Imipramine

280.41

280.41

200-042-1

OGG85SX4E4

169866

DTXSID1043881

C62039

White to off-white /hydrochloride/

N - Nervous system

2933990090

6.5

4.80

Solid

1.041g/cm3

174.5 °C

160 °C @ Press: 0.1 Torr

179.7ºC

1.574

18.23mg/L(24 ºC)

Odorless /hydrochloride/

9.4None

9.4

166.5 Ų [M+H]+ [CCS Type: TW, Method: Major Mix IMS/Tof Calibration Kit (Waters)]|165.3 Ų [M+H]+ [CCS Type: DT, Method: single field calibrated]

Imipramine hydrochloride turns yellowish or reddish on exposure to light; slight discoloration does not affect potency, but marked discoloration is associated with loss of potency. Solutions of imipramine hydrochloride are stable at pH 4-5. During storage, minute crystals may form in the injection; the efficacy of the preparation is unaltered if the crystals are redissolved by immersing the ampul in hot water for 1 minute. /Imipramine hydrochloride/

P264, P270, P273, P301+P312, P330, P391, P501

H302

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).

A REVIEW ON MECHANISM OF ACTION.[COSTA E ET AL; MOLECULAR MECHANISMS IN THE ACTION OF IMIPRAMINE; EXPERIENTIA 39(8) 855 (1983)]

|Warning|H302 (50%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P273, P301+P312, P330, P391, and P501|Aggregated GHS information provided by 8 companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

The anticholinergic actvity of imipramine can produce dry mucous membranes, blurred vision, increased intraocular pressure, hyperthermia, constipation, adynamic ileus, urinary retention, delayed micturition, and dilation of the urinary tract. Central nervous system and neuromuscular effects include drowsiness, lethargy, fatigue, agitation, excitement, nightmares, restlessness, insomnia, confusion, disturbed concentration, disorientation, delusions, and hallucinations. Effects on the GI tract include anorexia, nausea and vomiting, diarrhea, abdominal cramps, increases in pancreatic enzymes, epigastric distress, stomatitis, peculiar taste, and black tongue. Rarely agranulocytosis, thrombocytopenia, eosinophilia, leukopenia, and purpura have occured. Infants whose mothers were receiving tricyclic antidepressants prior to delivery have experienced cardiac problems, irritability, respiratory distress, muscle spasms, seizures, and urinary retention. Serotonin syndrome can occur when used in conjunction with other pro-serotonergic drugs. ### LD50 Values Rat - Oral 250 mg/kg - Intraperitoneal 79mg/kg - Subcutaneous 250 mg/kg - Intravenous 15.9 mg/kg Mouse - Oral 188 mg/kg - Intraperitoneal 51.6 mg/kg - Subcutaneous 195 μg/kg - Intravenous 21 mg/kg Human range of toxicity is considered to include single dosages greater than 5 mg/kg.|IDENTIFICATION: Imipramine is a tricyclic antidepressant drug. Properties of the substance: Imipramine hydrochloride is a white or slightly yellow, odorless or almost odorless, crystalline powder. It is soluble in water, alcohol, chloroform, and acetone; practically insoluble in ether. Indications: Treatment of depression; nocturnal enuresis in children HUMAN EXPOSURE: Main risks and target organs: Affects the parasympathetic nervous system, central nervous system, and cardiovascular system. Summary of clinical effects: Early symptoms: mydriasis, blurred vision, dry mouth, tachycardia, hyperpyrexia, urinary retention, decreased intestinal peristalsis, and CNS excitation. Extrapyramidal symptoms may occur. Later more serious features: convulsions, coma, hypotension, arrhythmias, and cardiorespiratory arrest. The progression from being alert with mild symptoms to life-threatening toxic effects may be extremely rapid. Contraindications: Epilepsy, organic brain damage, urine retention, heart diseases, acute glaucoma. Hyperthyroidism and liver diseases are a relative contraindication. Routes of entry: Oral: Preferred route of administration. Parenteral: In the initial stages of treatment, if administration by mouth is impracticable or inadvisable imipramine may be given by intramuscular injection. Absorption by route of exposure: Oral: absorption occurs in the small intestine with little or no absorption in the stomach. Absorption is virtually complete (95%). The peak plasma concentration occurs 2 to 6 hours after administration. Food does not affect absorption, peak concentration or time to peak concentration. Large doses may be absorbed more slowly due to delayed gastric emptying and reduced peristalsis. Large amounts of imipramine, including intact pill fragments, have been recovered at autopsy. Parenteral: absorption appears to be complete since recovery of urinary metabolites is the same after either oral or parenteral administration. Distribution by route of exposure: Imipramine is lipophilic and therefore widely distributed in the body. Distribution is influenced by the degree of binding to plasma proteins. Plasma protein binding of imipramine ranges from 60 to 96%. Biological half-life by route of exposure: The half-life of imipramine is approximately 20 hours. Its active metabolite desipramine has a half-life of up to 125 hours. Metabolism: Imipramine is metabolised almost exclusively in the liver, undergoing oxidation by microsomal enzymes, followed by conjugation with glucuronic acid. Imipramine is mainly metabolised by demethylation to an active metabolite desipramine, and to a lesser extent by aromatic 2-hydroxylation to 2-hydroxyimipramine. Desipramine is metabolised by aromatic 2-hydroxylation to 2-hydroxydesimipramine. Quantitatively, hydroxylation is the most important intermediate metabolic pathway and it is the rate-limiting step for the elimination of imipramine and desimipramine. The greater plasma elimination half-life for desimipramine compared with imipramine may be due to a lower rate of hydroxylation. Both imipramine and desimipramine undergo substantial and highly variable first-pass metabolism, the extent of which is determined by oxidative phenotype. In Caucasians, there are slow and fast metabolizers: at least 6.5 to 10% of the population are slow metabolizers. First-pass metabolism of imipramine and desimipramine is reduced in slow metabolizers. Smoking, alcohol ingestion and other drugs may influence imipramine and desimipramine metabolism by altering the mixed function oxidase system: Smokers have lower steady-state levels of imipramine than non-smokers. Alcoholics were found to have a 3-fold greater intrinsic clearance of imipramine. Cimetidine increases the bioavailability of imipramine by 40 to 75%. Some drugs, such as haloperidol, disulfiram, and morphine, may prolong toxicity by inhibiting hydroxylation. Elimination by route of exposure: Less than 5% of an oral dose of imipramine is excreted unchanged in the urine. In patients with chronic renal failure, disproportionate increases in hydroxymetabolite concentration may occur. Mode of action: Toxicodynamics: Anticholinergic effects: increased heart rate. Quinidine-like effects on the heart due to slowing of sodium influx and potassium efflux, resulting in slowing of conduction and repolarization. Slowing of conduction notably occurs at the His-Purkinje portion of the atrioventricular conduction system resulting in prolongation of the PR- and QRS- intervals. Prolonged depolarization results in lengthening of the QT-interval. Peripheral receptor blockade may cause orthostatic hypotension. Pharmacodynamics: The probable mechanism of antidepressant activity is central inhibition of biogenic amine reuptake, predominantly affecting norepinephrine and serotonin. In addition to its central effects, imipramine is also a competitive antagonist at histamine H1 and H2 receptors. Interactions: Effect on imipramine itself: potentiation due to reduced hepatic metabolism by: neuroleptic drugs, methylphenidate, and certain steroids, including oral contraceptives. Reduced effect due to enhanced hepatic metabolism by barbiturates, certain other sedatives, and cigarette smoking. Effect of imipramine on other substances. Potentiates the effect of alcohol and probably other CNS depressants. Potentiates the anticholinergic effects of anticholinergic drugs used in the treatment of Parkinson's disease. Potentiates the effect of biogenic amines, such as norepinephrine, which are normally removed from their site of action by neuronal reuptake. Blocks the effects of indirectly acting amines, such as tyramine. Prevents the action of adrenergic neuron blocking agents such as guanethidine. Potentiates central nervous stimulation by amphetamine but blocks its peripheral effects. A particularly severe interaction occurs with concurrent administration of an MAO inhibitor and a tricyclic antidepressant. The resultant syndrome can include severe CNS toxicity, marked by hyperpyrexia, convulsions and coma. Main adverse effects: Antimuscarinic effects include dry mouth, a sour or metallic taste, epigastric distress, constipation, dizziness, tachycardia, palpitations, blurred vision and urinary retention. Paradoxically, excessive sweating. Weakness and fatigue. Older patients suffer more from dizziness, postural hypotension, constipation, delayed micturition, oedema, and muscle tremors. In approximately 10% of treated patients and in over 30% of patients over age 50, manic reactions, confusion, or delirium may occur. Extrapyramidal reactions are rare, though tremor is not unusual. A withdrawal syndrome, may occur in children, who experience gastrointestinal symptoms.

Liver test abnormalities have been reported to occur in up to 20% of patients on long term therapy with imipramine, but elevations are uncommonly above 3 times the upper limit of normal. The aminotransferase abnormalities are usually mild, asymptomatic and transient, reversing even with continuation of medication. Rare instances of clinically apparent acute liver injury as well as prolonged jaundice have been reported due to imipramine. The onset of jaundice is usually with 1 to 8 weeks of starting therapy. The pattern of enzyme elevations varies from hepatocellular to mixed or cholestatic. Signs and symptoms of hypersensitivity (fever, rash, eosinophilia) are common, but usually not very prominent. Rapid recurrence with rechallenge is common. Autoantibody formation is rare. Rare instances of acute liver failure and death attributed to imipramine have been reported.

A PARTICULARLY SEVERE, BUT RARE, INTERACTION HAS BEEN NOTED FOLLOWING THE CONCURRENT ADMINISTRATION OF AN MAO /MONOAMINE OXIDASE/ INHIBITOR AND A TRICYCLIC ANTIDEPRESSANT. /TRICYCLIC ANTIDEPRESSANTS/|...INTERACTIONS INCL POTENTIATION OF CENTRAL DEPRESSANT DRUGS, BLOCKADE OF ANTIHYPERTENSIVE EFFECTS OF GUANETHIDINE, & AUGMENTATION OF PRESSOR EFFECTS OF SYMPATHOMIMETIC AMINES. INTERACTIONS WITH THYROID PREPN, METHYLPHENIDATE, & PHENOTHIAZINES, ALL OF WHICH MAY ENHANCE...EFFECT... /TRICYCLIC ANTIDEPRESSANTS/|CHRONIC ADMIN OF EITHER IMIPRAMINE OR DESMETHYLIMIPRAMINE SIGNIFICANTLY INCR THE CARDIOTOXICITY OF DIGOXIN...|THEY /TRICYCLIC COMPOUNDS/ POTENTIATE THE EFFECTS OF ANTIHISTAMINICS; ANTIMUSCARINICS, AND OTHER CENTRAL NERVOUS SYSTEM DEPRESSANTS... /TRICYCLIC ANTIDEPRESSANTS/|For more Interactions (Complete) data for IMIPRAMINE (26 total), please visit the HSDB record page.

LD50 Rat oral 250 mg/kg|LD50 Rat ip 79 mg/kg|LD50 Rat sc 250 mg/kg|LD50 Rat iv 15900 ug/kg|For more Non-Human Toxicity Values (Complete) data for IMIPRAMINE (8 total), please visit the HSDB record page.

Imipramine is 60-96% bound to plasma proteins in circulation. It is known to bind albumin, α1-acid glycoprotein, and lipoproteins.

For the relief of symptoms of depression and as temporary adjunctive therapy in reducing enuresis in children aged 6 years and older. May also be used off-label to manage panic disorders with or without agoraphobia, as a second line agent for ADHD in children and adolescents, to manage bulimia nervosa, for short-term management of acute depressive episodes in bipolar disorder and schizophrenia, for the treatment of acute stress disorder and posttraumatic stress disorder, and for symptomatic treatment of postherpetic neuralgia and painful diabetic neuropathy.|FDA Label

Imipramine is a tricyclic antidepressant that continues to be widely used in the therapy of depression. Imipramine can cause mild and transient serum enzyme elevations and is rare cause of clinically apparent acute cholestatic liver injury.

Antidepressant Agents

Adrenergic Uptake Inhibitors; Antidepressive Agents, Tricyclic|EFFECTIVE IN DEPRESSIVE SYNDROMES, PARTICULARLY THOSE ASSOC WITH MANIC-DEPRESSIVE & INVOLUTIONAL PSYCHOSES... /HYDROCHLORIDE/|2-HYDROXYIMIPRAMINE-HCL INHIBITED UPTAKE OF NOREPINEPHRINE & SEROTONIN BY RAT CEREBROCORTICAL SYNAPTOSOMES TO SAME EXTENT AS PARENT DRUGS.|METHODS OF TREATMENT OF ENURESIS IN CHILD ARE PRESENTED INCL IMIPRAMINE.|For more Therapeutic Uses (Complete) data for IMIPRAMINE (8 total), please visit the HSDB record page.

BECAUSE OF POSSIBLE CONGENITAL MALFORMATIONS ASSOC WITH USE OF THIS DRUG.../IT/ SHOULD NOT BE USED DURING FIRST TRIMESTER OF PREGNANCY. /IMIPRAMINE HYDROCHLORIDE/|TRICYCLIC COMPD ARE CONTRAINDICATED IN PT WITH CONGESTIVE HEART FAILURE, ANGINA PECTORIS, & PAROXYSMAL TACHYCARDIA; ALSO, THEY SHOULD BE USED WITH CAUTION IN PATIENTS WITH URINARY RETENTION, GLAUCOMA, DIABETES, IMPAIRED LIVER FUNCTION, ASTHMA, AND A HISTORY OF CONVULSIVE SEIZURES. /TRICYCLIC ANTIDEPRESSANTS/|OCCASIONAL PT WILL SHOW PHYSICAL DEPENDENCE ON TRICYCLIC ANTIDEPRESSANTS, WITH MALAISE, CHILLS, CORYZA, & MUSCLE ACHES FOLLOWING ABRUPT DISCONTINUATION OF HIGH DOSES OF IMIPRAMINE.|ALTHOUGH MOST FATAL CASES...HAVE OCCURRED AFTER INGESTION OF MORE THAN 1.5 G ... DEATH HAS BEEN REPORTED AFTER AS LITTLE AS 500 TO 750 MG AND RECOVERY HAS BEEN REPORTED AFTER INGESTION OF 5.4 G. /IMIPRAMINE HYDROCHLORIDE/|For more Drug Warnings (Complete) data for IMIPRAMINE (33 total), please visit the HSDB record page.

4. 4= VERY TOXIC: PROBABLE ORAL LETHAL DOSE (HUMAN) 50-500 MG/KG; BETWEEN 1 TEASPOON AND 1 OZ FOR 70 KG PERSON (150 LB).

Imipramine is a tricyclic antidepressant with general pharmacological properties similar to those of structurally related tricyclic antidepressant drugs such as amitriptyline and doxepin. While it acts to block both, imipramine displays a much higher affinity for the serotonin reuptake transporter than for the norepinephrine reuptake transporter. Imipramine produces effects similar to other monoamine targeting antidepressants, increasing serotonin- and norepinephrine-based neurotransmission. This modulation of neurotransmission produces a complex range of changes in brain structure and function along with an improvement in depressive symptoms. The changes include increases in hippocampal neurogenesis and reduced downregulation of this neurogenesis in response to stress. These implicate brain derived neurotrophic factor signalling as a necessary contributor to antidepressant effect although the link to the direct increase in monoamine neurotransmission is unclear. Serotonin reuptake targeting agents may also produce a down-regulation in β-adrenergic receptors in the brain.

Substances that contain a fused three-ring moiety and are used in the treatment of depression. These drugs block the uptake of norepinephrine and serotonin into axon terminals and may block some subtypes of serotonin, adrenergic, and histamine receptors. However the mechanism of their antidepressant effects is not clear because the therapeutic effects usually take weeks to develop and may reflect compensatory changes in the central nervous system. (See all compounds classified as Antidepressive Agents, Tricyclic.)|Drugs that block the transport of adrenergic transmitters into axon terminals or into storage vesicles within terminals. The tricyclic antidepressants (ANTIDEPRESSIVE AGENTS, TRICYCLIC) and amphetamines are among the therapeutically important drugs that may act via inhibition of adrenergic transport. Many of these drugs also block transport of serotonin. (See all compounds classified as Adrenergic Uptake Inhibitors.)

Rapidly and well absorbed (>95%) after oral administration. The primary site of absorption is the small intestine as the basic amine groups are ionized in the acidic environment of the stomach, preventing movement across tissues. Bioavailability ranges from 29-77% due to high inter-individual variability. Peak plasma concentration is usually attained 2-6 hours following oral administration. Absorption is unaffected by food.|Imipramine is primarily excreted in the urine with less than 5% present as the parent compound|Imipramine has a high apparent volume of distribution of 10-20 L/kg. The drug is known to accumulate in the brain at concentrations 30-40 times that in systemic circulation.|Imipramine has a mean clearance of 1 L/h/kg. Its active metabolite, desipramine has a mean clearance of 1.8 L/h/kg.|TRICYCLIC ANTIDEPRESSANTS ARE FAIRLY WELL ABSORBED AFTER ORAL ADMINISTRATION. ... ONCE ABSORBED /IT/ IS WIDELY DISTRIBUTED. ... ARE STRONGLY BOUND TO PLASMA PROTEIN AND TO THE CONSTITUENTS OF TISSUES./TRICYCLIC ANTIDEPRESSANTS|EXCRETION...IS RAPID... APPROX 40% OF DOSE OF RADIOACTIVE IMIPRAMINE APPEARS IN URINE IN 24 HR & TOTAL OF 70% DURING FIRST 72 HR. REMAINDER APPEARS IN FECES. SMALL PORTION...RECOVERED AS UNCHANGED DRUG OR AS ACTIVE DESMETHYL DERIV. LARGER PORTION...EXCRETED AS N-OXIDE OR AS NONCONJUGATED OR CONJUGATED 2-OH DERIV.|IN ANIMALS, PLACENTAL TRANSFER HAS BEEN OBSERVED WITH IMIPRAMINE & ITS DESMETHYL DERIVATIVE.|DISTRIBUTION OF IV ADMIN.../(14)C, IMIPRAMINE/ IN MICE...STUDIED USING WHOLE-BODY AUTORADIOGRAPHY. 5 MIN AFTER DOSING, HIGH UPTAKE OF (14)C OCCURRED IN BRAIN, MYOCARDIUM, LUNGS, ADRENALS & KIDNEYS, BUT (14)C IN BLOOD WAS LOW. IN 1 HR...(14)C /LEVELS/...HIGH IN SALIVARY GLANDS, INTESTINES, LIVER, GALL BLADDER, & URINARY BLADDER & 3 HR LATER...LARGELY CONFINED TO ORGANS CONCERNED WITH EXCRETION OF IMIPRAMINE...INTESTINES, LIVER, & KIDNEYS.|For more Absorption, Distribution and Excretion (Complete) data for IMIPRAMINE (8 total), please visit the HSDB record page.

Imipramine is nearly exclusively metabolized by the liver. Imipramine is converted to desipramine by CYP1A2, CYP3A4, CYP2C19. Both imipramine and desipramine are hydroxylated by CYP2D6. Desipramine is an active metabolite. Minor metabolic pathways include dealkylation to form an imidodibenzyl product as well as demethylation of desipramine to didemethylimipramine and subsequent hydroxylation. Less than 5% of orally administered imipramine is excreted unchanged.|...STUDY OF METABOLISM OF IMIPRAMINE & ITS METABOLITES BY RAT LIVER MICROSOMES...REVEALED OPERATION OF 16 METABOLIC PATHWAYS, INCL N-DEMETHYLATION, AROMATIC HYDROXYLATIONS, SIDE-CHAIN DEALKYLATIONS, N-OXIDATION, N-OXIDE REDUCTION, & CONJUGATION REACTIONS.|IMIPRAMINE N-OXIDE & IMINODIBENZYL...IDENTIFIED AS ADDITIONAL URINARY METABOLITES IN MAN.|...METABOLIZED IN HUMANS BY N-DEMETHYLATION & BY HYDROXYLATION IN ONE OF THE AROMATIC RINGS OR IN ETHYLENE BRIDGE TO GIVE DESMONOMETHYLIMIPRAMINE (DMI) & DESDIMETHYLIMIPRAMINE (DDMI) & THE 2-HYDROXY & 10-HYDROXY DERIVATIVES OF IMIPRAMINE, DMI & DDMI, TOGETHER WITH THEIR GLUCURONIDE CONJUGATES.|IMIPRAMINE (HALF-LIFE, 16 HOURS) IS BIOTRANSFORMED TO THE ACTIVE METABOLITE, DESIPRAMINE (HALF-LIFE, 18 HOURS).|Imipramine has known human metabolites that include 2-Hydroxyimipramine, Desipramine, and Imipramine N-glucuronide.

Imipramine has a mean half life of 12 h. Its active metabolite, desipramine has a mean half life of 22.5 h.|IMIPRAMINE (HALF-LIFE, 16 HOURS)...

Imipramine works by inhibiting the neuronal reuptake of the neurotransmitters norepinephrine and serotonin. It binds the sodium-dependent serotonin transporter and sodium-dependent norepinephrine transporter reducing the reuptake of norepinephrine and serotonin by neurons. Depression has been linked to a lack of stimulation of the post-synaptic neuron by norepinephrine and serotonin. Slowing the reuptake of these neurotransmitters increases their concentration in the synaptic cleft, producing knock-on effects in protein kinase signalling which is thought to contribute to changes in neurotransmission and brain physiology which relieves symptoms of depression.|MANNER IN WHICH IMIPRAMINE RELIEVES...DEPRESSION IS NOT CLEAR. ITS EFFECT HAS BEEN DESCRIBED AS DULLING OF DEPRESSIVE IDEATION... HOWEVER, REPORTS OF MANIC EXCITEMENT AS WELL AS EUPHORIA & INSOMNIA INDICATE THAT IMIPRAMINE DOES HAVE STIMULANT ACTION UNDER CERTAIN CIRCUMSTANCES.|TRICYCLIC ANTIDEPRESSANTS HAVE THREE PRIMARY PHARMACOLOGIC ACTIONS, INCLUDING ANTICHOLINERGIC EFFECTS, REUPTAKE BLOCKADE OF CATECHOLAMINES AT THE ADRENERGIC NEURONAL SITE AND QUINIDINE-LIKE EFFECTS ON THE CARDIAC TISSUE. /TRICYCLIC ANTIDEPRESSANTS/

TYPICAL PATTERN /OF TOXICITY/ IS BRIEF PHASE OF EXCITEMENT AND RESTLESSNESS, SOMETIMES WITH MYOCLONUS, TONIC-CLONIC SEIZURES, OR DYSTONIA, FOLLOWED BY RAPID DEVELOPMENT OF COMA, OFTEN WITH DEPRESSED RESPIRATION, HYPOXIA, DEPRESSED REFLEXES, HYPOTHERMIA, HYPOTENSION. ... ANTICHOLINERGIC EFFECTS ARE STRIKING, WITH MYDRIASIS, FLUSHED DRY SKIN & DRY MUCOSAE, ABSENT BOWEL SOUNDS, URINARY RETENTION, AND TACHYCARDIA. /TRICYCLIC ANTIDEPRESSANTS/|IMIPRAMINE HCL INDUCED ALTERATION IN FLUID LEVELS OF SEROTONIN METABOLITE, 5-HYDROXY-INDOLEACETIC ACID IN 15 DEPRESSED PATIENTS.|OVERDOSE OF PATIENTS BY INGESTION OF IMIPRAMINE, & 1 ON BOTH IMIPRAMINE & DESIPRAMINE, DOCUMENTED BY SERIAL MEASUREMENTS OF PLASMA LEVELS. SOME PT COMATOSE, SOME REQUIRED SUPPORTIVE RESPIRATION, 2 DIED.|Human systemic effects by ingestion: somnolence, hallucinations, distorted perceptions, changes in motor activity, ataxia (loss of muscle coordination), coma, nausea and vomiting, irritative dermatitis.|For more Human Toxicity Excerpts (Complete) data for IMIPRAMINE (6 total), please visit the HSDB record page.

4,4'-Methylenebis(3-hydroxy-2-naphthoic acid)-3-(10,11-dihydro-5H-dibenzo(b,f)azepin-5-yl)-N,N-dimethyl-1-propanamine (1:2)

INJECTION: 25 MG/2 ML; TABLETS: 10, 25, & 50 MG. /HYDROCHLORIDE/

LIQUID CHROMATOGRAPHY SEPARATION OF TRICYCLIC DRUGS.|IMPROVED ASSAY TECHNIQUES FOR TRICYCLIC ANTIDEPRESSANTS THAT ELIMINATE POSSIBLE SOURCES OF ERROR BY GAS CHROMATOGRAPHY/MASS SPECTROMETRY.

RAPID DETERMINATION OF SUBTHERAPEUTIC TO OVERDOSE LEVELS OF IMIPRAMINE IN BLOOD SERUM BY HIGH-PERFORMANCE LIQUID CHROMATOGRAPHY.

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Pharmaceuticals