Product Information
Registration Status: ActiveSIN03526P
SEMERIN COUGH SYRUP is approved to be sold in Singapore with effective from 1989-05-25. It is marketed by CENTRAL CHEMICAL & ENTERPRISES PTE LTD, with the registration number of SIN03526P.
This product contains Ammonium Chloride 100mg/5ml,Ephedrine 4mg/5ml, and Sodium Citrate 150mg/5ml in the form of SYRUP. It is approved for ORAL use.
This product is manufactured by SUNWARD PHARMACEUTICAL PTE LTD in SINGAPORE.
It is an Over-the-counter Medicine that can be freely obtained from any retailer
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
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.
Description
Sodium citrate is the sodium salt of citric acid. It is white, crystalline powder or white, granular crystals, slightly deliquescent in moist air, freely soluble in water, practically insoluble in alcohol. Like citric acid, it has a sour taste. From the medical point of view, it is used as alkalinizing agent. It works by neutralizing excess acid in the blood and urine. It has been indicated for the treatment of metabolic acidosis.
Indication
Used as an anticoagulant during plasmophoresis as well as a neutralizing agent in the treatment of upset stomach and acidic urine [FDA Label] [L788] [L789].
Mechanism of Action
Citrate chelates free calcium ions preventing them from forming a complex with tissue factor and coagulation factor VIIa to promote the activation of coagulation factor X [A19410] [A19411]. This inhibits the extrinsic initiation of the coagulation cascade. Citrate may also exert an anticoagulant effect via a so far unknown mechanism as restoration of calcium concentration does not fully reverse the effect of citrate [A19410]. Citrate is a weak base and so reacts with hydrochloric acid in the stomach to raise the pH. It it further metabolized to bicarbonate which then acts as a systemic alkalizing agent, raising the pH of the blood and urine [L790]. It also acts as a diuretic and increases the urinary excretion of calcium.
Pharmacokinetics
- Absorption
- Tmax of 98-130min [A19414].
- Distribution
- 19-39L [A19414].
- Metabolism
- Citrate is metabolized to bicarbonate in the liver and plays a role as an intermediate in the citric acid cycle [A19419] [L795].
- Elimination
Clearance
Total clearance of 313-1107mL/min [A19414].
Toxicity
Overdose toxicity is mainly due to alkalosis as well as tetany or depressed heart function due to lack of free calcium [L790].
Active Ingredient/Synonyms
Sodium citrate anhydrous | Sodium citrate, anhydrous | trisodium citrate anhydrous | Trisodium citrate, anhydrous | Sodium Citrate |
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.