Saroten - General Information:

Tricyclic antidepressant with anticholinergic and sedative properties. It appears to prevent the re-uptake of norepinephrine and serotonin at nerve terminals, thus potentiating the action of these neurotransmitters. Saroten also appears to antagonize cholinergic and alpha-1 adrenergic responses to bioactive amines. [PubChem]

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Elavil (Amitriptyline) is a tricyclic antidepressant used to treat depression. It may also be used to treat chronic pain and other conditions as determined by your doctor.

Pharmacology:

Saroten, a tertiary amine tricyclic antidepressant, is structurally related to both the skeletal muscle relaxant cyclobenzaprine and the thioxanthene antipsychotics such as thiothixene. It is extremely sedating, and thus improvement of sleep patterns can be the first benefit of treatment. Saroten exhibits strong anticholinergic activity, cardiovascular effects including orthostatic hypotension, changes in heart rhythm and conduction, and a lowering of the seizure threshold. As with other antidepressants, several weeks of therapy may be required in order to realize the full clinical benefit of amitriptyline. Although not a labelled indication, amitriptyline is widely used in the management of chronic nonmalignant pain (e.g., post-herpetic neuralgia, fibromyalgia).

Saroten for patients

While on therapy with amitriptyline HCl, patients should be advised as to the possible impairment of mental and/or physical abilities required for performance of hazardous tasks, such as operating machinery or driving a motor vehicle.

Saroten Interactions

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 7-10% 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, and paroxetine, inhibit P450 2D6, they may vary in the extent of inhibition. 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 coadministration 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 tricyclic antidepressants with drugs that can inhibit cytochrome P450 2D6 may require lower doses than usually prescribed for either the tricyclic antidepressant or the other drug. Furthermore, whenever one of these other drugs is withdrawn from co-therapy, an increased dose of tricyclic antidepressant may be required. It is desirable to monitor TCA plasma levels whenever a TCA is going to be coadministered with another drug known to be an inhibitor of P450 2D6.

Monoamine Oxidase Inhibitors: Guanethidine or similarly acting compounds; thyroid medication; alcohol, barbiturates and other CNS depressants; and disulfiram

When amitriptyline HCl is given with anticholinergic agents or sympathomimetic drugs, including epinephrine combined with local anesthetics, close supervision and careful adjustment of dosages are required.

Hyperpyrexia has been reported when amitriptyline HCl is administered with anticholinergic agents or with neuroleptic drugs, particularly during hot weather.

Paralytic ileus may occur in patients taking tricyclic antidepressants in combination with anticholinergic-type drugs.

Cimetidine is reported to reduce hepatic metabolism of certain tricyclic antidepressants, thereby delaying elimination and increasing steady-state concentrations of these drugs. Clinically significant effects have been reported with the tricyclic antidepressants when used concomitantly with cimetidine. Increases in plasma levels of tricyclic antidepressants, and in the frequency and severity of side effects, particularly anticholinergic, have been reported when cimetidine was added to the drug regimen. Discontinuation of cimetidine in well-controlled patients receiving tricyclic antidepressants and cimetidine may decrease the plasma levels and efficacy of the antidepressants.

Caution is advised if patients receive large doses of ethchlorvynol concurrently. Transient delirium has been reported in patients who were treated with one gram of ethchlorvynol and 75 - 150 mg of amitriptyline HCl.

Saroten Contraindications

Amitriptyline HCl is contraindicated in patients who have shown prior hypersensitivity to it.

It should not be given concomitantly with monoamine oxidase inhibitors. Hyperpyretic crises, severe convulsions, and deaths have occurred in patients receiving tricyclic antidepressant and monoamine oxidase inhibiting drugs simultaneously. When it is desired to replace a monoamine oxidase inhibitor with amitriptyline HCl, a minimum of 14 days should be allowed to elapse after the former is discontinued. Amitriptyline HCl should then be initiated cautiously with gradual increase in dosage until optimum response is achieved.

This drug is not recommended for use during the acute recovery phase following myocardial infarction.

Additional information about Saroten

Saroten Indication: For the treatment of anxiety, bipolar disorders, and depression.
Mechanism Of Action: Saroten is metabolized to nortriptyline which inhibits the reuptake of norepinephrine and serotonin almost equally. Saroten inhibits the membrane pump mechanism responsible for uptake of norepinephrine and serotonin in adrenergic and serotonergic neurons. Pharmacologically this action may potentiate or prolong neuronal activity since reuptake of these biogenic amines is important physiologically in terminating transmitting activity. This interference with the reuptake of norepinephrine and/or serotonin is believed by some to underlie the antidepressant activity of amitriptyline.
Drug Interactions: Altretamine Risk of severe hypotension
Atazanavir Atazanavir increases the effect and toxicity of tricyclics
Carbamazepine The tricyclics increases the effect of carbamazepine
Cimetidine Cimetidine increases the effect of tricyclic agent
Cisapride Increased risk of cardiotoxicity and arrhythmias
Grepafloxacin Increased risk of cardiotoxicity and arrhythmias
Clonidine The tricyclic decreases the effect of clonidine
Dihydroquinidine barbiturate Quinidine increases the effect of tricyclic agent
Dobutamine The tricyclic increases the sympathomimetic effect
Donepezil Possible antagonism of action
Dopamine The tricyclic increases the sympathomimetic effect
Duloxetine Possible increase in the levels of this agent when used with duloxetine
Epinephrine The tricyclic increases the sympathomimetic effect
Fenoterol The tricyclic increases the sympathomimetic effect
Fluconazole The imidazole increases the effect and toxicity of the tricyclic
Fluoxetine Fluoxetine increases the effect and toxicity of tricyclics
Fluvoxamine Fluvoxamine increases the effect and toxicity of tricyclics
Galantamine Possible antagonism of action
Guanethidine The tricyclic decreases the effect of guanethidine
Isocarboxazid Possibility of severe adverse effects
Isoproterenol The tricyclic increases the sympathomimetic effect
Ketoconazole The imidazole increases the effect and toxicity of the tricyclic
Metaraminol The tricyclic increases the sympathomimetic effect
Mesoridazine Increased risk of cardiotoxicity and arrhythmias
Methoxamine The tricyclic increases the sympathomimetic effect
Moclobemide Possible severe adverse reaction with this combination
Norepinephrine The tricyclic increases the sympathomimetic effect
Orciprenaline The tricyclic increases the sympathomimetic effect
Phenelzine Possibility of severe adverse effects
Phenylephrine The tricyclic increases the sympathomimetic effect
Phenylpropanolamine The tricyclic increases the sympathomimetic effect
Pirbuterol The tricyclic increases the sympathomimetic effect
Pseudoephedrine The tricyclic increases the sympathomimetic effect
Quinidine Quinidine increases the effect of tricyclic agent
Quinidine barbiturate Quinidine increases the effect of tricyclic agent
Rifabutin The rifamycin decreases the effect of tricyclics
Rifampin The rifamycin decreases the effect of tricyclics
Ritonavir Ritonavir increases the effect and toxicity of tricyclics
Rivastigmine Possible antagonism of action
Sibutramine Increased risk of CNS adverse effects
Sparfloxacin Increased risk of cardiotoxicity and arrhythmias
Terbutaline The tricyclic increases the sympathomimetic effect
Terfenadine Increased risk of cardiotoxicity and arrhythmias
Thioridazine Increased risk of cardiotoxicity and arrhythmias
Tranylcypromine Possibility of severe adverse effects
Ephedra The tricyclic increases the sympathomimetic effect
Ephedrine The tricyclic increases the sympathomimetic effect
Mephentermine The tricyclic increases the sympathomimetic effect
Procaterol The tricyclic increases the sympathomimetic effect
Rasagiline Possibility of severe adverse effects
Salbutamol The tricyclic increases the sympathomimetic effect
Food Interactions: Avoid alcohol.
Take with food to reduce irritation.
Avoid excessive quantities of coffee or tea (Caffeine).
Avoid St.John's Wort.
Generic Name: Amitriptyline
Synonyms: Amitriptyline Hydrochloride; Amitriptyline HCL; Amitriprolidine; Amitriptylin; Amitryptiline; Amitryptyline; Amytriptiline
Drug Category: Analgesics, Non-Narcotic; Antidepressive Agents, Tricyclic; Adrenergic Uptake Inhibitors
Drug Type: Small Molecule; Approved
Other Brand Names containing Amitriptyline: Adepress; Adepril; Amitid; Amitril; Damilan; Damilen; dAmitriptyline; Elanil; Elavil; Endep; Flavyl; Hexathane; Horizon; Lantron; Laroxil; Laroxyl; Lentizol; Proheptadiene; Redomex; Saroten; Sarotex; Seroten; Sylvemid; Triptanol; Triptilin; Triptisol; Tryptanol; Tryptizol;
Absorption: Rapidly and well absorbed following oral administration (bioavailability is 30-60% due to first pass metabolism).
Toxicity (Overdose): LD50=350 mg/kg (in mice). Symptoms of overdose include abnormally low blood pressure, confusion, convulsions, dilated pupils and other eye problems, disturbed concentration, drowsiness, hallucinations, impaired heart function, rapid or irregular heartbeat, reduced body temperature, stupor, and unresponsiveness or coma.
Protein Binding: Very highly protein bound (90% or more) in plasma and tissues
Biotransformation: Exclusively hepatic, with first pass effect. Amitriptyline is demethylated in the liver to its primary active metabolite, nortriptyline.
Half Life: 10 to 50 hours, with an average of 15 hours
Dosage Forms of Saroten: Tablet Oral
Chemical IUPAC Name: 3-(10,11-dihydro-5H-dibenzo-[a,d]cyclohepten-5-ylidene)-N,N-dimethyl-1-propanamine
Chemical Formula: C20H23N
Amitriptyline on Wikipedia: http://en.wikipedia.org/wiki/Amitriptyline
Organisms Affected: Humans and other mammals

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