Paracetamol

Effects

Overview

A common, over the counter, fever reducer and painkiller. It is mixed with many common opiates. Can cause liver damage and failure in higher doses. No recreational value. TS

Paracetamol, or acetaminophen, is an analgesic and antipyretic agent used to treat fever and mild to moderate pain. It is a widely available over-the-counter drug sold generically or under various brand names, including Tylenol and Panadol.[1][2] WP⚠ The source has a footnote here that is not shown.⚠ The source gives a pronunciation guide here that is not shown.

Paracetamol relieves pain in acute mild migraine and episodic tension headaches. At a standard dose, paracetamol slightly reduces fever, though it is inferior to ibuprofen in that respect: the benefits of its use for fever are unclear, particularly in the context of fever of viral origins. Paracetamol is effective for pain after wisdom tooth extraction, but it is less effective than ibuprofen. The combination of paracetamol and ibuprofen provides greater analgesic efficacy than either drug alone. The pain relief paracetamol provides in osteoarthritis is small and clinically insignificant. Evidence supporting its use in low back pain, cancer pain, and neuropathic pain is insufficient. Paracetamol is the first-line treatment for pain and fever in pregnancy; no causal association with neurodevelopmental disorders has been established, while untreated pain and fever can harm the mother and fetus.[1–20] WP

At a recommended maximum daily dose for an adult of three to four grams, paracetamol is safe and effective in the short term when used as directed, with uncommon adverse effects similar to those of ibuprofen. It is often used in patients who cannot tolerate nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen. Chronic consumption of paracetamol is in many cases not of benefit, and may result in abnormal liver function tests, and higher doses may lead to toxicity, including liver failure. Paracetamol poisoning is one of the leading causes of poisoning in high-income countries, and the foremost cause of acute liver failure in many countries.[12][13][21–27] WP

Paracetamol was first made in 1878 by Harmon Northrop Morse or possibly in 1852 by Charles Frédéric Gerhardt. It is the most commonly used medication for pain and fever in both the United States and Europe. It is on the World Health Organization's List of Essential Medicines. Paracetamol is available as a generic medication, with brand names including Tylenol and Panadol, among others. In 2023, it was the 112th most commonly prescribed medication in the United States, with more than 5 million prescriptions.[28–35] WP

History

History

Acetanilide was the first aniline derivative serendipitously found to possess analgesic as well as antipyretic properties, and was quickly introduced into medical practice under the name of Antifebrin by Cahn & Hepp in 1886. But its unacceptable toxic effects—the most alarming being cyanosis due to methemoglobinemia, an increase of hemoglobin in its ferric [Fe³⁺] state, called methemoglobin, which cannot bind oxygen, and thus decreases overall carriage of oxygen to tissue—prompted the search for less toxic aniline derivatives. Some reports state that Cahn & Hepp or a French chemist called Charles Gerhardt first synthesized paracetamol in 1852.[29][30][36][37] WP

Harmon Northrop Morse synthesized paracetamol at Johns Hopkins University via the reduction of p-nitrophenol with tin in glacial acetic acid in 1877, but it was not until 1887 that clinical pharmacologist Joseph von Mering tried paracetamol on humans. In 1893, von Mering published a paper reporting on the clinical results of paracetamol with phenacetin, another aniline derivative. Von Mering claimed that, unlike phenacetin, paracetamol had a slight tendency to produce methemoglobinemia. Paracetamol was then quickly discarded in favor of phenacetin. The sales of phenacetin established Bayer as a leading pharmaceutical company.[37–41] WP

Von Mering's claims remained essentially unchallenged for half a century until two teams of researchers from the United States analysed the metabolism of acetanilide and phenacetin. In 1947, David Lester and Leon Greenberg found strong evidence that paracetamol was a major metabolite of acetanilide in human blood, and in a subsequent study, they reported that large doses of paracetamol given to albino rats did not cause methemoglobinemia. In 1948, Bernard Brodie, Julius Axelrod and Frederick Flinn confirmed that paracetamol was the major metabolite of acetanilide in humans, and established that it was just as efficacious an analgesic as its precursor. They also suggested that methemoglobinemia is produced in humans mainly by another metabolite, phenylhydroxylamine. A follow-up paper by Brodie and Axelrod in 1949 established that phenacetin was also metabolized to paracetamol. This led to a "rediscovery" of paracetamol.[37][41–46] WP

Paracetamol was first marketed in the United States in 1950 under the name Trigesic, a combination of paracetamol, aspirin, and caffeine. Reports in 1951 of three users stricken with the blood disease agranulocytosis led to its removal from the marketplace, and it took several years until it became clear that the disease was unconnected. The following year, 1952, paracetamol returned to the U.S. market as a prescription drug. In the United Kingdom, marketing of paracetamol began in 1956 by Sterling-Winthrop Co. as Panadol, available only by prescription, and promoted as preferable to aspirin since it was safe for children and people with ulcers. In 1963, paracetamol was added to the British Pharmacopoeia, and has gained popularity since then as an analgesic agent with few side-effects and little interaction with other pharmaceutical agents.[39][47][48][49] WP

Concerns about paracetamol's safety delayed its widespread acceptance until the 1970s, but in the 1980s, paracetamol sales exceeded those of aspirin in many countries, including the United Kingdom. This was accompanied by the commercial demise of phenacetin, blamed as the cause of analgesic nephropathy and hematological toxicity. Available in the U.S. without a prescription since 1955 (1960, according to another source), paracetamol has become a common household drug. In 1988, Sterling Winthrop was acquired by Eastman Kodak which sold the over the counter drug rights to SmithKline Beecham in 1994.[37][47][50][51] WP⚠ Wikipedia itself has flagged this text: citation needed.

In June 2009, an FDA advisory committee recommended that new restrictions be placed on paracetamol use in the United States to help protect people from the potential toxic effects. The maximum single adult dosage would be decreased from 1000 mg to 650 mg, while combinations of paracetamol and other products would be prohibited. Committee members were particularly concerned by the fact that the then-present maximum dosages of paracetamol had been shown to produce alterations in liver function.[52] WP

In January 2011, the FDA asked manufacturers of prescription combination products containing paracetamol to limit its amount to no more than 325 mg per tablet or capsule and began requiring manufacturers to update the labels of all prescription combination paracetamol products to warn of the potential risk of severe liver damage. Manufacturers had three years to limit the amount of paracetamol in their prescription drug products to 325 mg per dosage unit.[53–56] WP

In November 2011, the Medicines and Healthcare products Regulatory Agency revised UK dosing of liquid paracetamol for children.[57] WP

In September 2013, "Use Only as Directed", an episode of the radio program This American Life highlighted deaths from paracetamol overdose. This report was followed by two reports by ProPublica alleging that the "FDA has long been aware of studies showing the risks of acetaminophen. So has the maker of Tylenol, McNeil Consumer Healthcare, a division of Johnson & Johnson" and "McNeil, the maker of Tylenol,... has repeatedly opposed safety warnings, dosage restrictions and other measures meant to safeguard users of the drug."[58][59][60] WP

In September 2025, US President Donald Trump and HHS Secretary Robert F. Kennedy Jr. claimed that Tylenol may cause autism and urged pregnant women to avoid it; whereas medical experts, major health organizations, and international studies strongly dispute any causal link, emphasizing that the drug remains safe for treating pain and fever in pregnancy.[61] WP

Legal status

Naming

Paracetamol is the Australian Approved Name and the British Approved Name as well as the international nonproprietary name that is used by the World Health Organization (WHO); acetaminophen is the United States Adopted Name and the Canadian and Japanese Accepted Name. Both paracetamol and acetaminophen are contractions of chemical names for the compound. The word paracetamol is a shortened form of para-acetylaminophenol, and was coined by Frederick Stearns & Co in 1956, while the word acetaminophen is a shortened form of N-acetyl-p-aminophenol (APAP), which was coined and first marketed by McNeil Laboratories in 1955. The initialism APAP is used by dispensing pharmacists in the United States.[62–68] WP

Pharmacology

Pharmacodynamics

Paracetamol appears to exert its effects through two mechanisms: the inhibition of cyclooxygenase (COX) and actions of its metabolite N-arachidonoylphenolamine (AM404).[69] WP

Supporting the first mechanism, pharmacologically and in its side effects, paracetamol is close to classical nonsteroidal anti-inflammatory drugs (NSAIDs) that act by inhibiting COX-1 and COX-2 enzymes and especially similar to selective COX-2 inhibitors, Paracetamol inhibits prostaglandin synthesis by reducing the active form of COX-1 and COX-2 enzymes. This occurs only when the concentration of arachidonic acid and peroxides is low; under these conditions, COX-2 is the predominant form of cyclooxygenase, which explains the apparent COX-2 selectivity of paracetamol. Under typical inflammation conditions, the concentration of peroxides is high, which counteracts the reducing anti-inflammatory effect of paracetamol, rendering it negligible; in situations where peroxide levels are low, such as for COX-2 in the CNS, this inhibition and its resulting anti-inflammatory effect remain high.[69][70] WP

The second mechanism centers on the paracetamol metabolite AM404. This metabolite has been detected in the brains of animals and cerebrospinal fluid of humans taking paracetamol. It is formed in the brain from another paracetamol metabolite 4-aminophenol by action of fatty acid amide hydrolase. AM404 is a weak agonist of cannabinoid receptors CB1 and CB2, an inhibitor of endocannabinoid transporter, and a potent activator of TRPV1 receptor. This and other research indicate that the endocannabinoid system and TRPV1 may play an important role in the analgesic effect of paracetamol.[69][71][72] WP

In 2018, Suemaru et al. found that, in mice, paracetamol exerts an anticonvulsant effect by activation of the TRPV1 receptors and a decrease in neuronal excitability by hyperpolarization of neurons. The exact mechanism of the anticonvulsant effect of paracetamol is not clear. According to Suemaru et al., acetaminophen and its active metabolite AM404 show a dose-dependent anticonvulsant activity against pentylenetetrazol-induced seizures in mice.[73][74] WP

In 2025, Maatuf et al. reported that AM404 is also produced by peripheral sensory neurons in vitro and blocks the action of pain-sensing Naᵥ1.8 and 1.7 channels at nanomolar concentrations. AM404 injected into the hind paw of rats increases the pain threshold for the treated paw, but not the untreated paw, confirming the peripheral nature of this effect. It also lowers pain responses in a few other in vivo models when injected directly into the affected area. Other tested metabolites of paracetamol do not block pain-sensing sodium channels in vitro.[75][76] WP

Pharmacokinetics

After being taken by mouth, paracetamol is rapidly absorbed from the small intestine, while absorption from the stomach is negligible. Thus, the rate of absorption depends on stomach emptying. Food slows the stomach's emptying and absorption, but the total amount absorbed stays the same. In the same subjects, the time to reach peak plasma concentration of paracetamol was 20 minutes in a fasting state, compared to 90 minutes in a fed state. Furthermore, a high-carbohydrate meal reduced the peak plasma concentration by approximately fourfold, an effect not observed with high-protein or high-fat meals.[77][78] WP

Paracetamol's bioavailability is dose-dependent: it increases from 63% for 500 mg dose to 89% for 1000 mg dose. Its plasma terminal elimination half-life is 1.9–2.5 hours, and volume of distribution is roughly 50 L. Protein binding is negligible, except under the conditions of overdose, when it may reach 15–21%. The concentration in serum after a typical dose of paracetamol usually peaks below 30 μg/mL (200 μmol/L). After 4 hours, the concentration is usually less than 10 μg/mL (66 μmol/L).[70][78][79] WP

Paracetamol is metabolized primarily in the liver, mainly by glucuronidation and sulfation, and the products are then eliminated in the urine (see the Scheme on the right). Only 2–5% of the drug is excreted unchanged in the urine. Glucuronidation by UGT1A1 and UGT1A6 accounts for 50–70% of the drug metabolism. Additional 25–35% of paracetamol is converted to sulfate by sulfation enzymes SULT1A1, SULT1A3, and SULT1E1.[78][80] WP

A minor metabolic pathway (5–15%) of oxidation by cytochrome P450 enzymes, mainly by CYP2E1, forms a toxic metabolite known as NAPQI (N-acetyl-p-benzoquinone imine). NAPQI is responsible for the liver toxicity of paracetamol. At usual doses of paracetamol, NAPQI is quickly detoxified by conjugation with glutathione. The non-toxic conjugate APAP-GSH is taken up in the bile and further degraded to mercapturic and cysteine conjugates that are excreted in the urine. In overdose, glutathione is depleted by a large amount of formed NAPQI, and NAPQI binds to mitochondria proteins of the liver cells, causing oxidative stress and toxicity.[80] WP

Yet another minor but important direction of metabolism is deacetylation of 1–2% of paracetamol to form p-aminophenol. p-Aminophenol is then converted in the brain by fatty acid amide hydrolase into AM404, a compound that may be partially responsible for the analgesic action of paracetamol.[70] WP

Chemistry

Formula

C8H9NO2 PC

CAS number

103-90-2 PC

Molar mass (g/mol)

151.16 PC

IUPAC name (computed by PubChem)

N-(4-hydroxyphenyl)acetamide PC

SMILES

CC(=O)NC1=CC=C(C=C1)O PC

InChIKey

RZVAJINKPMORJF-UHFFFAOYSA-N PC

PubChem CID

1983

Pop culture

No references added yet.

References

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