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アセチルサリチル酸 化学構造式
アセチルサリチル酸;アスピリン[商品名];アスピリン;2-アセトキシ安息香酸;o-アセトキシ安息香酸;アセチルサリチル酸標準品;アセチルサリチル酸【アスピリン】;アスパロン;アスパロン (JAN);アスピリン (JP17)
Acetylsalicylic acid
MOL File:

アセチルサリチル酸 物理性質

融点 :
134-136 °C(lit.)
沸点 :
272.96°C (rough estimate)
比重(密度) :
屈折率 :
1.4500 (estimate)
闪点 :
250 °C
貯蔵温度 :
Store at RT.
H2O: 10 mg/mL at 37 °C
外見 :
3.5(at 25℃)
水溶解度 :
3.3 g/L (20 ºC)
Merck :
Stable. Keep dry. Incompatible with strong oxidizing agents, strong bases, strong acids, various other compounds such as iodides, iron salts, quinine salts, etc.
CAS データベース:
50-78-2(CAS DataBase Reference)
Benzoic acid, 2-(acetyloxy)-(50-78-2)
Benzoic acid, 2-(acetyloxy)-(50-78-2)
  • リスクと安全性に関する声明
  • 危険有害性情報のコード(GHS)
主な危険性  Xn
Rフレーズ  22-36/37/38
Sフレーズ  26-36/37/39
WGK Germany  1
RTECS 番号 VO0700000
国連危険物分類  6.1
容器等級  III
HSコード  29182210
有毒物質データの 50-78-2(Hazardous Substances Data)
毒性 LD50 orally in mice, rats: 1.1, 1.5 g/kg (Hart)
化審法 (3)-1652
安衛法 57,57-2
注意喚起語 Warning
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
H301 飲み込むと有毒 急性毒性、経口 3 危険 P264, P270, P301+P310, P321, P330,P405, P501
H302 飲み込むと有害 急性毒性、経口 4 警告 P264, P270, P301+P312, P330, P501
H315 皮膚刺激 皮膚腐食性/刺激性 2 警告 P264, P280, P302+P352, P321,P332+P313, P362
H319 強い眼刺激 眼に対する重篤な損傷性/眼刺激 性 2A 警告 P264, P280, P305+P351+P338,P337+P313P
H334 吸入するとアレルギー、喘息または、呼吸困難 を起こすおそれ 感作性、呼吸器 1 危険 P261, P285, P304+P341, P342+P311,P501
H335 呼吸器への刺激のおそれ 特定標的臓器毒性、単回暴露; 気道刺激性 3 警告
H360 生殖能または胎児への悪影響のおそれ 生殖毒性 1A, 1B 危険
H371 臓器の障害のおそれ 特定標的臓器有害性、単回暴露 2 警告 P260, P264, P270, P309+P311, P405,P501
H373 長期にわたる、または反復暴露により臓器の障 害のおそれ 特定標的臓器有害性、単回暴露 2 警告 P260, P314, P501
P201 使用前に取扱説明書を入手すること。
P202 全ての安全注意を読み理解するまで取り扱わないこ と。
P260 粉じん/煙/ガス/ミスト/蒸気/スプレーを吸入しないこ と。
P261 粉じん/煙/ガス/ミスト/蒸気/スプレーの吸入を避ける こと。
P264 取扱い後は皮膚をよく洗うこと。
P264 取扱い後は手や顔をよく洗うこと。
P270 この製品を使用する時に、飲食または喫煙をしないこ と。
P280 保護手袋/保護衣/保護眼鏡/保護面を着用するこ と。
P284 呼吸用保護具を着用すること。
P304+P340 吸入した場合:空気の新鮮な場所に移し、呼吸しやすい 姿勢で休息させること。
P305+P351+P338 眼に入った場合:水で数分間注意深く洗うこと。次にコ ンタクトレンズを着用していて容易に外せる場合は外す こと。その後も洗浄を続けること。

アセチルサリチル酸 価格 もっと(32)

メーカー 製品番号 製品説明 CAS番号 包装 価格 更新時間 購入
富士フイルム和光純薬株式会社(wako) W01CAY70260
50-78-2 50g ¥2300 2018-12-26 購入
富士フイルム和光純薬株式会社(wako) W01CAY70260
50-78-2 100g ¥3500 2018-12-26 購入
東京化成工業 A2262 アセチルサリチル酸 >98.0%(GC)(T)
Acetylsalicylic Acid >98.0%(GC)(T)
50-78-2 500g ¥4200 2018-12-04 購入
東京化成工業 A2262 アセチルサリチル酸 >98.0%(GC)(T)
Acetylsalicylic Acid >98.0%(GC)(T)
50-78-2 25g ¥1600 2018-12-04 購入
関東化学株式会社(KANTO) 01058-00 アセチルサリチル酸 >99.0%(T)
Acetylsalicylic acid >99.0%(T)
50-78-2 500g ¥5000 2018-12-13 購入

アセチルサリチル酸 MSDS

Acetylsalicylic acid

アセチルサリチル酸 化学特性,用途語,生産方法




水に難溶。エタノール, アセトンに易溶。水に難溶、エタノール, アセトンに易溶、エーテル, 水酸化ナトリウム溶液に可溶。エタノール及びアセトンに溶けやすく、水に溶けにくい。




サリチル酸系化合物です。シ クロオキシゲナーゼ1(COX-1)を選択的に 阻害します。


シクロオキシゲナーゼ1 (COX-1)を選択的に阻害し、プロスタグラ ンジン生合成阻害作用を示します。




鎮痛薬, 抗炎症薬, 解熱薬, 抗リウマチ薬, 抗血小板薬, シクロオキシゲナーゼ阻害薬


アスピリン (バイエル薬品); アスピリン (マイラン製薬); アスピリン (丸石製薬); アスピリン (健栄製薬); アスピリン (吉田製薬); アスピリン (小堺製薬); アスピリン (山善製薬); アスピリン (日医工)


アセチルサリチル酸(アセチルサリチルさん、英: acetylsalicylic acid)は、代表的な消炎鎮痛剤のひとつで非ステロイド性抗炎症薬の代名詞とも言うべき医薬品。ドイツのバイエル社が名付けた商標名のアスピリン(独: Aspirin)がよく知られ、日本薬局方ではアスピリンが正式名称になっている。


Acetylsalicylic acid is a white crystalline powder commonly known by its common name as aspirin or ASA. Aspirin is the most widely used medication in the world.


Aspirin (USAN), also known as acetyl salicylic acid (abbreviated ASA ) , is a salicylate drug, often used as an analgesic to relieve minor aches and pains, as an antipyretic to reduce fever, and as an anti - inflammatory medication. Aspirin may be effective at preventing certain types of cancer, particularly colorectal cancer.
The main undesirable side effects of aspirin taken by mouth are gastrointestinal ulcers, stomach bleeding, and tinnitus, especially in higher doses. In children and adolescents, aspirin is no longer indicated to control flu - like symptoms or the symptoms of chickenpox or other viral illnesses, because of the risk of Reye's syndrome.
Aspirin is part of a group of medications called non steroidal anti - inflammatory drugs (NSAIDs), but differs from most other NSAIDs in the mechanism of action. Though it, and others in its group called the salicylates, have similar effects (antipyretic, antiinflammatory, analgesic) to the other NSAIDs and inhibit the same enzyme cyclooxygenase, aspirin (but not the other salicylates) does so in an irreversible manner and, unlike others, affects more the COX-1 variant than the COX-2 variant of the enzyme.
Today, aspirin is one of the most widely used medications in the world, with an estimated 40,000 tonnes of it being consumed each year . In countries where Aspirin is a registered trademark owned by Bayer, the generic term is acetylsalicylic acid (ASA).


Acetylsalicylic acid is a white crystalline solid with a slightly bitter taste. It is odorless but hydrolyzes in moist air to give an acetic acid odor


White Solid


Aspirin, an acetyl derivative of salicylic acid, is a white, crystalline, weakly acidic substance, with a melting point of 136 °C , and a boiling point of 140 °C .
The synthesis of aspirin is classified as an esterification reaction. Salicylic acid is treated with acetic anhydride, an acid derivative, causing a chemical reaction that turns salicylic acid's hydroxyl group into an ester group (R-OH → R-OCOCH3). This process yields aspirin and acetic acid, which is considered a byproduct of this reaction.
Polymorphism, or the ability of a substance to form more than one crystal structure, is important in the development of pharmaceutical ingredients. Many drugs are receiving regulatory approval for only a single crystal form or polymorph. For a long time, only one crystal structure for aspirin was known. That aspirin might have a second crystalline form was suspected since the 1960s. The elusive second polymorph was first discovered by Vishweshwar and coworkers in 2005 , and fine structural details were given by Bond et al. .


The use of salicylic acid goes back thousands of years, and there are numerous accounts of the medicinal properties of plants from the Salix (willow) and Myrtaceae (Myrtle) families. Writings from ancient civilizations indicate the use of willow bark in Mesopotamia and myrtle leaves in Egypt as medicines existing several thousand years b.c.e. Hippocrates (460–377 b.c.e. ) and the ancient Greeks used powdered willow bark and leaves to reduce fever (antipyretic) and as a pain reliever (analgesic). Willow and oil of wintergreen was used as medications by native Americans.
The chemical responsible for the medicinal properties in willow and oil of wintergreen are forms of salicylates, a general name to describe compounds containing the general structure of salicylic acid. Willows (genus Salix) contain salicin and oil of wintergreen contains methyl salicylate. Although the use of willow bark and oil of wintergreen as an accepted antipyretic and analgesic has occurred for at least 2,000 years, by the 19th century medicines were starting to be synthesized in chemical laboratories.


Aspirin’s original use as an analgesic, an antipyretic, and to reduce inflammation continues to this day. More recently there is some evidence that aspirin lessens the chance of heart attacks as a result of its effect as a blood “thinner.”




Axepim Cephalosporin antibiotic


Analgesic; antipyretic; anti-inflammatory; antithrombotic


ChEBI: A member of the class of benzoic acids that is salicylic acid in which the hydrogen that is attached to the phenolic hydroxy group has been replaced by an acetoxy group. A non-steroidal anti-inflammatory drug with moA cyclooxygenase inhibitor activity.


Aspirin is available as capsules, tablets, enteric-coated tablets (Ecotrin), timed-release tablets (ZORprin), buffered tablets (Ascriptin, Bufferin), and as rectal suppositories. Sodium salicylate is available generically. Other salicylates include choline salicylate (Arthropan), choline magnesium trisalicylate (Trilisate), and magnesium salicylate (Momentum).

brand name



Acetylsalicylic acid, a nonsteroidal anti-inflammatory, analgesic and antipyretic agent, was introduced into medicine in 1899 and has since been widely available in over-the-counter preparations. Recent studies carried out in the USA have shown an association between acetylsalicylic acid consumption in children and the development of Reye's syndrome (a rare condition characterized by a combination of encephalopathy and liver disorder and usually preceded by an acute viral illness, such as influenza, diarrhoea, or chickenpox). Many drug regulatory authorities have acted to caution against the use of the drug in children and young adults with febrile conditions. Even within this group the risk of exposure is remote and has been estimated to be of the order of 1.5 per million. This warning also concerns products containing other salicylates. The new indication of acetylsalicylic acid - prophylaxis of myocardial infarction due to its antithrombotic effect - requires loneterm use and may lead to serious adverse reactions, including cerebral haemorrhage. Acetylsalicylic acid retains a valuable place in medicine and remains in the WHO Model List of Essential Drugs.


Aspirin is one of the most important NSAIDs because it decreases pain at predominantly peripheral sites with little cortical interaction and thus has few CNS effects. The prototypical COX-2 inhibitors are celecoxib (Celebrex) and its chemical cousin, rofecoxib (Vioxx). In addition to a role in inflammatory processes,COX-2 seems to play a role in colon cancer and Alzheimer’s disease, providing potential additional uses for COX-2-selective drugs.


Aspirin, acetylsalicylic acid (Aspro, Empirin), was introducedinto medicine by Dreser in 1899.Aspirin occurs as white crystals or as a white crystallinepowder and must be kept under dry conditions. It is not advisableto keep aspirin products in the kitchen or bathroomcabinets, because aspirin is slowly decomposed into aceticand salicylic acids in the presence of heat and moisture.Several proprietaries (e.g., Bufferin) use compounds such as sodium bicarbonate, aluminum glycinate, sodium citrate,aluminum hydroxide, or magnesium trisilicate to counteractaspirin’s acidic property. One of the better antacids is dihydroxyaluminumaminoacetate. Aspirin is unusually effectivewhen prescribed with calcium glutamate. The more stable,nonirritant calcium acetylsalicylate is formed, and theglutamate portion (glutamic acid) maintains a pH of 3.5 to5. Practically all salts of aspirin, except those of aluminumand calcium, are unstable for pharmaceutical use. Thesesalts appear to have fewer undesirable side effects and induceanalgesia faster than aspirin. A timed release preparationof aspirin is available. It does not appear to offer anyadvantages over aspirin, except for bedtime dosage.


Aspirin, acetylsalicylic acid, has an inhibitoryeffect on platelet aggregation not only because of its abilityto inhibit cyclooxygenase (COX) but also because of its ability to acetylate the enzyme. Aspirin irreversibly inhibitsCOX (prostaglandin H synthase), which is the enzyme involvedin converting arachidonate to prostaglandin G2 andultimately thromboxane 2, an inducer of platelet aggregation.Aspirin’s mechanism of action includes not only the inhibitionin the biosynthesis of thromboxane 2, but also itsability to acetylate the serine residue (529) in the polypeptidechain of platelet prostaglandin H synthetase-1. Thisexplains why other nonsteroidal anti-inflammatory agentsthat are capable of inhibiting the COX enzyme do not act asantithrombotics—they are not capable of acetylating thisenzyme. Because platelets cannot synthesize new enzymes,aspirin’s ability to acetylate COX lasts for the life of theplatelet (7–10 days) and is, thus, irreversible.


Odorless white crystals or crystalline powder with a slightly bitter taste.


Slowly hydrolyzes in moist air. Has been involved in dust cloud explosions. Water insoluble. Solution in water is acid to methyl red indicator.


The active ingredient in common aspirin. Incompatible with oxidizers and strong acids. Also incompatible with strong bases. May react with water or nucleophiles (e.g. amines and hydroxy groups). May also react with acetanilide, amidopyrine, phenazone, hexamine, iron salts, phenobarbitone sodium, quinine salts, potassium and sodium iodides, alkali hydroxides, carbonates, stearates and paracetanol.


An allergen; may cause local bleeding espe- cially of the gums; 10-g dose may be fatal. May cause excessive biosynthesis of prostaglandins. Dust dispersed in air is serious explosion risk. Skin and eye irritant.


Acetylsalicylic acid is combustible.


Discovery of the mechanism
In 1971, British pharmacologist John Robert Vane, then employed by the Royal College of Surgeons in London, showed aspirin suppressed the production of prostaglandins and thromboxanes.
Suppression of prostaglandins and thromboxanes
Aspirin's ability to suppress the production of prostaglandins and thromboxanes is due to its irreversible inactivation of the cyclo oxygenase (PTGS) enzyme required for prostaglandin and thromboxane synthesis. Aspirin acts as an acetylating agent where an acetyl group is covalently attached to a serine residue in the active site of the PTGS enzyme.
COX-1 and COX-2 inhibition
There are at least two different types of cyclooxygenase: COX-1 and COX-2. Aspirin irreversibly inhibits COX-1 and modifies the enzymatic activity of COX-2. COX-2 normally produces prostanoids, most of which are proinflammatory. Aspirin-modified PTGS2 produces lipoxins, most of which are anti-inflammatory.
Additional mechanisms
Aspirin has been shown to have at least three additional modes of action. It uncouples oxidative phosphorylation in cartilaginous (and hepatic) mitochondria, by diffusing from the inner membrane space as a proton carrier back into the mitochondrial matrix, where it ionizes once again to release protons . In short, aspirin buffers and transports the protons. When high doses of aspirin are given, it may actually cause fever, owing to the heat released from the electron transport chain, as opposed to the antipyretic action of aspirin seen with lower doses.
Hypothalamic - pituitary - adrenal activity
Aspirin, like other medications affecting prostaglandin synthesis, has profound effects on the pituitary gland, which indirectly affects a number of other hormones and physiological functions.


Although aspirin itself is pharmacologically active, it is rapidly hydrolyzed to salicylic acid after its absorption, and it is the salicylate anion that accounts for most of the anti-inflammatory activity of the drug. The superior analgesic activity of aspirin compared with sodium salicylate implies that aspirin has an intrinsic activity that is not totally explainable by its conversion to salicylic acid. Aspirin inhibits COX-1 to a much greater extent than COX-2; sodium salicylate is more selective for COX-1. This, combined with the ability of aspirin to acetylate proteins, might account for some of the therapeutic and toxicological differences between aspirin and the other salicylates.
The binding of salicylic acid to plasma proteins varies with its plasma concentrations. At serum salicylic acid concentrations of less than 100 μg/mL, 90 to 95% is protein bound; at 100 to 400 μg/mL, 70 to 85% is protein bound; and at concentrations greater than 400 μg/mL, 20 to 60% is protein bound. The plasma concentration of salicylate that is associated with antiinflammatory activity (200–300 μg/mL) is about six times that needed to produce analgesia. At these higher concentrations, salicylate metabolism is reduced, resulting in a longer half-life for the drug. This reaction is a consequence of the saturable enzyme systems that metabolize salicylates. The plasma half-life for salicylate has been estimated to be 3 to 6 hours at the lower (analgesic) dosage and 15 to 30 hours at the higher (antiinflammatory) dosages.The rate of hydrolysis of aspirin to salicylic acid is not dose limited, and no differences in the absorption of aspirin have been observed between arthritic patients and normal individuals.


Salicylic acid is a weak acid, and very little of it is ionized in the stomach after oral administration. Acetylsalicylic acid is poorly soluble in the acidic conditions of the stomach, which can delay absorption of high doses for eight to 24 hours. The increased pH and larger surface area of the small intestine causes aspirin to be absorbed rapidly there, which in turn allows more of the salicylate to dissolve. Owing to the issue of solubility, however, aspirin is absorbed much more slowly during overdose, and plasma concentrations can continue to rise for up to 24 hours after ingestion.


Aspirin is used in the treatment of a number of conditions, including fever, pain, rheumatic fever, and inflammatory diseases, such as rheumatoid arthritis, pericarditis, and Kawasaki disease.
Asprin 325 MG for pain In most cases, aspirin is considered inferior to ibuprofen for the alleviation of pain, because aspirin is more likely to cause gastrointestinal bleeding . Aspirin is generally ineffective for those pains caused by muscle cramps, bloating, gastric distension, or acute skin irritation.
Aspirin, either by itself or in combined formulation, effectively treats some types of headache, but its efficacy may be questionable for others.
Aspirin or other overthe- counter analgesics are widely recognized as effective for the treatment of tension headache. Aspirin, especially as a component of an acetaminophen/aspirin/caffeine formulation (e.g., Excedrin Migraine), is considered a first - line therapy in the treatment of migraine, and comparable to lower doses of sumatriptan.
Like its ability to control pain, aspirin's ability to control fever is due to its action on the prostaglandin system through its irreversible inhibition of COX .
Heart attacks and strokes
For a subset of the population, aspirin may help prevent heart attacks and strokes. In lower doses, aspirin has been known to prevent the progression of existing cardiovascular disease, and reduce the frequency of these events for those with a history of them . ( This is known as secondary prevention.)
After percutaneous coronary interventions (PCIs), such as the placement of a coronary artery stent, a US Agency for Healthcare Research and Quality guideline recommends that aspirin be taken indefinitely.Frequently, aspirin is combined with an ADP receptor inhibitor, such as clopidogrel, prasugrel or ticagrelor to prevent blood clots. This is called dual anti-platelet therapy (DAPT).


Aspirin should not be taken by people who are allergic to ibuprofen or naproxen , or who have salicylate intolerance[70][71] or a more generalized drug intolerance to NSAIDs, and caution should be exercised in those with asthma or NSAID - precipitated bronchospasm.
Aspirin use has been shown to increase the risk of gastrointestinal bleeding . Although some enteric-coated formulations of aspirin are advertised as being "gentle to the stomach", in one study, enteric coating did not seem to reduce this risk. Combining aspirin with other NSAIDs has also been shown to further increase this risk.
Central effects
Large doses of salicylate, a metabolite of aspirin, have been proposed to cause tinnitus (ringing in the ears) based on experiments in rats, via the action on arachidonic acid and NMDA receptors cascade.
's syndrome
';s syndrome, a rare but severe illness characterized by acute encephalopathy and fatty liver, can occur when children or adolescents are given aspirin for a fever or other illnesses or infections.


The most common adverse effects produced by the salicylates are GI disturbances. Occult blood loss from the GI tract, peptic ulceration, and rarely, severe GI hemorrhage can occur. Because salicylic acid is highly bound to plasma proteins, it may be displaced by other highly protein-bound drugs such as oral anticoagulants, sulfonylureas, phenytoin, penicillins, and sulfonamides. The nonacetylated salicylates have greatly reduced effects on blood loss and produce fewer adverse GI effects. In addition, they may be somewhat kidney sparing. Salicylates may provoke hypersensitivity reactions and prolonged bleeding time in some individuals. Tinnitus, hearing impairment, blurred vision, and lightheadedness are indicators of toxic dosages. The use of aspirin in conjunction with any other NSAID is not recommended because of the lack of evidence that such combinations increase efficacy and because of the increased potential for an adverse reaction. Salicylates are contraindicated in children with febrile viral illnesses because of a possible increased risk of Reye’s syndrome.


Poison by ingestion, intraperitoneal, and possibly other routes. Human systemic effects by ingestion: acute pulmonary edema, body temperature increase, changes in kidney tubules, coma, constipation, dehydration, hematuria, hepatitis, nausea or vomiting, respiratory stimulation, somnolence, tinnitus, decreased urine volume. Implicated in aplastic anemia. A 10 gram dose to an adult may be fatal. A human teratogen. Human reproductive effects by ingestion and possibly other routes: menstrual cycle changes, parturition, various effects on newborn including Apgar score, developmental abnormalities of the cardlovascular and respiratory systems. Experimental animal reproductive effects. Human mutation data reported. An allergen; skin contact, inhalation, or ingestion can cause asthma, sneezing, irritation of eyes and nose, hves, and eczema. Combustible when exposed to heat or flame. When heated to decomposition it emits acrid smoke and fumes.


Used as an over-the counter and proprietary pharmaceutical and veterinary drug. Those engagedin manufacture of aspirin or, more likely, in its consumption in widespread use as an analgesic, antipyretic, and antiinflammatory agent


This first-in-class pain-relieving and fever-lowering anti-inflammatory agent (FWfree-acid = 180.16 g/mol; CAS 50-78-2; pKa = 3.49 at 25°C; Solubility = 3.3 mg/mL at 25°C; Symbol: ASA) is the original synthetic nonsteroidal anti-inflammatory drug, or NSAID. Aspirin exerts its effects by inactivating cyclooxygenase (or prostaglandin G/H synthase, or PGHS). It shows somewhat greater selectivity toward COX-1, the type-1 isozyme, with attendent inhibition of prostaglandin formation. Acetylsalicylic acid also inhibits platelet thromboxane synthesis as well as the ADP- and collagen-induced platelet release reaction. Low-dose aspirin is effective in preventing ~20% of atherothrombotic complications (including non-fatal myocardial infarction, non-fatal stroke, or vascular death) in patients with prior evidence of myocardial infarction, stroke, or transient cerebral ischemia. Mechanism of Action: That aspirin targets prostaglandin formation was first demonstrated by Piper & Vane, a finding that earned Vane the Nobel Prize in Physiology and Medicine in 1982. Aspirin selectively acetylates the hydroxyl group of Ser-530 in COX-1, irreversibly inhibiting the enzyme. This outcome requires de novo enzyme synthesis before prostanoid synthesis can resume. When purified PGHS is acetylated, its COX activity is inhibited, but not its hydroperoxidase activity. One acetyl group is incorporated per monomer of the dimeric enzyme. At low concentrations, aspirin acetylates PGHS rapidly (usually within minutes) in a highly selective reaction that prevents arachidonate binding. At higher concentrations, aspirin non-specifically acetylates a variety of proteins and even nucleic acids. Upon modification of COX-2, the latter produces lipoxins, of which most are anti-inflammatory. Pharmacokinetics & Metabolism: Aspirin is both a drug and prodrug, depending on its target. It is rapidly absorbed from the stomach and intestine by passive diffusion. Pertinent PK parameters for acetylsalicylate are: Oral Bioavailability = 68%; Clearance = 39 L/hour; Volume of Distribution = 10.5 L; and t1/2 = 0.25 hours. Acetylsalicylate is transformed into salicylate in stomach, intestinal mucosa, blood, and liver, the latter being the main site. Salicylate distributes rapidly into the body fluid compartments, binding to albumin within plasma. With increasing total plasma salicylate concentrations, the unbound fraction increases. Pertinent PK parameters for salicylate are: Clearance = 0.6-3.6 L/hour, depending on dose; Volume of Distribution = 11.5 L; and t1/2 = 2-30 hours, depending on aspirin dose. Salicylate also activates AMP-stimulated protein kinase (AMPK), a property likely to account for some of aspirin’s anti-cancer and anti-inflammatory effects. ASA can also be used during a heart attack to reduce the risk of dying from the heart attack. Chemical Synthesis: Acetylsalicylate was first synthesized from salicylate and acetyl chloride by Felix Hofmann at Friedrich Bayer & Co. in 1897, and its name universally known name, “aspirin”, was coined by then supervising pharmacologist, Heinrich Dreser, to avoid confusion with salicylic acid. The famously high purity and stability of the Bayer product is evident by the absence of a vinegary odor, long after the packaged product is first opened. Prolonged exposure to moisture, however, generates both acetate and salicylate, with the latter inhibiting some 20-30 enzymes (See Salicylate). Nonenzymatic Aspirin Hydrolysis: Hydrolysis of acetylsalicylic acid presents the interesting case where the reaction rate is pH-independent over range from 4 to 8. As shown nearly a half century ago, aspirin undergoes general base catalysis. Later work suggests that aspirin anion exists only fleetingly, rearranging by acetyl transfer to the ortho-carboxylate group, as indicated by IR, UV and NMR . The mixed anhydride then cyclizes to the more stable bicyclic orthoacetate isomer, a process facilitated by time and increasing pH. Target (s) : prostaglandin-endoperoxide synthase, or cyclooxygenase ; z-crystallin; creatine kinase, 15- hydroxyprostaglandin dehydrogenase; cyclooxygenase-16; cyclooxygenase-26; hemoglobin S polymerization, however, See Reference 13; glutamine:D-fructose-6-phosphate aminotransferase; ATPase, mitochondrial; aryl-acylamidase; palmitoyl-CoA hydrolase, or acyl-CoA hydrolase; phospholipase A2; estrone sulfotransferase; phenol sulfotransferase, or aryl sulfotransferase; IkB kinase; procollagen glucosyltransferase; N- hydroxyarylamine O-acetyltransferase; 1-alkylglycerophosphocholine O-acetyltransferase; thiopurine S-methyltransferase; 3- hydroxyanthranilate 3,4 dioxygenase.


Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In the case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. For minor skin contact, avoid spreading material on unaffected skin. Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves. Medical observation is recommended for 24 to 48 hours after breathing overexposure, as pulmonary edema may be delayed. As first aid for pulmonary edema, a doctor or authorized paramedic may consider administering a drug or other inhalation therapy.


UN2811 Toxic solids, organic, n.o.s., Hazard Class: 6.1; Labels: 6.1-Poisonous materials, Technical Name Required


Crystallise aspirin twice from toluene, wash it with cyclohexane and dry it at 60o under vacuum for several hours [Davis & Hetzer J Res Nat Bur Stand 60 569 1958]. It has been recrystallised from isopropanol and from diethyl ether/pet ether (b 40-60o). It crystallises from EtOH (m 143-144o), *C6H6 (m 143o), hexane (m 115o and 128o), octane (m 121o), and has m 110o after sublimation. It has pK2 6 3.69(H2O), 4.15(20% aqueous EtOH), 4.47(30% aqueous EtOH) and 4.94(40% aqueous EtOH). It is an analgesic. [Beilstein 10 H 67, 10 II 41, 10 III 102, 10 IV 138.]


Incompatible with oxidizers (chlorates, nitrates, peroxides, permanganates, perchlorates, chlorine, bromine, fluorine, etc.); contact may cause fires or explosions. Keep away from alkaline materials, strong bases, strong acids, oxoacids, epoxides, carbonates, moisture. Dust dispersed in air is explosive


May be flushed to sewer with large volumes of water.

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  • アセチルサリチル酸
  • アスピリン[商品名]
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  • アセチルサリチル酸【アスピリン】
  • アスパロン
  • アスパロン (JAN)
  • アスピリン (JP17)
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