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化工社化工社 化学情報印刷レポート · 研究参考用
HCID 3696作成日：2026年10月27日

イミプラミン

N-(γ-ジメチルアミノプロピル)イミノジベンジル · デスメチルトリミプラミン · N,N-ジメチル-10,11-ジヒドロ-5H-ジベンゾ[b,f]アゼピン-5-(プロパン-1-アミン) · 10,11-ジヒドロ-N,N-ジメチル-5H-ジベンゾ[b,f]アゼピン-5-(プロパン-1-アミン) · 10,11-ジヒドロ-5-(3-ジメチルアミノプロピル)-5H-ジベンゾ[b,f]アゼピン · 10,11-ジヒドロ-5-[3-(ジメチルアミノ)プロピル]-5H-ジベンゾ[b,f]アゼピン · N,N-ジメチル-10,11-ジヒドロ-5H-ジベンゾ[b,f]アゼピン-5-プロパン-1-アミン · 10,11-ジヒドロ-N,N-ジメチル-5H-ジベンゾ[b,f]アゼピン-5-プロパン-1-アミン

https://huagongshe.com/ja/chemical/3696

イミプラミン の分子構造式

識別子と物理属性

CAS No.50-49-7
分子式C19H24N2
平均分子量280.4 g/mol
単同位体質量280.19394877 g/mol
SMILESCN(C)CCCN1c2ccccc2CCc2ccccc21
InChIKeyBCGWQEUPMDMJNV-UHFFFAOYSA-N
PubChem CID3696
ChEMBLCHEMBL11
ChEBICHEBI:47499
EC No.200-042-1
DTXSIDDTXSID1043881
現地名イミプラミン

化学・物理的性質

XLogP4.8
極性表面積6.5
水素結合供与体数0
水素結合受容体数2
回転可能結合数4
重原子数21
形式電荷0
複雑度291
医薬品DEA NFLIS-Drug Category -> AntidepressantsPharmaceuticalsPharmaceuticals -> Listed in ZINC15Pharmaceuticals -> Tricyclic Antidepressants (TCAs)
LogP（分配係数）log Kow = 4.804.68
臭いOdorless /hydrochloride/
Color/FormWhite to off-white /hydrochloride/
溶解度CRYSTALS FROM ACETONEFREELY SOL IN WATER, LESS SOL IN ALCOHOL, SPARINGLY SOL IN ACETONE /HYDROCHLORIDE/In water, 18.2 mg/l @ 24 °C.18.2 mg/L at 24 °C18.23mg/L(24℃)
Human DrugsAntidepressants -> Tricyclic antidepressants (TCA)Breast FeedingLactationMilk, HumanAntidepressive AgentsAntidepressive Agents, TricyclicPharmaceuticals
沸点160 °C @ 0.1 MM HGbp0.1 160°
DecompositionWhen heated to decomposition it emits toxic fumes of nitroxides.
融点174-175174.5 °C174°C
Physical DescriptionSolid
Stability/Shelf LifeImipramine hydrochloride turns yellowish or reddish on exposure to lightslight 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 injectionthe efficacy of the preparation is unaltered if the crystals are redissolved by immersing the ampul in hot water for 1 minute. /Imipramine hydrochloride/
Dissociation Constants9.519.45
密度0.9935 (rough estimate)
屈折率1.5640 (estimate)
貯蔵条件Storage temp. 2-8°C
外観・状態Liquid
pKa（酸解離定数）pKa 9.66(H2O,t = 25,I=0.025) (Uncertain)
色Colorless to light yellow
Specific Activity60-90 Ci/mmol
BCS Class1
EPAの化学物質情報Imipramine (50-49-7)

安全性と法規制

GHS 分類This chemical does not meet GHS hazard criteria for 75% (6 of 8) of all reports.WarningH302 (12.5%): Harmful if swallowed [Warning Acute toxicity, oral]P264, P270, P273, P301+P317, P330, P391, and P501 (click each P-code to see the statement)Aggregated GHS information provided per 8 reports by companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
規制情報Status: Active Update: 08-03-2018 https://echa.europa.eu/registration-dossier/-/registered-dossier/20142Imipramine: Does not have an individual approval but may be used under an appropriate group standard
FDA 要件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 amended21 U.S.C. 321-392).
Special ReportsA REVIEW ON MECHANISM OF ACTION.[COSTA E ET ALMOLECULAR MECHANISMS IN THE ACTION OF IMIPRAMINEEXPERIENTIA 39(8) 855 (1983)]
Hazard Classes and CategoriesAcute Tox. 4 (12.5%)
処分方法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.
TreatmentObtain an ECG and immediately initiate cardiac monitoring. Protect the patient's airway, establish an intravenous line and initiate gastric decontamination. A minimum of 6 hours of observation with cardiac monitoring and observation for signs of CNS or respiratory depression, hypotension, cardiac dysrhythmias and/or conduction blocks, and seizures is necessary. If signs of toxicity occur at anytime during this period, extended monitoring is required. (L1712)
相互作用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/

用途

解説

イミプラミン，代表的な三環系抗うつ剤。内因性うつ病患者の抑うつ状態を取除くが，思考力や集中力の低下，抗不安作用も認められる。作用機序は中枢の視床下部，辺縁系，網様体での神経細胞から遊離した伝達物質のカテコールアミン，インドールアミンなどの再取込みの抑制による伝達物質の活性を持続延長させることにあるといわれ，一部，抗コリン作用の関与も考えられている。抗ヒスタミン，抗セロトニン作用も認められている。体内で側鎖の脱メチル化が起り，デスメチルイミプラミンと三環系抗うつ剤に属する活性代謝物となる。副作用には，ねむけ，かすみ目，口渇，便秘，眼圧亢進，起立性低血圧，錐体外路症状，黄疸などがある。 MAO (モノアミン酸化酵素) 阻害薬との併用は，全身けいれん，発熱，振戦などの症状を起すので禁忌である。

用途

三環系抗うつ薬うつ病やうつ状態の治療に用いられ，三環系抗うつ薬に分類される。ノルアドレナリンとセロトニンの神経終末への取込み阻害作用を持ち 。

使用

Imipramine is used in depression of various etiology accompanied by motor clumsiness and enuresis in children and Parkinson’s disease.

...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.
HepatotoxicityLiver 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.
有害作用Since imipramine acts on various receptors in the body, it can cause adverse effects on some organs and systems. In the central and autonomic nervous system, the antihistaminic effects of imipramine can lead to dizziness, sedation, confusion, delirium, seizures, increased appetite, and weight gain.
暴露経路Rapidly and well absorbed after oral administration. Bioavailability is approximately 43%. Peak plasma concentrations usually attained 1 - 2 hours following oral administration. Absorption is unaffected by food.
毒性の概要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 acetonepractically insoluble in ether. Indications: Treatment of depressionnocturnal 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.The risk of developing toxicity from imipramine and other tricyclics is greater upon increasing the dose. An overdose of imipramine can result in serious side effects, mainly cardiac dysrhythmia, critical hypotension, convulsions, coma, confusion, hyperactive reflexes, and hypothermia. Imipramine has type 1 antiarrhythmic effects as it blocks the fast sodium channel on the myocardium. Therefore, this will lead to inhibition of depolarization of the heart action potential, which will result in QRS prolongation, which can lead to cardiac arrhythmia.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 preventing or reducing the reuptake of norepinephrine and serotonin by nerve cells. 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, which is thought to contribute to relieving symptoms of depression. In addition to acutely inhibiting neurotransmitter re-uptake, imipramine causes down-regulation of cerebral cortical beta-adrenergic receptors and sensitization of post-synaptic serotonergic receptors with chronic use. This leads to enhanced serotonergic transmission.
Signs and SymptomsAntagonism of the histamine H<sub>1</sub> and &alpha<sub>1</sub> receptors can lead to sedation and hypotension. Antimuscarinic and anticholinergic side effects such as blurred vision, dry mouth, constipation and urine retention may occur. Cardiotoxicity may occur with high doses of imipramine. Cardiovascular side effects in postural hypotension, tachycardia, hypertension, ECG changes and congestive heart failure. Psychotoxic effects include impaired memory and delirium. Induction of hypomanic or manic episodes may occur in patients with a history of bipolar disorder. Withdrawal symptoms include GI disturbances (e.g. nausea, vomiting, abdominal pain, diarrhea), anxiety, insomnia, nervousness, headache and malaise.
Human Toxicity ExcerptsTYPICAL 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.
Carcinogen ClassificationNo indication of carcinogenicity to humans (not listed by IARC).
Drug Induced Liver InjuryBenchmark Dataset for the Liver Toxicity Knowledge Base (LTKB)imipramineTofranil®Antidepressants3less-DILI-concern drugs
Non-Human Toxicity Excerpts...IMIPRAMINE PRODUCES DEPRESSION OF SPONTANEOUS MOTOR ACTIVITY IN LAB ANIMALS. ...IT...DECR BODY TEMP, & CAUSES ATAXIA. IT IMPAIRS BOTH ACQUISITION & PERFORMANCE OF CONDITIONED AVOIDANCE RESPONSES.IMIPRAMINE LOWERS BLOOD PRESSURE IN ANESTHETIZED DOGS & OBTUNDS VARIOUS CARDIOVASCULAR REFLEXES, INCL CAROTID OCCLUSION REFLEX, BEZOLD-JARISCH REFLEX, & POSTURAL REFLEXES.Pregnant Wistar-Imamichi rats were given subcutaneous injections of 5 mg/kg of imipramine (IMI) daily from days 1 to 21 of gestation (IMI 1-21), or from days 15 to 21 of gestation (IMI 15-21). The control groups of rats received saline on 1-21 or 15-21 days of gestation. The basal body temperature (BBT) of the pups at 8 or 13 weeks of age was recorded. BBT of female pups was higher than that of male pups in both IMI and saline groups at 8 weeks of age, with a significant rise in temperature at 13 weeks of age. BBT of 13-wk-old IMI (1-21) male pups was significantly lower than that of saline controls and the BBT of 13-wk-old IMI (1-21) female pups was higher than that of controls. At 8 or 13 weeks of age, the pups were tested for thermic response to chlorpromazine (CPZ) injected intraperitoneally at a dose of 5 mg/kg. Male IMI (1-21) pups at 8 weeks of age showed hyperthermia for 1-2 hr after an injection of CPZ, with a significant increase of temperature at 13 weeks of age. Female IMI (1-21) pups at 8 or 13 weeks of age and the control male and female pups showed a marked hypothermia.
Effects During Pregnancy and Lactation◉ Summary of Use during Lactation◈ What is imipramine?
毒性A tertiary amine tricyclic antidepressant that is thought to exert its therapeutic effect by inhibiting the reuptake of serotonin and norepinephrine centrally. A major metabolite is N-desmethylimipramine (desipramine), also used as an antidepressant drug. Desipramine differs from imipramine in being a better blocker of norepinephrine, rather than serotonin, uptake. Side effects, including sedation and drowsiness, dry mouth, urinary retention, constipation, and orthostatic hypotension, are probably due to the anticholinergic, anti-α-adrenergic, and antihistaminergic receptor-blocking properties. Imipramine should not be used in conjunction with a monoamine oxidase inhibitor or other treatment that increases catecholamine concentrations (e.g., drugs containing sympathomimetic amines). Imipramine should be avoided in patients with cardiovascular disease or seizure disorder, or in those who may abuse alcohol, as imipramine lowers seizure threshold, can produce cardiovascular toxicity and may potentiate the effects of alcohol. Imipramine intoxication can include CNS abnormalities (e.g., drowsiness, stupor, coma, and extrapyramidal symptoms), cardiac arrhythmia, and respiratory depression. Children appear to be particularly vulnerable to the cardiotoxic and seizure-inducing effects of high doses of imipramine. The oral LD50 in female rats is 305 mg/kg.
有害物質データ50-49-7(Hazardous Substances Data)