Parvon N
Parvon N Uses, Dosage, Side Effects, Food Interaction and all others data.
Dextropropoxyphene is an opioid analgesic manufactured by Eli Lilly and Company. It is used in the symptomatic treatment of mild pain. It displays antitussive and local anaesthetic actions. Due to the risk of cardiac arrhythmias and overdose, possibly leading to death, dextropropoxyphene has been withdrawn from the market in Europe and the United States. The drug is often referred to as the general form, "propoxyphene", however only the dextro-isomer (dextropropoxyphene) has any analgesic effect. The levo-isomer appears to exhibit a very limited antitussive effect.
Propoxyphene, a synthetic opiate agonist, is structurally similar to methadone. Its general pharmacologic properties are those of the opiates as a group. The analgesic effect of propoxyphene is due to the d-isomer, dextropropoxyphene. It binds to the opiate receptors and leads to a decrease of the perception of pain stimuli. Propoxyphene possesses little to no antitussive activity and no antipyretic action.
| Trade Name | Parvon N |
| Generic | Dextropropoxyphene + Paracetamol / Acetaminophen |
| Weight | 32mg, |
| Type | Capsule |
| Therapeutic Class | |
| Manufacturer | Jagsonpal Pharmaceuticals Ltd |
| Available Country | India |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Dextropropoxyphene is an opioid analgesic used to treat mild to moderate pain.
For the relief of mild to moderate pain.
Parvon N is also used to associated treatment for these conditions: Pain
How Parvon N works
Propoxyphene acts as a weak agonist at OP1, OP2, and OP3 opiate receptors within the central nervous system (CNS). Propoxyphene primarily affects OP3 receptors, which are coupled with G-protein receptors and function as modulators, both positive and negative, 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 such as propoxyphene also inhibit the release of vasopressin, somatostatin, insulin, and glucagon. 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.
Toxicity
Coma, respiratory depression, circulatory collapse, and pulmonary edema. Seizures occur more frequently in patients with propoxyphene intoxication than in those with opiate intoxication. LD50=230mg/kg (orally in rat, Emerson)
Volume of Distribution
- 16 L/kg
Half Life
6-12 hours
Clearance
- 2.6 L/min
Elimination Route
The major route of metabolism is cytochrome CYP3A4 mediated N-demethylation to norpropoxyphene, which is excreted by the kidneys. In 48 hours, approximately 20% to 25% of the administered dose of propoxyphene is excreted via the urine, most of which is free or conjugated norpropoxyphene.
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