. "Dextropropoxyph\u00E8ne"@en . . . . . . . . "Destropropossifene"@en . . . "For the relief of mild to moderate pain"@en . . . . . . "withdrawn"@en . . . . . . . . "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."@en . . . . . . . . . . . . . . . . . . . . . . "Dextropropoxyphen"@en . . . . . . . . . . . . "Dextropropoxyphene is an analgesic in the opioid category, patented (1955) and manufactured by Eli Lilly and Company. It is intended to treat mild pain and also has antitussive and local anaesthetic effects. The drug has been taken off the market in Europe and the US due to concerns of fatal overdoses and heart arrhythmias. An estimated 10 million patients have used these products. 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."@en . . . . . . . . . . . . . . "Dextropropoxyphene"@en . "469-62-5"@en . . . . . "Dextropropoxyphenum"@en . "# Coda BA, Rudy AC, Archer SM, Wermeling DP: Pharmacokinetics and bioavailability of single-dose intranasal hydromorphone hydrochloride in healthy volunteers. Anesth Analg. 2003 Jul;97(1):117-23, table of contents. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/12818953"@en . . "* 16 L/kg"@en . . . "Carl R. White, \"Synthesis and purification of d-propoxyphene hydrochloride.\" U.S. Patent US4661625, issued April, 1973."@en . . . . "Humans and other mammals"@en . "6-12 hours"@en . . . . . . . "Dextropropoxifeno"@en . . . . "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."@en . "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)"@en . . . . . . " "@en . . . . . . . . . . . "approved"@en . . . . . . . "d-Propoxyphene"@en . . . . . . . . . . . . . . "illicit"@en . . " "@en . . "* 2.6 L/min"@en . . . . . . . . . . . . . "Take without regard to meals. Avoid alcohol."@en . . . . . . . . . . . . . . . . . . . .