"Desmethylcitalopram"

Serum N-Desmethylcitalopram Concentrations are Associated with the Clinical Response to Citalopram of Patients with Major Depression Citalopram (CITA) is a widely used and well-tolerated selective serotonin reuptake inhibitor. The aim of the study was to evaluate the possible influences of serum concentrations of CITA and its major metabolite n-desmethylcitalopram (NDCITA) on the efficacy

A population pharmacokinetic model for R- and S-citalopram and desmethylcitalopram in Alzheimer’s disease patients with agitation The citalopram for Alzheimer's disease trial evaluated citalopram for the management for agitation in Alzheimer's disease patients. Sparse data was available from this elderly patient population. A nonlinear mixed effects population pharmacokinetic modeling approach was used to describe the pharmacokinetics of R- and S-citalopram and their primary metabolite (desmethylcitalopram). A structural model with 4 compartments (one compartment/compound) with linear oral absorption and elimination described the data adequately. Overall, the model showed that clearance of the R-enantiomer was slower than the clearance of the S-enantiomer. Without accounting for any patient

contained 123 mcg/L and 131 mcg/L, respectively. The samples also contained 25 mcg/L and 31 mcg/L of desmethylcitalopram in foremilk and hindmilk, respectively.[10]Two women treated with citalopram 5 or 10 mg daily during the third trimester of pregnancy and during breastfeeding provided trough milk samples during the first week postpartum. The citalopram milk levels were 62.6 mcg/L with the 5 mg dose

to be about 13% that of citalopram.[3]Maternal Levels. Eight women taking escitalopram in an average dosage of 199 mcg/kg daily (10 to 20 mg daily) had 6 to 8 milk steady-state milk samples analyzed over the 24-hour interval after their single daily dose. The average dosage that an exclusively breastfed infant would receive was calculated to be 7.6 mcg/kg of escitalopram and 3 mcg/kg of desmethylcitalopram . The samples also contained 21 mcg/L and 24 mcg/L of S -desmethylcitalopram in foremilk and hindmilk, respectively.[7]Eighteen lactating women taking escitalopram in a mean daily dosage of 10 mg (range 2.5 to 30 mg [mean 0.2 mg/kg daily]) donated 3 to 5 random milk samples over a 24-hour period (n = 104 samples). The mean peak milk levels were 84.3 and 84.7 mcg/L for the 10 and 20 mg daily doses

, and the expressions of proteins in serum were verified using western boltting analysis. Moreover, effects of KXS on serum lipid and lipid metabolism-related hormone levels in CUMS rats were detected by enzyme-linked immunosorbent assay and enzymatic method. We validated that the levels of six serum lipid metabolites (N-Desmethylcitalopram (HMDB14021), PC(14:1(9Z)/24:0) (HMDB07926), PC(P-18:1(11Z)/20:0) (HMDB11281

± SD age: 14.8 ± 1.7 years) or placebo (n = 25, mean ± SD age: 14.9 ± 1.6 years) for 8 weeks. Outcomes were the change in scores on the Pediatric Anxiety Rating Scale (PARS) and Clinical Global Impressions (CGI) scales as well as vital signs and adverse events. Plasma escitalopram and desmethylcitalopram area under the curve during 24 hours (AUC0-24) and maximum concentration (Cmax) were determined

a washout period raltegravir 400 mg twice daily for 5 days. Intensive steady-state pharmacokinetic blood sampling was performed. Geometric mean ratios (GMRs) of the combination versus the reference treatment and 90% CIs were calculated for the area under the plasma concentration-time curve (AUC). CYP2C19 genotyping was performed because it influences N-demethylation of citalopram to desmethylcitalopram . A total of 22 healthy volunteers completed the trial. GMRs (90% CI) were 1.00 (0.98, 1.03) for citalopram AUC0-24 h, 0.99 (0.88, 1.12) for desmethylcitalopram AUC0-24 h and 0.77 (0.50, 1.19) for raltegravir AUC0-12 h. Raltegravir plasma concentration 12 h after intake (C12 h) did not change with concomitant use of citalopram. Within each CYP2C19 phenotype subgroup the citalopram metabolite-to-parent

by the parent compounds for inhibition of wild-type mSERT over M172 mSERT, whereas desvenlafaxine and desmethylcitalopram retained selectivity. Furthermore, we show that the metabolite desmethylcitalopram accumulates in the brain and that the metabolites desmethylcitalopram, norfluoxetine, and desvenlafaxine inhibit serotonin uptake in wild-type mSERT at potencies similar to those of their parent compounds

maternal administration on gestational days (GD)14 and GD18, as well as the fetal brain drug disposition. The results show that pregnancy affects the pharmacokinetics of CIT and that maternal drug clearance increases as gestation progresses. The data further show that CIT and its primary metabolite desmethylcitalopram (DCIT) readily cross the placenta into the fetal compartment, and fetal exposure to CIT

1. Sexual Dysfunction in 10-15% of cases 2. Similar to Luvox and Effexor in terms of this effect 3. See Antidepressant Induced Sexual Dysfunction VIII. Adverse Effects: Overdose 1. See SSRI Overdose 2. P450 Metabolism to di-desmethylcitalopram 1. Di-desmethylcitalopram is cardiotoxic (inhibits cardiac Potassium and Calcium channels) 3. Overdose presentation (esp

1. Sexual Dysfunction in 10-15% of cases 2. Similar to Luvox and Effexor in terms of this effect 3. See Antidepressant Induced Sexual Dysfunction VIII. Adverse Effects: Overdose 1. See SSRI Overdose 2. P450 Metabolism to di-desmethylcitalopram 1. Di-desmethylcitalopram is cardiotoxic (inhibits cardiac Potassium and Calcium channels) 3. Overdose presentation (esp

plasma concentrations (L/D ratios) of S- and R-citalopram and S-sertraline, and the corresponding primary chiral metabolites S- and R-desmethylcitalopram and N-desmethylsertra-line were assessed. The samples were analyzed for concentrations of stereospecific parent drug and metabolites. The study was conducted from 2003 to 2006. Three women received citalopram, 2 women were treated with escitalopram

and desmethylcitalopram, and the inhibitory effect of serum on serotonin uptake by fresh platelets, were assessed once weekly during the trial. The serum concentrations of citalopram were highly correlated with inhibition of serotonin uptake. Less of the metabolite was found, it being detected only in the higher dose groups. Steady state levels of citalopram, attained after 1 week, were linearly related to dose

(metabolic ratio dextromethorphan/dextrorphan greater than 0.3 = PM (poor metabolizer); mephenytoin/4-OH-mephenytoin greater than 5.6, or mephenytoin S/R greater than 0.8 = PM). Citalopram plasma levels: Plasma levels of citalopram, desmethylcitalopram and didesmethylcitalopram are determined by gas chromatography--mass spectrometry. RESULTS OF THE PILOT STUDY. The investigation has been preceded

[Citalopram and desmethylcitalopram for psychiatric patients]. Serum samples were selected randomly from blood samples drawn in the morning for other reasons in patients treated with citalopram, and the serum concentrations of citalopram (S-citalopram) and its major metabolite desmethylcitalopram were determined. A total of 44 patients, 13 males and 31 females, with a median age of 38.5 years may at least partly be due to treatment with 600 mg/day of carbamazepine, which is known to accelerate the metabolism of other drugs. The serum concentration of the major metabolite desmethylcitalopram averaged 28% of S-citalopram and is most likely without clinical importance. It is concluded that determination of S-citalopram may be considered if there is doubt about the compliance of the patient

Citalopram causes no significant alterations in plasma neuroleptic levels in schizophrenic patients. Steady-state plasma concentrations of commonly used neuroleptic drugs were measured in 90 schizophrenic patients before and after adding placebo or citalopram (40 mg/day) to their treatment regimen. Plasma concentrations of citalopram and its main metabolite, desmethylcitalopram, were also of haloperidol, chlorpromazine, zuclopenthixol, levomepromazine, thioridazine or perphenazine during the study. Plasma concentrations of citalopram and desmethylcitalopram were well within the levels reported previously with monotherapy, and remained stable throughout the study. None of the 15 patients analysed for the CYP2D6 genotype was a poor metabolizer. It is concluded that clinically important

. Similarly, the pharmacokinetics of the metabolite desmethylcitalopram were unaltered by ketoconazole. No changes in pharmacokinetics of citalopram were observed after coadministration of ketoconazole, suggesting that ketoconazole and other CYP3A4 inhibitors may be administered safely with citalopram. Furthermore, no adjustment of citalopram dosage should be necessary in most patients who receive the drug

and for the metabolites desmethylcitalopram and didesmethylcitalopram. A significant correlation was found between the estimation of creatinine clearance and concentration-dose ratio of citalopram. Poor metabolizers, who had been prescribed an antidepressant drug that are substrate for the cytochrome P450 isoenzyme examined, have higher concentrations of prescribed antidepressant drug than do non-poor metabolizers