Product Information
Registration Status: ActiveFEDAC COMPOUND LINCTUS is approved to be sold in Singapore with effective from 1989-01-06. It is marketed by DRUG HOUSES OF AUSTRALIA PTE LTD, with the registration number of SIN03195P.
This product contains Codeine 10mg/5ml,Pseudoephedrine 30mg/5ml, and Triprolidine 1.25mg/5ml in the form of ELIXIR. It is approved for ORAL use.
This product is manufactured by DRUG HOUSES OF AUSTRALIA PTE LTD in SINGAPORE.
It is a Pharmacy Only Medicine that can be obtained from a pharmacist at a retail pharmacy.
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
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.
Description
First generation histamine H1 antagonist used in allergic rhinitis; asthma; and urticaria. It is a component of cough and cold medicines. It may cause drowsiness.
Indication
For the symptomatic relief of seasonal or perennial allergic rhinitis or nonallergic rhinitis; allergic conjunctivitis; and mild, uncomplicated allergic skin manifestations of urticaria and angioedema. Also used in combination with other agents for the symptomatic relief of symptoms associated with the common cold.
Mechanism of Action
Triprolidine 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
- Rapidly absorbed in the intestinal tract.
- Distribution
- Metabolism
- Elimination
Toxicity
Symptoms of overdose include drowsiness, weakness, inco-ordination, difficulty with micturition, respiratory depression, hypotension, agitation, irritability, convulsions, hypertension, palpitation and tachycardia.
Active Ingredient/Synonyms
Tripolidina | Triprolidin | Triprolidine | Triprolidinum | Triprolidine |
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.