CAS: 90-34-6; 8-(4-Amino-1-Methylbutylamino)-6-Methoxyquinoline
该化合物是一种抗疟药物,主要用于治疗和预防疟疾,特别是抗疟和卵巢感染的复发;它被归类为8-氨基氮化合物,并因其能够针对疟疾寄生虫的肝脏阶段而闻名;原虫的化学配方为C15H18N3O,其分子重量约为245.33克/摩尔;该化合物通常以磷酸盐形式施用,这增加了其溶性;普里马昆的特点是其水溶性相对较低,但在有机溶剂中可溶性较强;其行动机制涉及生成活性氧物种,损害寄生虫细胞成分;尽管其有效,初质可导致葡萄糖-6-磷酸盐-脱氢酶缺乏症(G6PD)的人出现血糖性贫血症,但需要事先检查.此外,它有几小时的半衰期,需要多剂量才能得到有效的治疗.
- 英文名称8-(4-Amino-1-Methylbutylamino)-6-Methoxyquinoline
- 中文名称伯氨喹
- IUPAC名称N4-(6-methoxyquinolin-8-yl)pentane-1,4-diamine
- 其它别名8-(4-Amino-1-methylbutylamino)-6-methoxyquinoline; N-(6-Methoxyquinolin-8-yl)pentane-1,4-diamine
- CAS编号90-34-6
- MFCD编号:MFCD00598906
- EINECS号:201-987-2
- FDA UNII编号:MVR3634GX1
- 分子式:C15H21N3O分子量:259.35
- 产品CID: 1935954
- 产品分类有机原料→分子砌块→芳杂环类化合物→喹啉类化合物
相似化合物
90-52-8 525-61-1 77229-67-5物理性质
- 熔点25 °C
- 沸点175-179 °C at 760 mmHg
- 闪点226.6±28.7 °C
- 密度1.1±0.1 g/cm3
- pKa:pKa 3.74/9.99(H2O,t =25) (Uncertain)
- PSA:60.17
- LogP:2.7827
- 折射率1.616
- 蒸汽压0.0±1.1 mmHg at 25°C
- 溶解性Chloroform (Slightly), Methanol (Slightly)
- 外观形态深黄色至深橙色油状物
- 储存条件冰箱
- 产品应用对间日疟原虫红外期及各型疟原虫配子体有较强的杀虫作用,是根治间日疟疾与阻断各型疟疾传播的有效药物.伯氨喹对红内期裂殖体的作用弱,对f性疟原虫的红内期裂殖体则无效,因此,不能用于控制症状.用于控制间日疟与三日疟的复发和传播以及防止f性疟的传播.
- 性质描述粘性液体.沸点175-179°C(0.0266kPa),溶于醚.其磷酸盐(C15H21N3O·2H3PO4,[63-45-6])为橙红色结晶性粉末.熔点197-198°C.不溶于氯仿或乙醚,溶于水,水溶液显酸性反应.无臭,味苦.
MSDS等安全信息
- GHS象形图
- GHS符号GHS08 & GHS06;
注释: Health hazard & Skull and crossbones - 危险类别生殖毒性 类别2
急性毒性 类别3(经口) - 警示词Danger(危险)
- 危险描述H361d |怀疑对胎儿造成损害.
H301 |吞咽会中毒. - 防范说明P264-P270-P280-P330-P405-P501
- 危险等级6.1
- UN编号2810.0
- 危险品标志Xn
- 包装等级Ⅲ
- 安全声明IDENTIFICATION: Primaquine phosphate is used to treat malaria caused by Plasmodium virax. Primaquine is an orange-red, odorless crystalline powder which has a bitter taste It is soluble in water and it is practically insoluble in alcohol, chloroform and ether. For elimination of primary and secondary exoerythrocytic stages of Plasmodium vivax, Plasmodium malariae and Plasmodium ovale and the primary exoerythrocytic forms only of Plasmodium falciparum. Primaquine must always be given in conjunction with full doses of a 4-aminoquinoline. HUMAN EXPOSURE: Main risks and target organs: Target organs are: cardiovascular, hematological system, and gastrointestinal. Acute, dose-dependent methemoglobinemia and hemolytic anemia occurs in persons with a deficiency of glucose-6-phosphate dehydrogenase (G6PD); leucopenia or agranulocytosis may also occur. Adverse effects with therapeutic doses are usually mild. Summary of clinical effects: Toxic manifestations include cardiovascular disturbances, especially ventricular dysrhythmias, abdominal cramps, vomiting, burning epigastric distress, headache, confusion, cyanosis, methemoglobinemia, leucocytosis or leucopenia, and anemia. Granulocytopenia, acute hemolytic anemia and acute hemolysis may occur in individuals who are hypersensitive to primaquine. Contraindications: The balance of risk and benefit should be considered when primaquine is administered under the following conditions: in acutely ill patients suffering from systemic disease characterized by a tendency to granulocytopenia (for example, patients with arthritis or lupus erythematosus). Agents capable of depressing the myeloid elements of the bone marrow (antineoplastic agents, colchicine, gold salts, penicillamine, phenylbutazone, quinacrine). Individuals who have shown previous idiosyncratic reaction to primaquine, individuals with a history of favism or acute haemolytic anaemia. Individuals with G6PD deficiency or NADH methemoglobin reductase deficiency; primaquine should be discontinued immediately if hemolysis occurs. Routes of entry: Oral: Oral absorption is the only common cause of intoxication. Absorption by route of exposure: Primaquine is readily absorbed from the gastrointestinal tract. The plasma concentration peaks within 1 to 3 hr after ingestion but is negligibly low after 24 hr Considerable inter-individual variation in peak plasma concentrations of primaquine has been reported with the same dose of the drug. Distribution by route of exposure: Primaquine is extensively distributed into body tissues. About 75% of primaquine in plasma is bound to proteins and high concentrations occur in erythrocytes. Primaquine crosses the placenta but it is uncertain whether significant amounts occur in breast milk. Biological half-life by route of exposure: Primaquine has a plasma elimination half-life of 3.7 to 9.6 hr in healthy adults. Metabolism: Primaquine is not subject to extensive first pass metabolism. However, it is readily metabolized in the liver to three metabolites: 8-(3-carboxyl-1-methyl-propylamino)-6-methoxy-quinoline, 5-hydroxy primaquine and 5-hydroxy-6-desmethyl-primaquine. The carboxyl derivative is the major metabolite found in plasma; it accumulates during repeated administration, when the plasma concentration greatly exceeds that of unchanged primaquine. These metabolites have appreciably less antimalarial activity than primaquine but their haemolytic activity, as assessed by formation of methemoglobin in vitro, is greater than that of the parent compound. Elimination by route of exposure: Only 3.6% of the dose of primaquine is excreted as unchanged drug. The principal metabolite is carboxyprimaquine. Mode of action: Toxicodynamics: Primaquine may cause hemolysis and methemoglobinemia. Certain ethnic groups, especially those arising in the Mediterranean basin, are more susceptible to these effects and primaquine sensitivity occurs in persons with G6PD deficiency. G6PD deficiency is genetically acquired; there are a large number of variants in which the extent of the deficiency differs. The sensitivity of individuals to primaquine therefore varies. G6PD is an enzyme which protects the erythrocyte from the direct oxidative effects of some drugs and chemicals by maintaining intracellular stores of reduced glutathione. In people who are G6PD deficient, oxidation of hemoglobin leads to precipitation within the cell, producing characteristic inclusions called Heinz bodies; increased oxidation of hemoglobin also produces methemoglobinemia. There is an increase in the generation of free radicals which also contribute to cellular damage. These effects ultimately cause hemolysis. Pharmacodynamics: The exact mechanism of anti-malarial activity of primaquine has not been determined, but the drug appears to bind to plasmodial DNA and interfere with its function. Human data: Adults: The toxicity of primaquine phosphate is dose-dependent; weekly administration (in combination with chloroquine) is less toxic than daily administration. Serious hematologic reactions may occur in some people with a G6PD deficiency even at the low weekly doses of primaquine used in combination with chloroquine for the prophylaxis of malaria. This occurs primarily in patients with a family or personal history of favism. Methemoglobinemia is more common in individuals with nicotinamide adenine dinucleotide methemoglobin reductase deficiency. About 10% of the black population with G6PD deficiency develop anaemia due to intravascular hemolysis at daily dose levels of 15 mg (base) and higher. Some darker-skinned Mediterranean populations are more sensitive than blacks. Teratogenicity: No reports are available to associate primaquine with congenital defects. Interactions: Primaquine should not be administered concurrently with any other drug that is likely to induce hemolysis or bone marrow depression (see section 4.3) as this may increase the risk of toxicity. Concurrent use of primaquine with bone marrow depressants may increase the risk of leukopenia. If concurrent use is essential, close observation for myelotoxicity should be considered. The toxicity of primaquine appears to be potentiated by antimalarial agents that are structurally similar (for example, quinacrine). Primaquine should not be administered to patients who have received quinacrine within the previous 3 months. Although primaquine inhibits the elimination of drugs which undergo oxidative metabolism (for example, antipyrine), therapeutic doses have no effect on paracetamol metabolism. The combination of chloroquine and primaquine with dapsone may prevent hemolysis in G6PD deficient subjects. The antimalarial effects of quinacrine and primaquine in various test organisms are synergistic with many antibiotics. After administration of primaquine, the metabolism of antipyrine (calculated from 0 to 24 h) to its 3 main metabolites, 3 hydroxymethyl-antipyrine, 4 hydroxy-antipyrine and norantipyrine, is significantly reduced. There is no selective effect on a particular metabolic pathway. Main adverse effects: Gastrointestinal tract: Dose-related gastrointestinal symptoms include anorexia, nausea, vomiting, epigastric distress, and abdominal cramps. Hematological system: Acute hemolytic anemia occurs most frequently in G6P Ddeficient individuals. It is usually self-limiting but in severe cases blood transfusion may be necessary. Methemoglobinemia, agranulocytosis, granulocytopenia and leucopenia are also reported. Methemoglobinemia can be severe in people who are nicotinamide dinucleotide (NADH) methemoglobin reductase deficient. Cardiovascular system: Hypertension and arrhythmias have been reported. Other: Headache, interference with visual accommodation and pruritus have been reported with primaquine. Adverse CNS effects, including depression and confusion, can also occur. Clinical effects: Acute poisoning: Ingestion: Toxic manifestations such as methemoglobinemia and cyanosis occur in most subjects; adverse gastrointestinal effects occur at higher doses. These doses also cause severe hematologic reactions such as leucopenia, anemia and intravascular hemolysis. Chronic poisoning: Ingestion: The adverse effects associated with chronic administration are similar to those which occur in acute poisoning. Course, prognosis, cause of death: Course: Commonly, symptoms of overdoses are nausea, abdominal pain, sometimes vomiting and jaundice. Hemolytic anemia may occur in G6PD deficiency but is usually self-limiting. Prognosis: If patient survives for 48 h recovery is likely. Death: Cardio-circulatory arrest may occur within 1 to 2 h of ingestion due to ventricular dysrhythmia or asystole. Hypotension is common and may progress rapidly to cardiogenic shock with increased central venous pressure. Hypertension and cardiac arrhythmias have been reported on rare occasions. Systematic description of clinical effects Cardiovascular: Based on its anti-arrhythmic activity in mice, primaquine is predicted to have quinidine like cardiotoxicity. Hypertension and cardiac arrhythmias have been reported on rare occasions. Respiratory: Respiratory arrest secondary to circulatory arrest or severe shock may occur within 1 to 2 hr following overdose. Neurological: CNS: In severe cases, headache, mental depression and confusion occur, especially in persons with prior exposure to chloroquine. Gastrointestinal: Abdominal cramps and epigastric distress have been reported. Hepatic: Hepatic function is unaffected. Dermatological: Pruritus and urticaria. Eye, ear, nose, throat: local effects: Diplopia; visual disturbances; blurred vision; irreversible changes to the cornea and retina; optic neuritis. Hematological: Toxic doses of primaquine induce marked bone marrow depression, methemoglobinemia, agranulocytosis and hemolytic anemia. Hemolytic anemia is commonest in persons with G6PD deficiency. The effects are more pronounced in the B-type G6PD deficiency (the Mediterranean type) than in the A-type (the type mainly present among black American and African populations) Immunological: Primaquine may also cause immunosuppression Metabolic: Fluid and electrolyte disturbances: Hypokalemia is common in severe intoxication. Others: Hypo- or hyperthermia and hypo- or hyperglycemia have been reported. Special risks: Pregnancy: Primaquine should be withheld from women with G6PD deficiency who are pregnant. If prophylaxis or treatment is essential, the possible benefits should outweigh the potential risks. Transplacental transfer of primaquine to a fetus with G6PD deficiency may result in life-threatening anemia and methemoglobinemia in utero. Breast-feeding: It is not known whether primaquine is excreted in breast milk. However, problems in man have not been documented. Enzyme deficiency: Primaquine should be used with caution in patients with G6PD deficiency who are receiving other drugs likely to induce hemolysis, (for example, nitrites, sulfonamides). /Primaquine phosphate/
- WGK Germany3
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ECHA物质C&L通报REACH预注册上下游产品
CAS号3396-99-4 α-甲基-D-半乳糖苷 | CAS号1185934-52-4 8-(4-ethoxycarb... | CAS号1355340-90-7 8-[4-(2-ethoxyc... | CAS号1355340-81-6 8-[4-(2,2,2-tri... | CAS号1355340-83-8 8-[4-(4-methoxy... | CAS号1355340-85-0 8-(4-phenoxycar... | CAS号1355340-87-2 8-[4-(4-chlorop... | CAS号1355340-89-4 8-[4-(4-nitroph... | CAS号63-45-6 磷酸伯安喹 | CAS号93245-26-2 bis(trifluoroac...合成工艺路线路线简述
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参考文献:Chemistry - A European Journal 日期:2004 卷标:10(7) 页码:1625-1636]
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90-34-6 = 90-34-6
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参考文献:Arzneimittel Forschung 日期:2010 卷标:60(10) 页码:627-635]
86166-06-5 = 90-34-6
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90-34-6 = 90-34-6
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83532-78-9 = 90-34-6
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90-34-6 = 90-34-6 [标题:Reaction Conditions
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作者:Rajic,Zrinka; Kos,Gabrijela; Zorc,Branka; Singh,Prati Pal; Singh,Savita
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📜8-[4-(2-Ethoxycarbonylmethoxycarbonyl)Amino-1-Methylbutylamino]-6-Methoxyquinoline置于sodium Hydroxide体系中,用 水,乙腈 作为反应溶剂,化学反应生成 伯氨喹
参考文献:基于氨基甲酸酯的伯氨喹前药的方法:抗疟疾活性,化学稳定性和酶促活化
标题:基于氨基甲酸酯的伯氨喹前药的方法:抗疟疾活性,化学稳定性和酶促活化
摘要:合成了抗疟疾药物伯氨喹的o-烷基和o-芳基氨基甲酸酯衍生物,作为潜在的前药,可以防止非活性代谢产物羧基伯氨喹的氧化脱氨作用.既ø-烷基和ö-芳基氨基甲酸盐进行水解在碱性和ph为7.4的磷酸盐缓冲液为母药,与ö-芳基氨基甲酸盐是约 10 6-10 10比其o-烷基对应物更具反应性.在人血浆ø烷基氨基甲酸酯是稳定的,而与此相反的ø芳基对应物迅速释放出相应的苯酚产物,而伯氨喹在较长的孵育时间内仅缓慢释放.人体血浆中o-芳基氨基甲酸酯的活化似乎由丁酰胆碱酯酶(buche)催化,该酶导致酶催化丝氨酸的氨基甲酰化,随后发生缓慢的酶再活化和母体药物释放.在大鼠肝匀浆中,大多数o-芳基和o-烷基氨基甲酸酯被激活,半衰期为9至15小时,而4-硝基苯基氨基甲酸酯的水解速度太快,无法确定准确的速率常数.使用由伯氏疟原虫,Balb C小鼠和斯蒂芬斯按蚊(anopheles Stephensi)蚊子.与对照
DOI:10.1016/j.Bmc.2011.11.059
海关参考信息
- 2905110000-甲醇
2933310010-吡啶
2908199090-其他酚的卤化衍生物
2908999090-其他酚的硝化衍生物 - 💡 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-10968174-B2
优先权日:2016-12-21
标题:Synthesis of a thiosulfonic acid by a step of periodate mediated oxidative coupling of a thiosulfonic acid with an aniline
发明人：SINCLAIR JAMES PETER; NICOLL SARAH LOUISE; STOREY JOHN MERVYN DAVID; LARCH CHRISTOPHER PAUL
权利人:WISTA LAB LTD
摘要:The present invention pertains generally to the field of chemical synthesis, and more particularly to methods for the chemical synthesis of a thiosulfonic acid of Formula (1) by a step of periodate mediated oxidative coupling of a thiosulfonic acid of Formula (2) with an aniline of Formula (3), as described herein. The present invention also relates to such methods which incorporate one or more additional (subsequent and/or preceding) steps, for example, to prepare compounds of Formula (5) from compounds of Formula (1); to prepare compounds of Formula (6) from compounds of Formula (5); and to prepare compounds of Formula (2) from compounds of Formula (4), as described herein.
专利号:WO-2006046949-A1
优先权日:2004-10-22
标 题 :SYNTHESIS AND ANTIMALARIAL ACTIVITY OF PYRROLO[3,2-f]QUINAZOLINE-1,3- DIAMINE DERIVATIVES
发明人：AI J LIN; JIAN GUAN; QUAN ZHANG; SKILLMAN DONALD R
权利人:WALTER REED ARMY INST OF RES W; AI J LIN; JIAN GUAN; QUAN ZHANG; SKILLMAN DONALD R
摘要:The invention relates to derivatives of pyrroloquinazolinediamine, more specifically derivatives of 7-(substituted)-7H-pyrrolo[3,2-F] quinazoline-1,3-diamines that are non-toxic and are also effective in the treatment of malaria, including P. falciparum and P.vivax strains. The derivatives are certain carbamate derivatives, succinimide derivatives, alkylcarboxamides derivatives and acetamide derivative, phthalimides, alkylamines and all other amide and imide derivatives and their 1-hydroxy analogs,. The derivatives of the present invention are also soluble in common organic solvents to facilitate the purification in a large scale synthesis of the composition.
专利号:US-2012100555-A1
优先权日:2009-06-29
标题 :Synthesis And Use Of Fluorophore-Tagged Antimalarials
发明人：LEAR MARTIN JAMES; TAN KEVIN SHYONG WEI
权利人:LEAR MARTIN JAMES; TAN KEVIN SHYONG WEI
摘要:This invention includes a fluorophore-tagged antimalarial represented by the following structural formula (1) or a salt thereof. This invention relates to the synthesis of fluorophore-tagged antimalarials and describes the synthesis of a fluorophore-tagged antimalarial. These fluorophore-tagged antimalarials can be used to image live cells to determine the location of the antimalarial in the cell, identify drug resistance and growth related pathways in Plasmodium isolates, identify new drug targets and chemo-sensitizers to reverse drug resistance.
专利号:US-7253177-B2
优先权日:2004-10-22
标 题:Synthesis and antimalarial activity of pyrrolo[3,2-f]quinazoline-1,3-diamine derivatives
发明人：LIN AI J; GUAN JIAN; ZHANG QUAN; SKILLMAN DONALD R
权利人:US ARMY
摘要:The invention relates to derivatives of pyrroloquinazolinediamine, more specifically derivatives of 7-(substituted)-7H-pyrrolo[3,2-F] quinazoline-1,3-diamines that are non-toxic and are also effective in the treatment of malaria, including P. falciparum and P. vivax strains. The derivatives are certain carbamate derivatives, succinimide derivatives, alkylcarboxamides derivatives and acetamide derivative, phthalimides, alkylamines and all other amide and imide derivatives and their 1-hydroxy analogs. The derivatives of the present invention are also soluble in common organic solvents to facilitate the purification in a large scale synthesis of the composition.
专利号:US-9409879-B2
优先权日:2011-03-29
标 题 :Total synthesis of redox-active 1.4-naphthoquinones and their metabolites and their therapeutic use as antimalarial and schistomicidal agents
发明人：DAVIOUD-CHARVET ELISABETH; LANFRANCHI DON ANTOINE; JOHANN LAURE; WILLIAMS DAVID LEE; CESAR RODO ELENA
权利人:DAVIOUD-CHARVET ELISABETH; LANFRANCHI DON ANTOINE; JOHANN LAURE; WILLIAMS DAVID LEE; CESAR RODO ELENA; CENTRE NAT RECH SCIENT
摘要:Naphthoquinones, azanaphthoquinones and benxanthones, their process of synthesis and methods of their use as antimalarial or antischistosomal agents.
专利号:US-7541172-B2
优先权日:1998-08-27
标题:Transgenic amorpha-4, 11-diene synthesis
发明人：WALLAART THORVALD EELCO; BOUWMEESTER HENDRIK JAN
权利人:INST ONEWORLD HEALTH
摘要:The present invention relates to an isolated DNA sequence encoding a polypeptide having the biological activity of amorpha-4,11-diene synthase. This DNA sequence can be used for the transformation of bacteria, yeasts and plants for the production of amorpha-4,11-diene, a specific precursor in the synthesis of artemisinin, in the respective organisms. The invention also relates to these organisms.
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📌 第三方产品分析报告
主要参考文献
1: Zorc B, Perković I, Pavić K, Rajić Z, Beus M. Primaquine derivatives: Modifications of the terminal amino group. Eur J Med Chem. 2019 Nov 15;182:111640. doi: 10.1016/j.ejmech.2019.111640. Epub 2019 Aug 23.
2: Baird JK, Hoffman SL. Primaquine therapy for malaria. Clin Infect Dis. 2004 Nov 1;39(9):1336-45. doi: 10.1086/424663. Epub 2004 Oct 12.
13:418. doi: 10.1186/1475-2875-13-418.
合成参考文献
参考文献:10.1186/1475-2875-10-185|10.1186/1475-2875-10-198
摘要:Menan H, Faye O, Same-Ekobo A, Oga ASS, Faye B, Kiki Barro CP, Kuete T, N'diaye J, Vicky A, Tine R, Yavo W, Kane D, Kassi KF, Kone M. Comparative study of the efficacy and tolerability of dihydroartemisinin - piperaquine - trimethoprim versus artemether - lumefantrine in the treatment of uncomplicated Plasmodium falciparum malaria in Cameroon, Ivory Coast and Senegal. Malaria Journal. 2011 Jul 08;10(1):185. doi: 10.1186/1475-2875-10-185.
参考文献:10.1086/498536
摘要:Renia L, Maranon C, Hosmalin A, Gruner AC, Silvie O, Snounou G. Do apoptotic Plasmodium-infected hepatocytes initiate protective immune responses J Infect Dis. 2006 Jan 01;193(1):163–4; author reply 164. doi: 10.1086/498536.
📝 需求与反馈
尽可能描述清楚需求与问题信息
