Product Information
Registration Status: ActiveSIN07643P
DEXCOPHAN COUGH LINCTUS PLUS is approved to be sold in Singapore with effective from 1993-12-15. It is marketed by GOLDPLUS UNIVERSAL PTE LTD, with the registration number of SIN07643P.
This product contains Ammonium Chloride 150mg/5ml,Dextromethorphan 10mg/5ml, and Ephedrine 6.25mg/5ml in the form of ELIXIR. It is approved for ORAL use.
This product is manufactured by HOVID BHD in MALAYSIA.
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
The d-isomer of the codeine analog of levorphanol. Dextromethorphan shows high affinity binding to several regions of the brain, including the medullary cough center. This compound is an NMDA receptor antagonist (receptors, N-methyl-D-aspartate) and acts as a non-competitive channel blocker. It is one of the widely used antitussives, and is also used to study the involvement of glutamate receptors in neurotoxicity. [PubChem]
Indication
For treatment and relief of dry cough.
Mechanism of Action
Dextromethorphan is an opioid-like drug that binds to and acts as antagonist to the NMDA glutamatergic receptor, it is an agonist to the opioid sigma 1 and sigma 2 receptors, it is also an alpha3/beta4 nicotinic receptor antagonist and targets the serotonin reuptake pump. Dextromethorphan is rapidly absorbed from the gastrointestinal tract, where it enters the bloodstream and crosses the blood-brain barrier. The first-pass through the hepatic portal vein results in some of the drug being metabolized into an active metabolite of dextromethorphan, dextrorphan, the 3-hydroxy derivative of dextromethorphan.
Pharmacokinetics
- Absorption
- Rapidly absorbed from the gastrointestinal tract.
- Distribution
- Metabolism
- Hepatic. Rapidly and extensively metabolized to dextrorphan (active metabolite). One well known metabolic catalyst involved is a specific cytochrome P450 enzyme known as 2D6, or CYP2D6.
- Elimination
Active Ingredient/Synonyms
(+)-dextromethorphan | D-methorphan | delta-Methorphan | Dex | Dextromethorfan | Dextromethorphan | Dextrométhorphane | Dextromethorphanum | Dextrometorfano | DM | Dextromethorphan |
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.