metabolic inhibition could account for this increase. Moreover, there was a greater rise in risperidone concentrations in subjects with more capacity for CYP2D6-dependent 9-hydroxylation of risperidone. [Pg.366]


See other pages where Thioridazine metabolism is mentioned: [Pg.564]    [Pg.97]    [Pg.112]    [Pg.126]    [Pg.185]    [Pg.218]    [Pg.399]    [Pg.54]    [Pg.60]    [Pg.335]    [Pg.243]    [Pg.126]    [Pg.187]    [Pg.97]    [Pg.60]    [Pg.259]    [Pg.608]    [Pg.317]    [Pg.210]    [Pg.200]    [Pg.363]    [Pg.365]    [Pg.366]   
See also in sourсe #XX -- [ Pg.563 ]

See also in sourсe #XX -- [ Pg.59 ]




SEARCH



Thioridazin

Thioridazine

© 2024 chempedia.info