Product Information
Registration Status: ActiveSIN03100P
COUGHLAX FORTE SYRUP is approved to be sold in Singapore with effective from 1989-05-06. It is marketed by BEACONS PHARMACEUTICALS PTE LTD, with the registration number of SIN03100P.
This product contains Ammonium Chloride 62.5mg/5ml,Chlorpheniramine 5mg/5ml,Codeine 10mg/5ml, and Ephedrine 5mg/5ml in the form of SYRUP. It is approved for ORAL use.
This product is manufactured by BEACONS PHARMACEUTICALS PTE LTD in SINGAPORE.
It is a Pharmacy Only Medicine that can be obtained from a pharmacist at a retail pharmacy.
Product Reference
Important Note: For generic product, the SPC/PIL provided may not be brand specific.
{{/items}} {{^items}}Description
Ammonium chloride is an inorganic compound with the formula NH4Cl and a white crystalline salt that is highly soluble in water. Solutions of ammonium chloride are mildly acidic.
Indication
1. Expectorant in cough syrups. 2. The ammonium ion (NH4+) in the body plays an important role in the maintenance of acid-base balance. The kidney uses ammonium (NH4+) in place of sodium (Na+) to combine with fixed anions in maintaining acid-base balance, especially as a homeostatic compensatory mechanism in metabolic acidosis. The therapeutic effects of Ammonium Chloride depend upon the ability of the kidney to utilize ammonia in the excretion of an excess of fixed anions and the conversion of ammonia to urea by the liver, thereby liberating hydrogen (H+) and chloride (Cl–) ions into the extracellular fluid. Ammonium Chloride Injection, USP, after dilution in isotonic sodium chloride injection, may be indicated in the treatment of patients with: (1) hypochloremic states and (2) metabolic alkalosis.
Mechanism of Action
1. Increases acidity by increasing the amount of hydrogen ion concentrations. 2. Ammonium chloride is used as an expectorant in cough medicine. Its expectorant action is caused by irritative action on the bronchial mucosa, which causes the production of excess respiratory tract fluid and make it easier to cough it up.
Pharmacokinetics
- Absorption
- Completely absorbed within 3–6 h. In healthy persons, absorption of ammonium chloride given by mouth was practically complete. Only 1 to 3% of the dose was recovered in the feces.
- Distribution
- Data not found.
- Metabolism
- Ammonium ion is converted to urea in the liver; chloride ion replaces bicarbonate.
- Elimination
Clearance
Data not found.
Toxicity
LD50 "Rat" after oral administration is: 1650 mg/kg. Overdosage of Ammonium Chloride has resulted in a serious degree of metabolic acidosis, disorientation, confusion and coma. If metabolic acidosis occur following overdosage, the administration of an alkalinizing solution such as sodium bicarbonate or sodium lactate will serve to correct the acidosis. Patients administering Ammonium chloride should be watched to the signs of ammonia toxicity including (pallor, sweating, irregular breathing, bradycardia, cardiac arrhythmias, local and general twitching, tonic convulsions and coma). It should be used with caution in patients with high total CO2 and buffer base secondary to primary respiratory acidosis. Intravenous administration should be slow to avoid local irritation and toxic effects.
Active Ingredient/Synonyms
Ammonium chloride | Ammonium chloride |
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
A histamine H1 antagonist used in allergic reactions, hay fever, rhinitis, urticaria, and asthma. It has also been used in veterinary applications. One of the most widely used of the classical antihistaminics, it generally causes less drowsiness and sedation than promethazine. [PubChem]
Indication
For the treatment of rhinitis, urticaria, allergy, common cold, asthma and hay fever.
Mechanism of Action
Chlorpheniramine binds to the histamine H1 receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine.
Pharmacokinetics
- Absorption
- Well absorbed in the gastrointestinal tract.
- Distribution
- Metabolism
- Primarily hepatic via Cytochrome P450 (CYP450) enzymes.
- Elimination
Toxicity
Oral LD50 (rat): 306 mg/kg; Oral LD50 (mice): 130 mg/kg; Oral LD50 (guinea pig): 198 mg/kg [Registry of Toxic Effects of Chemical Substances. Ed. D. Sweet, US Dept. of Health & Human Services: Cincinatti, 2010.] Also a mild reproductive toxin to women of childbearing age.
Active Ingredient/Synonyms
1-(p-chlorophenyl)-1-(2-pyridyl)-3-dimethylaminopropane | 1-(p-chlorophenyl)-1-(2-pyridyl)-3-N,N-dimethylpropylamine | 2-[p-chloro-α-[2-(dimethylamino)ethyl]benzyl]pyridine | 3-(p-chlorophenyl)-3-(2-pyridyl)-N,N-dimethylpropylamine | Chlorophenylpyridamine | Chlorphenamin | Chlorphenaminum | Chlorpheniramine | Chlorpheniramine polistirex | Chlorpheniraminum | Clorfenamina | Clorfeniramina | γ-(4-chlorophenyl)-N,N-dimethyl-2-pyridinepropanamine | γ-(4-chlorophenyl)-γ-(2-pyridyl)propyldimethylamine | Chlorphenamine |
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 opioid analgesic related to morphine but with less potent analgesic properties and mild sedative effects. It also acts centrally to suppress cough.
Indication
For treatment and management of pain (systemic). It is also used as an antidiarrheal and as a cough suppressant.
Mechanism of Action
Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Codeine's analgesic activity is, most likely, due to its conversion to morphine. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability.
Pharmacokinetics
- Absorption
- Well absorbed following oral administration with a bioavailability of approximately 90%. Maximum plasma concentration occurs 60 minutes post-administration. Food does not effect the rate or extent of absorption of codeine.
- Distribution
- Apparent volume of distribution = 3-6 L/kg
- Metabolism
- Hepatic. Codeine is a prodrug, itself inactive, but demethylated to the active morphine by the liver enzyme CYP2D6 to morphine. 70-80% of the dose undergoes glucuronidation to form codeine-6-glucuronide. This process is mediated by UDP-glucuronosyltransferase UGT2B7 and UGT2B4. 5-10% of the dose undergoes O-demethylation to morphine and 10% undergoes N-demethylation to form norcodeine. CYP2D6 mediates the biotransformation to morphine. CYP3A4 is the enzyme that mediates the conversion to norcodiene. Morphine and norcodeine are further metabolized and undergo glucuronidation. The glucuronide metabolites of morphine are morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G). Both morphine and morphine-6-glucuronide are active and have analgesic activity. Norcodiene and M3G do not have any analgesic properties.
- Elimination
Toxicity
Respiratory depression, sedation and miosis and common symptoms of overdose. Other symptoms include nausea, vomiting, skeletal muscle flaccidity, bradycardia, hypotension, and cool, clammy skin. Apnea and death may ensue.
Active Ingredient/Synonyms
(−)-Codeine | (5alpha,6alpha)-7,8-Didehydro-4,5-epoxy-3-methoxy-17-methylmorphinan-6-ol | (5α,6α)-7,8-didehydro-4,5-epoxy-3-methoxy-17-methylmorphinan-6-ol | 3-Methylmorphin | 3-methylmorphine | 7,8-didehydro-4,5alpha-epoxy-3-methoxy-17-methylmorphinan-6alpha-ol | 7,8-didehydro-4,5α-epoxy-3-methoxy-17-methylmorphinan-6α-ol | Codein | Codeína | Codéine | Codeine anhydrous | Codeine polistirex | Codeinum | L-Codeine | Methylmorphine | morphine 3-methyl ether | Morphine monomethyl ether | morphine monomethyl ether | morphine-3-methyl ether | O(3)-methylmorphine | Codeine |
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
Ephedrine commonly used as a stimulant, appetite suppressant, concentration aid, decongestant, and to treat hypotension associated with anaesthesia.
Mechanism of Action
Ephedrine is a sympathomimetic amine - that is, its principal mechanism of action relies on its direct and indirect actions on the adrenergic receptor system, which is part of the sympathetic nervous system. Ephedrine increases post-synaptic noradrenergic receptor activity by (weakly) directly activating post-synaptic α-receptors and β-receptors, but the bulk of its effect comes from the pre-synaptic neuron being unable to distinguish between real adrenaline or noradrenaline from ephedrine. The ephedrine, mixed with noradrenaline, is transported through the noradrenaline reuptake complex and packaged (along with real noradrenaline) into vesicles that reside at the terminal button of a nerve cell. Ephedrine's action as an agonist at most major noradrenaline receptors and its ability to increase the release of both dopamine and to a lesser extent, serotonin by the same mechanism is presumed to have a major role in its mechanism of action.
Pharmacokinetics
- Absorption
- 85%
- Distribution
- Metabolism
- Elimination
Toxicity
Cardiovascular: tachycardia, cardiac arrhythmias, angina pectoris, vasoconstriction with hypertension
Active Ingredient/Synonyms
(-)-Ephedrine | (1R,2S)-1-Phenyl-1-hydroxy-2-methylaminopropane | L-Ephedrine | L-erythro-2-(Methylamino)-1-phenylpropan-1-ol | L(−)-ephedrine | Ephedrine |
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.