Product Information
Registration Status: ActiveSIN15394P
SKUDEXA FILM-COATED TABLET 75 MG/25 MG is approved to be sold in Singapore with effective from 2017-12-13. It is marketed by A. MENARINI SINGAPORE PTE LTD, with the registration number of SIN15394P.
This product contains Dexketoprofen 25mg, and Tramadol 75mg in the form of TABLET, FILM-COATED. It is approved for ORAL use.
This product is manufactured by MENARINI - VON HEYDEN GmbH in GERMANY.
It is a Prescription Only Medicine that can only be obtained from a doctor or a dentist, or a pharmacist with a prescription from a Singapore-registered doctor or dentist.
Product Reference
Important Note: For generic product, the SPC/PIL provided may not be brand specific.
{{/items}} {{^items}}Description
Dexketoprofen is a non-steroidal anti-inflammatory drug. It is available in the various countries in Europe, Asia and Latin America. It has analgesic, antipyretic and anti-inflammatory properties [L1298].
Indication
For short-term treatment of mild to moderate pain, including dysmenorrhoea, musculoskeletal pain and toothache [L1302].
Mechanism of Action
It is a non-steroidal anti-inflammatory drug (NSAID) that reduces prostaglandin synthesis via inhibition of cyclooxygenase pathway (both COX-1 and COX-2) activity [L1299].
Pharmacokinetics
- Absorption
- After oral ingestion, the Dexketoprofen onset of action is within 30 minutes. The plasma half-life of Dexketoprofen is about 4-6 hours. The Cmax is about 30 minutes [L1204]
- Distribution
- Metabolism
- Dexketoprofen is highly lipophilic, and is metabolized in the liver by glucuronidation [L1304]. In one study, after oral administration of 25 mg of dexketoprofen to young healthy adults, Tmax was approximately 30 min for a Cmax of 3.7 ± 0.72 mg/l [L1305]. Dexketoprofen trometamol is metabolized by the hepatic cytochrome P450 enzymes (CYP2C8 and CYP2C9) [L1305]. Dexketoprofen trometamol has a number of metabolites, with hydroxyl derivatives making up the greatest volume [L1305]. In humans, hydroxylation plays a minor role. Dexketoprofen is primarily conjugated to an acyl-glucuronide [L1305]
- Elimination
Clearance
Mainly cleared via glucuronide conjugation and followed by renal excretion, mainly unchanged [L1299].
Toxicity
Nausea and/or vomiting, stomach pain, diarrhea, digestive problems (dyspepsia) are the most common symptoms of toxicity. More toxicity symptoms include dizziness, sleepiness, disturbed sleep, nervousness, headache, palpitations, flushing, stomach problems, constipation, dry mouth, flatulence, skin rash, tiredness, pain, feeling feverish and shivering, and malaise. Severe toxicity can lead to thrombocytopenia and anemia with bleeding episodes. Dexketoprofen is associated with a small increased risk of myocardial infarction [L1302].
Active Ingredient/Synonyms
Dexketoprofen | Dexketoprofen |
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 narcotic analgesic proposed for moderate to severe pain. It may be habituating. Tramadol is also prepared as a variable release capsules, marketed under the brand name ConZip. For example, a 150 mg capsule will contain 37.5 mg of the immediate release form and 112.5 mg of the extended release form.
Indication
Indicated in the treatment of moderate to severe pain. Consider for those prone to constipation or respiratory depression. Tramadol is used to treat postoperative, dental, cancer, and acute musculosketetal pain and as an adjuvant to NSAID therapy in patients with osteoarthritis.
Mechanism of Action
Tramadol and its O-desmethyl metabolite (M1) are selective, weak OP3-receptor agonists. 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. 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. The analgesic properties of Tramadol can be attributed to norepinephrine and serotonin reuptake blockade in the CNS, which inhibits pain transmission in the spinal cord. The (+) enantiomer has higher affinity for the OP3 receptor and preferentially inhibits serotonin uptake and enhances serotonin release. The (-) enantiomer preferentially inhibits norepinephrine reuptake by stimulating alpha(2)-adrenergic receptors.
Pharmacokinetics
- Absorption
- Racemic tramadol is rapidly and almost completely absorbed after oral administration. The mean absolute bioavailability of a 100 mg oral dose is approximately 75%. The mean peak plasma concentration of racemic tramadol and M1 occurs at two and three hours, respectively, after administration in healthy adults.
- Distribution
- * 2.6 L/kg [male, 100 mg intravenous dose] * 2.9 L/kg [female, 100 mg intravenous dose]
- Metabolism
- Hepatic. The major metabolic pathways appear to be N- and O- demethylation and glucuronidation or sulfation in the liver. One metabolite (O-desmethyltramadol, denoted M1) is pharmacologically active in animal models. CYP3A4 and CYP2B6 facilitates the biotransformation of tramadol to N-desmethyl-tramadol. CYP2D6 facilitates the biotransformation of tramadol to O-desmethyl-tramadol.
- Elimination
Clearance
* 5.9 mL/min/Kg [Healthy Adults, 100 mg qid, MD p.o] * 8.5 mL/min/Kg [Healthy Adults, 100 mg SD p.o] * 6.89 mL/min/Kg [Geriatric, (
Toxicity
LD50=350mg/kg (orally in mice)
Active Ingredient/Synonyms
(+)-Tramadol | (+)-trans-2-(Dimethylaminomethyl)-1-(m-methoxyphenyl)cyclohexanol | Tramadol |
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.