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PANADOL FOR COLD RELIEF CAPLET

Product Information

Registration Status: Active

SIN09985P

PANADOL FOR COLD RELIEF CAPLET is approved to be sold in Singapore with effective from 1998-03-09. It is marketed by GSK CONSUMER HEALTHCARE SINGAPORE PTE LTD, with the registration number of SIN09985P.

This product contains Paracetamol 500mg, and Pseudoephedrine 30mg in the form of TABLET. It is approved for ORAL use.

This product is manufactured by STERLING DRUG (MALAYA) SDN BHD in MALAYSIA.

It is an Over-the-counter Medicine that can be freely obtained from any retailer

Product Reference
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Description

Acetaminophen, also known as paracetamol, is commonly used for its analgesic and antipyretic effects. Its therapeutic effects are similar to salicylates, but it lacks anti-inflammatory, antiplatelet, and gastric ulcerative effects.

Indication

For temporary relief of fever, minor aches, and pains.

Mechanism of Action

Acetaminophen is thought to act primarily in the CNS, increasing the pain threshold by inhibiting both isoforms of cyclooxygenase, COX-1, COX-2, and COX-3 enzymes involved in prostaglandin (PG) synthesis. Unlike NSAIDs, acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, thus, has no peripheral anti-inflammatory affects. While aspirin acts as an irreversible inhibitor of COX and directly blocks the enzyme's active site, studies have found that acetaminophen indirectly blocks COX, and that this blockade is ineffective in the presence of peroxides. This might explain why acetaminophen is effective in the central nervous system and in endothelial cells but not in platelets and immune cells which have high levels of peroxides. Studies also report data suggesting that acetaminophen selectively blocks a variant of the COX enzyme that is different from the known variants COX-1 and COX-2. This enzyme is now referred to as COX-3. Its exact mechanism of action is still poorly understood, but future research may provide further insight into how it works. The antipyretic properties of acetaminophen are likely due to direct effects on the heat-regulating centres of the hypothalamus resulting in peripheral vasodilation, sweating and hence heat dissipation.

Pharmacokinetics

Absorption
Rapid and almost complete
Distribution
Metabolism
Acetaminophen primarily undergoes glucuronidation (45-55% of the dose) in which this process is facilitated by UGT1A1, UGT1A6, UGT1A9, UGT2B15 in the liver or UGT1A10 in the gut. 30-35% of the dose undergoes sulfation. This biotransformation is facilitated by SULT1A1, SULT1A3, SULT1A4, SULT1E1 and SULT2A1. A small percentage of acetaminophen is oxidized by CYP2E1 to form N-acetyl-p-benzo-quinone imine (NAPQI), a toxic metabolite which is then conjugated to glutathione and excreted renally. Studies suggest that CYP3A4 and CYP2E1 are the primary cytochrome P450 isozymes responsible for the generation of toxic metabolites. Accumulation of NAPQI may occur if primary metabolic pathways are saturated.
Elimination

Toxicity

Oral, mouse: LD50 = 338 mg/kg; Oral, rat: LD50 = 1944 mg/kg. Acetaminophen is metabolized primarily in the liver, where most of it is converted to inactive compounds by conjugation with glucuronic acid and, to a lesser extent, sulfuric acid. Conjugates are then excreted by the kidneys. Only a small portion is excreted in unchanged in urine or oxidized via the hepatic cytochrome P450 enzyme system (CYP2E1). Metabolism via CYP2E1 produces a toxic metabolite, N-acetyl-p-benzoquinoneimine (NAPQI). The toxic effects of acetaminophen are due to NAPQI, not acetaminophen itself nor any of the major metabolites. At therapeutic doses, NAPQI reacts with the sulfhydryl group of glutathione to produce a non-toxic conjugate that is excreted by the kidneys. High doses of acetaminophen may cause glutathione depletion, accumulation of NAPQI and hepatic necrosis. The maximum daily dose of acetaminophen is 4 g. Liver failure has been observed at doses as low as 6 g per day. As such, the maximum daily and single dose of acetaminophen is currently being reviewed in some countries. N-acetyl-cysteine, a precursor of glutathione, may be administered in the event of acetaminophen toxicity.

Active Ingredient/Synonyms

4-(Acetylamino)phenol | 4-acetamidophenol | 4'-hydroxyacetanilide | Acenol | acetaminofén | Acetaminophen | acétaminophène | APAP | N-acetyl-p-aminophenol | p-acetamidophenol | p-acetaminophenol | p-Acetylaminophenol | p-hydroxy-acetanilid | p-hydroxyacetanilide | p-hydroxyphenolacetamide | Paracétamol | Paracetamol | Paracetamolum | Acetaminophen |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


Description

An alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. It has been used in the treatment of several disorders including asthma, heart failure, rhinitis, and urinary incontinence, and for its central nervous system stimulatory effects in the treatment of narcolepsy and depression. It has become less extensively used with the advent of more selective agonists.

Indication

For the treatment of nasal congestion, sinus congestion, Eustachian tube congestion, and vasomotor rhinitis, and as an adjunct to other agents in the optimum treatment of allergic rhinitis, croup, sinusitis, otitis media, and tracheobronchitis. Also used as first-line therapy of priapism.

Mechanism of Action

Pseudoephedrine acts directly on both alpha- and, to a lesser degree, beta-adrenergic receptors. Through direct action on alpha-adrenergic receptors in the mucosa of the respiratory tract, pseudoephedrine produces vasoconstriction. Pseudoephedrine relaxes bronchial smooth muscle by stimulating beta2-adrenergic receptors. Like ephedrine, pseudoephedrine releasing norepinephrine from its storage sites, an indirect effect. This is its main and direct mechanism of action. The displaced noradrenaline is released into the neuronal synapse where it is free to activate the postsynaptic adrenergic receptors.

Pharmacokinetics

Absorption
Pseudoephedrine is readily and almost completely absorbed from the GI tract and there is no evidence of first-pass metabolism.
Distribution
Metabolism
Hepatic.
Elimination

Toxicity

Common adverse reactions include nervousness, restlessness, and insomnia. Rare adverse reactions include difficult/painful urination, dizziness/lightheadedness, heart palpitations, headache, increased sweating, nausea/vomiting, trembling, troubled breathing, unusual paleness, and weakness.

Active Ingredient/Synonyms

(+) threo-2-(methylamino)-1-phenyl-1-propanol | (+)-(1S,2S)-Pseudoephedrine | (+)-Pseudoephedrine | (+)-psi-Ephedrine | (+)-threo-Ephedrine | d-Isoephedrine | d-Pseudoephedrine | d-psi-2-Methylamino-1-phenyl-1-propanol | d-psi-Ephedrine | Isoephedrine | L-(+)-Pseudoephedrine | L(+)-psi-Ephedrine | Pseudoefedrina | pseudoéphédrine | Pseudoephedrine D-form | Pseudoephedrinum | Psi-ephedrin | Psi-ephedrine | trans-Ephedrine | ψ-ephedrine | Pseudoephedrine |


Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.

References

  1. Health Science Authority of Singapore - Reclassified POM
  2. Drugbank

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