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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 1935作成日：2026年10月27日

タクリン

ロモタール · テトラヒドロアミノアクリジン · 1,2,3,4-テトラヒドロ-9-アミノアクリジン · 9-アミノ-1,2,3,4-テトラヒドロアクリジン · テトラヒドロアミノクリン · 1,2,3,4-テトラヒドロ-9-アクリジンアミン · 5,6,7,8-テトラヒドロアクリジン-9-アミン · テトラヒドロアミナクリン

https://huagongshe.com/ja/chemical/1935

タクリン の分子構造式

識別子と物理属性

CAS No.206658-92-6
分子式C13H14N2
平均分子量198.26 g/mol
単同位体質量198.11569846 g/mol
SMILESNc1c2c(nc3ccccc13)CCCC2
InChIKeyYLJREFDVOIBQDA-UHFFFAOYSA-N
PubChem CID1935
ChEMBLCHEMBL1337960
ChEBICHEBI:45980
EC No.206-291-2
DTXSIDDTXSID1037272
現地名タクリン

化学・物理的性質

XLogP2.7
極性表面積38.9
水素結合供与体数1
水素結合受容体数2
回転可能結合数0
重原子数15
形式電荷0
複雑度229
医薬品Pharmaceuticals -> Listed in ZINC15
LogP（分配係数）2.22.71
溶解度1.36e-01 g/LDMSO (Slightly), Methanol (Slightly)
融点183.5 °C183.5℃
Physical DescriptionSolid
Dissociation Constants9.89.859.95 (at 20 °C)
Collision Cross Section142.7 Ų [M+H]+ [CCS Type: DTBuffer gas: N2Ionization: ESI+Dataset: TOXCASTSource Identifier: DTXSID1037272]148.62 Ų [M+K]+ [CCS Type: TWMethod: calibrated with polyalanine and drug standards]
沸点325.59°C (rough estimate)
密度0.9827 (rough estimate)
屈折率1.4400 (estimate)
貯蔵条件4°C, away from moisture and light
外観・状態Solid
pKa（酸解離定数）9+-.0.20(Predicted)
色White to Pale Yellow
CAS データベース321-64-2(CAS DataBase Reference)

安全性と法規制

GHS 分類DangerH301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]P203, P261, P262, P264, P264+P265, P270, P271, P280, P301+P316, P302+P352, P304+P340, P305+P351+P338, P316, P318, P319, P321, P330, P332+P317, P337+P317, P361+P364, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)Aggregated GHS information provided per 40 reports by companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
Hazard Classes and CategoriesAcute Tox. 3 (100%)
TreatmentIf the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.
健康影響Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

用途

説明

In the 1950s, tacrine was used experimentally to reverse cholinergic coma in animals. In the 1960s, tacrine was used to reverse the effects of phencyclidine-like drugs. It was also marketed for many years as a respiratory stimulant. In 1993, the US Food and Drug Administration approved tacrine for the treatment of symptoms of mild to moderate Alzheimer’s disease.

使用

The current use of tacrine is limited due to its poor oral bioavailability, the necessity for four daily doses, and serious side effects (including nausea, vomiting, dry mouth, indigestion, diarrhea, loss of appetite, urinary incontinence, collapse, convulsions, and hepatotoxicity). Currently, newer cholinesterase inhibitors (such as donepezil, rivastigmine, and galantamine) are preferred over tacrine.

HepatotoxicityStrikingly, therapy with tacrine was associated with serum aminotransferase elevations in almost half of patients. These elevations usually arose within 6 to 8 weeks of starting therapy and rapidly resolved when therapy was stopped. Elevations above 3 times the upper limit of the normal range (ULN) occurred in 25%, above 10 times ULN in 6% and above 20 times ULN in 2% of patients. Accompanying elevations in alkaline phosphatase and bilirubin were rare, and the ALT abnormalities were usually asymptomatic and resolved rapidly when therapy was stopped or with dose reduction. Monitoring of serum aminotransferase levels during tacrine therapy was recommended, with dose modification for ALT elevations above 3 times the ULN and discontinuation if levels rose above 5 times the ULN. In prelicensure studies, no instances of clinically apparent acute liver injury with jaundice were reported. Subsequently, however, several cases of acute hepatocellular injury with jaundice attributed to tacrine were reported, generally arising within 2 to 8 weeks of starting therapy and usually resolving rapidly with discontinuation. Eosinophilia often accompanied the hepatic injury due to tacrine, but rash and fever were uncommon as were autoantibodies. Rechallenge often led to recurrence of the hepatic injury with a somewhat shorter latency but similar or milder course. In many patients, the serum aminotransferase elevations resolved even without drug discontinuation or dose modification. Nevertheless, fatal cases of liver injury attributed to tacrine were reported to the sponsor. Routine monitoring of serum aminotransferase levels for the first six months of therapy was recommended. However, the availability of other oral anticholinesterase inhibitors that are given only once or twice daily, do not require ALT monitoring and only rarely cause liver enzyme elevations has led to the withdrawal of tacrine from clinical use in the United States.
暴露経路Oral. Tacrine is rapidly absorbed. Absolute bioavailability of tacrine is approximately 17%.
毒性の概要Tacrine is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.
Signs and SymptomsOverdosage with cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved.
Carcinogen ClassificationNo indication of carcinogenicity to humans (not listed by IARC).
Drug Induced Liver InjuryBenchmark Dataset for the Liver Toxicity Knowledge Base (LTKB)tacrineCognex®Cholinergics7most-DILI-concern
注意喚起語危険
危険有害性情報コード 危険有害性情報 危険有害性クラス 区分 注意喚起語 シンボル P コード H315