Database : MEDLINE
Search on : D02.241.223.100.050.500.625 [DeCS Category]
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PMID:23562328
Author:Mohamed AN; Abdelhady AM; Spencer D; Sowinski KM; Tisdale JE; Overholser BR
Title:Pharmacokinetic modeling and simulation of procainamide and N-acetylprocainamide in a patient receiving continuous renal replacement therapy: a novel approach to guide renal dose adjustments.
Source:Am J Kidney Dis; 61(6):1046-8, 2013 Jun.
ISSN:1523-6838
Country of publication:United States
Language:eng
Publication type:CASE REPORTS; LETTER; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
Name of substance:0 (Anti-Arrhythmia Agents); 910Q707V6F (Acecainide); L39WTC366D (Procainamide)


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PMID:22894712
Author:Ghosh SC; Ngiam JS; Seayad AM; Tuan DT; Chai CL; Chen A
Address:Institute of Chemical and Engineering Sciences, Agency for Science, Technology and Research (A*STAR), 8 Biomedical Grove, Neuros 07-01, Singapore 138665.
Title:Copper-catalyzed oxidative amidation of aldehydes with amine salts: synthesis of primary, secondary, and tertiary amides.
Source:J Org Chem; 77(18):8007-15, 2012 Sep 21.
ISSN:1520-6904
Country of publication:United States
Language:eng
Abstract:A practical method for the amidation of aldehydes with economic ammonium chloride or amine hydrochloride salts has been developed for the synthesis of a wide variety of amides by using inexpensive copper sulfate or copper(I) oxide as a catalyst and aqueous tert-butyl hydroperoxide as an oxidant. This amidation reaction is operationally straightforward and provides primary, secondary, and tertiary amides in good to excellent yields for most cases utilizing inexpensive and readily available reagents under mild conditions. In situ formation of amine salts from free amines extends the substrate scope of the reaction. Chiral amides are also synthesized from their corresponding chiral amines without detectable racemization. The practicality of this amide formation reaction has been demonstrated in an efficient synthesis of the antiarrhythmic drug N-acetylprocainamide.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Name of substance:0 (Aldehydes); 0 (Amides); 0 (Amines); 0 (Anti-Arrhythmia Agents); 0 (Salts); 789U1901C5 (Copper); 910Q707V6F (Acecainide); 955VYL842B (tert-Butylhydroperoxide)


  3 / 257 MEDLINE  
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PMID:18489081
Author:Siraki AG; Deterding LJ; Bonini MG; Jiang J; Ehrenshaft M; Tomer KB; Mason RP
Address:Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, National Institutes of Health, 111 Alexander Dr., Research Triangle Park, NC 27709, USA. sirakia@niehs.nih.gov
Title:Procainamide, but not N-acetylprocainamide, induces protein free radical formation on myeloperoxidase: a potential mechanism of agranulocytosis.
Source:Chem Res Toxicol; 21(5):1143-53, 2008 May.
ISSN:1520-5010
Country of publication:United States
Language:eng
Abstract:Procainamide (PA) is a drug that is used to treat tachycardia in postoperative patients or for long-term maintenance of cardiac arrythmias. Unfortunately, its use has also been associated with agranulocytosis. Here, we have investigated the metabolism of PA by myeloperoxidase (MPO) and the formation of an MPO protein free radical. We hypothesized that PA oxidation by MPO/H 2O 2 would produce a PA cation radical that, in the absence of a biochemical reductant, would lead to the free radical oxidation of MPO. We utilized a novel anti-DMPO antibody to detect DMPO (5,5-dimethyl-1-pyrroline N-oxide) covalently bound to protein, which forms by the reaction of DMPO with a protein free radical. We found that PA metabolism by MPO/H 2O 2 induced the formation of DMPO-MPO, which was inhibited by MPO inhibitors and ascorbate. N-acetyl-PA did not cause DMPO-MPO formation, indicating that the unsubstituted aromatic amine was more oxidizable. PA had a lower calculated ionization potential than N-acetyl-PA. The DMPO adducts of MPO metabolism, as analyzed by electron spin resonance spectroscopy, included a nitrogen-centered radical and a phenyl radical derived from PA, either of which may be involved in the free radical formation on MPO. Furthermore, we also found protein-DMPO adducts in MPO-containing, intact human promyelocytic leukemia cells (HL-60). MPO was affinity-purified from HL-60 cells treated with PA/H 2O 2 and was found to contain DMPO using the anti-DMPO antibody. Mass spectrometry analysis confirmed the identity of the protein as human MPO. These findings were also supported by the detection of protein free radicals with electron spin resonance in the cellular cytosolic lysate. The formation of an MPO protein free radical is believed to be mediated by free radical metabolites of PA, which we characterized by spin trapping. We propose that drug-induced free radical formation on MPO may play a role in the origin of agranulocytosis.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL
Name of substance:0 (Enzyme Inhibitors); 0 (Free Radicals); 0 (Ions); 910Q707V6F (Acecainide); BBX060AN9V (Hydrogen Peroxide); EC 1.11.1.7 (Peroxidase); L39WTC366D (Procainamide); PQ6CK8PD0R (Ascorbic Acid)


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PMID:17616997
Author:Dasgupta A; Hovanetz M; Olsen M; Wells A; Actor JK
Address:Department of Pathology and Laboratory Medicine, University of Texas-Houston Medical School, 6431 Fannin, MSB 2.292, Houston, TX 77030, USA. Amitava.Dasgupta@uth.tmc.edu
Title:Drug-herb interaction: effect of St John's wort on bioavailability and metabolism of procainamide in mice.
Source:Arch Pathol Lab Med; 131(7):1094-8, 2007 Jul.
ISSN:1543-2165
Country of publication:United States
Language:eng
Abstract:CONTEXT: St John's wort induces the activity of the cytochrome P450 enzyme system causing treatment failure because of increased metabolism of many drugs. Procainamide is metabolized by a different pathway to N-acetyl procainamide. OBJECTIVE: To study St John's wort-procainamide interaction using a mouse (Swiss Webster) model. DESIGN: One group of mice (group A, 4 mice in each group) was fed St John's wort each day for 2 weeks (last dose 1 day before administration of procainamide); another group (group B) received the same dose of St John's wort for 1 week. The third group (group C) received only a single dose 1 hour before administration of procainamide, and the control group (group D) received no St John's wort. All groups later received a single oral dose of procainamide. Blood was drawn 1, 4, and 24 hours after administration of procainamide and concentrations in serum of procainamide as well as N-acetyl procainamide were measured using immunoassays. RESULTS: The procainamide concentrations 1 hour after administration was highest in group C (mean, 11.59 microg/mL) followed by group A (9.92 microg/mL), whereas group B (7.44 microg/mL) and control group D (7.36 microg/mL) showed comparable values. The concentration in group C was significantly greater than the control group D (P = .03, 2-tailed independent t test). N-Acetyl procainamide concentrations and estimated half-life of procainamide among groups were comparable. In a separate experiment when mice were fed purified hypericin, the active component of St John's wort, a significant increase in bioavailability (53%) of procainamide was observed compared with the control group. CONCLUSIONS: St John's wort has an acute effect to increase bioavailability of procainamide but has no effect on its metabolism.
Publication type:JOURNAL ARTICLE
Name of substance:5QD5427UN7 (Perylene); 7V2F1075HD (hypericin); 910Q707V6F (Acecainide); L39WTC366D (Procainamide)


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PMID:17125432
Author:Moffett BS; Cannon BC; Friedman RA; Kertesz NJ
Address:Department of Pharmacy, Texas Children's Hospital, Houston, Texas 77030. bsmoffet@texaschildrenshospital.org
Title:Therapeutic levels of intravenous procainamide in neonates: a retrospective assessment.
Source:Pharmacotherapy; 26(12):1687-93, 2006 Dec.
ISSN:0277-0008
Country of publication:United States
Language:eng
Abstract:STUDY OBJECTIVES: To evaluate dosing and pharmacokinetic parameters of intravenous continuous-infusion procainamide in neonates, and to identify dosage regimens and factors leading to therapeutic procainamide levels and minimal adverse events. DESIGN: Retrospective, observational study. SETTING: Pediatric hospital. PATIENTS: . Twenty-one patients (seven preterm, 14 full term) younger than 30 days who received continuous-infusion procainamide therapy for more than 15 hours or had two consecutive therapeutic procainamide levels obtained while receiving therapy between June 1, 2002, and December 31, 2005. MEASUREMENTS AND MAIN RESULTS: Data on demographics, dosing, drug levels, and adverse effects were collected. Doses that achieved therapeutic levels were documented, and procainamide clearance was calculated and evaluated with regard to renal function and gestational age in patients who were at steady state. Mean clearance and mean N-acetylprocainamide (NAPA):procainamide ratios were compared between preterm and term neonates. No patients experienced hemodynamic instability or other adverse effects due to procainamide. Procainamide was given as a mean +/- SD 9.6 +/- 1.5-mg/kg bolus in 20 of 21 patients before continuous infusion. The mean +/- SD dose at which two therapeutic levels were achieved was 37.56 +/- 13.52 microg/kg/minute. Procainamide clearance was 6.36 +/- 8.85 ml/kg/minute and correlated with creatinine clearance (r=0.78, p<0.00001) and age at day of sampling (r=0.49, p<0.00001). The NAPA:procainamide ratio at steady state was 0.84 +/- 0.53; two patients were determined to be fast acetylators (ratio > 1). Preterm infants had lower mean clearance rates (p<0.001) but higher NAPA:procainamide ratios (p<0.01) than those of term infants. Five patients experienced seven supratherapeutic levels while receiving therapy; four of these patients were preterm, and all had creatinine clearances less than 30 ml/minute/1.73 m(2). Three patients had four pairs of levels obtained after discontinuation of procainamide, and elimination rate constant and half-life were calculated. CONCLUSION: Procainamide can be safely used in neonates, with no short-term adverse effects. The dosage regimen for intravenous procainamide required to achieve therapeutic levels in neonates is similar to that of older infants and children. Doses may need to be reduced in premature infants and in those with renal dysfunction.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Anti-Arrhythmia Agents); 910Q707V6F (Acecainide); AYI8EX34EU (Creatinine); L39WTC366D (Procainamide)


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PMID:16221756
Author:Brightman FA; Leahy DE; Searle GE; Thomas S
Address:Cyprotex Discovery Ltd., Macclesfield, Cheshire, United Kingdom, SK10 2DR.
Title:Application of a generic physiologically based pharmacokinetic model to the estimation of xenobiotic levels in human plasma.
Source:Drug Metab Dispos; 34(1):94-101, 2006 Jan.
ISSN:0090-9556
Country of publication:United States
Language:eng
Abstract:Estimation of xenobiotic kinetics in humans frequently relies upon extrapolation from experimental data generated in animals. In an accompanying paper, we have presented a unique, generic, physiologically based pharmacokinetic model and described its application to the prediction of rat plasma pharmacokinetics from in vitro data alone. Here we demonstrate the application of the same model, parameterized for human physiology, to the estimation of plasma pharmacokinetics in humans and report a comparative evaluation against some recently published predictive methods that involve scaling from in vivo animal data. The model was parameterized through an optimization process, using a training set of in vivo data taken from the literature, and validated using a separate test set of published in vivo data. On average, the vertical divergence of the predicted plasma concentrations from the observed data, on a semilog concentration-time plot, was 0.47 log unit. For the training set, more than 80% of the predicted values of a standardized measure of the area under the concentration-time curve were within 3-fold of the observed values; over 70% of the test set predictions were within the same margin. Furthermore, in terms of predicting human clearance for the test set, the model was found to match or exceed the performance of three published interspecies scaling methods, all of which showed a distinct bias toward overprediction. We conclude that the generic physiologically based pharmacokinetic model, as a means of integrating readily determined in vitro and/or in silico data, is potentially a powerful, cost-effective tool for predicting human xenobiotic kinetics in drug discovery and risk assessment.
Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE
Name of substance:0 (Xenobiotics); 0FRP6G56LD (Biperiden); 7S5I7G3JQL (Dexamethasone); 910Q707V6F (Acecainide); CJ0O37KU29 (Verapamil)


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PMID:15793163
Author:Bauer LA; Black DJ; Lill JS; Garrison J; Raisys VA; Hooton TM
Address:Department of Pharmacy, Box 357630, University of Washington, Seattle, WA 98195. labauer@u.washington.edu.
Title:Levofloxacin and ciprofloxacin decrease procainamide and N-acetylprocainamide renal clearances.
Source:Antimicrob Agents Chemother; 49(4):1649-51, 2005 Apr.
ISSN:0066-4804
Country of publication:United States
Language:eng
Abstract:Ten healthy adults participated in a randomized, crossover drug interaction study testing procainamide only, procainamide plus levofloxacin, and procainamide plus ciprofloxacin. During levofloxacin therapy, most procainamide and N-acetylprocainamide (NAPA) pharmacokinetic parameters, including decreased renal clearances and renal clearance/creatinine clearance ratios, changed (P < 0.05). During ciprofloxacin treatment, only procainamide and NAPA renal clearances decreased significantly.
Publication type:CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
Name of substance:0 (Anti-Arrhythmia Agents); 0 (Anti-Bacterial Agents); 5E8K9I0O4U (Ciprofloxacin); 6GNT3Y5LMF (Levofloxacin); 910Q707V6F (Acecainide); A4P49JAZ9H (Ofloxacin); L39WTC366D (Procainamide)


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PMID:15732917
Author:Flarakos J; Morand KL; Vouros P
Address:Barnett Institute and Department of Chemistry and Chemical Biology, Northeastern University, Boston, Massachusetts 02115, USA.
Title:High-throughput solution-based medicinal library screening against human serum albumin.
Source:Anal Chem; 77(5):1345-53, 2005 Mar 01.
ISSN:0003-2700
Country of publication:United States
Language:eng
Abstract:High-throughput screening of combinatorial libraries has evolved from studying large diverse libraries to analyzing small, structurally similar, focused libraries. This paradigm shift has generated a need for rapid screening technologies to screen both diverse and focused libraries in a simple, efficient, and inexpensive manner. We have proactively addressed these needs by developing a high-throughput, solution-based method combining size exclusion (SEC), two-dimensional liquid chromatography (2-D LC), and mass spectrometry (MS) for determining the relative binding of drug candidates in small, focused medicinal libraries against human serum albumin (HSA). Two types of libraries were used to evaluate the performance of the system. The first consisted of five diverse ligands with a wide range of hydrophobicities and whose association constants to HSA cover 3 orders of magnitude. A beta-lactam library composed of structurally similar compounds was used to further confirm the validity of the methodology. The ability to distinguish site-specific interactions of drugs competing for individual domains of the HSA receptor is also demonstrated. Comparison of chromatographic profiles of the library components before and after incubation with the receptor using multiple reaction monitoring allowed a ranking of the ligands according to their relative binding affinities. The observed rankings correlate closely with literature values of the association constants between the respective ligands and HSA. This simple, rugged methodology can screen a wide spectrum of chemical entities from combinatorial mixtures in less than 6 min.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
Name of substance:0 (Dansyl Compounds); 0 (Pharmaceutical Preparations); 0 (Serum Albumin); 0 (beta-Lactams); 1093-96-5 (dansylsarcosine); 5Q7ZVV76EI (Warfarin); 8DUH1N11BX (Tryptophan); 910Q707V6F (Acecainide); ITX08688JL (Quinidine); OGG85SX4E4 (Imipramine); XXE1CET956 (Indomethacin); Z711V88R5F (Sarcosine)


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PMID:11566320
Author:Lindgren H; Pero RW; Ivars F; Leanderson T
Address:Department of Cell and Molecular Biology, Section for Immunology, BMC I:13, Lund University, S-221 84, Lund, Sweden. hanna.lindgren@immuno.lu.se
Title:N-substituted benzamides inhibit nuclear factor-kappaB and nuclear factor of activated T cells activity while inducing activator protein 1 activity in T lymphocytes.
Source:Mol Immunol; 38(4):267-77, 2001 Aug.
ISSN:0161-5890
Country of publication:England
Language:eng
Abstract:N-substituted benzamides are compounds that have recently been reported to inhibit nuclear factor-kappaB (NF-kappaB) activity and induce apoptosis in a pre-B cell line. In this study, we focused on the effects of N-substituted benzamides on transcriptional regulation in Jurkat T cells. We used a model system where the cells can be stimulated either through TCR/CD28 or by treatment of the cells with PMA and ionomycin to induce transcription factors typical for T lymphocyte activation. Treatment of the Jurkat cells with procainamide did not influence the transcription factor profile of stimulated cells, while treatment with a derivative having an acetyl group in position 4 of the aromatic ring inhibited NF-kappaB and nuclear factor of activated T cells (NFAT) activity. Declopramide, which contains a chloride in position 3 of the aromatic ring, was inactive in this system, whereas also the acetylated derivative of this compound inhibited NF-kappaB and NFAT activity. In contrast, the transcriptional activity and nuclear expression of activator protein 1 induced by TCR/CD28 stimulation or PMA and ionomycin treatment was enhanced by the acetylated variants of the N-substituted benzamides. Finally, we investigated the effect of N-substituted benzamides on intact promoters for two genes central in immune regulation; the CD40 ligand (CD40L) and IL-2 promoters. The transcriptional activity of the CD40L promoter as well as surface expression of the CD40L induced by signaling through TCR/CD28 was inhibited by addition of acetylated N-substituted benzamides, while the transcriptional activity of the IL-2 promoter was enhanced. Taken together, these data indicate that derivatives of N-substituted benzamides are potential drug candidates for quantitative as well as qualitative modulation of immune functions.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Name of substance:0 (Benzamides); 0 (DNA-Binding Proteins); 0 (Interleukin-2); 0 (N-acetyldeclopramide); 0 (NF-kappa B); 0 (NF-kappa B p50 Subunit); 0 (NFATC Transcription Factors); 0 (Nuclear Proteins); 0 (Transcription Factor AP-1); 0 (Transcription Factors); 147205-72-9 (CD40 Ligand); 910Q707V6F (Acecainide); 916GJF577D (declopramide); L39WTC366D (Procainamide)


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PMID:11384853
Author:He YL; Kitada N; Yasuhara M; Hori R
Address:Department of Anaesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, Boston, MA 02114, USA. Yhe@partners.org
Title:Quantitative estimation of renal clearance of N-acetylprocainamide in rats with various experimental acute renal failure.
Source:Eur J Pharm Sci; 13(3):303-8, 2001 Jun.
ISSN:0928-0987
Country of publication:Netherlands
Language:eng
Abstract:The dosage regimen of a drug eliminated predominantly through the kidney need to be adjusted for the patients with renal disease. The objective of the present study was to establish a quantitative approach to precisely predicting the renal clearances of basic drugs using N-1-methylnicotinamide (NMN). A variety of experimental acute renal failure (ARF) in rats were prepared and N-acetylprocainamide (NAPA) was used as a model drug. The renal clearances of NAPA were significantly decreased in rats with ARF, resulting in significantly increased plasma concentrations. Remarkable reduction in clearance ratios (CL(ratio)) was observed, indicating that the impairment in tubular and glomerular function did not proceed in a parallel manner. The renal clearance of NAPA (CL(rNAPA)) was better predicted from the renal clearance of NMN (CL(rNMN)) than from GFR. A mathematical equation was also constructed to estimate the CL(rNMN) from the NMN plasma concentration. Therefore, the renal clearance of basic drugs excreted predominantly from the kidney can be easily and more accurately estimated based on the concentrations of endogenous NMN to provide a precise dosage regimen for patients with renal failure.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Blood Proteins); 910Q707V6F (Acecainide)



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