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Generic Anafranil is a tricyclic antidepressant. Generic Anafranil is used to treat symptoms of obsessive-compulsive disorder (recurrent thoughts or feelings and repetitive actions). Generic Anafranil works by affecting chemicals in the brain that may become unbalanced.

Other names for this medication:

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Anafranil SR, Clopran, Doxepin, Cymbalta, Elavil


Also known as:  Clomipramine.


Generic Anafranil is used to treat symptoms of obsessive-compulsive disorder (recurrent thoughts or feelings and repetitive actions).

Generic Anafranil is a tricyclic antidepressant.

Anafranil is also known as Clomipramine, Clonil, Clofranil, Clopram, Clopran, Clopress, Equinorm, Hydiphen.

Generic Anafranil works by affecting chemicals in the brain that may become unbalanced.

Generic name of Generic Anafranil is Clomipramine.

Brand name of Generic Anafranil is Anafranil.


Take Generic Anafranil orally.

Do not take Generic Anafranil in large amounts.

Take Generic Anafranil with food.

Take Generic Anafranil up to 4 weeks.

The dosage of tablets depends on the disease and its prescribed treatment.

If you want to achieve most effective results do not stop taking Generic Anafranil suddenly.


If you overdose Generic Anafranil and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Anafranil overdosage: uneven heart rate, extreme drowsiness, confusion, agitation, vomiting, blurred vision, sweating, muscle stiffness, increased or decreased urination, swelling, shortness of breath, blue lips or fingernails, feeling light-headed, fainting, seizure.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Anafranil are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Anafranil if you are allergic to Generic Anafranil components.

Do not take Generic Anafranil if you're pregnant or you plan to have a baby, or you are a nursing mother.

Do not take Generic Anafranil if you had recent heart attack.

Do not take Generic Anafranil if you use MAO inhibitor such as isocarboxazid (Marplan), phenelzine (Nardil), rasagiline (Azilect), selegiline (Eldepryl, Emsam) or tranylcypromine (Parnate) within the past 14 days.

Be careful with Generic Anafranil if you have heart disease or a history of heart attack, bipolar disorder, schizophrenia or other mental illness, kidney or liver disease, overactive thyroid or adrenal gland tumor, glaucoma, problems with urination.

Avoid using other medicines that make you sleepy while using Generic Anafranil.

Avoid drinking grapefruit juice and eating grapefruit while using Generic Anafranil.

Avoid exposure to sunlight or artificial UV rays while using Generic Anafranil.

Be careful if you drive or do anything that requires you to be awake and alert while using Generic Anafranil.

Avoid alcohol.

Do not stop taking Generic Anafranil suddenly.

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There is currently available evidence that suggests that drugs combining 2 synergistic mechanisms of action (e.g., enhancement of both noradrenergic and serotonergic neurotransmission) may yield superior therapeutic efficacy compared with a single therapeutic mechanism of highly selective agents such as selective serotonin reuptake inhibitors (SSRIs). The differences in antidepressant efficacy favoring dual-acting drugs may exist in particular for 3 difficult-to-treat groups of patients: those with endogenous depression, those with severe depression, or hospitalized depressed patients. Mirtazapine differs from other new dual-acting antidepressants by not being a reuptake inhibitor. Its antidepressant activity may be related to a direct enhancement of noradrenergic neurotransmission by blockade of alpha2-autoreceptors. The rapid increase in serotonin (5-HT) synaptic levels by blockade of alpha2-heteroreceptors indirectly enhances 5-HT1A-mediated neurotransmission since 5-HT2 and 5-HT3 are blocked by mirtazapine. The antidepressant efficacy of mirtazapine was established in several placebo-controlled trials. Currently available evidence suggests that mirtazapine is effective in all levels of severity of depressive illness, as well as is in a broad range of symptoms associated with depression.

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Glial fibrillary acidic protein (GFAP) is the major intermediate filament protein of astrocytes in the vertebrate central nervous system. Increased levels of GFAP are the hallmark feature of gliosis, a non-specific response of astrocytes to a wide variety of injuries and disorders of the CNS, and also occur in Alexander disease where the initial insult is a mutation within the coding region of GFAP itself. In both settings, excess GFAP may cause or exacerbate astrocyte dysfunction. With the goal of finding drugs that reduce the expression of GFAP, we have devised screens to detect changes in GFAP promoter activity or protein levels in primary cultures of mouse astrocytes in a 96-well format. We have applied these screens to libraries enriched in compounds that are already approved for human use by the FDA. We report that several compounds are active at micromolar levels in suppressing the expression of GFAP. Treatment of mice for 3 weeks with one of these drugs, clomipramine, causes nearly 50% reduction in the levels of GFAP protein in brain.

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A clear improvement was observed in the active treatment period. No placebo or carry-over effects were observed.

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To investigate the antidepressant-like effect of an alkaloid extract from the aerial parts of Annona cherimola (TA) in mice.

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A study has been made in rodents of the interactions between a range of psychotropic drugs, narcotic agonist and partial agonist analgesics, and pain. In rodents, tricyclic antidepressants do not alone reduce pain responses but, in combination with morphine or pentazocine, clomipramine enhances analgesic activity after single doses yet increases the onset and degree of tolerance to morphine on repeated injection. The tricyclic antidepressant maprotiline, in contrast, reduced both the rate of development and extent of morphine tolerance. In morphine-dependent rats, repeated injections of clomipramine or maprotiline exerted a mixed effect upon the abstinence syndrome, some behavioural signs being potentiated whilst others were suppressed. These studies suggest that combining maprotiline with morphine will improve the control of chronic pain states.

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The excitability of hypoglossal (XII) motoneurons innervating genioglossal muscles is markedly suppressed during the rapid-eye-movement (REM) stage of sleep. This may contribute to airway obstructions in sleep apnea patients. Based on our earlier studies in decerebrate cats using injections of carbachol into the pons to induce a REM sleep-like atonia and microinjections of serotonin (5HT) into the XII motor nucleus, we hypothesized that a sleep-related withdrawal of the serotonergic excitatory input to XII motoneurons may play a major role in these processes. To test one aspect of this hypothesis, we inserted microdialysis probes into the XII nucleus region of decerebrate, paralyzed, vagotomized and artificially ventilated cats. The probes were perfused without or with the addition of a 5HT reuptake blocker, clomipramine. The levels of 5HT and its metabolite, 5-hydroxyindoleacetic acid (5HIAA), were determined using HPLC and electrochemical detection in dialysate samples collected over successive 20 min periods under four successive experimental conditions: control (at least 2 h after probe insertion); during the postural atonia and respiratory depression produced by pontine microinjection of carbachol; recovery from the effects of carbachol produced by pontine microinjection of atropine; and, to verify that the presence of 5HT in the dialysate was related to the activity of serotonergic cells of the brainstem, following administration of 8-OH-DPAT, a 5HT 1A receptor agonist known to suppress activity in the serotonergic cells of the raphe system. After correcting for recovery rates of individual probes, the mean control 5HT level in the extracellular space of the XII nucleus region was 7.9 +/- 4.4 nM (S.D.) in eight experiments without reuptake blockers. During the carbachol-induced depression, it was reduced to 70 +/- 20% of the pre-carbachol level. It increased to the original control level 98 +/- 27% after pontine injection of atropine. 8-OH-DPAT reduced the 5HT level to 43 +/- 14% of the post-atropine level. Changes in the 5HIAA level were not as consistent as for 5HT and did not reach statistical significance under any of the experimental conditions. Thus, a functionally significant amount of 5HT is present in the extracellular space within the XII nucleus region, and its decrement during carbachol-induced, REM sleep-like atonia is likely to reflect that occurring during natural REM sleep; this may contribute to the decreased tone of upper airway muscles and airway patency.

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Antinociceptive responses were determined before and 30, 60, 90, 120 min after drug injection by tail-flick (TFT) and hot-plate (HPT) tests. Results for each treatment group are given as mean %MPE +/- SEM (Student's t-test, ANOVA).

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The effects of intravenous 1 and 2 mg./Kg. duloxetine or clomipramine on lower urinary tract function were studied in a total of 32 male and 32 female rabbits, under nonirritative conditions (intravesical infusion of saline) and in a model of bladder irritation (i.e., transvesical infusion of 0.5% acetic acid). A transurethral double-lumen catheter in male rabbits, and a subcutaneous cystostomy in female rabbits, were used for liquid infusion and recording of intravesical pressure during a cystometrogram. Simultaneously, SAS-EMG was recorded through electromyography electrodes placed in the perianal striated muscle.

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Tricyclic antidepressive agents are widely used in suicide attempts and present a variety of deleterious effects. Rhabdomyolysis is a rare complication of such poisoning.

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The plasma protein binding of amitriptyline, imipramine, clomipramine, and their primary demethylated metabolites were studied by means of a method combining dialysis and gas chromatography. Equilibrium in dialysis of serum containing amitriptyline and its metabolite nortriptyline was attained in about 0.5 h with the drug dissolved in the serum compartment, and in about 2 h with the drug passing from the buffer to the serum compartment. The calculation of free fractions was influenced by variations with dialysis time in the volumes of serum and buffer. Increase of pH in serum increased the protein binding of the weakly basic drugs studied, and made the Donnan distribution effects more pronounced. At pH 7.4, the Donnan effect was negligible. Binding parameters for the 6 tricyclic antidepressant substances studied were estimated for the binding to alpha 1-acid glycoprotein and for total binding in serum. For alpha 1-acid glycoprotein, the k-values ranged from 1 X 10(5) to 8 X 10(5) M-1, and for pooled serum from 0.4 X 10(5) to 8 X 10(5) M-1. The determined number of binding sites on the alpha 1-acid glycoprotein was, on average 0.87 for the 6 substances. In serum, the binding capacity was 2-14 times the concentration of alpha 1-acid glycoprotein.

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To measure opiate receptor sensitivity, the effects of naloxone on beta-endorphin and cortisol serum levels were determined before and after 3 weeks of clomipramine treatment (75 mg/day i.v.) in 12 patients with major depressive disorder. The opiate antagonist significantly increased both hormonal levels. The only significant endocrine differences between pre- and post-treatment were basal and maximal cortisol levels, which were elevated before antidepressant therapy. The rise in the cortisol or beta-endorphin serum level after naloxone injection was not affected by clomipramine treatment. There was no significant relationship between depression score and basal or stimulated endocrine variables. These data do not indicate a distinct effect of antidepressants on opiate receptor sensitivity.

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The relative cytotoxic effects of ten psychotropic drugs were assessed in rat hepatocyte monolayer cultures. Clear concentration-related toxicity was seen in the narrow range of 10(-5) M to 5 X 10(-5) M. The four cytotoxicity endpoints chosen were: release of the cytosolic enzyme, lactate dehydrogenase, and impairment of biosynthesis and secretion of proteins, bile acids and glycerolipids. LDH leakage and inhibition of protein secretion into the culture medium proved to be the parameters which allowed the best differentiation between the test compounds. The inhibition of glycerolipid secretion was the most sensitive test in relation to concentration and time of exposure. Based on the effects of these endpoints, the following ranking of relative in vitro toxicity, using equimolar drug concentrations, could be established: clomipramine greater than imipramine = thioridazine greater than chlorpromazine greater than amitriptyline = fluperlapine greater than haloperidol greater than promazine greater than clozapine much greater than sulpiride. This ranking order of in vitro cytotoxicity correlated well with the potential of the drugs to impair liver function in man. Only clozapine had to be classified as a false negative. There was, however, no correlation between the cytotoxicity and the intracellular accumulation of the test drugs. Furthermore, the comparison of the data obtained with psychotropics with the data from five other amphiphilic cationic drugs was consistent with the widely accepted concept of a direct toxic interaction of the drugs with cytomembranes. This nonspecific toxicity of the membrane-active drugs was further corroborated by a positive correlation between their potential to induce LDH leakage in hepatocytes and their ability to induce hemolysis in red cells. In conclusion, the results obtained in our study strongly suggest that it is possible to assess the relative cytotoxicity of psychotropic drugs in rat hepatocyte cultures. It is proposed that this in vitro system provides a useful tool to evaluate new drugs at an early stage of their development, and to identify the most promising candidates within a class of structurally related compounds. In addition, it allows information to be obtained on possible mechanisms of cytotoxicity.

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In an open, uncontrolled trial flupenthixol was administered to 45 patients with endogenous depression. The drug was markedly effective in eight patients, effective in nine patients, fairly effective in 12 patients, and ineffective or aggravating in 16 patients. Four patients showed transient manic symptoms. Dosage was 1-3 mg daily. In 36 patients flupenthixol was used in combination with previously administered tricyclic antidepressants, and in nine patients it was used alone. Clinical effect was quickly apparent. It appeared within 1 week in 63% and within 2 weeks in 93% of subjects. Side-effects were observed in 13 patients: insomnia, five patients; slight extrapyramidal symptoms, nine patients. Sedative-hypnogenic effects were rarely seen. In 71% of 17 patients in whom the drug was found to be markedly effective or effective, flupenthixol's influence on psychomotor retardation was particularly striking. Other clear benefits were relief of depressive mood, psychic anxiety, and agitation. It is recommended that flupenthixol is given, as supplementary medication, to patients (1) whose depressive symptoms other than psychomotor retardation have already improved with current tricyclic antidepressants, and (2) in whom, before antidepressant medication, psychomotor retardation is a principal feature.

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Fluvoxamine is the selective serotonin re-uptake inhibitor with the largest database in the treatment of obsessive-compulsive disorder, a severe, and often chronic, anxiety disorder associated with substantial impairment in functioning. The selective serotonin re-uptake inhibitors represent a first-line treatment in patients with obsessive-compulsive disorder. These agents work primarily by blocking the re-uptake of serotonin into the presynaptic nerve terminal, which is believed to be mediated by their effects on the serotonin transport system. In the last two decades, the anti-obsessional effect of fluvoxamine has been tested in several double-blind, placebo-controlled and active-comparison studies, demonstrating its superior efficacy over obsessions and compulsions compared with non-serotonergic antidepressants (i.e., desipramine) and equal efficacy to clomipramine (a tricyclic antidepressant with potent serotonin re-uptake inhibition) and other selective serotonin re-uptake inhibitors (paroxetine and citalopram). However, compared with clomipramine, the selective serotonin re-uptake inhibitor fluvoxamine showed fewer side effects and better tolerability. This reflects the poor affinity of this compound for adrenergic, muscarinic, cholinergic or histaminergic receptors.

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A case of akinesia and mutism is described in a menopausal, depressed woman with onset following a mood challenge with 40 mg of methylphenidate taken orally over a 3-hour period. Various diagnoses are considered with preference given on clinical grounds to conversion disorder precipitated by drug-induced dysphoria. It is suggested that increased susceptibility to dysphoria may have been related to prior clomipramine administration and hypoestrogenism.

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The aim of this study was to test the hypothesis of noradrenergic and serotoninergic depressive subtypes. For this purpose, the correlation between three variables was investigated: urinary 3-methoxy-4-hydroxyphenylglycol (MHPG), dexamethasone suppression test (DST), and clinical response profiles to clomipramine and maprotiline, the effects of which are relatively selective on the uptake of noradrenaline (NA) and 5-hydroxytryptamine (5HT). Our results showed no correlation between these measures. Therefore, the hypothesis of two subtypes of depression was not supported. The only significant finding in this study was the obvious decrease in MHPG excretion during the antidepressant treatment in the group with high pretreatment MHPG.

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Several concerns have been raised regarding the reproductive safety of the antidepressants most frequently used in clinical practice, such as selective serotonin reuptake inhibitors (SSRIs).

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Several compounds of pharmaceutical importance from a variety of chemical families, for example chlorpromazine and clomipramine, have been found to form charge-transfer complexes with iodine. We have investigated the influence of dietary iodine on thyroid-gland dysfunction induced by clomipramine, chlorpromazine or 2-thiazoline-2-thiol. We suggest that iodine is partly diverted from its metabolic pathway by complexation with drugs, and so the urinary concentration of iodide is increased. Both chlorpromazine and clomipramine, at doses which do not inhibit thyroperoxidase, enhanced urinary iodine excretion when dietary iodine was restricted (3.944+/-0.96 microg/day for chlorpromazine-tested rats, 3.43+/-1.33 microg/day for clomipramine-tested rats, compared with 2.34+/-0.11 microg/day in control rats). Concurrently, these pharmaceutical compounds increased the level of free thyroid-stimulating hormone (TSH) in comparison with controls and induced histological modifications in, and enlargement of, the thyroid gland. We have demonstrated that drug-induced loss of iodine in the urine was associated with antithyroid action when iodine intake was limited.

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The neuroendocrine responsivity to an acute serotonergic challenge with low-dose i.v. clomipramine was studied in seven drug-free depressed patients and seven age-matched healthy control subjects. The depressed patients had higher baseline prolactin concentrations than the healthy subjects, and their prolactin response to clomipramine, assessed as either the percent of baseline or the log-transformed concentration, was significantly different (delayed and blunted peak response) compared to healthy controls. The growth hormone response was exaggerated in the depressed patients, and there were also trends toward blunting in their cortisol and adrenocorticotropic hormone responses. These results are consistent with previous findings of altered neuroendocrine responses to a variety of putative serotonin agonists in depressed patients.

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We describe a case of severe serotonin syndrome. The patient was simultaneously taking the atypical antidepressant olanzapine and a tricyclical antidepressant, clomipramine. Symptoms included altered mental state resulting in coma, myoclonus, hyperreflexia, diaphoresis, diarrhoea, disorientation and fever. After suspension of antidepressant drugs, intensive symptomatic treatment and administration of biperiden and cyproheptadine, the patient's condition improved.

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The various clinical types of depression may correspond to biochemically distinct forms of the condition. If these could be characterized, antidepressant treatment might be tailored to correction of the underlying biochemical change(s) in individual patients. In particular, the selective actions of clomipramine and maprotiline on the serotonergic and noradrenergic systems respectively might be exploited therapeutically. Studies of the clinical response to these two antidepressants included tests of urinary 5-hydroxy-indoleacetic acid (5-HIAA) excretion and of serum thyroxine levels. While thyroid stimulation tests may prove of value for investigating depressed patients, urinary 5-HIAA levels are inconvenient, subject to extraneous influences and hard to interpret in terms of brain chemistry. (An alternative is proposed in the next paper.)

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Randomized controlled multicenter clinical trial.

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The present study was undertaken to investigate the spontaneous epileptiformic activity induced by antidepressants using amygdala-kindled rats. The intraperitoneal injection of imipramine and amitriptyline resulted in potent behavioral and electroencephalogram (EEG)-detected seizures in amygdala-kindled rats compared with those seen in sham rats (non-kindled rats). Almost the same findings were observed with clomipramine and maprotiline. On the other hand, paroxetine caused no or little behavioral or EEG seizures in either amygdala-kindled or sham rats, even at a dose of 50 mg/kg. In conclusion, our results indicate that epileptiformic activity induced by kindling increases the susceptibility to cyclic antidepressant-induced seizures.

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The fortuitous detection of SIADH is described in a patient receiving clomipramine therapy.

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Treatment-resistant depression (TRD) is a major health concern. More than 40% of patients treated for major depressive disorder with an appropriate antidepressant dose for an adequate duration fail to respond. Further, approximately half of adults with major depressive disorder fail to achieve sustained remission despite various medication trials. The utilization of monoamine oxidase inhibitors (MAOIs) for the treatment of depression in clinical practice today is low due to their widely known adverse effects, some of which may be life threatening, and the risk for dietary and drug interactions. For these reasons, MAOIs are not recommended to be prescribed along with other antidepressants or certain prescription or nonprescription drugs. Pharmacologic options are limited for individuals with TRD, however, and there is a paucity of data on the efficacy of MAOIs in combination with other antidepressants for the management of TRD. We performed a search of the PubMed database (inception through January 25, 2015) to identify cases that illustrate the potential utility, as well as risks, of combination treatment with MAOIs and other antidepressants for the management of TRD; 18 articles met the criteria for our search. In addition, we performed a retrospective case series by reviewing the medical records of 29 adults treated for depression with an MAOI plus another psychotropic agent (an antidepressant or stimulant medication) between 2003 and 2012 at a large Midwestern teaching hospital. We compared the findings of the published experience with our local experience to allow for more informed decisions regarding pharmacotherapy in patients with TRD. We separated the local experience into two groups: 15 cases with the selective MAO type B inhibitor selegiline combined with medications presumed to increase the risk of serotonin syndrome and 14 cases with nonselective MAOIs (phenelzine and tranylcypromine) combined with other contraindicated medications. Although risks of combination treatment certainly exist with selective serotonin reuptake inhibitors, serotonin and norepinephrine reuptake inhibitors, or clomipramine, the current literature supports cautious use of combining MAOIs with other antidepressants in patients with TRD who have failed multiple treatment modalities. In addition, the data from the 29 patients receiving combination therapy with an MAOI and another antidepressant or stimulant medication revealed that 21% improved significantly, with no complications. This case series and literature review suggest that when used under close supervision and under the care of an experienced clinician in psychiatry, combination therapy may be a consideration for the management of TRD in patients not responding to monotherapy or other combinations of antidepressants.

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NCB-20 cells (neuroblastoma X fetal Chinese hamster brain hybrids) are equipped with a [3H]5-hydroxytryptamine [( 3H]5-HT) uptake system and [3H]imipramine recognition sites. Approximately 80% of the radioactivity taken up by cells incubated with [3H]5-HT was identified with 5-HT. [3H]5-HT uptake was temperature-dependent, partially sodium-dependent, saturable (Km = 7.3 +/- 0.6 microM; Vmax = 2.0 +/- 0.6 pmol/min/mg), and inhibited by clomipramine, imipramine, fluoxetine, and desipramine, but not by iprindole, mianserin, or opipramol. Lineweaver-Burk plots showed a competitive type of inhibition by imipramine and fluoxetine. [3H]5-HT uptake was not inhibited by nisoxetine or benztropine. [3H]Imipramine binding sites had a KD of 12 +/- 2 nM and a Bmax of 22 +/- 7 pmol/mg protein. The binding was sodium-sensitive although to a lesser extent than that found with brain membranes. Imipramine binding was displaced by tricyclic antidepressants with the following order of potency: clomipramine greater than imipramine greater than fluoxetine greater than desipramine much greater than iprindole = mianserin greater than opipramol. These results suggest that imipramine binding sites are present together with the 5-HT uptake sites in NCB-20 cells and that these sites interact functionally but are different biochemically.

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Neonatal treatment with CLI reliably produces enhanced levels of REM (p < 0.01) and reduced sexual activity (p < 0.05). Theta power was enhanced during NREM sleep in the CLI group (p = 0.02). CLI-treated animals experienced increased frequency at the NRT (p < 0.01), as well as additional epileptiform activity of continuous (CTS; p < 0.05) and petite-continuous (P-CTS; p < 0.01) types, across the sleep-wake cycle. There is a strong temporal correlation with increased REM sleep duration, increased frequency of NRT bursts, and increased theta power during NREM sleep in CLI-treated animals.

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anafranil 25mg prices 2017-11-11

Although both protocols significantly decreased the scores of the Yale-Brown obsessive-compulsive scale over the buy anafranil trial period, the combination of clomipramine and nortriptyline showed a significant superiority over clomipramine alone in the treatment of OCD.

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Atypical, stereotypic motor and locomotor behavior was observed in 3 dogs. In 1 dog, the behavior included circling, vocalization, and snapping; in another, circling associated with pica and aerophagia; and in a third, gradually intensifying locomotor behavior stimulated by bright light. This behavior interfered with normal interaction between their owners and the dogs, and has been associated buy anafranil with obsessive-compulsive disorders. Treatment with clomipramine, along with other psychotropic medications and behavioral modification, suppressed the inappropriate behavior in all dogs; in 2 of the 3 dogs, the condition worsened when clomipramine treatment was withdrawn. Clomipramine may be helpful in treatment of such behavioral disorders, but one should consider the ability of such drugs to mask or worsen metabolic or neurologic problems, to induce toxicoses when used at inappropriate dosages, and to be abused by human beings.

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Thus, we demonstrate that hippocampal LTP is decreased in this animal model of depression, possibly explaining the learning deficits. Further, the reversal of learning and electrophysiological impairments by escitalopram reveals the buy anafranil important therapeutic effects of escitalopram that could benefit patients suffering from depression.

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A retrospective review elicited 12 patients who met DSM-III-R diagnostic criteria for both OCD and buy anafranil social phobia and were treated in our clinic last year with adequate trials of serotonin reuptake blockers or MAOIs.

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Thirty affected subjects were placed into three groups: two buy anafranil received an intravenous dose of 25 mg clomipramine or 40 mg citalopram, and one received an injection of a placebo. Motor cortex excitability was studied by single and paired TMS before and after 3.5, 8, and 24 hours from administration of the drugs and placebo. Motor cortical excitability was measured using different TMS parameters: resting motor threshold (RMT), motor-evoked potential (MEP) amplitude, intracortical inhibition (ICI), and intracortical facilitation (ICF).

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The reaction was studied in control liver microsomes in the presence of antidepressants, as well as buy anafranil in microsomes from rats treated intraperitoneally (ip) with pharmacological doses of the tested drugs (imipramine, amitriptyline, clomipramine, nefazodone - 10 mg/kg ip; desipramine, fluoxetine, sertraline - 5 mg/kg ip; mirtazapine - 3 mg/kg ip) for one day or two weeks (twice a day), in the absence of antidepressants in vitro.

anafranil 10 mg 2016-08-10

Chronic treatment with selective 5-HT reuptake inhibitors (SSRI) are therapeutic in obsessive compulsive disorder, depression, anxiety, bulimia nervosa and migraine. In the present study the possibility that SSRI's act by desensitizing 5-HT2C/5-HT2B receptors was assessed using a putative in vivo model of 5-HT2C/5-HT2B receptor function, mCPP-induced hypolocomotion. mCPP (2, 4 and 6 mg/kg i.p. 20 min pretest) reduced locomotion and rears in rats treated acutely or chronically with saline. Acute oral administration of the SSRI's fluoxetine (10 mg/kg), paroxetine (10 mg/kg), or clomipramine (70 mg/kg) or the noradrenaline reuptake inhibitor, desipramine (10 mg/kg), all 1 hr pretest, did not prevent mCPP-induced hypolocomotion. In contrast, chronic treatment with the SSRI's paroxetine and fluoxetine (both 10 mg/kg p.o. daily x 21 buy anafranil days), significantly attenuated the effect of mCPP (4 and 6 mg/kg i.p.) on locomotion and rears 24 hr after the last pretreatment dose. Chronic clomipramine (70 mg/kg p.o. daily x 21 days) also significantly attenuated the effect of mCPP (4 mg/kg i.p.) on rears and tended to reduce the hypolocomotor response. However, chronic treatment with desipramine, (10 mg/kg p.o. daily x 21) had no effect on any of the parameters measured. As chronic fluoxetine and paroxetine did not reduce brain mCPP levels (determined by HPLC 30 min after 4 mg/kg i.p.) the results suggest that chronic SSRI's, but not desipramine, reduce 5-HT2C/5-HT2B receptor responsivity. If this occurs in man, it may mediate or contribute to their reported therapeutic efficacy in depression, anxiety, bulimia, migraine and alcoholism. It may also be of particular relevance to their unique efficacy in OCD.

anafranil dose range 2015-05-23

When considering the buy anafranil risk-benefit profile of antidepressants in the acute treatment of major depressive disorder, these drugs do not seem to offer a clear advantage for children and adolescents. Fluoxetine is probably the best option to consider when a pharmacological treatment is indicated.

anafranil 600 mg 2016-04-17

The effects of a 10 day administration of clomipramine (25-50 mg t.i.d.), alprazolam (0.25-0.75 mg t.i.d.) and placebo were assessed in normal volunteers in a double-blind cross-over study. A battery of physiological, psychomotor and cognitive tests was administered both before and 3 h after drug on days 1, 5 and 10. The effects of alprazolam on EEG and evoked potentials were characteristic of benzodiazepines; clomipramine had little effect. In contrast, reaction speed was markedly slowed by clomipramine but little affected by alprazolam. Neither drug produced any accumulation of effect on a buy anafranil verbal recall task but neither did tolerance develop to the acute impairments produced by active treatments. Alprazolam produced an increase in levels of forgetting, especially on day 5. Subjective ratings for mood and bodily symptoms were adversely affected by clomipramine but little altered by alprazolam. It is suggested that some of the differences between drug treatments may be due to differences in the speed of onset of tolerance.

anafranil 225 mg 2017-08-17

Sixty outpatients meeting DSM-II-R or DSM-IV criteria for OCD were followed up for 1 to 5 years (mean = 2.5 years). All of them received prolonged pharmacologic therapy buy anafranil with an SRI.

anafranil user reviews 2016-06-19

This is the first demonstration of multiple symptoms consistent with an OCD-like profile in animals. Moreover, these behaviors are accompanied by biochemical changes in brain regions previously identified as relevant to OCD. This novel model buy anafranil of OCD demonstrates that drug exposure during a sensitive period can program disease-like systems permanently, which could have implications for current and future therapeutic strategies for this and other psychiatric disorders.

anafranil ocd dose 2017-08-15

Panic disorder is a common psychiatric disorder characterized by recurrent anxiety attacks and anticipatory anxiety. Due to buy anafranil the severity of the symptoms of the panic attacks and the frequent additional occurrence of agoraphobia, panic disorder is an often debilitating disease. Elevation of central serotonin levels by drugs such as clomipramine represents one of the most effective treatment options for panic disorder. This points to an important role of dysregulation of the serotonergic system in the genetic etiology of panic disorder. The novel brain-specific 5-HT synthesizing enzyme, tryptophan hydroxylase-2 (TPH2), which represents the rate-limiting enzyme of 5-HT production in the brain, may therefore be of particular importance in panic disorder. We focused on the putative transcriptional control region of TPH2 and identified two novel common single nucleotide polymorphisms (SNPs) of TPH2 in and close to this region. Moreover, a recently described loss-of-function mutation of TPH2 which results in an 80% reduction of serotonin production, was assessed. In an analysis of the putative transcriptional control region SNPs in a sample of panic disorder patients and controls no association of the disorder with the TPH2 SNPs or haplotypes was found. Moreover, the loss-of-function R441H mutation of TPH2 was not present in the panic disorder patients. The results of this first study of TPH2 in panic disorder argue against an importance of allelic variation of TPH2 in the pathogenesis of panic disorder with or without agoraphobia.

anafranil 40 mg 2015-10-13

In 1997, we described a new automated method of scoring the pain behaviors in the formalin test. The algic behavior was automatically measured with the help of a video-analysis system. The time during which the animal grooms, licks, or bites itself was used as the parameter of pain. In the present study, we tested various analgesics to realize a pharmacological validation of the system. The effect of opiate analgesic (morphine, i.v.), nonsteroidal anti-inflammatory drugs (paracetamol, i.v., piroxicam, i.v., indomethacin, i.v.), antidepressant drugs (clomipramine, desipramine, nortryptyline, and paroxetine, i.p.), and serotonin (i.t.) were analyzed. A dose of 1.25 mg/kg of morphine induced a decrease in the scores of phases 1 and 2. Naloxone (0.25 mg/kg) reversed the effect of morphine (2.5 mg/kg). A 20-mg/kg dose of indomethacin induced a decrease in the second phase, and paracetamol induced a decrease in both phases ( buy anafranil analgesic doses were 400 mg/kg and 200 mg/kg for first and second phases, respectively). Piroxicam had no effect on the pain scores. Clomipramine, desipramine, and paroxetine at a dose of 5 mg/kg induced a significant decrease in the second phase. Nortriptyline had no effect on the pain scores. A dose of 75 microg of serotonin induced a decrease in both phases 1 and 2. This study demonstrated that this system shows a good pharmacological sensitivity, although it is lower than that of manual assessment.

anafranil cost 2016-09-02

Inhibition of distinct ubiquitin E3 ligases might represent a powerful therapeutic tool. ITCH is a HECT domain-containing E3 ligase that promotes the ubiquitylation and degradation of several proteins, including p73, p63, c-Jun, JunB, Notch and c-FLIP, thus affecting cell fate. Accordingly, ITCH depletion potentiates the effect of chemotherapeutic drugs, revealing ITCH as a potential pharmacological target in cancer therapy. Using high throughput screening of ITCH auto-ubiquitylation, we identified several putative ITCH inhibitors, one of which is clomipramine--a clinically useful antidepressant drug. Previously, we have shown that clomipramine inhibits autophagy by blocking autophagolysosomal fluxes and thus could potentiate chemotherapy in vitro. Here, we found that clomipramine specifically blocks ITCH auto-ubiquitylation, as well as p73 ubiquitylation. By screening structural homologs of clomipramine, we identified several ITCH inhibitors and putative molecular moieties that are essential for ITCH inhibition. Treating a panel of breast, prostate and bladder cancer cell lines with clomipramine, or its homologs, we found that they reduce cancer cell growth, and synergize with gemcitabine or mitomycin in killing cancer cells by blocking autophagy. We also discuss a potential mechanism of inhibition. Together, our study (i) demonstrates the feasibility of using high throughput screening to identify E3 ligase inhibitors and (ii) provides insight into how clomipramine and its structural homologs might interfere with ITCH and other HECT E3 ligase catalytic activity Valtrex Y Alcohol in (iii) potentiating chemotherapy by regulating autophagic fluxes. These results may have direct clinical applications.

anafranil dosing 2017-01-13

These data provide evidence of dopaminergic mechanisms in drug-seeking following extinction of MDMA Bystolic Reviews self-administration. Because tissue levels of 5-HT were significantly decreased following MDMA self-administration, we suggest that MDMA begins to preferentially activate dopaminergic substrates to potentiate the drug-seeking response.

anafranil capsules 2016-06-26

Plasma concentrations and response to antidepressants vary considerably between patients treated with similar dosages. Most antidepressants and also antipsychotics are metabolized by the polymorphic debrisoquine/sparteine hydroxylase, i.e., cytochrome P450 (CYP)2D6. About 7% of Caucasians are poor metabolizers (PM), and such patients might develop adverse drug reactions when treated with recommended doses of, for example, tricyclic antidepressants. In contrast, ultrarapid metabolizers with multiple CYP2D6 genes might require high doses of such drugs for optimal therapy. The mean CYP2D6 activity is lower in Oriental than in Caucasian populations, because of a frequent mutation causing decreased enzyme activity. Drugs metabolized by the same enzyme may interact with each other. For example, the potent CYP2D6 inhibitor fluoxetine increases the plasma concentrations of tricyclic antidepressants. Another enzyme catalyzing the metabolism of antidepressants is the polymorphic S-mephenytoin hydroxylase. CYP2C19, which catalyses the metabolism of, for example, citalopram, clomipramine and moclobemide. Various probe drugs may be used for phenotyping CYP2D6 (debrisoquine, dextromethorphan and sparteine) and CYP2C19 (mephenytoin and omeprazole). Allele-specific polymerase chain reaction (PCR)-based methods are now available for genotyping using Bactrim 240 Mg leukocyte DNA. A major advantage of genotyping compared with phenotyping is that the former may be performed in blood samples from patients irrespective of treatment.

anafranil 5 mg 2017-04-15

Fluvoxamine and clomipramine were equally effective in the treatment of obsessive compulsive disorder. Both agents were well tolerated Effexor 250 Mg ; fluvoxamine produced fewer anticholinergic side effects and caused less sexual dysfunction than clomipramine, but more reports of headache and insomnia.

anafranil patient reviews 2016-03-09

Abuse of anabolic androgenic steroids (AASs) is frequently associated with changes in mood, including depression. However, the nature of this association is still largely unexplored. As a model of AAS abuse, we used male adult rats injected for 4 weeks with either nandrolone or stanozolol at daily doses (5 mg/kg, s.c.) that are considered equivalent to those abused by humans on a milligram per kilogram of body weight basis. AAS treatment reduced levels of brain-derived neurotrophic factor in the hippocampus and prefrontal cortex, reduced the expression of low-affinity glucocorticoid receptors in the hippocampus, and increased morning trough basal plasma corticosterone levels. All these changes have been related to the pathophysiology of major depressive disorder. Accordingly, rats treated with nandrolone or stanozolol showed an increased immobility time in the forced swim test, which is widely used for the screening of antidepressant drugs. All effects produced by AASs Nexium Reviews Uk were prevented by co-administration with the classical antidepressant, chlorimipramine. The evidence that supraphysiological doses of AASs induce changes indicative of a depressive state in normal rats, raises the concern that AAS abuse in humans may cause depression regardless of exposure to stress or other risk factors.

anafranil drug reviews 2016-06-10

We report two female patients who deteriorated to depressive-catatonic state after interepisode recovery from a hypomanic episode induced by corticosteroid treatment. Their symptoms developed during maintenance treatment with a low dose of prednisolone in Case 1 and after discontinuation of betamethasone in Case 2. Intravenous clomipramine successfully relieved their symptoms including reduction in contact and reactivity, immobility and mutism. These two patients showed no schizophrenic symptoms such as hallucinations and delusions. Corticosteroid-induced mood disorder can deteriorate into depressive stupor, Risperdal Maximum Dosage severe depressive episode with catatonic features in DSM-IV. Clomipramine, a tricyclic antidepressant with relatively stronger serotonin reuptake inhibition, is one of the useful treatment options for corticosteroid-induced depression even in severe cases.

anafranil online 2017-11-10

In a large, open, multicentre trial, Reglan 800 Mg conducted in general practice, 765 patients suffering from agoraphobia or social phobias were treated with clomipramine (Anafranil, Geigy Pharmaceuticals). Four hundred and eight patients completed a twelve-week course of treatment. Of 285 withdrawals, 139 were due to side-effects. Good results were obtained on all measures of phobias in those patients who completed the study, the improvements being of the order of 70-80%, and over 50% of patients being symptom-free.

anafranil 20 mg 2016-01-02

This paper explores a possible connection between neurochemistry and cognitions in eating disorders (ED). Cognitions play an important role in ED. However, a possible neurochemical origin of these cognitions has not been explored. Obsessive-compulsive disorder (OCD) is known as a disorder of thinking. Extensive neurochemical research conducted on this disorder indicates a connection between serotonin (5-HT) dysregulation and cognitions in OCD. This study used research done on OCD as a template to interpret the available research findings in ED and their possible meaning in terms of neurochemical origin of cognitions in ED. This paper suggests that the neurochemical and behavioral expression of both ED and Neurontin 600mg Pill OCD occur on a continuum. At one end of the continuum, ED and OCD are expressed through constrained behaviors of an avoidant quality. This pole is also characterized by high levels of serotonin markers. At the other end, both disorders are characterized by disinhibited approach behavior. This end of the continuum is characterized by low levels of 5-HT markers. It is suggested that these levels of 5-HT generate cognitions that may in turn promote specific behaviors.

anafranil therapeutic dose 2016-12-11

Disturbances in sleep are encountered in the majority of patients with depression. To elucidate the possible molecular mechanisms behind this relationship we examined gene expression changes in a rodent model for depression and disturbed sleep. Animals were treated with daily injections of clomipramine in their early infancy, after which gene expression in basal forebrain was examined using Affymetrix Rat 230.2 chips. We tested the levels of both single transcripts and involved pathways, and searched for common nominators (i.e. transcription factors) that could explain these changes. We identified 72 differentially expressed gene transcripts Arava 40 Mg , many of which are involved in epigenetic regulation, such as DNMT2. Analysis of functional pathways revealed statistically significant changes of the biological process of synaptic transmission, the cellular compartment of the synapse and the molecular function of GABA signalling, showing that transcripts with altered expression are functionally related. Finally, promoter analysis of the differentially expressed genes showed a clear enrichment of binding sites for the transcription factor CREB1, a molecule also involved in epigenetic regulation (cAMP response element-binding protein induces histone modifications). These results indicate that CREB1 may constitute one of the major links between disturbed sleep and mood. The results also highlight the molecular mechanisms in the murine clomipramine model, previously shown to be a valid model for depression.

anafranil pill 2015-11-24

The most critical point in pharmacotherapy of OCD is the need for the high-dose and long-term use of drugs. In OCD, generally the higher doses of applicable drugs than those Zyrtec Pill used in depression are required, often exceeding the recommended maximum dose. Moreover, such high doses should be given for at least 10 - 12 weeks to ensure the adequate treatment duration for the clinical effects to emerge. This long-term high-dose maintenance therapy increases the risk of drug toxicity and adverse effects. Physicians should take extra care in periodical assessment of signs and symptoms of metabolic and toxicological complications in patients. Subjective symptoms reported by patients should be carefully assessed and not attributed to obsessive nature of the patients.

anafranil dosage information 2017-01-15

Anxiety is common in the Mild Cognitive Impairment (MCI) stage of Alzheimer's disease (AD) and the pre-motor stages of Parkinson's disease (PD). A concomitant and possible cause of this anxiety is microglial activation, also considered a key promoter of neurodegeneration in MCI and early PD via inflammatory mechanisms and the generation of degenerative proinflammatory cytokines. Psychiatric disorders, prevalent in AD and PD, are often treated with psychiatric drugs (psychotropics), raising the question of whether psychotropics might therapeutically affect microglial activation, MCI, and PD. The literature of common psychotropics used in treating psychiatric disorders was reviewed for preclinical and clinical findings regarding microglial activation. Findings potentially compatible with reduced microglial activation or reduced microglial inflammogen release were evident for: antipsychotics including neuroleptics (chlorpromazine, thioridazine, loxapine) and atypicals (aripiprazole, olanzapine, quetiapine, risperidone, ziprasidone); mood stabilizers (carbamazepine, valproate, lithium); antidepressants including tricyclics (amitriptyline, clomipramine, imipramine, nortriptyline), SSRIs (citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline), venlafaxine, and bupropion; benzodiazepine anxiolytics (clonazepam, diazepam); cognitive enhancers (donepezil, galantamine, memantine); and other drugs (dextromethorphan, quinidine, amantadine). In contrast, pramipexole and methylphenidate might promote microglial activation. The most promising replicated findings of reduced microglial activation are for quetiapine, valproate, lithium, fluoxetine, donepezil, and memantine but further study is needed and translation of their microglial effects to human disease still requires investigation. In AD-relevant models, risperidone, valproate, lithium, fluoxetine, bupropion, donepezil, and memantine have therapeutic microglial effects in need of replication. Limited clinical data Protonix Dose Po suggest some support for lithium and donepezil in reducing MCI progression, but other drugs have not been studied. In PD-relevant models, lamotrigine, valproate, fluoxetine, dextromethorphan, and amantadine have therapeutic microglial effects whereas methylphenidate induced microglial activation and pramipexole promoted NO release. Clinical data limited to pramipexole do not as of yet indicate faster progression of early PD while the other drugs remain to be investigated. These tantalizing psychotropic neuroprotective findings now invite replication and evidence in AD-and PD-specific models under chronic administration, followed by consideration for clinical trials in MCI and early stage PD. Psychiatric features in early disease may provide opportunities for clinical studies that also employ microglial PET biomarkers.

anafranil generic name 2016-05-03

Genetically determined activity ofCYP2D6 may be modified by some drugs through inhibition processes. Inhibition properties of TCA's were confirmed mainly in in vitro studies. The aim of the study was to assess the influence of clomipramine on CYP2D6 activity in vivo.

anafranil dosage 2017-07-21

Clomipramine, by acutely elevating synaptic monoamine levels, could exacerbate absence seizures.

anafranil tablet 2015-03-31

Side effect profile and drug-drug interactions largely determine the choice of SRI. Those who fail to respond to one SRI trial may well respond to another SRI trial. Clomipramine is recommended if 2-3 trials of SRIs fail to produce response. Atypical antipsychotics are the first-line augmenting agents in SRI non-responders. CBT should be considered in all patients with OCD and is a potential option in SRI non-responders.

anafranil 100 mg 2015-11-12

The relationship between the debrisoquine oxidation status and the metabolism of clomipramine was studied in nine healthy volunteers (five rapid hydroxylators, three slow hydroxylators and one of intermediate status). The hydroxylation of clomipramine and demethylclomipramine were found to covary with that of debrisoquine, whereas demethylation of clomipramine seemed to be independent of the debrisoquine hydroxylation phenotype. The steady-state blood concentrations of clomipramine and its three main metabolites were measured in 122 depressed patients. Thirteen patients who concomitantly received a neuroleptic tended to have higher levels of demethylclomipramine and clomipramine, whereas the levels of the hydroxylated metabolites were hardly affected. Benzodiazepine co-administration did not modify the pharmacokinetics of clomipramine. The results suggest that benzodiazepines rather than levomepromazine should be used in depressed patients with anxiety and/or agitation in combination with the antidepressant treatment.