Disease relevance of Norpropoxyphene

• A woman with portacaval shunt and essentially complete renal failure was also studied; she exhibited the highest propoxyphene peak concentration in this investigation and had no detectable norpropoxyphene in plasma [1].
• Plasma concentrations of propoxyphene and its major metabolite, norpropoxyphene, were determined over at least 12 hr after oral administration of 130 mg dextropropoxyphene hydrochloride to eight men with hepatic cirrhosis, of whom four had a surgically constructed portacaval shunt, and to seven healthy men [1].
• In an attempt to design a liver function test which takes into account both portal-systemic shunting and hepatocellular dysfunction, we investigated a group of patients with cirrhosis with or without surgical porta-caval shunt for d-propoxyphene and its major metabolite, norpropoxyphene kinetics [2].
• Norpropoxyphene also showed opioid activity in the rat tail heat and guinea-pig ileum tests, but exhibited nonopioid activity in the mouse abdominal constriction and acute toxicity studies [3].
• 2) A reduced metabolism DP to NP during hypocapnia [4].

Psychiatry related information on Norpropoxyphene

• The ratios of propoxyphene to norpropoxyphene do not appear to differ markedly between drug abuse deaths and nonabuse deaths [5].

High impact information on Norpropoxyphene

• Propoxyphene (P) and norpropoxyphene (NP) excretion in breast milk was studied in six healthy nursing mothers [6].
• Propoxyphene and norpropoxyphene kinetics after single and repeated doses of propoxyphene [7].
• Propoxyphene and norpropoxyphene plasma concentrations after oral propoxyphene in cirrhotic patients with and without surgically constructed portacaval shunt [1].
• CONCLUSION: FL and NORP block the current of cTBAK-1 channels differently, the latter modified the selectivity of the channel pore [8].
• Our mutagenesis study revealed that NORP interacts with the selectivity filter of cTBAK-1 [8].

Biological context of Norpropoxyphene

• These data suggest that the norpropoxyphene/d-propoxyphene AUC ratio reflects both shunting and reduced hepatocellular function.(ABSTRACT TRUNCATED AT 250 WORDS)[2]
• Point mutations in the channel resulted in two distinct phenotypes of cTBAK-1: the mutant Y105F channel lost its selectivity and was unaffected by NORP, in contrast to the F211Y mutant [8].

Anatomical context of Norpropoxyphene

• As d-propoxyphene is a high extraction drug and since the production of norpropoxyphene should reflect the amount of d-propoxyphene available to the hepatocytes, we tested the hypothesis that norpropoxyphene/d-propoxyphene AUC ratios should reflect both the degree of portal-systemic shunting and the severity of hepatocyte dysfunction [2].
• Propoxyphene and norpropoxyphene depressed axonal conduction in isolated peripheral nerve and were comparable in potency to standard local anesthetic agents [3].

Associations of Norpropoxyphene with other chemical compounds

• Urine is treated with sodium hydroxide in order to rearrange, by base catalysis, norpropoxyphene to norpropoxyphene amide, which is then extracted with these columns and chromatographed [9].
• The effect of ethanol (10 and 60 mM) on propoxyphene (2 microM) and norpropoxyphene (2 microM) metabolism in suspensions of isolated rat hepatocytes was studied [10].
• Citralopram, a new selective serotonin reuptake inhibitor, cocaine, oxycodone, promethazine, propoxyphene, and norpropoxyphene were identified and quantitated in the postmortem samples by gas chromatography-mass spectrometry [11].
• Propoxyphene, norpropoxyphene, and cyclic dinorpropoxyphene concentrations in the sera of eight opiate addicts were measured by gas chromatography [12].
• The plasma concentrations of propoxyphene, its major metabolite norpropoxyphene, salicylic acid and phenazone were determined by mass fragmentography, spectrofluorimetry and gas chromatography [13].

Gene context of Norpropoxyphene

• Norpropoxyphene-induced cardiotoxicity is associated with changes in ion-selectivity and gating of HERG currents [14].
• TPP results from 160 urine specimens screened for PPY and/or NP were compared to those obtained by testing with DRI enzyme immunoassay, Emit II plus immunoassay, Abuscreen Online immunoassay and gas chromatography-mass spectrometry (GC-MS) [15].
• Preliminary assays showed that the limit of detection for PPX is below 1.0 ng/mg hair, the limit of detection for the metabolite NPPX being significantly higher (1.5 ng/mg) [16].
• Propoxyphene and norpropoxyphene quantitation in the same solid-phase extraction using Toxi-Lab Spec VC MP3 system [17].
• A method for the identification and quantification of dextropropoxyphene, norpropoxyphene, and methaqualone in plasma by GC/NPD is presented [18].

Analytical, diagnostic and therapeutic context of Norpropoxyphene

• Blood propoxyphene and norpropoxyphene levels were determined repeatedly during the sixth dosing interval (before hemodialysis) and during the seventh dosing interval (during hemodialysis) [19].
• Simultaneous determination of propoxyphene and norpropoxyphene in biological samples by gas chromatography using an on-column injection technique with a fused-silica capillary column [20].
• A sensitive and specific high-performance liquid chromatographic (HPLC) procedure was developed for determination of propoxyphene and norpropoxyphene in plasma and breast milk [21].
• The high concentrations of NPPX, relative to those of PPX, found in all of the clinical samples suggest that laboratories that currently confirm for PPX should confirm for NPPX in order to obtain a better correlation between immunoassay results and GC-MS confirmations [22].
• In fact, autoinduction, resulting in significantly lower plasma concentrations after treatment for 1 week was found for NP and was indicated for DP [23].

References