Benzphetamine: A sympathomimetic agent with properties similar to DEXTROAMPHETAMINE. It is used in the treatment of obesity. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1222)Ethylmorphine: A narcotic analgesic and antitussive. It is metabolized in the liver by ETHYLMORPHINE-N-DEMETHYLASE and used as an indicator of liver function.Aniline Hydroxylase: A drug-metabolizing, cytochrome P-450 enzyme which catalyzes the hydroxylation of aniline to hydroxyaniline in the presence of reduced flavoprotein and molecular oxygen. EC 1.14.14.-.NADPH-Ferrihemoprotein Reductase: A flavoprotein that catalyzes the reduction of heme-thiolate-dependent monooxygenases and is part of the microsomal hydroxylating system. EC 1.6.2.4.Cytochrome P-450 Enzyme System: A superfamily of hundreds of closely related HEMEPROTEINS found throughout the phylogenetic spectrum, from animals, plants, fungi, to bacteria. They include numerous complex monooxygenases (MIXED FUNCTION OXYGENASES). In animals, these P-450 enzymes serve two major functions: (1) biosynthesis of steroids, fatty acids, and bile acids; (2) metabolism of endogenous and a wide variety of exogenous substrates, such as toxins and drugs (BIOTRANSFORMATION). They are classified, according to their sequence similarities rather than functions, into CYP gene families (>40% homology) and subfamilies (>59% homology). For example, enzymes from the CYP1, CYP2, and CYP3 gene families are responsible for most drug metabolism.Microsomes, Liver: Closed vesicles of fragmented endoplasmic reticulum created when liver cells or tissue are disrupted by homogenization. They may be smooth or rough.Cytochromes b5: Cytochromes of the b group that are found bound to cytoplasmic side of ENDOPLASMIC RETICULUM. They serve as electron carrier proteins for a variety of membrane-bound OXYGENASES. They are reduced by the enzyme CYTOCHROME-B(5) REDUCTASE.Oxidoreductases, N-DemethylatingCytochrome P-450 CYP2B1: A major cytochrome P-450 enzyme which is inducible by PHENOBARBITAL in both the LIVER and SMALL INTESTINE. It is active in the metabolism of compounds like pentoxyresorufin, TESTOSTERONE, and ANDROSTENEDIONE. This enzyme, encoded by CYP2B1 gene, also mediates the activation of CYCLOPHOSPHAMIDE and IFOSFAMIDE to MUTAGENS.Phenobarbital: A barbituric acid derivative that acts as a nonselective central nervous system depressant. It potentiates GAMMA-AMINOBUTYRIC ACID action on GABA-A RECEPTORS, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations.Phenacetin: A phenylacetamide that was formerly used in ANALGESICS but nephropathy and METHEMOGLOBINEMIA led to its withdrawal from the market. (From Smith and Reynard, Textbook of Pharmacology,1991, p431)Phenethylamines: A group of compounds that are derivatives of beta- aminoethylbenzene which is structurally and pharmacologically related to amphetamine. (From Merck Index, 11th ed)Aniline CompoundsAppetite Depressants: Agents that are used to suppress appetite.Acetone: A colorless liquid used as a solvent and an antiseptic. It is one of the ketone bodies produced during ketoacidosis.Aryl Hydrocarbon Hydroxylases: A large group of cytochrome P-450 (heme-thiolate) monooxygenases that complex with NAD(P)H-FLAVIN OXIDOREDUCTASE in numerous mixed-function oxidations of aromatic compounds. They catalyze hydroxylation of a broad spectrum of substrates and are important in the metabolism of steroids, drugs, and toxins such as PHENOBARBITAL, carcinogens, and insecticides.Spectrophotometry: The art or process of comparing photometrically the relative intensities of the light in different parts of the spectrum.Methylcholanthrene: A carcinogen that is often used in experimental cancer studies.Steroid Hydroxylases: Cytochrome P-450 monooxygenases (MIXED FUNCTION OXYGENASES) that are important in steroid biosynthesis and metabolism.Hydroxylation: Placing of a hydroxyl group on a compound in a position where one did not exist before. (Stedman, 26th ed)Mixed Function Oxygenases: Widely distributed enzymes that carry out oxidation-reduction reactions in which one atom of the oxygen molecule is incorporated into the organic substrate; the other oxygen atom is reduced and combined with hydrogen ions to form water. They are also known as monooxygenases or hydroxylases. These reactions require two substrates as reductants for each of the two oxygen atoms. There are different classes of monooxygenases depending on the type of hydrogen-providing cosubstrate (COENZYMES) required in the mixed-function oxidation.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.Immunodiffusion: Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction.Substrate Specificity: A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.Kinetics: The rate dynamics in chemical or physical systems.Microsomes: Artifactual vesicles formed from the endoplasmic reticulum when cells are disrupted. They are isolated by differential centrifugation and are composed of three structural features: rough vesicles, smooth vesicles, and ribosomes. Numerous enzyme activities are associated with the microsomal fraction. (Glick, Glossary of Biochemistry and Molecular Biology, 1990; from Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)NADP: Nicotinamide adenine dinucleotide phosphate. A coenzyme composed of ribosylnicotinamide 5'-phosphate (NMN) coupled by pyrophosphate linkage to the 5'-phosphate adenosine 2',5'-bisphosphate. It serves as an electron carrier in a number of reactions, being alternately oxidized (NADP+) and reduced (NADPH). (Dorland, 27th ed)Aminorex: An amphetamine-like anorectic agent. It may cause pulmonary hypertension.Emetics: Agents that cause vomiting. They may act directly on the gastrointestinal tract, bringing about emesis through local irritant effects, or indirectly, through their effects on the chemoreceptor trigger zone in the postremal area near the medulla.Fenfluramine: A centrally active drug that apparently both blocks serotonin uptake and provokes transport-mediated serotonin release.DNA Barcoding, Taxonomic: Techniques for standardizing and expediting taxonomic identification or classification of organisms that are based on deciphering the sequence of one or a few regions of DNA known as the "DNA barcode".Radiographic Image Interpretation, Computer-Assisted: Computer systems or networks designed to provide radiographic interpretive information.Weight Loss: Decrease in existing BODY WEIGHT.Tablets: Solid dosage forms, of varying weight, size, and shape, which may be molded or compressed, and which contain a medicinal substance in pure or diluted form. (Dorland, 28th ed)Dizziness: An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness.Alcohol Drinking: Behaviors associated with the ingesting of alcoholic beverages, including social drinking.Alcoholic Beverages: Drinkable liquids containing ETHANOL.Glucagon-Like Peptide 1: A peptide of 36 or 37 amino acids that is derived from PROGLUCAGON and mainly produced by the INTESTINAL L CELLS. GLP-1(1-37 or 1-36) is further N-terminally truncated resulting in GLP-1(7-37) or GLP-1-(7-36) which can be amidated. These GLP-1 peptides are known to enhance glucose-dependent INSULIN release, suppress GLUCAGON release and gastric emptying, lower BLOOD GLUCOSE, and reduce food intake.Whistleblowing: The reporting of observed or suspected PROFESSIONAL MISCONDUCT or incompetence to appropriate authorities or to the public.Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level.Receptors, Glucagon: Cell surface receptors that bind glucagon with high affinity and trigger intracellular changes which influence the behavior of cells. Activation of glucagon receptors causes a variety of effects; the best understood is the initiation of a complex enzymatic cascade in the liver which ultimately increases the availability of glucose to body organs.Glucagon-Like Peptides: Peptides derived from proglucagon which is also the precursor of pancreatic GLUCAGON. Despite expression of proglucagon in multiple tissues, the major production site of glucagon-like peptides (GLPs) is the INTESTINAL L CELLS. GLPs include glucagon-like peptide 1, glucagon-like peptide 2, and the various truncated forms.Complex Mixtures: Mixtures of many components in inexact proportions, usually natural, such as PLANT EXTRACTS; VENOMS; and MANURE. These are distinguished from DRUG COMBINATIONS which have only a few components in definite proportions.Reference Standards: A basis of value established for the measure of quantity, weight, extent or quality, e.g. weight standards, standard solutions, methods, techniques, and procedures used in diagnosis and therapy.Liquid Phase Microextraction: Miniaturized methods of liquid-liquid extraction.Explosive Agents: Substances that are energetically unstable and can produce a sudden expansion of the material, called an explosion, which is accompanied by heat, pressure and noise. Other things which have been described as explosive that are not included here are explosive action of laser heating, human performance, sudden epidemiological outbreaks, or fast cell growth.Triazines: Heterocyclic rings containing three nitrogen atoms, commonly in 1,2,4 or 1,3,5 or 2,4,6 formats. Some are used as HERBICIDES.Drug and Narcotic Control: Control of drug and narcotic use by international agreement, or by institutional systems for handling prescribed drugs. This includes regulations concerned with the manufacturing, dispensing, approval (DRUG APPROVAL), and marketing of drugs.Oenothera: A plant genus of the family ONAGRACEAE. Members contain oenotheins.Viola: A plant genus of the family VIOLACEAE. Some species in this genus are called bouncing bet which is a common name more often used with SAPONARIA OFFICINALIS. Members contain macrocyclic peptides.Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges.Central Nervous System Stimulants: A loosely defined group of drugs that tend to increase behavioral alertness, agitation, or excitation. They work by a variety of mechanisms, but usually not by direct excitation of neurons. The many drugs that have such actions as side effects to their main therapeutic use are not included here.

Demethylation capacity of human fetal adrenal mitochondrial cytochrome P-450 in vitro. (1/36)

AIM: To explore the capacity and characteristics of adrenal mitochondria to metabolize xenobiotics in vitro in human fetus. METHODS: Subcellular fractions of fetal adrenal were prepared by differential centrifugation. Mitochondrial P-450 system was proved by spectral analyses and SDS-PAGE. The formaldehyde formation contents were measured with Nash reagent. RESULTS: The erythromycin N-demethylation linearly increased in the protein concentration (1-4 mg)- and incubation time (10-30 min)-dependent manners. A typical concentration-effect relationship appeared with erythromycin 0.067-1 mmol.L-1 and a positive correlation (r = 0.641, P < 0.05) existed between erythromycin N-demethylation and gestation months. The N-demethylation values (nmol.s-1/g protein) of erythromycin (2.7 +/- 0.8), benzfetamine (1.1 +/- 0.5), and aminophenazone (0.9 +/- 0.4) in mitochondria were 89% (P > 0.05), 162% (P < 0.01), and 62% (P < 0.01), respectively, of those in microsomes. There was correlation between mitochondria and microsomes in the N-demethylation of erythromycin (r = 0.708, P < 0.05) and benzfetamine (r = 0.707, P < 0.05). Troleandomycin stimulated erythromycin N-demethylation in adrenal mitochondria as well as in adrenal and liver microsomes in vitro. CONCLUSION: Fetal adrenal mitochondria, with multiple P-450 isoforms and greater capacity of demethylation, play a role in drug-metabolism during fetal development.  (+info)

Metabolic production of amphetamine following multidose administration of clobenzorex. (2/36)

The interpretation of urine drug-testing results can have important forensic and legal implications. In particular, drugs that are metabolized to amphetamine or methamphetamine or both pose significant concerns. In this study, clobenzorex, an anorectic drug that is metabolized to d-amphetamine, was administered to five subjects. Each subject took 30 mg daily for seven days, and individual urine samples were collected ad lib for 14 days beginning on the first day the drug was administered. Urine pH, specific gravity, and creatinine values were determined for each sample. Gas chromatography-mass spectrometry (GC-MS) was used to determine the excretion profile of amphetamine and clobenzorex using a standard procedure for amphetamines with additional monitoring of ions at m/z 118, 125, and 364 for the detection of clobenzorex. Peak concentrations of amphetamine were found at 82 to 168 h after the first dose and ranged from approximately 2900 to 4700 ng/mL amphetamine. The use of a regioisomer (3-Cl-benzylamphetamine) as internal standard allowed for accurate quantitation of the parent drug. Peak concentrations of clobenzorex were found at 50 to 120 h after the first dose and ranged from approximately 8 to 47 ng/mL clobenzorex. However, in many samples, clobenzorex was not detected at all. This analysis revealed that the metabolite, (amphetamine) is present in much higher concentrations than the parent compound, clobenzorex. Yet even at peak amphetamine concentrations, the parent was not always detected (limit of detection 1 ng/mL). Thus, in the interpretation of amphetamine-positive drug-testing results, the absence of clobenzorex in the urine sample does not exclude the possibility of its use.  (+info)

Multiple forms of cytochrome P-450 in phenobarbital- and 3-methylcholanthrene-treated rats. Separation and spectral properties. (3/36)

Multiple forms of liver microsomal cytochrome P-450 isolated from immature male rats pretreated with phenobarbital or 3-methylcholanthrene are described. Afraction of low specific content (Fraction A. 1.7 TO 4.0 nmol of cytochrome P-450 per mg of protein) and a fraction substantially purified (Fraction B, 9.0 TO 11.0 NMOL of cytochrome P-450 per mg of protein) are obtained by DEAE-cellulose chromatography of a partially purified cytochrome P-450 preparation in the presence of Emulgen 911. Shifts in the absorption maxima in the CO-reduced and ethyl isocyanide difference spectra are observed in the fractions derived from 3-methylcholanthrene-treated rats. The fractions derived from phenobarbital-treated rats exhibit different 455:430 ratios and pH intercepts in the ethyl isocyanide difference spectra. The absolute oxidized spectra and n-octylamine binding spectra at room temperature and EPR analysis at the temperature of liquid helium characterize all the fractions, except the Fraction A from 3-methylcholanthrene-treated rats, as low spin ferric hemeproteins. The A hemeprotein fractions from both 3-methylcholanthrene- and phenobarbital-treated rats have poor catalytic activity for the metabolism of benzphentamine and 3,4-benzo-[a]pyrene in comparison to the B hemeprotein fractions which may be due to the presence of a high concentration of Emulgen 911 in the A fractions. However, the presence of Emulgen 911 cannot account for the spectral differences among the fractions.  (+info)

Purified liver microsomal cytochrome P-450. Separation and characterization of multiple forms. (4/36)

During the purification of rabbit liver microsomal cytochrome P-450 (P-450LM), evidence was obtained for the occurrence of at least four distinct forms. These were distinguished by polyacrylamide gel electrophoresis after treatment with sodium dodecyl sulfate in the presence or absence of mercaptoethanol and were shown to have characteristic spectra as the reduced carbon monoxide complexes. They are designated by their relative electrophoretic mobilities. P-450LM2, which was purified to apparent homogeneity, is induced by phenobarbital and has a subunit molecular weight of 50,000. P-450LM4, which was also extensively purified, is induced by beta-naphthoflavone and has a molecular weight of 54,000. P-450LM1,7, which is induced neither by phenobarbital nor beta-naphthoflavone, is a mixtureMIXTURE OF ABOUT EQUAL AMOUNTS OF TWO FORMS WITH MOLECULAR WEIGHTS OF 47,000 AND 60,000 RESPECTIVELY. Some preparations were obtained containing primarily P-450LM1 or P-450LM7. Benzphetamine, ethylmorphine, and p-nitroanisole are hydroxylated preferentially by P-450LM2, and benzpyrene by P-450LM1,7. Biphenyl is hydroxylated in both positions 2 and 4 by all of the preparations, but the latter position is strongly favored by the action of P-450LM2. Testosterone is hydroxylated primarily in position 16alpha by P-450LM2 and in position 6beta by P-450LM1,7. Although the occurrence of additional forms of the cytochrome with highly similar electrophoretic behavior is not ruled out, it appears that the presence of these forms differing in subunit molecular weight may account for the variety of catalytic activities attributed to this pigment of liver microsomes.  (+info)

Evidence supporting the interaction of CYP2B4 and CYP1A2 in microsomal preparations. (5/36)

Recent studies have demonstrated that the catalytic behavior of one cytochrome P450 (P450) enzyme can be influenced by the presence of a second P450. This effect has been observed using reconstituted systems containing reductase, CYP2B4, and CYP1A2, primarily at subsaturating reductase. Addition of 1A2 caused a 75% inhibition of CYP2B4-dependent 7-pentoxyresorufin-O-dealkylation (PROD). Conversely, CYP2B4-dependent benzphetamine (bzp) demethylation did not exhibit this response after CYP1A2 addition. Addition of CYP2B4 to a reconstituted system containing reductase and CYP1A2 caused synergism of CYP1A2-dependent 7-ethoxyresorufin-O-dealkylation (EROD). This behavior was consistent with the formation of heteromeric CYP1A2-CYP2B4 complexes with altered catalytic properties. Although such responses have been documented in reconstituted systems, they have not been demonstrated in microsomal preparations. The goal of the present study was to determine whether such interactions were observed in rabbit liver microsomes. In an effort to detect such changes, we took advantage of the differential effect of CYP1A2 on CYP2B4-selective PROD and bzp metabolism. Rabbits were treated with phenobarbital (PB), beta-naphthoflavone (betaNF), and both PB + betaNF-conditions that enrich microsomes with CYP2B4, CYP1A2, or both enzymes, respectively. Benzphetamine demethylation activity was equivalently elevated in both the PB and the PB + betaNF groups, consistent with the induction of CYP2B4 in both groups. In contrast, PROD activity in the PB + betaNF group was less than 25% of that found in the PB-treated rabbits. These results demonstrate that the interactions observed in reconstituted systems are not an artifact of reconstitution but are observed under the more natural conditions of the microsomal membrane.  (+info)

Effects of vinyl chloride exposures to rats pretreated with phenobarbital. (6/36)

Male rats were exposed to 10 consecutive days, 6 hr/day, to vinyl chloride vapors at an average concentration of 13,500 ppm. The exposed rats were divided into three groups of eight rats each: one group was pretreated with 3-methylcholanthrene, one group was pretreated with phenobarbital, and the third group received no treatment. Half the animals in each group were sacrificed 18 hr after the last exposure and half were sacrificed 4 days later. In a second experiment, four rats pretreated with phenobarbital were exposed to vinyl chloride vapors at a concentration of 17,300 ppm for 2 days and sacrificed about 9 A.M. on the third day. In both experiments control animals, also treated with phenobarbital or 3-methylcholanthrene, were exposed to air only. At the time of sacrifice, lungs, kidneys, spleen, heart, and a small piece of liver from each animal were preserved for histological examination. The remainder of the liver was processed for assay of microsomal enzyme activity. The following parameters were investigated: growth rate, organ weights, morphological changes, and both benzphetamine-N-demethylase activity and cytochrome P-450 content of microsomes prepared from the livers. In both experiments the only marked difference noted in any group was a decrease in the growth rate of the animals exposed to vinyl chloride and treated with phenobarbital. This decreased growth rate was particularly apparent on the third day of the vinyl chloride exposures. Occasional morphological changes were also seen in the livers of the animals treated with phenobarbital and exposed to vinyl chloride.  (+info)

Evidence for the presence of active cytochrome P450 systems in Schistosoma mansoni and Schistosoma haematobium adult worms. (7/36)

Extracts of the adult worms of both Schistosoma mansoni and Schistosoma haematobium can metabolise some typical P450 substrates but to differing degrees. S. mansoni worm extracts displayed a approximately 12-fold higher specific activity for an aminopyrine substrate than rat liver microsomes. At 4 mM substrate concentration the demethylation reaction with N-nitrosodimethylamine (NDMA) (5 nmol HCHO/mg protein/min) was only half that of rat liver microsomes, whereas in extracts of S. haematobium, no detectable activity was found towards NDMA. Using ethylmorphine as substrate the demethylation activity of S. mansoni extracts (1.82 nmol HCHO/mg protein/min) was 5.5-fold lower than that of rat liver microsomes. Benzphetamine demethylase activity was also readily detectable in S. mansoni worm extracts at 6.79 nmol HCHO/mg protein/min compared with 10.20 nmol HCHO/mg protein/min in the case of rat liver microsomes. When aniline was used as substrate, surprisingly, no activity was found in worm extracts of either S. mansoni or S. haematobium, whereas rat liver microsomes showed high activity towards this amine. The anti-P450 2E1 and 2B1/2 cross-reacted with both worm homogenates and gave a specific band corresponding to a protein of molecular weight of approximately 50.0 kDa. A study with anti-P450 IVA antibody revealed that while this protein was strongly expressed in S. haematobium worm extracts, no immunoreactivity was observed with extracts of S. mansoni. Immunoblotting analyses with anti-P450 IIIA and P450 1A1 did not detect immunoreactive protein in either S. mansoni or S. haematobium.  (+info)

Metabolism of N,N',N"-triethylenethiophosphoramide by CYP2B1 and CYP2B6 results in the inactivation of both isoforms by two distinct mechanisms. (8/36)

The anticancer drug N,N,"N"-triethylenethiophosphoramide (tTEPA) inactivated CYP2B6 and CYP2B1 in the reconstituted system in a time-, concentration-, and NADPH-dependent manner indicative of mechanism-based inactivation. The KI value for the inactivation of CYP2B1 was 38 microM, the kinact was 0.3 min(-1), and the t1/2 value was 2.5 min. Spectral carbon monoxide (CO) binding and high-performance liquid chromatography heme studies of the tTEPA-inactivated CYP2B1 suggest that the loss in the enzymatic activity was primarily due to the binding of a reactive tTEPA intermediate to the 2B1 apoprotein. Inactivation by tTEPA in the presence of 7-ethoxycoumarin, an alternate substrate, reduced the rate of inactivation of CYP2B1. Incubations with tTEPA and NADPH resulted in greater than 90% loss in the 7-ethoxy-4-(trifluoromethyl)coumarin O-deethylation and testosterone hydroxylation activity of CYP2B1. In contrast, benzphetamine metabolism was significantly less inhibited (47%). CYP2B6 was inactivated by tTEPA with a KI value of 50 microM, a k inact value of 0.1 min(-1), and a t1/2 value of 14 min. However, unlike CYP2B1, the tTEPA-inactivated human isoform showed losses in the cytochrome P450 (P450) CO spectrum, the pyridine hemochrome spectrum, and in the amount of native heme that were comparable with the loss in the 7-EFC and benzphetamine activity, suggesting that activity loss was brought about by a tTEPA-reactive intermediate damaging the CYP2B6 heme. CYP2B6 could only be protected from the tTEPA-dependent inactivation by the 2B6-specific substrate bupropion but not by other substrates of CYP2B such as benzphetamine, testosterone, or 7-ethoxycoumarin. The data indicate that tTEPA metabolism by these two 2B isoforms results in inactivation of the P450s by two distinct mechanisms.  (+info)

*Benzphetamine

... should not be given to patients who are in an agitated state or who have a history of drug abuse. Benzphetamine ... Benzphetamine also slightly increases metabolism. Benzphetamine is a sympathomimetic amine and is classified as an anorectic. ... Benzphetamine (brand name Didrex) is a substituted amphetamine used short-term along with a doctor-approved, reduced-calorie ... "Benzphetamine". Toxnet. AHC Media, LLC (17 March 2014). Pediatric Trauma Care II: A clinical reference for physicians and ...

*List of dopaminergic drugs

Benzphetamine • Buphedrone • Butylone • Cathine • Cathinone • Clobenzorex • Clortermine • D-Deprenyl • Dimethoxyamphetamine ( ...

*Furfenorex

Marsel, J; Döring, G; Remberg, G; Spiteller, G (1972). "Methamphetamine--a metabolite of the anorectics Benzphetamine and ...

*Controlled Substances Act

Benzphetamine HCl (Didrex), a stimulant designed for use as an anorexiant. Fast-acting barbiturates such as secobarbital ( ...

*CYP4F11

... is active in metabolism of many drugs including benzphetamine, ethylmorphine, chlorpromazine, imipramine, and ...

*Drug Trafficking Safe Harbor Elimination Act

According to the DEA List of Scheduled Substances, examples include: Suboxone, benzphetamine, ketamine, and less than 15 ...

*Amphetamine

Several prescription drugs produce amphetamine as a metabolite, including benzphetamine, clobenzorex, famprofazone, fenproporex ...

*Opium Law

... allobarbital alprazolam amobarbital amfepramone aminorex barbital benzphetamine bromazepam brotizolam buprenorphine butalbital ...

*Convention on Psychotropic Substances

... amfepramone aminorex benzphetamine etilamfetamine fencamfamine fenproporex mazindol mefenorex mesocarb pemoline phendimetrazine ...

*Controlled Drugs and Substances Act

Benzphetamine (N-benzyl-N,α-dimethylbenzeneethanamine) N-Propyl-3,4-methylenedioxy- amphetamine (α-methyl-N-propyl-1,3- ...

*Misuse of Drugs Act (Ireland)

Benzphetamine Buprenorphine Butorphanol Codeine Dexamphetamine Dextropropoxyphene Dihydrocodeine Ethylmorphine (3-ethylmorphine ...

*Benzedrone

Substituted cathinone Benzphetamine 4-MEC Mephedrone EMCDDA Annual Report 2010 Research on Head Shop drugs in Dublin: Part 2 An ...

*List of adrenergic drugs

Amfecloral Amfepentorex Amfepramone Amphetamine dextroamphetamine levoamphetamine Amphetaminil β-Me-PEA BDB Benzphetamine BOH ...

*Norepinephrine releasing agent

... benzphetamine, phenmetrazine, aminorex As wakefulness-promoting agents in the treatment of narcolepsy - e.g., amphetamine, ...

*Misuse of Drugs Act (Singapore)

Benzphetamine Chlorphentermine Flunitrazepam (Rohypnol) Flutoprazepam (Restas) Mephentermine Pipradrol Triazolam (Halcion) For ...

*Substituted amphetamine

A variety of prodrugs of amphetamine and/or methamphetamine exist, and include amfecloral, amphetaminil, benzphetamine, ...

*List of banned substances in baseball

Amiphenazole Amphetamine Amphetaminil Armodafinil Benfluorex Benzphetamine Benzylpiperazine Bromantan Carphedon Cathine ( ...

*List of MeSH codes (D02)

... benzphetamine MeSH D02.092.471.683.152.660 --- 3,4-methylenedioxyamphetamine MeSH D02.092.471.683.152.670 --- n-methyl-3,4- ...

*Etilamfetamine

... and benzphetamine, and was largely discontinued once newer drugs such as phenmetrazine were introduced. The molecular structure ...

*Monoamine oxidase inhibitor

... benzphetamine, cathine, cathinone, diethylcathinone, ephedrine, levmetamfetamine, lisdexamfetamine, MDMA ("Ecstasy"), ...

*Psychotropic Substances Act (Thailand)

Benzphetamine (N-benzyl-N, α -dimethylphenethylamine) Bromazepam (7-bromo-1,3-dihydro-5-(2-pyridyl)-2H-1,4- benzodiazepin-2-one ...
To start, 25 to 50 mg once a day. Usually taken in midmorning or midafternoon. The dose can be increased up to 150 mg per day, taken in 3 doses, if necessary and if the patient can tolerate this dosage without severe side effects. The magnitude of the increased weight loss associated with benzphetamine is a fraction of a pound a week, with the weight loss greatest in the first weeks of therapy ...
Didrex is a prescription diet drug in a brand name form, which is intended for use by certain obese individuals who must lower their body fat levels in order to improve their health and lower their risk of various medical conditions. The generic form of this pill is called benzphetamine.. This pill is an appetite suppressant that is available only when prescribed by a licensed doctor. It functions by stimulating the central nervous system so that the heart rate and blood pressure will rise. The outcome is often a decline in the individuals hunger. Continue reading →. ...
Visit your doctor or health care professional for regular checks on your progress.. This medicine may affect your concentration, or hide signs of tiredness. Do not drive, use machinery, or do anything that needs mental alertness until you know how this medicine affects you. Do not stand or sit up quickly, especially if you are an older patient. This reduces the risk of dizzy or fainting spells. Alcohol may increase dizziness and drowsiness. Avoid alcoholic drinks.. This medicine is intended to be used in addition to a healthy diet and exercise. The best results are achieved this way. This medicine is only indicated for short-term use. Tell your doctor or health care professional if this medicine loses its effects, or if you feel you need to take more than the prescribed amount. Do not change the dose without advice from your doctor or health care professional.. ...
Comprehensive alcohol & food interactions for Didrex (benzphetamine). Includes High Blood Pressure (Hypertension), High Blood Pressure (Hypertension)
Background Human fetal adrenal glands are highly active and, with the placenta, regulate circulating progesterone, estrogen and corticosteroids in the fetus. At birth the adrenals are essential for...
Induction of cytochrome P-450-dependent monooxygenases with phenobarbital (PB) or other hepatic drug-metabolizing enzyme inducers in the rat is associated with enhanced cocaine hepatotoxicity both in vivo and in cultured rat hepatocytes. To demonstrate whether the major PB-inducible P-450 subfamily (P-450IIB) could be involved in the metabolic activation of cocaine, rates of cocaine N-demethylation (the first step of cocaine bioactivation) and the rate of irreversible (covalent) binding of tritiated cocaine to hepatic microsomal proteins (a measure for the overall bioactivation) were determined in microsomes from saline or PB-pretreated rats. PB pretreatment augmented Vmax (6-fold), but not KM, of cocaine N-demethylation. Similarly, the rate of irreversible protein binding was 3-fold increased in microsomes from PB-pretreated rats as compared with those from saline controls. Addition of benzphetamine, a substrate of P-450IIB, markedly inhibited cocaine irreversible binding. In addition, various ...
Studies were done to determine the mechanism(s) responsible for the thermal lability of adrenal microsomal monooxygenases. Preincubation of guinea pig adrenal microsomal suspensions at 37 degrees C caused large time-dependent declines in benzo(a)pyrene (BP) hydroxylase and benzphetamine (BZ) demethylase activities. Similar preincubations with hepatic microsomes had little effect on enzyme activities. The decreases in adrenal enzyme activities were completely prevented by co-incubation of microsomes with cytosol, but were not diminished by reduced glutathione, ascorbic acid, or bovine serum albumin. Partial protection was afforded by EDTA, suggesting that lipid peroxidation might be involved, but malonaldehyde production was not demonstrable and MnCl2, a potent inhibitor of lipid peroxidation, did not affect the decline in enzyme activities. The decreases in the rates of BP and BZ metabolism were prevented by including NADPH or NADP+ in the preincubation medium. The preincubation conditions ...
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Human fetal adrenal glands are highly active and, with the placenta, regulate circulating progesterone, estrogen and corticosteroids in the fetus. At birth the adrenals are essential for neonate salt retention through secretion of aldosterone, while adequate glucocorticoids are required to prevent adrenal insufficiency. The objective of this study was to carry out the first comprehensive analysis of adrenal steroid levels and steroidogenic enzyme expression in normal second trimester human fetuses. This was an observational study of steroids, messenger RNA transcripts and proteins in adrenals from up to 109 second trimester fetuses (11 weeks to 21 weeks) at the Universities of Aberdeen and Glasgow. The study design was balanced to show effects of maternal smoking. Concentrations of 19 intra-adrenal steroids were quantified using liquid chromatography and mass spectrometry. Pregnenolone was the most abundant steroid while levels of 17α-hydroxyprogesterone, dehydroepiandrosterone sulphate (DHEAS) and
1. Cimetidine pretreatment of male Sprague-Dawley rats caused a significant increase in the specific content of total hepatic cytochrome P-450, supporting the hypothesis that this H2-receptor antagonist has monooxygenase induction effects. 2. Quantitative ultrastructural studies of liver of cimetidine-pretreated animals also supported this hypothesis in showing a significant proliferation of smooth endoplasmic reticulum. These ultrastructural changes were qualitatively similar to those produced by treatment of rats with phenobarbital, a well-characterized monooxygenase-inducing agent whose effects were studied for comparative purposes. 3. Competitive inhibition of metoprolol αhydroxylation by cimetidine in liver microsomes prepared from untreated animals (Ki = 18.8 μM) was also demonstrated. 4. These results allowed testing of the hypothesis (Burnet el al. 1986) that inhibition of a defined monooxygenase should lead to induction of the synthesis of the relevant cytochrome P-450 isozyme. 5. The ...
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Hey everyone, really curious on any evidence or anecdotal reports of the likelihood that Selegiline dosing (mg a day) could result in a false positive drug test. I know that due to the metabolites it is advised to discontinue use when anticipating a test, but unfortunately tests are completely random. J Forensic Sci. Nov;40(6) Methamphetamine and amphetamine derived from the metabolism of selegiline. Romberg RW(1), Needleman SB, Snyder JJ, Greedan A. Author information: (1)Navy Drug Screening Laboratory, Great Lakes, IL, USA. Routine methamphetamine testing identified a urine specimen with.. Methamphetamine (MAMP) is a nap of abuse in the Structural States that is bad by urine drug testing (1). The sky cohort was filtered to identify agents with the MAMP medications benzphetamine (Didrex), selegiline (Eldepryl, Emsam and Zelapar), or MAMP (Desoxyn or Vicks Float Inhaler) selegiline drug test. Selegiline, also known as L-deprenyl, is a bit phenethylamine. At selegiline drug test clinical trials, ...
1. Actions of CRH on the Fetal Adrenal Gland As discussed in Chapter 3 (see Fetal Adrenal Glands), the human fetal adrenal glands are morphologically, functionally, and physiologically remarkable organs. At term, the fetal adrenal glands weigh the same as those in the adult and are similar in size to the adjacent fetal kidney. The…
Tolerance to the drugs effects develops fast. That is why ethylmorphine is normally used only as a temporary medicine to treat e.g. cough. Patients may develop addiction. Side effects, which are rare for medical doses but normal for recreational doses, include the classical opiate side-effects: nausea, vomiting, urinary retention, miosis and constipation. Also, some people are hypersensitive or allergic to ethylmorphine and should never take it. Additionally, the same dose of ethylmorphine can have completely different effects on two different people because of large individual differences in metabolism. Opioids are known of causing severe physical addiction, in addition to psychological addiction. This type of addiction is hard to treat. Taking ethylmorphine in combination with alcohol or other drugs that have a suppressive effect on the central nervous system boosts both drugs effects, creating a dangerous combination. Possible outcome is death through respiratory arrest. In recreational use ...

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PBSS is a novel surveillance system that allows public health officials to characterize the use and misuse of controlled prescription drugs. PBSS provides timely, population-based measures by both demographic characteristics and state. This report highlights the wide variations among states in multiple measures.. State ranks for prescribing of opioids, benzodiazepines, and stimulants in PBSS are consistent with their ranks in commercial prescription data (16,17). For example, California had the lowest opioid and benzodiazepine rates in this study and in a similar study that used data from IMS Health, a company that estimates state rates from a sample of pharmacies (http://www.imshealth.com/portal/site/imshealth). Population characteristics, such as ethnicity and socioeconomic status, and the availability of prescribers can explain only a small fraction of the variation in prescribing rates for opioid analgesics. Nor does the variation reflect variation in the prevalence of conditions for which ...
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  • In addition, neither pseudoephedrine nor benzphetamine sodium at customizing the highest radiation doses used showed an effect on pregnancy. (utidur.com)
  • Benzphetamine should not be used with any other central nervous stimulant drug. (wholehealthmd.com)
  • Benzphetamine should not be given to patients who are in an agitated state or who have a history of drug abuse. (wikipedia.org)
  • Benzphetamine is unique in its classification as a Schedule III drug in the United States. (wikipedia.org)
  • When properly used Benzphetamine can help the grossly obese lose weight, however it is a potent drug and shouldn't be used if you just have a few pounds to lose. (theathlete.org)
  • The magnitude of the increased weight loss associated with benzphetamine is a fraction of a pound a week, with the weight loss greatest in the first weeks of therapy. (wholehealthmd.com)
  • Benzphetamine is only part of a complete program of treatment that may also include diet, exercise, and weight control. (carolinapainandspine.com)
  • Benzphetamine is used short-term along with a doctor-approved, reduced-calorie diet, exercise, and behavior change program to help you lose weight. (drugs-track.online)
  • Some side effects of benzphetamine may occur that usually do not need medical attention. (drugs.com)
  • Using benzphetamine with alcohol can increase the risk of cardiovascular side effects such as increased heart rate, chest pain, or blood pressure changes. (drugs.com)
  • The generic form of this pill is called benzphetamine. (diet-pills.cc)
  • benzphetamine no generic 25-50 mg/day Available in trade available formulation only. (thefreedictionary.com)
  • Benzphetamine is contraindicated in patients with advanced arteriosclerosis, symptomatic cardiovascular disease, moderate to severe hypertension, hyper-thyroidism, known hypersensitivity or idiosyncrasy to sympathomimetic amines, and glaucoma, or who have recently used a MAOI. (wikipedia.org)
  • Although the clinical significance of this interaction is not been known, pentazocine should be used cautiously in patients receiving benzphetamine. (mariosathanasiou.com)
  • Benzphetamine is classified as a Schedule III controlled substance. (theathlete.org)
  • Treatment continued with intranasal benzphetamine 40 mcg nightly for 5 months but had recently been supplemented first with emedastine 25 mg. (mariosathanasiou.com)