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About CAS 103-90-2 Acetaminophen

2024-05-10 09:37:28
Melting point 168-172 °C(lit.)
Boiling point 273.17°C (rough estimate)
density 1,293 g/cm3
vapor pressure 0.008Pa at 25℃
refractive index 1.5810 (rough estimate)
Fp 11 °C
storage temp. Inert atmosphere,Room Temperature
solubility ethanol: soluble0.5M, clear, colorless
pka 9.86±0.13(Predicted)
form Crystals or Crystalline Powder
color White
Acetaminophen, also known as paracetamol, is a chemical compound with the molecular formula C8H9NO2. It is a medication that falls under the class of analgesics (pain relievers) and antipyretics (fever reducers). Structurally, acetaminophen is a para-aminophenol derivative. In terms of physical properties, acetaminophen is a white crystalline powder that is sparingly soluble in water. It is commonly available in various formulations, including tablets, capsules, and liquid suspensions, for oral administration.

Acetaminophen is widely used to alleviate pain and reduce fever. It is known for its effectiveness in relieving mild to moderate pain, such as headaches, muscle aches, and toothaches. Unlike nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen does not have significant anti-inflammatory properties.
The exact mechanism of action of acetaminophen is not fully understood, but it is believed to involve the inhibition of an enzyme called cyclooxygenase (COX) in the central nervous system. This enzyme is involved in the production of prostaglandins, which play a role in pain perception and regulation of body temperature.
Acetaminophen is considered a safer option for pain relief in individuals who cannot tolerate NSAIDs due to factors such as gastric ulcers or bleeding disorders. 

Related research:
In vitro studies In vitro, acetaminophen caused a 4.4-fold selectivity for COX-2 inhibition (IC50 for COX-1, 113.7 μM; IC50 for COX-2, 25.8 μM). After oral administration, maximum ex vivo inhibition was 56% (COX-1) and 83% (COX-2). Acetaminophen plasma concentrations remained above the in vitro IC50 of COX-2 for at least 5 hours after dosing. The ex vivo IC50 values of acetaminophen (COX-1: 105.2 μM; COX-2: 26.3 μM) compare favorably with its in vitro IC50 values. Contrary to previous notions, acetaminophen inhibits COX-2 by more than 80%, a degree comparable to nonsteroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors. However, no >95% COX-1 blockade has been associated with inhibition of platelet function [1]. MTT assay showed that acetaminophen (APAP) at a dose of 50mM significantly (p <0.001) reduced cell viability to 61.5±6.65%. Interestingly, a significant (p < 0.01) increase in cell viability to 79.7 ± 2.47% was observed in acetaminophen/HV110 co-treated cells compared with acetaminophen-treated cells.
In vivo studies: Administration of acetaminophen (250 mg/kg, orally) to mice resulted in significant (p < 0.001) liver damage and cell necrosis, serum liver enzyme alanine aminotransferase (ALT), aminotransferase ( AST), alkaline phosphatase (ALP), and γ-glutamyl transferase (γGT) were elevated compared with the normal group. On the contrary, the effect of pretreatment with different doses of citral (125, 250 and 500 mg/kg) showed a significant (p < 0.05) reduction in serum activities of ALT (91.79%, 93.07% and 95.61%, respectively), AST (93.40%, respectively). 91.89% and 96.52%), ALP (39.29%, 37.07% and 59.80%, respectively) and γGT (92.83%, 91.59% and 93.0%, respectively), compared with the acetaminophen group. SLM pretreatment had similar effects on ALT activity (95.90%), AST (95.03%), ALP (70.52%) and γGT (92.69%).