CAS: 50-49-7; 3-(10,11-Dihydro-5H-Dibenzo[b,F]Azepin-5-yl)-N,N-Dimethylpropan-1-Amine
- 英文名称3-(10,11-Dihydro-5H-Dibenzo[b,F]Azepin-5-yl)-N,N-Dimethylpropan-1-Amine
- 中文名称米帕明
- IUPAC名称3-(10,11-dihydro-5H-dibenzo[b,f]azepin-5-yl)-N,N-dimethylpropan-1-amine
- 其它别名Dimipressin; Tofranil (Hydrochloride); 3-(5,6-Dihydrobenzo[b][1]Benzazepin-11-yl)-N,N-Dimethylpropan-1-Amine; Intalpram; Declomipramine; Imizine (Salt/mix); Ogg85Sx4E4; 10,11-Dihydro-N,N-Dimethyl-5H-Dibenz[b,F]Azepine-5-Propanamine; 5H
- CAS编号50-49-7
- MFCD编号:MFCD00242921
- EINECS号:200-042-1
- FDA UNII编号:OGG85SX4E4
- 分子式:C19H24N2分子量:280.41
- 产品CID: 2291068
- 同类组份化合物CAS93980-91-7 (maleate)67246-27-9 (HBr)10075-24-8 (pamoate)113-52-0 (HCl)50-49-7 (free base)
- 产品分类原料药 → 神经系统用药 → 抗抑郁、躁狂药
物理性质
- 熔点174 °C
- 沸点403.1 °C at 760mmHg
- 闪点179.7 °C
- 密度1.041g/cm3
- pKa:pKa 9.66(H2O,t = 25,I=0.025) (Uncertain)
- PSA:6.48
- LogP:3.94
- 折射率1.574
- 蒸汽压1.04E-06 mmHg at 25 °C
- 溶解性18.2 mg/L (at 24 °C)
- 外观形态固体-粉末
- 储存条件本品密封保存避光干燥环境保存。
- 产品应用本药为常用三环类抗抑郁药.目前认为抑制症的发生与脑内NE和5-HT含量的减少有关.丙咪嗪能阻止神经末梢突触前膜对NE,5-HT的再摄取,使突触膜间隙这两种递质的含量增加,从而发挥抗抑郁作用,丙咪嗪还能提高中枢神经系统中NE受体和5-HT受体的敏感性.临床用于各种类型的抑郁症,对内源性抑郁症,反应性抑郁症疗效好,对更年期抑郁症,神经官能症的抑郁症及强迫症也有效.尚可用于小儿遗尿症.
- 性质描述为白色或淡黄色结晶性粉末,无臭,味灼而麻.溶于水,乙醇;几乎不溶于乙醚.
MSDS等安全信息
- GHS象形图
- GHS符号GHS07;
注释: Exclamation mark - 危险类别急性毒性 类别4(经口)
- 警示词Warning(警告)
- 危险描述H302 |吞咽有害.
- 防范说明P260-P261-P264-P270-P271-P280-P304+P340-P307+P311-P312-P321-P391-P403+P233-P405-P501-
- 安全声明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. | 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. | Acute management must begin with an assessment of airway, breathing, and circulation in addition to ECG monitoring and vital signs. The initial management should primarily focus on the correction of hypoxia and acidosis if present. Treatment with sodium bicarbonate will reverse the fast sodium channel function on the myocardium, which will reverse the cardiotoxicity and will also help in increasing the pH, which can enhance the excretion of TCAs. Therefore, continuous monitoring of imipramine is important to prevent cardiotoxicity and to prevent morbidity and mortality. If patients develop seizures, the recommendation is to use benzodiazepines as first-line therapy. However, dose adjustment is necessary for certain medical conditions as hepatic or renal impairment. | 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.
欧盟法规
REACH注册ECHA物质C&L通报REACH预注册上下游产品
CAS号494-19-9 亚氨基二苄 | CAS号109-54-6 3-氯-1-(N,N-二甲基)丙胺 | CAS号6829-98-7 氧丙咪嗪 | CAS号876124-39-9 N'-(4-carbometh... | CAS号50-47-5 盐酸去甲咪嗪 | CAS号124-38-9 二氧化碳 | CAS号58-28-6 去甲丙咪嗪盐酸盐 | CAS号79-22-1 氯甲酸甲酯 | CAS号50-47-5 盐酸去甲咪嗪 | CAS号6829-98-7 氧丙咪嗪 | CAS号10075-24-8 米帕明双羟萘酸盐 | CAS号796-28-1 10-hydroxyimipramine | CAS号303-70-8 11-[3-(dimethyl...合成工艺路线路线简述
📜丙咪嗪置于sodium Hydroxide体系中,用 水 作为反应溶剂,化学反应生成 米帕明
参考文献:Method Of Preparation Of Imipramine Pamoate And Novel Crystalline Form Of Imipramine Pamoate Thereof
标题:Method Of Preparation Of Imipramine Pamoate And Novel Crystalline Form Of Imipramine Pamoate Thereof
摘要:本发明涉及通过简单的两步过程制备盐酸地普拉明.该过程提供了新形式的盐酸地普拉明.本发明具有成本效益,涉及温和条件以反应生成所述化合物.
海关参考信息
- 2902600000-乙苯
2921440000-二苯胺 - 💡 提示：海关信息按照顺序优先匹配，如需确认的海关信息，请参考相关资料。
- 详情请参考：📖 海关编码查询和海关进出口税则
专利信息
专利号:US-2012177593-A1
优先权日:2009-07-20
标 题 :Synthesis of dendrimer conjugates
发明人：BAKER JR JAMES R; ZHANG YUEHUA; THOMAS THOMMEY P; DESAI ANKUR MAHESH
权利人:BAKER JR JAMES R; ZHANG YUEHUA; THOMAS THOMMEY P; DESAI ANKUR MAHESH; UNIV MICHIGAN
摘要:The present invention relates to novel methods of synthesis of therapeutic and diagnostic dendrimers. In particular, the present invention is directed to novel dendrimer conjugates, novel methods of synthesizing the same, compositions comprising the conjugates, as well as systems and methods utilizing the conjugates (e.g., in diagnostic and/or therapeutic settings (e.g., for the delivery of therapeutics, imaging, and/or targeting agents (e.g., in disease (e.g., cancer, inflammatory disease) diagnosis and/or therapy, pain therapy, etc.)). Accordingly, dendrimer conjugates of the present invention may further comprise at least two different components for targeting, imaging, sensing, and/or providing a therapeutic or diagnostic material and/or monitoring response to therapy. Furthermore, the novel synthesis methods of certain embodiments of the present invention provide significant advantages with regard to total reaction time and simplicity.
专利号:WO-2024260325-A1
优先权日:2023-06-19
标题 :Synthesis of macrocyclic compound and medical use of macrocyclic compound
发明人：LU HONGFU; DING XIAO; REN FENG
权利人:INSILICO MEDICINE IP LTD
摘要:Provided in the present invention are the synthesis of a macrocyclic compound and the medical use of the macrocyclic compound. Specifically, provided in the present invention are a compound as show in formula (II), a stereoisomer thereof or a pharmaceutically acceptable salt thereof, which can be used as a CDK7 inhibitor.
专利号:US-10005720-B2
优先权日:2013-04-05
标题:Compounds useful for the treatment of metabolic disorders and synthesis of the same
发明人：SEXTON JONATHAN Z; BRENMAN JAY E; MUSSO DAVID L
权利人:NORTH CAROLINA CENTRAL UNIV; UNIV NORTH CAROLINA CHAPEL HILL
摘要:The present invention provides compounds of Formula (I): wherein variables X, Y, Z and R1 are as described herein. Some of the compounds described herein are glutamate dehydrogenase activators. The invention is also directed to pharmaceutical compositions comprising these compounds, uses of these compounds and compositions in the treatment of metabolic disorders as well as synthesis of the compounds.
专利号:WO-2015194928-A1
优先权日:2014-06-17
标 题:Method for the isolation and synthesis of 3-(1´, 1´- dimethylallyl)-herniarin, as well as (e)-3-(1´,1´-dimethyl-3´nitro-allyl-herniarin, from casimiroa pubescens, and use thereof as an antidepressant
发明人：MARTÃ?NEZ VÃ?ZQUEZ MARIANO; ESTRADA REYES ROSA; UBALDO SUÃ?REZ DENISSE; DE LA ROSA SIERRA ROBERTO
权利人:UNIV NAC AUTÓNOMA DE MÉXICO
摘要:The invention relates to the compounds 3-(1´,1´ -dimethylallyl)-herniarin (1) y 3- (1,1´-dimethyl-3´ nitro allyl-herniarin] (3) (NHR) derived from coumarin, which have excellent antidepressant activity. The compound 3- (1,1´-dimethyl-3´ nitro allyl-herniarin] (3) (NHR) is synthesised by means of a nitration reaction of the compound 3-(1´,1´-dimethylallyl)-herniarin. The present invention also relates to the method for the isolation and synthesis of the compound 3 -(1´,1´-dimethylallyl)-herniarin.
专利号:US-9315483-B2
优先权日:2007-09-13
标题 :Synthesis of deuterated catechols and benzo[D][1,3]dioxoles and derivatives thereof
发明人：JONES ANDREW D; ZELLE ROBERT E; SILVERMAN I ROBERT
权利人:CONCERT PHARMACEUTICALS INC
摘要:The present invention provides a convenient and efficient process for the synthesis of d 2 -benzo[d][1,3]dioxoles.
专利号:US-12234200-B2
优先权日:2019-04-16
标 题:Synthetic methods of preparing esketamine
发明人：CHEN CHENG YI
权利人:JANSSEN PHARMACEUTICA NV
摘要:The present invention is directed to methods for the asymmetric synthesis of esketamine. The present invention is further directed to key intermediates in the asymmetric esketamine synthesis. In one embodiment, the invention is an asymmetric synthesis of esketamine comprising the conversion of (S)-2′-chloro-2-methoxy-3,4,5,6-5 tetrahydro-[1, 1′-biphenyl]-3-yl carbamate to (S)-2′-chloro-1-isocyanato-6-methoxy-1,2,3,4-tetrahydro-1,1′-biphenyl.
供应商参考报价(招募中)
品牌试剂参考报价(招募中)
📌 第三方产品分析报告
主要参考文献
1: Agabio R, Trogu E, Pani PP. Antidepressants for the treatment of people with co-occurring depression and alcohol dependence. Cochrane Database Syst Rev. 2018 Apr 24;4:CD008581. doi: 10.1002/14651858.CD008581.pub2. Review. Available from http://www.ncbi.nlm.nih.gov/books/NBK476277/ doi: 10.1016/j.jad.2017.11.020. Epub 2017 Nov 7. Review. Available from http://www.ncbi.nlm.nih.gov/books/NBK447974/ Review.
6: Shamim D, Laskowski M. Inhibition of Inflammation Mediated Through the Tumor Necrosis Factor α Biochemical Pathway Can Lead to Favorable Outcomes in Alzheimer Disease. J Cent Nerv Syst Dis. 2017 Jul 28;9:1179573517722512. doi: 10.1177/1179573517722512. eCollection 2017. Review.
7: Euwema MS, Swanson TJ. Toxicity, Deadly Single Dose Agents. 2017 Oct 6. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2018 Jan-. Available from http://www.ncbi.nlm.nih.gov/books/NBK441849/ doi: 10.1016/j.seizure.2017.06.022. Epub 2017 Jun 27. Review. doi: 10.1016/j.euroneuro.2017.05.007. Epub 2017 Jun 24. Review. doi: 10.1177/0269881117711709. Epub 2017 Jun 21. Review. Available from http://www.ncbi.nlm.nih.gov/books/NBK425164/ doi: 10.3233/JAD-161247. Review.
合成参考文献
参考文献:10.2165/11592070-000000000-00000
摘要:Watkins CC, Pieper AA, Treisman GJ. Safety considerations in drug treatment of depression in HIV-positive patients: an updated review. Drug Saf. 2011 Aug 01;34(8):623–39. doi: 10.2165/11592070-000000000-00000.
参考文献:10.1007/s00535-005-1687-8
摘要:Hojo M, Miwa H, Yokoyama T, Ohkusa T, Nagahara A, Kawabe M, Asaoka D, Izumi Y, Sato N. Treatment of functional dyspepsia with antianxiety or antidepressive agents: systematic review. J Gastroenterol. 2005 Nov;40(11):1036–42. doi: 10.1007/s00535-005-1687-8.
参考文献:10.1016/j.brainres.2011.05.033
摘要:Crespi F. Influence of Neuropeptide Y and antidepressants upon cerebral monoamines involved in depression: an in vivo electrochemical study. Brain Res. 2011 Aug 17;1407():27–37. doi: 10.1016/j.brainres.2011.05.033.
📝 需求与反馈
尽可能描述清楚需求与问题信息
