Product Information
Registration Status: InactiveTHIS PRODUCT HAS BEEN DEREGISTERED!
YINCHI BRAND FEVER & COLD'S TABLET is approved to be sold in Singapore with effective from 1992-02-27. It is marketed by TIENTSIN DA-CHONG TRADING, with the registration number of SIN06851P.
This product contains Caffeine 30mg,Paracetamol 250mg, and Phenylephrine 5mg in the form of TABLET, SUGAR-COATED. It is approved for ORAL use.
This product is manufactured by BEACONS PHARMACEUTICALS PTE LTD in SINGAPORE.
It is an Over-the-counter Medicine that can be freely obtained from any retailer
Description
A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes smooth muscle, stimulates cardiac muscle, stimulates diuresis, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide phosphodiesterases, antagonism of adenosine receptors, and modulation of intracellular calcium handling.
Indication
For management of fatigue, orthostatic hypotension, and for the short term treatment of apnea of prematurity in infants.
Mechanism of Action
Caffeine stimulates medullary, vagal, vasomotor, and respiratory centers, promoting bradycardia, vasoconstriction, and increased respiratory rate. This action was previously believed to be due primarily to increased intracellular cyclic 3′,5′-adenosine monophosphate (cyclic AMP) following inhibition of phosphodiesterase, the enzyme that degrades cyclic AMP. It is now thought that xanthines such as caffeine act as antagonists at adenosine-receptors within the plasma membrane of virtually every cell. As adenosine acts as an autocoid, inhibiting the release of neurotransmitters from presynaptic sites but augmenting the actions of norepinephrine or angiotensin, antagonism of adenosine receptors promotes neurotransmitter release. This explains the stimulatory effects of caffeine. Blockade of the adenosine A1 receptor in the heart leads to the accelerated, pronounced "pounding" of the heart upon caffeine intake.
Pharmacokinetics
- Absorption
- Readily absorbed after oral or parenteral administration. The peak plasma level for caffeine range from 6-10mg/L and the mean time to reach peak concentration ranged from 30 minutes to 2 hours.
- Distribution
- * 0.8 to 0.9 L/kg [infants] * 0.6 L/kg [adults]
- Metabolism
- Hepatic cytochrome P450 1A2 (CYP 1A2) is involved in caffeine biotransformation. About 80% of a dose of caffeine is metabolized to paraxanthine (1,7-dimethylxanthine), 10% to theobromine (3,7-dimethylxanthine), and 4% to theophylline (1,3-dimethylxanthine).
- Elimination
Toxicity
LD50=127 mg/kg (orally in mice)
Active Ingredient/Synonyms
1-methyltheobromine | 1,3,7-trimethyl-2,6-dioxopurine | 1,3,7-trimethylpurine-2,6-dione | 1,3,7-trimethylxanthine | 3,7-Dihydro-1,3,7-trimethyl-1H-purin-2,6-dion | 7-methyltheophylline | Anhydrous caffeine | Cafeína | Caféine | Caffeinum | Coffein | Coffeinum | Guaranine | Koffein | Mateína | Methyltheobromine | teína | Thein | Theine | Caffeine |
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
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
Phenylephrine is a sympathomimetic amine that acts predominantly on α-adrenergic receptors. It is mainly used to treat nasal congestion, but may also be useful in treating hypotension and shock, hypotension during spinal anaesthesia, prolongation of spinal anaesthesia, paroxysmal supraventricular tachycardia, symptomatic relief of external or internal hemorrhoids, and to increase blood pressure as an aid in the diagnosis of heart murmurs.
Indication
Phenylephrine is mainly used to treat nasal congestion, but may also be useful in treating hypotension and shock, hypotension during spinal anaesthesia, prolongation of spinal anaesthesia, paroxysmal supraventricular tachycardia, symptomatic relief of external or internal hemorrhoids, and to increase blood pressure as an aid in the diagnosis of heart murmurs.
Mechanism of Action
In general, α1-adrenergic receptors mediate contraction and hypertrophic growth of smooth muscle cells. α1-receptors are 7-transmembrane domain receptors coupled to G proteins, Gq/11. Three α1-receptor subtypes, which share approximately 75% homology in their transmembrane domains, have been identified: α1A (chromosome 8), α1B (chromosome 5), and α1D (chromosome 20). Phenylephrine appears to act similarly on all three receptor subtypes. All three receptor subtypes appear to be involved in maintaining vascular tone. The α1A-receptor maintains basal vascular tone while the α1B-receptor mediates the vasocontrictory effects of exogenous α1-agonists. Activation of the α1-receptor activates Gq-proteins, which results in intracellular stimulation of phospholipases C, A2, and D. This results in mobilization of Ca2+ from intracellular stores, activation of mitogen-activated kinase and PI3 kinase pathways and subsequent vasoconstriction. Phenylephrine produces its local and systemic actions by acting on α1-adrenergic receptors peripheral vascular smooth muscle. Stimulation of the α1-adrenergic receptors results in contraction arteriolar smooth muscle in the periphery. Phenylephrine decreases nasal congestion by acting on α1-adrenergic receptors in the arterioles of the nasal mucosa to produce constriction; this leads to decreased edema and increased drainage of the sinus cavities.
Pharmacokinetics
- Absorption
- Completely absorbed after oral administration. It has a reduced bioavailability (compared to pseudoephedrine) following oral administration due to significant first-pass metabolism in the intestinal wall. Compared to IV administration, bioavailability is approximately 38%. Peak serum concentrations are achieved approximately 0.75-2 hours following oral administration. Phenylephrine should be administered parenterally to achieve cardiovascular effects. Occasionally, systemic effects are observed following oral inhalation.
- Distribution
- Metabolism
- Undergoes extensive first-pass metabolism in the intestinal wall and extensive metabolism in the liver. Sulfate conjugation, primarily in the intestinal wall, and oxidative metabolism by monoamine oxidase (MAO) represent the principle routes of metabolism. Glucuronidation occurs to a lesser extent. Phenylephrine and its metabolites are mainly excreted in urine/ .
- Elimination
Active Ingredient/Synonyms
(-)-m-Hydroxy-alpha-(methylaminomethyl)benzyl alcohol | (-)-m-Hydroxy-α-(methylaminomethyl)benzyl alcohol | Benzenemethanol, 3-hydroxy-.alpha.-[(methylamino)methyl]-, (R)- | Benzenemethanol, 3-hydroxy-alpha-((methylamino)methyl)-, (R)- | Benzyl alcohol, m-hydroxy-alpha-((methylamino)methyl)-, (-)- | Fenilefrina | l-(3-Hydroxyphenyl)-N-methylethanolamine | Phenylephrine | Phenylephrinum | R(-)-Phenylephrine | Phenylephrine |
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.