CAS 50-78-2 Acetylsalicylic Acid , Popular Products C9H8O4 cas 50-78-2 Acetylsalicylic acid

Aspirin

Benzoic acid,2-(acetyloxy)-;Rhodine;Salicylic acid acetate;2-(Acetyloxy)benzoic acid;Aceticyl;Acetilum acidulatum;Acetophen;Acetosal;Acetosalic acid;Acetosalin;o-Acetoxybenzoic acid;2-Acetoxybenzoic acid;Acetylin;Acetylsal;Acidum acetylsalicylicum;Acylpyrin;Aspirin;Aspirine;Aspro;Asteric;A.S.A. Empirin;Helicon;Measurin;Salacetin;Salcetogen;Saletin;Xaxa;Acetylsalicylic acid;Asagran;Rhonal;Acenterine;SP 189;ASA;Duramax;Ecotrin;Entrophen;Enterosarine;Neuronika;Endydol;Acetisal;Colfarit;Acisal;Dolean pH 8;AC 5230;Acesal;Polopiryna;o-Carboxyphenyl acetate;Triple-sal;Rheumintabletten;Idragin;Yasta;Benaspir;Temperal;Bialpirina;2-Carboxyphenyl acetate;Globentyl;Novid;Globoid;O-Acetylsalicylic acid;Micristin;Acetysal;Acetard;Medisyl;Caprin;ECM;Empirin;Istopirin;o-(Acetyloxy)benzoic acid;Endosprin;Aspro Clear;Kapsazal;Aspropharm;Zorprin;Aspirina 03;Rhodine NC RP;Acesan;Miniasal;Aspirin Protect 100;Aspirin Protect 300;Melhoral;Claradin;Coricidin;Contrheuma Retard;Aspalon;Aspergum;Bialpirinia;Enterophen;Solpyron;Easprin;Darvon Compound;Extren;Gelprin;Nu-seals;Supac;Acetyonyl;Persistin;Acimetten;Coricidin D;Aspirdrops;Salycylacetylsalicylic acid;Ascriptin;Crystar;Ascoden 30;Asatard;Entericin;Albyl E;Adiro;Cardioaspirina;Ewin;Dominal;Toldex;NSC 27223;NSC 406186;Ascolong;Aspirin-Direkt;Asaflow;Trombyl;Magnecyl;Lysoprin (pharmaceutical);Salospir;Rhodine 2312;Astrix;Mycropyrin;Colsprin;Ecosprin;2349-94-2;11126-35-5;11126-37-7;26914-13-6;98201-60-6;2087491-38-9

50-78-2

C9H8O4

BSYNRYMUTXBXSQ-UHFFFAOYSA-N

180.16

180.16

200-064-1

Monoclinic tablets or needle-like crystals; Colorless to white, crystalline powder.

3004909090

Inorganic Salts

63.60000

Acetylsalicylic acid appears as odorless white crystals or crystalline powder with a slightly bitter taste. (NTP, 1992); Odorless, colorless to white, crystal-line powder. [aspirin] [Note: Develops the vinegar-like odor of acetic acid on contact with moisture.]; Solid; COLOURLESS-TO-WHITE CRYSTALS OR WHITE CRYSTALLINE POWDER WITH CHARACTERISTIC ODOUR.; Odorless, colorless to white, crystal-line powder.

1.18

Acetylsalicylic acid appears as odorless white crystals or crystalline powder with a slightly bitter taste. (NTP, 1992)

1.4 (NTP, 1992) - Denser than water; will sink; 1.40; 1.4 g/cm³; 1.35

275 °F (NTP, 1992); 138-140; 135 °C (rapid heating); 135 °C; 275 °F

284 °F at 760 mmHg (decomposes) (NTP, 1992); 140; 284 °F (decomposes); 284 °F (Decomposes)

250ºC

1.551

less than 1 mg/mL at 73 °F (NTP, 1992); 10; 1 g sol in: 300 mL water at 25 °C, 100 mL water at 37 °C, 5 mL alcohol, 17 mL chloroform, 10-15 mL ether; less sol in anhydrous ether; In water, 4,600 mg/L at 25 °C; Solubility in water, g/100ml at 15 °C: 0.25 (poor); (77 °F): 0.3%

Chewable aspirin tablets containing 81 mg of the drug should be stored in child-resistant containers holding not more than 36 tablets each in order to limit the potential toxicity associated with accidental ingestion in children. Aspirin suppositories should be stored at 2-15 °C.

0 mmHg (approx) (NIOSH, 2024); 2.52X10-5 mm Hg at 25 °C (calc); Vapor pressure, Pa at 25 °C: ~ 0.004; 0 mmHg (approx)

100 mg/kg) and with salicylate levels of greater than 25 mg/dL, but mild-to-moderate ALT elevations occur with even lower doses and lower serum levels. These abnormalities resolve rapidly with discontinuation of aspirin, but instances of resolution despite continuation of aspirin in the same or lower doses (adaptation) have also been described. The hepatotoxicity of aspirin is usually mild and asymptomatic, although with higher doses symptoms of nausea, anorexia and abdominal pain and even encephalopathy with signs of hepatic dysfunction (hyperammonemia and coagulopathy) can occur. Bilirubin elevations are usually mild or absent. Mild eosinophilia may accompany the enzyme elevations, but rash, fever and other allergic manifestations are rare. Liver biopsy histology generally shows minimal injury despite the height of the enzyme elevations; electron microscopy may reveal fat and mitochondrial abnormalities. Aspirin can often be continued in lower doses safely. Likelihood score: A[HD] (well known cause of clinically apparent liver injury when given in high doses). Drug Induced Liver Injury Rank (DILIrank 2.0) Aspirin vLess-DILI-concern 0 No match DOI:10.1016/j.drudis.2016.02.015 Drug-Induced Liver Injury Severity and Toxicity (DILIst) aspirin DILI Positive Oral DOI:10.1016/j.drudis.2019.09.022 No indication of carcinogenicity to humans (not listed by IARC). Might i">IDENTIFICATION: Acetylsalicylic acid is colorless or white crystals or white crystalline powder or granules; odorless or almost odorless with a slight acid taste. It is soluble in water. Indications: It is used as an analgesic for the treatment of mild to moderate pain, as an anti-inflammatory agent for the treatment of soft tissue and joint inflammation, and as an antipyretic drug. In low doses salicylate is used for the prevention of thrombosis. HUMAN EXPOSURE: The toxic effects of salicylate are complex. The following appear to be the principal primary effects of salicylate in overdose: Stimulation of the respiratory center; inhibition of citric acid cycle (carbohydrate metabolism); stimulation of lipid metabolism; inhibition of amino acid metabolism; and uncoupling of oxidative phosphorylation. Respiratory alkalosis, metabolic acidosis, water and electrolyte loss occur as the principal secondary consequences of salicylate intoxication. Central nervous system toxicity (including tinnitus, hearing-loss, convulsions and coma), hypoprothrombinemia and non-cardiogenic pulmonary edema may also occur, though for some the mechanism remains uncertain. Target organs: The target organs are: all tissues (whose cellular metabolism is affected), but in particular the liver, kidneys, lungs and the VIIIth cranial nerve. Summary of clinical effects: the following are symptoms of intoxication: Nausea, vomiting, epigastric discomfort, gastrointestinal bleeding (typically with chronic and rarely with acute intoxication); tachypnea and hyperpnea; tinnitus, deafness, sweating, vasodilatation, hyperpyrexia (rare), dehydration; irritability, tremor, blurring of vision, subconjunctival haemorrhages. The following are the effects on blood glucose: hyper- or hypoglycemia; effects on blood: hypoprothrombinemia; effects on liver: increased serum aminotransferase activities (SGOT and SGPT). Non-cardiogenic pulmonary edema; confusion, delirium, stupor, asterixis, coma, cerebral edema (with severe intoxication only); acute renal failure; cardio-respiratory arrest (with severe intoxication only). Absorption by route of exposure: After oral administration, 80 - 100% will be absorbed in the stomach and in the small intestine. However, bioavailability is lower because partial hydrolysis occurs during absorption and there is a "first-pass" effect in the liver. The non-protein bound fraction of salicylate increases with the total plasma concentration, and the binding capacity of albumin is partially saturated at therapeutic concentrations of salicylate. The greater proportion of unbound drug found at high concentrations will mean that greater toxicity will result than would be expected from the total salicylate concentration. Absorption after rectal administration is slow and unpredictable. Timed-release preparations are therapeutically of limited value because of the prolonged half-life of elimination of salicylate. Contraindications: Acetylsalicylic acid is contraindicated for the following: Absorption of enteric-coated tablets is sometimes incomplete. Active peptic ulcer, febrile/post-febrile illness in children, hemostatic disorders, including anticoagulant and thrombolytic treatment, hypoproteinemia; hypersensitivity; and asthma induced by acetylsalicylic acid or other non-steroidal anti-inflammatory drugs. Caution is indicated in patients with: a history of peptic ulceration or gastro-intestinal hemorrhage, hepatic or renal insufficiency, asthma, children < 2 years, especially in those who are dehydrated Routes of entry: The route of entry is oral. Distribution by route of exposure: Salicylic acid is a weak acid; following oral administration, almost all salicylate is found in the unionized form in the stomach. About 50 - 80% of salicylate in the blood is bound by protein while the rest remain in the active, ionized state; protein binding is concentration-dependent. Saturation of binding sites leads to more free salicylate and increased toxicity. Metabolism: approximately 80% of small doses of salicylic acid is metabolised in the liver. Conjugation with glycine forms salicyluric acid and with glucuronic acid forms salicyl acyl and phenolic glucuronide. These metabolic pathways have only a limited capacity. Small amounts of salicylic acid are also hydroxylated to gentisic acid. With large salicylate doses the kinetics switch from first order to zero order. Elimination by route of exposure: salicylates are excreted mainly by the kidney as salicyluric acid, free salicylic acid, salicylic phenol and acyl glucuronides, and gentisic acid. The analgesic, antipyretic, and anti-inflammatory effects of acetylsalicylic acid are due to actions by both the acetyl and the salicylate portions of the intact molecule as well as by the active salicylate metabolite. Acetylsalicylic acid directly and irreversibly inhibits the activity of both types of cyclooxygenase (COX-1 and COX-2) to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. This makes acetylsalicylic acid different from other NSAIDS (such as diclofenac and ibuprofen) which are reversible inhibitors. Salicylate may competitively inhibit prostaglandin formation. Acetylsalicylic acid's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms; the therapeutic effects are not due to pituitary-adrenal stimulation. The platelet aggregation-inhibiting effect of acetylsalicylic acid specifically involves the compound's ability to act as an acetyl donor to cyclooxygenase; the nonacetylated salicylates have no clinically significant effect on platelet aggregation. Irreversible acetylation renders cyclooxygenase inactive, thereby preventing the formation of the aggregating agent thromboxane A2 in platelets. Since platelets lack the ability to synthesize new proteins, the effects persist for the life of the exposed platelets (7-10 days). Acetylsalicylic acid may also inhibit production of the platelet aggregation inhibitor, prostacyclin (prostaglandin I2), by blood vessel endothelial cells; however, inhibition prostacyclin production is not permanent as endothelial cells can produce more cyclooxygenase to replace the non-functional enzyme. Patients on long term, moderate-to-high dose aspirin therapy frequently have elevations in serum ALT levels. With high doses, ALT elevations are common and can be marked and associated with mild increases in alkaline phosphatase and bilirubin. The more dramatic examples of aspirin hepatotoxicity usually occur with doses of 1,800 to 3,200 mg daily (>100 mg/kg) and with salicylate levels of greater than 25 mg/dL, but mild-to-moderate ALT elevations occur with even lower doses and lower serum levels. These abnormalities resolve rapidly with discontinuation of aspirin, but instances of resolution despite continuation of aspirin in the same or lower doses (adaptation) have also been described. The hepatotoxicity of aspirin is usually mild and asymptomatic, although with higher doses symptoms of nausea, anorexia and abdominal pain and even encephalopathy with signs of hepatic dysfunction (hyperammonemia and coagulopathy) can occur. Bilirubin elevations are usually mild or absent. Mild eosinophilia may accompany the enzyme elevations, but rash, fever and other allergic manifestations are rare. Liver biopsy histology generally shows minimal injury despite the height of the enzyme elevations; electron microscopy may reveal fat and mitochondrial abnormalities. Aspirin can often be continued in lower doses safely. Likelihood score: A[HD] (well known cause of clinically apparent liver injury when given in high doses). Drug Induced Liver Injury Rank (DILIrank 2.0) Aspirin vLess-DILI-concern 0 No match DOI:10.1016/j.drudis.2016.02.015 Drug-Induced Liver Injury Severity and Toxicity (DILIst) aspirin DILI Positive Oral DOI:10.1016/j.drudis.2019.09.022 No indication of carcinogenicity to humans (not listed by IARC). Might i

Combustible Powder; explosion hazard if dispersed in air.

Odorless, but in moist air it is gradually hydrolyzed and acquires odor of acetic acid; Odorless [Note: Develops the vinegar-like odor of acetic acid on contact with moisture].

3.5None

3.47; 3.5; pKa = 3.49 at 25 °C

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. (NTP, 1992)

Combustible Powder; explosion hazard if dispersed in air.

Dust explosion possible if in powder or granular form, mixed with air.