Depramine Uses

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What is Depramine?

Depramine is used to treat obsessive compulsive disorder (OCD). OCD is a nervous condition where a person has recurring thoughts or ideas, or does repetitive things because they are anxious.

Depramine is a tricyclic antidepressant (TCA). It is thought to work in the brain by increasing the activity of the chemical serotonin.

Depramine is available only with your doctor's prescription.

Depramine indications

An indication is a term used for the list of condition or symptom or illness for which the medicine is prescribed or used by the patient. For example, acetaminophen or paracetamol is used for fever by the patient, or the doctor prescribes it for a headache or body pains. Now fever, headache and body pains are the indications of paracetamol. A patient should be aware of the indications of medications used for common conditions because they can be taken over the counter in the pharmacy meaning without prescription by the Physician.
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Depramine™ (Depramine hydrochloride) Capsules USP is indicated for the treatment of obsessions and compulsions in patients with Obsessive-Compulsive Disorder (OCD). The obsessions or compulsions must cause marked distress, be time-consuming, or significantly interfere with social or occupational functioning, in order to meet the DSM-III-R (circa 1989) diagnosis of OCD.

Obsessions are recurrent, persistent ideas, thoughts, images, or impulses that are ego-dystonic. Compulsions are repetitive, purposeful, and intentional behaviors performed in response to an obsession or in a stereotyped fashion, and are recognized by the person as excessive or unreasonable.

The effectiveness of Depramine for the treatment of OCD was demonstrated in multicenter, placebo-controlled, parallel-group studies, including two 10-week studies in adults and one 8-week study in children and adolescents 10 to 17 years of age. Patients in all studies had moderate-to-severe OCD (DSM-III), with mean baseline ratings on the Yale-Brown Obsessive Compulsive Scale (YBOCS) ranging from 26 to 28 and a mean baseline rating of 10 on the NIMH Clinical Global Obsessive Compulsive Scale (NIMH-OC). Patients taking CMI experienced a mean reduction of approximately 10 on the YBOCS, representing an average improvement on this scale of 35% to 42% among adults and 37% among children and adolescents. CMI-treated patients experienced a 3.5 unit decrement on the NIMH-OC. Patients on placebo showed no important clinical response on either scale. The maximum dose was 250 mg/day for most adults and 3 mg/kg/day (up to 200 mg) for all children and adolescents.

The effectiveness of Depramine for long-term use (i.e., for more than 10 weeks) has not been systematically evaluated in placebo-controlled trials. The physician who elects to use Depramine for extended periods should periodically reevaluate the long-term usefulness of the drug for the individual patient.

How should I use Depramine?

Use Depramine as directed by your doctor. Check the label on the medicine for exact dosing instructions.

Ask your health care provider any questions you may have about how to use Depramine.

Uses of Depramine in details

There are specific as well as general uses of a drug or medicine. A medicine can be used to prevent a disease, treat a disease over a period or cure a disease. It can also be used to treat the particular symptom of the disease. The drug use depends on the form the patient takes it. It may be more useful in injection form or sometimes in tablet form. The drug can be used for a single troubling symptom or a life-threatening condition. While some medications can be stopped after few days, some drugs need to be continued for prolonged period to get the benefit from it.
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Use: Labeled Indications

Obsessive-compulsive disorder: Treatment of obsessive-compulsive disorder

Off Label Uses

Major depressive disorder

Data from randomized, double-blind studies supports the use of Depramine in the treatment of major depressive disorder. Additional trials may be necessary to further define the role of Depramine in this condition.

According to the American Psychiatric Association treatment guidelines, Depramine is effective and recommended for the management of major depressive disorder. Although the WFSBP treatment guidelines also recommend Depramine, particularly for patients with severe depression or concomitant obsessive-compulsive disorder, the guidelines recommend prescribing a limited supply for severely depressed patients at risk of overdose.

Panic disorder

Data from randomized, double-blind, placebo-controlled studies supports the use of Depramine in the management of panic disorder with or without agoraphobia to decrease severity of anxiety and phobias, as well as severity and frequency of panic attacks. Additional trials may be necessary to further define the role of Depramine in this condition.

Based on the American Psychiatric Association guidelines for the treatment of panic disorder, selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), and benzodiazepines all have roughly comparable efficacy in the treatment of panic disorder, but SSRIs are likely to have the most favorable balance of efficacy and adverse effects for most patients. Based on the Canadian Psychiatric Association guidelines for the management of anxiety disorders, TCAs like Depramine are second-line choices for panic disorder. Based on the World Federation of the Societies of Biological Psychiatry guidelines for the management of anxiety disorders, TCAs are recommended in panic disorder in patients who have not responded to SSRIs or SNRIs.

Depramine description

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Depramine, the 3-chloro analog of imipramine, is a dibenzazepine-derivative tricyclic antidepressant (TCA). TCAs are structurally similar to phenothiazines. They contain a tricyclic ring system with an alkyl amine substituent on the central ring. In non-depressed individuals, Depramine does not affect mood or arousal, but may cause sedation. In depressed individuals, Depramine exerts a positive effect on mood. TCAs are potent inhibitors of serotonin and norepinephrine reuptake. Tertiary amine TCAs, such as Depramine, are more potent inhibitors of serotonin reuptake than secondary amine TCAs, such as nortriptyline and desipramine. TCAs also down-regulate cerebral cortical β-adrenergic receptors and sensitize post-synaptic serotonergic receptors with chronic use. The antidepressant effects of TCAs are thought to be due to an overall increase in serotonergic neurotransmission. TCAs also block histamine-H1 receptors, α1-adrenergic receptors and muscarinic receptors, which accounts for their sedative, hypotensive and anticholinergic effects (e.g. blurred vision, dry mouth, constipation, urinary retention), respectively. See toxicity section below for a complete listing of side effects. Depramine may be used to treat obsessive-compulsive disorder and disorders with an obsessive-compulsive component (e.g. depression, schizophrenia, Tourette’s disorder). Unlabeled indications include panic disorder, chronic pain (e.g. central pain, idiopathic pain disorder, tension headache, diabetic peripheral neuropathy, neuropathic pain), cataplexy and associated narcolepsy, autistic disorder, trichotillomania, onchophagia, stuttering, premature ejaculation, and premenstrual syndrome. Depramine is rapidly absorbed from the gastrointestinal tract and demethylated in the liver to its primary active metabolite, desmethylclomipramine.

Depramine dosage

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Depramine Dosage

Generic name: Depramine HYDROCHLORIDE 25mg

Dosage form: capsule

The information at Drugs.com is not a substitute for medical advice. Always consult your doctor or pharmacist.

The treatment regimens described below are based on those used in controlled clinical trials of Depramine in 520 adults, and 91 children and adolescents with OCD. During initial titration, Depramine should be given in divided doses with meals to reduce gastrointestinal side effects. The goal of this initial titration phase is to minimize side effects by permitting tolerance to side effects to develop or allowing the patient time to adapt if tolerance does not develop.

Because both CMI and its active metabolite, DMI, have long elimination half-lives, the prescriber should take into consideration the fact that steady-state plasma levels may not be achieved until 2 to 3 weeks after dosage change. Therefore, after initial titration, it may be appropriate to wait 2 to 3 weeks between further dosage adjustments.

Initial Treatment/Dose Adjustment (Adults)

Treatment with Depramine should be initiated at a dosage of 25 mg daily and gradually increased, as tolerated, to approximately 100 mg during the first 2 weeks. During initial titration, Depramine should be given in divided doses with meals to reduce gastrointestinal side effects. Thereafter, the dosage may be increased gradually over the next several weeks, up to a maximum of 250 mg daily. After titration, the total daily dose may be given once daily at bedtime to minimize daytime sedation.

Initial Treatment/Dose Adjustment (Children and Adolescents)

As with adults, the starting dose is 25 mg daily and should be gradually increased (also given in divided doses with meals to reduce gastrointestinal side effects) during the first 2 weeks, as tolerated, up to a daily maximum of 3 mg/kg or 100 mg, whichever is smaller. Thereafter, the dosage may be increased gradually over the next several weeks up to a daily maximum of 3 mg/kg or 200 mg, whichever is smaller. As with adults, after titration, the total daily dose may be given once daily at bedtime to minimize daytime sedation.

Maintenance/Continuation Treatment (Adults, Children, and Adolescents)

While there are no systematic studies that answer the question of how long to continue Depramine, OCD is a chronic condition and it is reasonable to consider continuation for a responding patient. Although the efficacy of Depramine after 10 weeks has not been documented in controlled trials, patients have been continued in therapy under double-blind conditions for up to 1 year without loss of benefit. However, dosage adjustments should be made to maintain the patient on the lowest effective dosage, and patients should be periodically reassessed to determine the need for treatment. During maintenance, the total daily dose may be given once daily at bedtime.

Switching a Patient To or From a Monoamine Oxidase Inhibitor (MAOI) Intended to Treat Psychiatric Disorders

At least 14 days should elapse between discontinuation of an MAOI intended to treat psychiatric disorders and initiation of therapy with Depramine. Conversely, at least 14 days should be allowed after stopping Depramine before starting an MAOI intended to treat psychiatric disorders.

Use of Depramine With Other MAOIs, Such as Linezolid or Methylene Blue

Do not start Depramine in a patient who is being treated with linezolid or intravenous methylene blue because there is increased risk of serotonin syndrome. In a patient who requires more urgent treatment of a psychiatric condition, other interventions, including hospitalization, should be considered.

In some cases, a patient already receiving Depramine therapy may require urgent treatment with linezolid or intravenous methylene blue. If acceptable alternatives to linezolid or intravenous methylene blue treatment are not available and the potential benefits of linezolid or intravenous methylene blue treatment are judged to outweigh the risks of serotonin syndrome in a particular patient, Depramine should be stopped promptly, and linezolid or intravenous methylene blue can be administered. The patient should be monitored for symptoms of serotonin syndrome for two weeks or until

24 hours after the last dose of linezolid or intravenous methylene blue, whichever comes first. Therapy with Depramine may be resumed 24 hours after the last dose of linezolid or intravenous methylene blue.

The risk of administering methylene blue by non-intravenous routes (such as oral tablets or by local injection) or in intravenous doses much lower than 1 mg/kg with Depramine is unclear. The clinician should, nevertheless, be aware of the possibility of emergent symptoms of serotonin syndrome with such use.

More about Depramine (Depramine)

Consumer resources

Professional resources

Related treatment guides

Depramine interactions

See also:
What other drugs will affect Depramine?

The risks of using Depramine in combination with other drugs have not been systematically evaluated. Given the primary CNS effects of Depramine, caution is advised in using it concomitantly with other CNS-active drugs. Depramine should not be used with MAO inhibitors.

Close supervision and careful adjustment of dosage are required when Depramine is administered with anticholinergic or sympathomimetic drugs.

Several tricyclic antidepressants have been reported to block the pharmacologic effects of guanethidine, clonidine, or similar agents, and such an effect may be anticipated with CMI because of its structural similarity to other tricyclic antidepressants.

The plasma concentration of CMI has been reported to be increased by the concomitant administration of haloperidol; plasma levels of several closely related tricyclic antidepressants have been reported to be increased by the concomitant administration of methylphenidate or hepatic enzyme inhibitors (e.g., cimetidine, fluoxetine) and decreased by the concomitant administration of hepatic enzyme inducers (e.g., barbiturates, phenytoin), and such an effect may be anticipated with CMI as well. Administration of CMI has been reported to increase the plasma levels of phenobarbital, if given concomitantly.

Drugs Metabolized By P450 2D6

The biochemical activity of the drug metabolizing isozyme cytochrome P450 2D6 (debrisoquin hydroxylase) is reduced in a subset of the Caucasian population (about 7% to 10% of Caucasians are so-called “poor metabolizers”); reliable estimates of the prevalence of reduced P450 2D6 isozyme activity among Asian, African and other populations are not yet available. Poor metabolizers have higher than expected plasma concentrations of tricyclic antidepressants (TCAs) when given usual doses. Depending on the fraction of drug metabolized by P450 2D6, the increase in plasma concentration may be small, or quite large (8 fold increase in plasma AUC of the TCA). In addition, certain drugs inhibit the activity of this isozyme and make normal metabolizers resemble poor metabolizers. An individual who is stable on a given dose of TCA may become abruptly toxic when given one of these inhibiting drugs as concomitant therapy. The drugs that inhibit cytochrome P450 2D6 include some that are not metabolized by the enzyme (quinidine; cimetidine) and many that are substrates for P450 2D6 (many other antidepressants, phenothiazines, and the Type 1C antiarrhythmics propafenone and flecainide). While all the selective serotonin reuptake inhibitors (SSRIs), e.g., fluoxetine, sertraline, paroxetine, and fluvoxamine, inhibit P450 2D6, they may vary in the extent of inhibition. Fluvoxamine has also been shown to inhibit P450 1A2, an isoform also involved in TCA metabolism. The extent to which SSRI-TCA interactions may pose clinical problems will depend on the degree of inhibition and the pharmacokinetics of the SSRI involved. Nevertheless, caution is indicated in the co-administration of TCAs with any of the SSRIs and also in switching from one class to the other. Of particular importance, sufficient time must elapse before initiating TCA treatment in a patient being withdrawn from fluoxetine, given the long half-life of the parent and active metabolite (at least 5 weeks may be necessary). Concomitant use of agents in the tricyclic antidepressant class (which includes Depramine) with drugs that can inhibit cytochrome P450 2D6 may require lower doses than usually prescribed for either the tricyclic antidepressant agent or the other drug. Furthermore, whenever one of these drugs is withdrawn from co-therapy, an increased dose of tricyclic antidepressant agent may be required. It is desirable to monitor TCA plasma levels whenever an agent of the tricyclic antidepressant class including Depramine is going to be co-administered with another drug known to be an inhibitor of P450 2D6 (and/or P450 1A2).

Because Depramine is highly bound to serum protein, the administration of Depramine to patients taking other drugs that are highly bound to protein (e.g., warfarin, digoxin) may cause an increase in plasma concentrations of these drugs, potentially resulting in adverse effects. Conversely, adverse effects may result from displacement of protein-bound Depramine by other highly bound drugs.

Monoamine Oxidase Inhibitors (MAOIs )

Serotonergic Drugs

Depramine side effects

See also:
What are the possible side effects of Depramine?

Applies to Depramine: oral capsule, oral tablet

In addition to its needed effects, some unwanted effects may be caused by Depramine (the active ingredient contained in Depramine). In the event that any of these side effects do occur, they may require medical attention.

Major Side Effects

You should check with your doctor immediately if any of these side effects occur when taking Depramine:

More common:

Less common:

Minor Side Effects

Some of the side effects that can occur with Depramine may not need medical attention. As your body adjusts to the medicine during treatment these side effects may go away. Your health care professional may also be able to tell you about ways to reduce or prevent some of these side effects. If any of the following side effects continue, are bothersome or if you have any questions about them, check with your health care professional:

More common:

Less common:

Depramine contraindications

See also:
What is the most important information I should know about Depramine?

Depramine is contraindicated in patients with a history of hypersensitivity to Depramine or other tricyclic antidepressants.

Monoamine Oxidase Inhibitors (MAOIs)

The use of MAOIs intended to treat psychiatric disorders with Depramine or within 14 days of stopping treatment with Depramine is contraindicated because of an increased risk of serotonin syndrome. The use of Depramine within 14 days of stopping an MAOI intended to treat psychiatric disorders is also contraindicated.

Starting Depramine in a patient who is being treated with linezolid or intravenous methylene blue is also contraindicated because of an increased risk of serotonin syndrome.

Myocardial Infarction

Depramine is contraindicated during the acute recovery period after a myocardial infarction.

Active ingredient matches for Depramine:

Clomipramine in Pakistan.


Unit description / dosage (Manufacturer)Price, USD
DEPRAMINE 2MG TABLET 1 strip / 10 tablets each (RKG Pharma)$ 0.14
DEPRAMINE 5MG TABLET 1 strip / 10 tablets each (RKG Pharma)$ 0.14
DEPRAMINE 75MG TABLET 1 strip / 10 tablets each (RKG Pharma)$ 0.56
Depramine 5mg Tablet (RKG Pharma)$ 0.01
Depramine 75mg Tablet (RKG Pharma)$ 0.06

List of Depramine substitutes (brand and generic names):

Depnil 75mg Tablet (Tas Med (I) Pvt. Ltd.)$ 0.49
Tablet; Oral; Clomipramine Hydrochloride 25 mg
Tablet; Oral; Clomipramine Hydrochloride 50 mg
Dom-clomipramine tablet 25 mg (Dominion Pharmacal (Canada))
Dom-clomipramine tablet 50 mg (Dominion Pharmacal (Canada))
For-You 25 mg
Tablet; Oral; Clomipramine Hydrochloride 10 mg
Tablet; Oral; Clomipramine Hydrochloride 25 mg
Tablet; Oral; Clomipramine Hydrochloride 50 mg
Tablet; Oral; Clomipramine Hydrochloride 25 mg
Dragee; Oral; Clomipramine Hydrochloride 25 mg (Arzneimittelwerk Dresden)
Tablet, Film-Coated; Oral; Clomipramine Hydrochloride 10 mg (Arzneimittelwerk Dresden)
10 mg x 100's (Sunrise)$ 3.02
25 mg x 100's (Sunrise)$ 5.16
50 mg x 100's (Sunrise)$ 8.73
75 mg x 100's (Sunrise)$ 13.89
Imi-CI 10mg TAB / 100 (Sunrise)$ 3.02
Imi-CI 25mg TAB / 100 (Sunrise)$ 5.16
Imi-CI 50mg TAB / 100 (Sunrise)$ 8.73
Imi-CI 75mg TAB / 100 (Sunrise)$ 13.89
IMI-CI tab 10 mg x 10's (Sunrise)$ 0.30
IMI-CI tab 25 mg x 10's (Sunrise)$ 0.52
IMI-CI tab 50 mg x 10's (Sunrise)$ 0.87
IMI-CI tab 75 mg x 10's (Sunrise)$ 1.39
Imi-CI 10mg TAB / 100 (Sunrise)$ 3.02
Imi-CI 25mg TAB / 100 (Sunrise)$ 5.16
Imi-CI 50mg TAB / 100 (Sunrise)$ 8.73
Imi-CI 75mg TAB / 100 (Sunrise)$ 13.89
KLOMIN 25MG TABLET 1 strip / 10 tablets each (RKG Pharma)$ 0.56
KLOMIN 50MG TABLET 1 strip / 10 tablets each (RKG Pharma)$ 0.95
Klomin 50mg Tablet (RKG Pharma)$ 0.10
Mario 25mg TAB / 10 (Esma)$ 0.60
25 mg x 10's (Esma)$ 0.60
MARIO tab 25 mg x 10's (Esma)$ 0.60
Tablet; Oral; Clomipramine Hydrochloride 25 mg (Unipharm)

References

  1. PubChem. "Depramine". https://pubchem.ncbi.nlm.nih.gov/com... (accessed September 17, 2018).
  2. PubChem. "clomipramine". https://pubchem.ncbi.nlm.nih.gov/com... (accessed September 17, 2018).
  3. DrugBank. "clomipramine". http://www.drugbank.ca/drugs/DB01242 (accessed September 17, 2018).

Reviews

The results of a survey conducted on ndrugs.com for Depramine are given in detail below. The results of the survey conducted are based on the impressions and views of the website users and consumers taking Depramine. We implore you to kindly base your medical condition or therapeutic choices on the result or test conducted by a physician or licensed medical practitioners.

User reports

1 consumer reported useful

Was the Depramine drug useful in terms of decreasing the symptom or the disease?
According to the reports released by ndrugs.com website users, the below mentioned percentages of users say the drug is useful / not useful to them in decreasing their symptoms/disease. The usefulness of the drug depends on many factors, like severity of the disease, perception of symptom, or disease by the patient, brand name used [matters only to a certain extent], other associated conditions of the patient. If the drug is not effective or useful in your case, you need to meet the doctor to get re-evaluated about your symptoms/disease, and he will prescribe an alternative drug.
Users%
Useful1
100.0%


Consumer reported price estimates

No survey data has been collected yet


1 consumer reported time for results

To what extent do I have to use Depramine before I begin to see changes in my health conditions?
As part of the reports released by ndrugs.com website users, it takes 1 month and a few days before you notice an improvement in your health conditions.
Please note, it doesn't mean you will start to notice such health improvement in the same time frame as other users. There are many factors to consider, and we implore you to visit your doctor to know how long before you can see improvements in your health while taking Depramine. To get the time effectiveness of using Depramine drug by other patients, please click here.
Users%
1 month1
100.0%


2 consumers reported age

Users%
46-602
100.0%


Consumer reviews


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Information checked by Dr. Sachin Kumar, MD Pharmacology

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