• Raw Material Powder Phenacetin Reduce Pain Phenacetin
  • Raw Material Powder Phenacetin Reduce Pain Phenacetin
  • Raw Material Powder Phenacetin Reduce Pain Phenacetin
  • Raw Material Powder Phenacetin Reduce Pain Phenacetin
  • Raw Material Powder Phenacetin Reduce Pain Phenacetin

Raw Material Powder Phenacetin Reduce Pain Phenacetin

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10 G

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Product Description


  • CAS: 62-44-2
  • MF: C10H13NO2
  • MW: 179.22
  • EINECS: 200-533-0
  • Chemical name: Phenacetin; Acetophenetidin; N-(4-Ethoxyphenyl)acetamide;Acetphenetidin; Acetophenetidine
  • Appearance: White or almost white crystalline powder

Phenacetin is a synthetic, white crystalline solid that is slightly soluble in water and benzene, soluble in acetone and very soluble in pyrimidine. It is used in research as the preferred marker for detecting CYP1A2-based inhibition potential in vitro. Human ingestion of phenacetin can result in a bluish discoloration of the skin due to a lack of oxygen in the blood (cyanosis), dizziness and respiratory depression. 
Phenacetin is one of the first commercially produced  synthetic pharmaceuticals and the first non-opioid analgesic; it was widely distributed in A.P.C. cold tablets since it was frequently mixed with aspirin and caffeine. This compound is representative of a class of acetanilide-based analogues known to have analgesic and antipyretic properties. Other compounds within this class are paracetamol (acetaminophen), lidocaine and highly potent opioid analgesic acetylfentanyl. Like the parent compound acetanilide, phenacetin is metabolized into paracetamol in the human body. Phenacetin was first withdrawn from market use in Canada in 1978 as it was found to be carcinogenic and cause kidney damage, with most countries withdrawing its use in over-the-counter medications in the subsequent years. Drugs utilizing phenacetin were reformulated with paracetamol, which was found to have similar pain and fever reducing properties but is non-carcinogenic.

Since their synthesis in the late 1800s paracetamol (acetaminophen) and phenacetin have followed divergent pathways with regard to their popularity as mild analgesic/antipyretic drugs. Initially, paracetamol was discarded in favour of phenacetin because the latter drug was supposedly less toxic. Today the opposite is true, and paracetamol, along with aspirin, has become one of the two most popular 'over-the-counter' non-narcotic analgesic agents. This marked increase in the wide approval attained by paracetamol has been accompanied by the virtual commercial demise of phenacetin because of its role, albeit somewhat circumstantial, in causing analgesic nephropathy. Both paracetamol and phenacetin are effective mild analgesics, suitable for treating mild to moderate pain, and their actions are broadly comparable with those of aspirin and related salicylates, although they do not appear to possess significant anti-inflammatory activity. Since a major portion of a dose of phenacetin is rapidly metabolised to paracetamol, it seems possible that phenacetin owes some of its therapeutic activity to its main metabolite, paracetamol, whereas its most troublesome side effect (methaemoglobinaemia) is due to another metabolite, p-phenetidine. The mechanism of action of paracetamol is poorly defined, although it has been speculated that it may selectively inhibit prostaglandin production in the central nervous system, which would account for its analgesic/antipyretic properties. The lack of any significant influence on peripheral cyclooxygenase would explain the absence of anti-inflammatory activity. At therapeutic doses paracetamol is well tolerated and produces fewer side effects than aspirin. The most frequently reported adverse effect associated with paracetamol is hepatotoxicity, which occurs after acute overdosage (usually doses greater than 10 to 15g are needed) and, very rarely, during long term treatment with doses at the higher levels of the therapeutic range. Paracetamol damages the liver through the formation of a highly reactive metabolite which is normally inactivated by conjugation with glutathione. Overdoses of paracetamol exhaust glutathione stores, thus allowing the accumulation of this toxic metabolite which covalently binds with vital cell elements and can result in liver necrosis.  

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