Big Chemical Encyclopedia

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

Articles Figures Tables About

Fluoxetine specificity

However, the specific serotonin uptake inhibitor fluoxetine failed to produce an MBDB-like cue and failed to block the stimulus effects of MBDB when it was given prior to a training dose of MBDB. Table 3 summarizes results of fluoxetine testing in MBDB-trained rats. In other exploratory studies, pretreatment of MDMA-trained rats with either methysergide or ketanserin failed to block completely the MDMA-discriminative stimulus. [Pg.12]

Examples of specific methods important to neurochemists include separation and quantification of R- and S-fluoxetine and R- and S-norfluoxetine in brain tissue and body fluids using derivatization with (—)-(S)-N-(trifluoracetyl)prolyl chloride, a chiral derivatizing agent (Torok-Both et al., 1992 Aspeslet et al., 1994). A similar method has been used to separate the enantiomers of 3,4-methylenedioxyamphetamine (MDA) and 3,4-methylenedioxymethamphetamine (MDMA) (Hegadoren et al., 1993). Eluoxetine and norfluoxetine enantiomers have also been separated on a chiral column in series with a nonchiral column with NPD detections (Ulrich, 2003). Reviews of the analysis of enantiomers of several drugs of abuse are available (Jirovsky et al., 1998 Tao and Zeng, 2002 Liu and Liu, 2002). [Pg.6]

A breakthrough in the treatment of major depression was the discovery of fluoxetine, marketed as Prozac. Fluoxetine has a mechanism of action similar to that of imipramine with an important exception. It is a selective serotonin reuptake inhibitor, an SSRI. This strongly suggests that, in some sense, the symptoms of major depression result from a deficit in serotonin specifically. By inhibiting its reuptake from the synapse, the activity of serotonin is enhanced. Two other important drugs for major depression, sertraline (Zoloft) and paroxetine (Paxil), among several others,... [Pg.303]

Specific Serotonin Reuptake inhibitors (SSRis). To date, the only SSRI studied in AN is fluoxetine (Prozac). During the acute refeeding phase of treatment, fluoxetine shows modest improvement in weight gain while a larger controlled study during the maintenance phase of treatment demonstrated effectiveness in the prevention of relapse. From the standpoint of side effects and toxicity, the SSRIs are clearly... [Pg.214]

It should be possible to treat the disease by increasing the concentration of the neurotransmitter in the synaptic cleft. There are, in principle, three ways in which this could be achieved, (i) Neurotransmitter synthesis could be increased, (ii) The rate of exocytosis could be increased, (iii) Removal of neurotransmitter from the synapse could be inhibited. Drugs that affect process (iii) have been developed. The tricyclic antidepressants and the specific serotonin (5-hydroxytryptamine) reuptake inhibitors (abbreviated to SSRIs) inhibit uptake of the neurotransmitter into the presynaptic on postsynaptic neurone. The most prescribed SSRI is fluoxetine (Prozac). [Pg.321]

The radiosynthesis of [ F] fluoxetine, a selective serotonine uptake inhibitor (Scheme 62), is one of the rare examples in which a Br atom has been substituted for an F isotope [248]. It suffers from a low specific radioactivity due to decomposition of starting material. [Pg.247]

Serotonin-specific inhibitors (SSRI) include fluoxetine, paroxetine, sertraline, citalopram and others. They are not more effective than the tricyclic antidepressants but may suit some patients better and are generally safer in overdose (see Geddes et al., 1999). While the SSRIs are devoid of the cardiac effects (membrane stabilisation, inhibition of conduction) of the tricyclics in overdose, they increase the risk of hemorrhage into the gut or brain. [Pg.680]

In general, the SSRIs have a more tolerable side effect profile than the tricyclic antidepressants with their anticholinergic effects. Review of the rate that subjects in the controlled studies discontinued a SSRI because of adverse effects provides some perspective on how well tolerated the medications are, although the specifics may vary according to dosage and design (e.g., forced titration) and are not directly comparable. The rate of discontinuation was reported to be 12% (4/48) for fluoxetine (Emslie et ah, 1997), 9.7% for paroxetine (Keller et ah, 2001), 13% (12/92) for sertraline (March et ah, 1998), and 33% (19/57) (Riddle et ah, 2001) and 7.9% (5/63) for fluvoxamine (Walkup et ah, 2001). [Pg.276]

All SSRIs (e.g., Feonard et ah, 1997) and in particular fluoxetine, Fluvosamine and paroxetine are metabolized by hepatic cytochrome P450 enzymes. Therefore, it is important to be aware of the possibility that the therapeutic or toxic effects of other medications metabolized by the cytochrome P450 isoenzyme system can be increased. Substantial inhibition of these isoenzymes converts a normal metabolizer into a slow metabolizer with regard to this specific pathway. Inhibition of the hepatic oxidative isoenzymes has been associated with a reduction, to a varying extent, in the clearance of many therapeutic agents, including the TCAs, several neuroleptics, antiarrhythmics, theophy-lene, terfenadine, benzodiazepines, carbamazepine, and warfarin (for a complete list, see Nemeroff et ak, 1996). [Pg.469]

Tricyclic antidepressants are still prescribed today, but some patients experience side effects such as dry mouth, blurry vision, constipation, and other uncomfortable conditions. Other antidepressants have since been found that induce fewer side effects. One of the most popular is fluoxetine, which is marketed under the trade name Prozac. This drug, along with Zoloft and other antidepressants, are known to inhibit reuptake proteins specifically for serotonin. As a result, these drugs are called selective serotonin reuptake inhibitors, or SSRIs. Although some concerns have appeared because of a possible risk of suicide in young patients who take Prozac, these drugs are commonly prescribed and have proved highly effective in millions of patients. [Pg.86]

The olanzapine-fluoxetine combination is currently the only medication approved by the FDA specifically for the treatment of depression in patients with bipolar disorder. This indication was based on data from a double-bhnd, randomized study in which the combination was superior to both olanzapine monotherapy and placebo (Tohen et al. 2003). Treatment-emergent mania or hypomania did not occur more frequently in the olanzapine-fluoxetine combination group than in the placebo group during the acute trial. [Pg.160]

The side effects of antidepressants, sometimes very unpleasant, olten lead patients to interrupt their treatment or to reduce the drug dose, which involves a great risk in view of the high relapse rate and danger of suicide in depression. The newer antidepressants, such as trazodone, fluoxetine and other SSRIs and moclobemide, are characterized by better tolerability and lower toxicity and are therefore preferred in the treatment of outpatients and elderly patients (Rudorfer and Potter, 1989). A detailed list of general and specific common side effects associated with the newer generation of antidepressants is seen in Table 1.7. [Pg.15]

Another approach to correct neurotransmission is to inhibit the reuptake of the neurotransmitters into their presvnaptic endings. If the presynaptic reuptake mechanism of a neurotransmitter is blocked then more of the neurotransmitter will stay in the synaptic cleft and be functionally available. Many antidepressant drugs, called reuptake inhibitors , are thought to act via this mechanism. If selective for serotonin they are called selective serotonin reuptake inhibitors (SSRIs, Chapter 1), but if selective for both serotonin and noradrenaline they are called serotonin noradrenaline reuptake inhibitors (SNRIs). Most older antidepressants, such as the tricyclic compounds amitriptyline, imipramine and clomipramine, have little specificity for any of the neurotransmitters fluoxetine, paroxetine, citalopram and a few others are specific for serotonin venlafaxine is a representative of the SNRIs. A more recent mixed-uptake inhibitor is mirtazepine, and some similar compounds are about to be launched. [Pg.126]

A larger set of placebo-controlled studies show conclusively that imipramine is also effective for the treatment of panic disorders. Other agents shown to be effective in panic disorders include the SSRIs paroxetine, sertraline, fluvoxamine, fluoxetine and citalopram. Generally, initial treatment of moderate to severe panic disorders may require the initiation of a short course of benzodiazepines e.g. clonazepam (0.5 1 mg twice daily), and an SSRI. The patient will obtain immediate relief from panic attacks with the benzodiazepine whereas the SSRI may take 1 6 weeks to become effective. Once a patient is relieved of initial panic attacks, clonazepam should be tapered and discontinued over several weeks and SSRI therapy continued thereafter. There are no pharmacological treatments available for specific phobias, however controlled trials have shown efficacy for several agents, e.g. phenelzine, moclobemide. clonazepam, alprazolam, fluvoxamine. sertraline and paroxetine in the treatment of social phobia (Roy-Byrne and Cowlev, 2002). [Pg.293]

An alternative approach with antidepressants is to use the specific serotonergic re-uptake inhibitors such as fluoxetine (Covi et al. 1995). Serotonin transmission is affected... [Pg.83]

Treatment of psychiatric complications should generally be along standard lines for the respective conditions. Some syndromes appear to be brief and self-limiting once ecstasy use stops, but a more chronic course may also be seen, with cases in the literature of psychoses which prove resistant to treatment (Vecellio et al. 2003). Whichever psychiatric syndrome occurs, there is possibly a theoretical indication for specific serotonergic re-uptake inhibitors such as fluoxetine, sertraline or citalopram, given the effect of ecstasy in reducing serotonin transmission. This would purely be a pragmatic approach which has not yet been properly tested, and it may be that the transmission abnormalities are not amenable to this kind of enhancement. [Pg.94]

In contrast to anticonvulsants and alcohol, drugs such as bupropion, fluoxetine, fluvoxamine, nefazodone, quinidine, paroxetine, and some antipsychotics can inhibit specific CYP enzymes (7, 11, 36, 37, 41, 42, 43 and 44). Thus, TCAs, certain BZDs, bupropion, some steroids, and antipsychotics can all have their metabolism inhibited by drugs such as fluoxetine. For example, fluoxetine at 20 mg/day produces on average a 500% increase in the levels of coprescribed drugs which are principally dependent on CYP 2D6 for their clearance. That can lead to serious or even life-threatening toxicity if the drug has a narrow therapeutic index and the dose is not adjusted for the change in clearance caused by the coadministration of fluoxetine. [Pg.37]


See other pages where Fluoxetine specificity is mentioned: [Pg.269]    [Pg.112]    [Pg.203]    [Pg.290]    [Pg.295]    [Pg.68]    [Pg.118]    [Pg.181]    [Pg.449]    [Pg.111]    [Pg.148]    [Pg.165]    [Pg.53]    [Pg.39]    [Pg.253]    [Pg.680]    [Pg.683]    [Pg.148]    [Pg.436]    [Pg.515]    [Pg.295]    [Pg.520]    [Pg.661]    [Pg.202]    [Pg.209]    [Pg.261]    [Pg.292]    [Pg.172]    [Pg.87]    [Pg.126]    [Pg.12]    [Pg.40]    [Pg.132]   
See also in sourсe #XX -- [ Pg.126 , Pg.161 ]




SEARCH



Fluoxetin

Fluoxetine

Fluoxetine receptor specificity

© 2024 chempedia.info