An antidepressive agent and monoamine oxidase inhibitor related to PARGYLINE.
A chemically heterogeneous group of drugs that have in common the ability to block oxidative deamination of naturally occurring monoamines. (From Gilman, et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p414)
A selective, irreversible inhibitor of Type B monoamine oxidase. It is used in newly diagnosed patients with Parkinson's disease. It may slow progression of the clinical disease and delay the requirement for levodopa therapy. It also may be given with levodopa upon onset of disability. (From AMA Drug Evaluations Annual, 1994, p385) The compound without isomeric designation is Deprenyl.
An enzyme that catalyzes the oxidative deamination of naturally occurring monoamines. It is a flavin-containing enzyme that is localized in mitochondrial membranes, whether in nerve terminals, the liver, or other organs. Monoamine oxidase is important in regulating the metabolic degradation of catecholamines and serotonin in neural or target tissues. Hepatic monoamine oxidase has a crucial defensive role in inactivating circulating monoamines or those, such as tyramine, that originate in the gut and are absorbed into the portal circulation. (From Goodman and Gilman's, The Pharmacological Basis of Therapeutics, 8th ed, p415) EC 1.4.3.4.
A monoamine oxidase inhibitor with antihypertensive properties.
1,4-Diethylene dioxides. Industrial solvents. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), dioxane itself may "reasonably be anticipated to be a carcinogen." (Merck Index, 11th ed)
A propylamine formed from the cyclization of the side chain of amphetamine. This monoamine oxidase inhibitor is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in panic and phobic disorders. (From AMA Drug Evaluations Annual, 1994, p311)
A benzodioxane-linked imidazole that has alpha-2 adrenoceptor antagonist activity.
A group of compounds that are derivatives of beta- aminoethylbenzene which is structurally and pharmacologically related to amphetamine. (From Merck Index, 11th ed)
An indirect sympathomimetic. Tyramine does not directly activate adrenergic receptors, but it can serve as a substrate for adrenergic uptake systems and monoamine oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals. Tyramine may be a neurotransmitter in some invertebrate nervous systems.
An MAO inhibitor that is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in the treatment of panic disorder and the phobic disorders. (From AMA, Drug Evaluations Annual, 1994, p311)
Receptors of CLONIDINE and other IMIDAZOLINES. Activity of the ligands was earlier attributed to ADRENERGIC ALPHA-2 RECEPTORS. Endogenous ligands include AGMATINE, imidazoleacetic acid ribotide, and harman.
A deaminated metabolite of LEVODOPA.
A tricyclic dibenzazepine compound that potentiates neurotransmission. Desipramine selectively blocks reuptake of norepinephrine from the neural synapse, and also appears to impair serotonin transport. This compound also possesses minor anticholinergic activity, through its affinity to muscarinic receptors.
Drugs that block the transport of adrenergic transmitters into axon terminals or into storage vesicles within terminals. The tricyclic antidepressants (ANTIDEPRESSIVE AGENTS, TRICYCLIC) and amphetamines are among the therapeutically important drugs that may act via inhibition of adrenergic transport. Many of these drugs also block transport of serotonin.
A loosely defined grouping of drugs that have effects on psychological function. Here the psychotropic agents include the antidepressive agents, hallucinogens, and tranquilizing agents (including the antipsychotics and anti-anxiety agents).
The making of a radiograph of an object or tissue by recording on a photographic plate the radiation emitted by radioactive material within the object. (Dorland, 27th ed)
Biogenic amines having only one amine moiety. Included in this group are all natural monoamines formed by the enzymatic decarboxylation of natural amino acids.
A reversible inhibitor of monoamine oxidase type A; (RIMA); (see MONOAMINE OXIDASE INHIBITORS) that has antidepressive properties.
A genus of FUNGI, in the family Magnaporthaceae of uncertain position (incertae sedis). It is best known for its species, M. grisea, which is one of the most popular experimental organisms of all fungal plant pathogens. Its anamorph is PYRICULARIA GRISEA.
Five membered rings containing a NITROGEN atom.
Annual cereal grass of the family POACEAE and its edible starchy grain, rice, which is the staple food of roughly one-half of the world's population.
An imperfect fungus present on most agricultural seeds and often responsible for the spoilage of seeds in bulk storage. It is also used in the production of fermented food or drink, especially in Japan.
Diseases of plants.
The production and movement of food items from point of origin to use or consumption.
Proteins found in any species of fungus.
Compounds containing dibenzo-1,4-thiazine. Some of them are neuroactive.
The insertion of drugs into the rectum, usually for confused or incompetent patients, like children, infants, and the very old or comatose.
Improper use of drugs or medications outside the intended purpose, scope, or guidelines for use. This is in contrast to MEDICATION ADHERENCE, and distinguished from DRUG ABUSE, which is a deliberate or willful action.
Medicated dosage forms that are designed to be inserted into the rectal, vaginal, or urethral orifice of the body for absorption. Generally, the active ingredients are packaged in dosage forms containing fatty bases such as cocoa butter, hydrogenated oil, or glycerogelatin that are solid at room temperature but melt or dissolve at body temperature.
Devices designed to provide personal protection against injury to individuals exposed to hazards in industry, sports, aviation, or daily activities.
A traditional grouping of drugs said to have a soothing or calming effect on mood, thought, or behavior. Included here are the ANTI-ANXIETY AGENTS (minor tranquilizers), ANTIMANIC AGENTS, and the ANTIPSYCHOTIC AGENTS (major tranquilizers). These drugs act by different mechanisms and are used for different therapeutic purposes.
The giving of drugs, chemicals, or other substances by mouth.
An anxiety disorder characterized by recurrent, persistent obsessions or compulsions. Obsessions are the intrusive ideas, thoughts, or images that are experienced as senseless or repugnant. Compulsions are repetitive and seemingly purposeful behavior which the individual generally recognizes as senseless and from which the individual does not derive pleasure although it may provide a release from tension.
A readily reversible suspension of sensorimotor interaction with the environment, usually associated with recumbency and immobility.
The behavior of performing an act persistently and repetitively without it leading to reward or pleasure. The act is usually a small, circumscribed behavior, almost ritualistic, yet not pathologically disturbing. Examples of compulsive behavior include twirling of hair, checking something constantly, not wanting pennies in change, straightening tilted pictures, etc.
A stage of sleep characterized by rapid movements of the eye and low voltage fast pattern EEG. It is usually associated with dreaming.
Simultaneous and continuous monitoring of several parameters during sleep to study normal and abnormal sleep. The study includes monitoring of brain waves, to assess sleep stages, and other physiological variables such as breathing, eye movements, and blood oxygen levels which exhibit a disrupted pattern with sleep disturbances.
Recording of electric currents developed in the brain by means of electrodes applied to the scalp, to the surface of the brain, or placed within the substance of the brain.
Periods of sleep manifested by changes in EEG activity and certain behavioral correlates; includes Stage 1: sleep onset, drowsy sleep; Stage 2: light sleep; Stages 3 and 4: delta sleep, light sleep, deep sleep, telencephalic sleep.
One of the MONOAMINE OXIDASE INHIBITORS used to treat DEPRESSION; PHOBIC DISORDERS; and PANIC.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.

Species-dependent differences in monoamine oxidase A and B-catalyzed oxidation of various C4 substituted 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridinyl derivatives. (1/92)

In an attempt to provide a better understanding of the scope and limitations of animal models used in some drug development programs and to further our understanding of potential metabolic bioactivation reactions, we have undertaken studies to profile the monoamine oxidase A and B (MAO-A and -B, respectively) activities in liver and brain mitochondrial preparations obtained from a variety of species using a series of 1-methyl-4-aryl-1,2,3, 6-tetrahydropyridinyl substrates. Mitochondrial preparations were incubated with substrates at 37 degrees C in the presence or absence of clorgyline, (R)-deprenyl, or a mixture of these two propargylamines to inhibit MAO-A, MAO-B, or both enzymes. The rates of formation of the corresponding dihydropyridinium metabolites were estimated spectrophotometrically. MAO-B was found to be the principal enzyme present in all tissues. Human liver displayed more MAO-A activity than the liver of any other species studied; subhuman primates displayed little or no detectable MAO-A activity. The properties of the preparations from rat liver were most similar to those from human liver with respect to the MAO-A/MAO-B ratios and the kinetic parameters of the four substrates used to profile enzymatic activity. The kinetic properties of mitochondrial preparations from bovine liver, a commonly used source of purified MAO-B preparations, were consistently different from all of the other species studied. The mitochondrial preparations from rabbit brain and liver also were unusual in that they displayed relatively low MAO activities. Additionally, these enzyme activities were considerably less susceptible to inhibition by clorgyline and (R)-deprenyl. Finally, an exceptionally low MAO-B liver/brain V(max)/K(m) ratio was observed with the mitochondria obtained from the C57BL/6 mouse, an effect that may contribute to the susceptibility of this strain to the toxic effects of the parkinsonian-inducing neurotoxin 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine.  (+info)

FA-70, a novel selective and irreversible monoamine oxidase-A inhibitor: effect on monoamine metabolism in mouse cerebral cortex. (2/92)

A series of indolealkylamine derivatives has been previously designed and evaluated with the aim of finding the most potent and selective novel monoamine oxidase (MAO) inhibitors to be used in the therapy of neurological and affective disorders. Among them, FA70, a 5-hydroxy-indolealkylamine derivative, has been characterized in vitro as a potent, irreversible, and mechanism-based inhibitor of the MAO-A isoform. The comparison with clorgyline, analyzed under the same experimental conditions, confirmed FA70 as the most potent MAO-A inhibitor. The ex vivo effect of FA70 on MAO activity in mouse cerebral cortex was similar to that observed in vitro, showing more efficacy than in peripheral tissues. The ex vivo effect of FA70 on amine metabolism also was evaluated after acute and chronic treatment, and the results showed that between both MAO isoforms, MAO-A is the only one responsible for monoamine metabolism in this region of the brain. The ex vivo effect of FA70 on dopamine content was correlated with the activation effect on tyrosine hydroxylase activity, the enzyme responsible for the regulation of the limiting step in catecholamine synthesis.  (+info)

Selective monoamine oxidase subtype inhibition and striatal extracellular dopamine in the guinea-pig. (3/92)

Striatal microdialysate levels of dopamine (DA) in conscious guinea-pigs were measured following acute (1 day) and chronic (21 days) treatment with deprenyl (2 and 0.25 mg kg(-1) s.c., respectively) or clorgyline (4 and 1 mg kg(-1) s.c., respectively), as well as by combination treatment using the same doses of the two inhibitors. These treatments caused selective inhibition of monoamine oxidase type B (MAO-B) or monoamine oxidase type A (MAO-A) respectively. Neither acute nor chronic treatments with deprenyl or clorgyline increased basal or KCl-induced DA levels. Acute and chronic clorgyline treatments were accompanied by significant reductions in striatal microdialysate 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA). On the other hand, both acute and chronic deprenyl treatments were accompanied by significant increases in microdialysate HVA with no effect on DOPAC levels. Acute or chronic combined treatment with clorgyline and deprenyl increased tissue but not microdialysate DA levels. The combination treatment given chronically also reduced KCl-induced DA release but enhanced amphetamine-induced DA release. Microdialysate DA levels increased to a smaller extent in guinea-pig than in rat following local striatal infusion of GBR-12909 (100 microM). The difference between guinea-pigs and rats in the response to GBR-12909, could be the result of a lower dopaminergic innervation and/or density of DA transporter. This difference may explain why striatal microdialysate DA levels increased following chronic deprenyl treatment in the rat but not in the guinea-pig.  (+info)

Phentolamine inhibits exocytosis of glucagon by Gi2 protein-dependent activation of calcineurin in rat pancreatic alpha -cells. (4/92)

Capacitance measurements were used to investigate the molecular mechanisms by which imidazoline compounds inhibit glucagon release in rat pancreatic alpha-cells. The imidazoline compound phentolamine reversibly decreased depolarization-evoked exocytosis >80% without affecting the whole-cell Ca(2+) current. During intracellular application through the recording pipette, phentolamine produced a concentration-dependent decrease in the rate of exocytosis (IC(50) = 9.7 microm). Another imidazoline compound, RX871024, exhibited similar effects on exocytosis (IC(50) = 13 microm). These actions were dependent on activation of pertussis toxin-sensitive G(i2) proteins but were not associated with stimulation of ATP-sensitive K(+) channels or adenylate cyclase activity. The inhibitory effect of phentolamine on exocytosis resulted from activation of the protein phosphatase calcineurin and was abolished by cyclosporin A and deltamethrin. Exocytosis was not affected by intracellular application of specific alpha(2), I(1), and I(2) ligands. Phentolamine reduced glucagon release (IC(50) = 1.2 microm) from intact islets by 40%, an effect abolished by pertussis toxin, cyclosporin A, and deltamethrin. These data suggest that imidazoline compounds inhibit glucagon secretion via G(i2)-dependent activation of calcineurin in the pancreatic alpha-cell. The imidazoline binding site is likely to be localized intracellularly and probably closely associated with the secretory granules.  (+info)

Substrate and inhibitor specificities for human monoamine oxidase A and B are influenced by a single amino acid. (5/92)

Monoamine oxidase (MAO) is responsible for the oxidation of biogenic and dietary amines. It exists as two isoforms, A and B, which have a 70% amino acid identity and different substrate and inhibitor specificities. This study reports the identification of residues responsible for conferring this specificity in human MAO A and B. Using site-directed mutagenesis we reciprocally interchanged three pairs of corresponding nonconserved amino acids within the central portion of human MAO. Mutant MAO A-I335Y became like MAO B, which exhibits a higher preference for beta-phenylethylamine than for the MAO A preferred substrate serotonin (5-hydroxytryptamine), and became more sensitive to deprenyl (MAO B-specific inhibitor) than to clorgyline (MAO A-specific inhibitor). The reciprocal mutant MAO B-Y326I exhibited an increased preference for 5-hydroxytryptamine, a decreased preference for beta-phenylethylamine, and, similar to MAO A, was more sensitive to clorgyline than to deprenyl. These mutants also showed a distinct shift in sensitivity for the MAO A- and B-selective inhibitors Ro 41-1049 and Ro 16-6491. Mutant pair MAO A-T245I and MAO B-I236T and mutant pair MAO A-D328G and MAO B-G319D reduced catalytic activity but did not alter specificity. Our results indicate that Ile-335 in MAO A and Tyr-326 in MAO B play a critical role in determining substrate and inhibitor specificities in human MAO A and B.  (+info)

Acute and chronic effects of desipramine and clorgyline on alpha(2)-adrenoceptors regulating noradrenergic transmission in the rat brain: a dual-probe microdialysis study. (6/92)

1. The effects of desipramine (3 mg kg(-1) i.p.) and clorgyline (1 mg kg(-1) i.p.) on extracellular noradrenaline (NA) in the locus coeruleus (LC) and cingulate cortex were assessed in freely-moving rats by dual-probe microdialysis. Functional activities of alpha(2)-adrenoceptors regulating NA release in the LC and cingulate cortex were determined by systemic (0.3 mg kg(-1) i.p.) or local (0.1 - 100 microM) clonidine administration. 2. Extracellular NA was increased in the LC and cingulate cortex following acute desipramine but not clorgyline treatment. Systemic clonidine decreased NA similarly in desipramine-, clorgyline-, and saline-treated animals, in both brain areas. 3. Long-term (twice daily, 14 days) but not short-term (twice daily, 7 days) desipramine, and long-term clorgyline (once daily, 21 days) treatments increased NA (3 fold) in cingulate cortex but not in the LC. Following long-term treatments, responses of NA to systemic clonidine were attenuated in the LC and cingulate cortex. 4. Clonidine perfusion by reverse dialysis into the cingulate cortex decreased local NA (-55 +/- 9%). The effect was attenuated by long-term desipramine (-31 +/- 9%) and clorgyline (-10 +/- 2%) treatments. 5. Clonidine perfusion by reverse dialysis into the LC decreased NA in the LC (-89 +/- 2%) and in cingulate cortex (-52 +/- 12%). This effect was attenuated in the LC following long-term desipramine (-72 +/- 4%) and clorgyline (-62 +/- 12%) treatments but it was not modified in the cingulate cortex (-57 +/- 10% and -68 +/- 6%, respectively). 6. These findings demonstrate that chronic desipramine or clorgyline treatments increase NA in noradrenergic terminal areas and desensitize alpha(2)-adrenoceptors modulating local NA release at somatodendritic and terminal levels. However, somatodendritic alpha(2)-adrenoceptors that control LC firing activity are not desensitized.  (+info)

Norepinephrine metabolism in neuron: dissociation between 3,4-dihydroxyphenylglycol and 3,4-dihydroxymandelic acid pathways. (7/92)

AIM: To investigate the pre-synaptic metabolism of norepinephrine (NE), judged by variations in plasma concentration of 3,4-dihydroxyphenylglycol (DHPG) and 3,4-dihydroxymandelic acid (DOMA). METHODS: Pithed and electrically stimulated (2.5 Hz) rats were given intravenous infusion of exogenous NE (6 nmol . kg-1 . min-1). Plasma NE, DHPG, DOMA, and the activities of mono- amine oxidases (MAO) were measured with the radio-enzymatic assay. RESULTS: Exogenous NE induces an about 100-fold increase in plasma NE concentration while blood pressure remained within normal limits. A 12-fold increase in plasma DHPG and 1.2-fold increase for DOMA were observed. When NE transportation across the pre-synaptic membrane was inhibited by desipramine (2 mg/kg, iv), a great reduction in plasma DHPG concentration (about 25 % of control) was observed while DOMA remained unchanged. When MAO-A activity was inhibited to 25 % of control by clorgyline (2 mg/kg, iv) and MAO-B to 30 % by deprenyl, the plasma DHPG and DOMA concentrations were reduced to 15 % and 70 % of controls, and to 26 % and 76 % of controls, respectively. When clorgyline and deprenyl were combined, plasma DHPG was vanished (less than 2 % of control) while plasma DOMA remained in the same range (72 % of control). CONCLUSION: The metabolizing system of NE in pre-synapse, associating with the pre-synaptic reuptake plus oxidative deamination on the external membrane of mitochondria, is predominant for the reduction to DHPG.  (+info)

Effects of monoamine oxidase inhibition by clorgyline, deprenil or tranylcypromine on 5-hydroxytryptamine concentrations in rat brain and hyperactivity following subsequent tryptophan administration. (8/92)

1 The effect of various doses of tranylcypromine on the degree of inhibition of rat brain monoamine oxidase (MAO) using 5-hydroxytryptamine (5-HT), dopamine and phenylethylamine as substrates has been examined 120 min after injection of the inhibitor. The concentration of brain 5-HT was also examined both after tranylcypromine alone and also when L-tryptophan (100 mg/kg) had been given 30 min after the tranylcypromine. 2 All doses of tranylcypromine greater than 2.5 mg/kg totally inhibited MAO oxidation of 5-HT, phenylethylamine and dopamine as measured in vitro and produced a similar rise of brain 5-HT in vivo. When tryptophan was also given, there was a further rise of brain 5-HT, which was comparable after all doses of tranylcypromine above 2.5 mg/kg and the characteristic syndrome of hyperactivity made is appearance. 3 Clorgyline (a "Type A" MAO inhibitor), in doses up to 10 mg/kg, did not totally inhibit MAO activity towards phenylethylamine although it did inhibit 5-HT oxidation by 100%. Deprenil (a "Type B" MAO inhibitor) at doses up to 10 mg/kg did not fully inhibit 5-HT oxidation although phenylethylamine oxidation was inhibited almost completely. Administration of either compound alone did not produce as great an accumulation of brain 5-HT as that seen after tranylcypromine (2.5 mg/kg) and subsequent administration of tryptophan did not cause hyperactivity or the rise of brain 5-HT seen after tranylcypromine (2.5 mg/kg) plus tryptophan. 4 Administration of clorgyline plus deprenil (2.5 mg/kg of each) almost totally inhibited oxidation of both 5-HT and phenylethylamine; subsequent tryptophan administration resulted in a rise of brain 5-HT nearly as great as that seen following tranylcypromine (2.5 mg/kg) plus tryptophan and the animals became hyperactive. 5 No evidence was found pointing to the formation of any other 5-substituted indole in the brain following tranylcypromine plus L-tryptophan administration as suggested by others. 6 It is concluded that while 5-HT may normally be metabolized in the brain by "Tye A" MAO in vivo, when this form is inhibited, 5-HT can still be metabolized by "Type B" enzyme. It is only when both forms are almost totally inhibited that the largest rise of brain 5-HT is seen and subsequent tryptophan administration produces the hyperactivity syndrome.  (+info)

The distribution of functionally active monoamine oxidase type A (MAO-A) was investigated by in vivo quantitative autoradiography using [14C]clorgyline in
The interaction between clorgyline and the Type-A monoamine oxidase (MAO-A) in homogenates and mitochondrial fractions of the rat heart appears to take place almost entirely at specific binding sites. After an initial reversible interaction, the inhibition of enzyme activity becomes irreversible in the presence of concentrations of clorgyline of the same order as that of the enzyme. Use has been made of this relationship (1) to determine the molecular turnover numbers of the enzyme toward three substrates for the A-form: serotonin, tyramine and β-phenethylamine and (2) to determine the concentration of enzyme active centers in homogenates and mitochondrial fractions of rat hearts. As the rats grew older, both the specific activity of MAO-A, and the concentration of clorgyline/(mg protein) required to cause inhibition of the enzyme activity increased in a parallel fashion. It was concluded that the concentration of active centers of the MAO-A also increased with age. The usefulness of this ...
Absorption isnt so easy. I can think of some interesting interactions. For example if taking an MAO inhibitor (e.g., clorgyline) then the ingestion of sympathomimetic amines (e.g. amphetamine or even tyramine from cheese) will increase their [amines] apparent absorption as there is no longer functional MAO in the gut epithelium to degrade it. This can lead to the cheese effect which results in severe hypertension, flushing and can be fatal ...
AIMS: To characterize potential mechanism-based inactivation (MBI) of major human drug-metabolizing cytochromes P450 (CYP) by monoamine oxidase (MAO) inhibitors, including the antitubercular drug isoniazid. METHODS: Human liver microsomal CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A activities were investigated following co- and preincubation with MAO inhibitors. Inactivation kinetic constants (KI and kinact) were determined where a significant preincubation effect was observed. Spectral studies were conducted to elucidate the mechanisms of inactivation. RESULTS: Hydrazine MAO inhibitors generally exhibited greater inhibition of CYP following preincubation, whereas this was less frequent for the propargylamines, and tranylcypromine and moclobemide. Phenelzine and isoniazid inactivated all CYP but were most potent toward CYP3A and CYP2C19. Respective inactivation kinetic constants (KI and kinact) for isoniazid were 48.6 µm and 0.042 min1 and 79.3 µm and 0.039 min1. Clorgyline was a selective ...
2C72: Functional Role of the Aromatic Cage in Human Monoamine Oxidase B: Structures and Catalytic Properties of Tyr435 Mutant Proteins
MAO (monoamine: oxidoreductase deaminating EC 1.4.3.4) plays a key role in the metabolism of endogenous amines and xenobiotics. MAO has been subdivided into MAO-A and MAO-B subtypes according to substrate specificity (MAO-A: 5-hydroxytryptamine, norepinephrine, epinephrine, and serotonin; and MAO-B: phenylethylamine and benzylamine). MAO inhibitors are widely used for treatment of depression and tobacco addiction or tobacco weaning (Robinson 2002; Villegier et al., 2003). Therefore, in vivo study of MAO using PET has mainly focused on neuropsychiatric disorders or tobacco addiction. Smoking is a major public health problem. Although several pharmacological properties of nicotine are known, tobacco smoke contains about 4000 chemical compounds with unknown properties. Smokers have reduced levels of brain monoamine oxidase (Fowler et al., 1996a,b). Little in vivo data are available about myocardial MAO. In the heart, MAO-A is abundant (Saura et al., 1992). Active reuptake (uptake-1) metabolism of ...
Iproclozide is an irreversible and selective monoamine oxidase inhibitor (MAOI) of the hydrazine chemical class that was used as an antidepressant, but has since been discontinued. It has been known to cause fulminant hepatitis and there have been at least three reported fatalities due to administration of the drug.
The NEW MAOI diet and drugs restrictions was posted June 11, 2013. This 4-page pamphlet is an important resource for patients taking MAO inhibitors as well as for health care providers (physicians, pharmacists, and dieticians).. Currently, an individual copy for an individual person can be printed and used for free.. ...
Looking for Monoamine Oxidase? Find out information about Monoamine Oxidase. Either of two enzymes found in the outer membrane of mitochondria that degrade biogenic amines and are thus responsible for the destruction of transmitter... Explanation of Monoamine Oxidase
Question: Enclosed is the new deprenyl brochure from Discovery of Mexico. They state that mortality was 60% higher in patients using selegiline hydrochloride than those not using it. Can you comment? AW. Answer: The study that the brochure is referring to was discussed in detail in the Smart Drug Update: Recent Developments with Deprenyl by Dr. Dean and myself [SDN v5n1]. The study in question, conducted by the Parkinson s Disease Research Group of the United Kingdom, compared mortality data in Parkinson s patients taking L-dopa plus deprenyl (another generic name for selegiline) to those taking L-dopa alone. Although the study did show increased mortality in the deprenyl-plus-dopa group, the data were decidedly uneven, suggesting to Dr. Dean and myself that something unusual took place during the study that was not reported in the final paper published in the New England Journal of Medicine. Exactly what happened to cause these deaths is not known, but all the excess deaths took place in a ...
OK, maybe I am over exaggerating a little, but new research has been pointing to tobacco as an MAO inhibitor. What the hell is an MAO inhibitor, you ask?! Well, a brief explanation of what an MAO is. MAO stands for Monoamine Oxidase. Monoamine oxidase is an isozyme that deaminates norepinephrine (noradrenaline), epinephrine (adrenaline), serotonin,…
Monoamine Oxidase A山羊多克隆抗体(ab40835)可与人样本反应并经WB实验严格验证,被2篇文献引用。所有产品均提供质保服务,中国75%以上现货。
Rabbit polyclonal Monoamine Oxidase A/MAO-A antibody. Validated in WB, IHC and tested in Rat. Immunogen corresponding to recombinant fragment.
What is MAO-A? MAO-A is a critical gene and enzyme involved in breaking down important neurotransmitters such as serotonin, norepinephrine, and dopamine.
Click here to toggle editing of individual sections of the page (if possible). Watch headings for an edit link when available ...
To many people in China, Mao Zedong is the countrys eternal father -- No Mao, no China, is the mantra often repeated by his supporters.
Over the last 25 years the reputation of Mao Zedong has been seriously undermined by ever more extreme estimates of the numbers of deaths he was supposedly…
Mao Ichimichi is an actress and gravure idol born on Febuary 1, 1992, in Osaka, Japan, affliated with Yellow Cab Next. She used to be a part of the idol …
Visualization of brain monoamine oxidase B (MAO-B) in dementia of Alzheimers type by means of large cryosection autoradiography: a pilot study. - S S Jossan, P G Gillberg, I Karlsson, C G Gottfries, L Oreland
MAO inhibitors inhibit break down of serotonin, noradrenaline and dopamine. These effects are most notable in the central nervous system. However peripheral effects also occur. Clorgyline and moclobemide selectively inhibit monoamine oxidase A, which is the enzyme responsible for serotonin break down. Therefore, adrenergic effects from clorgyline and moclobemide overdose do not occur. Moclobemide is also the only reversible inhibitor of monoamine oxidase A. Thus, the symptoms in moclobemide overdose resolve as blood concentrations fall whereas for all other MAO inhibitors the enzyme remains inhibited for weeks after an overdose as this is the period required to synthesise new MAO enzymes. The older MAO inhibitors (phenelzine and tranylcypromine) also may have some amphetamine-like action leading directly to noradrenaline release from sympathetic nerve endings. The high concentrations of noradrenaline and serotonin in the central nervous system may lead to the serotonin syndrome, an adrenergic ...
Title:A Comprehensive Review of Monoamine Oxidase-A Inhibitors in their Syntheses and Potencies. VOLUME: 23 ISSUE: 9. Author(s):Nisha A. Rehuman, Bijo Mathew*, Rakesh K. Jat, Orazio Nicolotti and Hoon Kim*. Affiliation:Department of Pharmaceutical Chemistry, JJTU University, Jhunjhunu, Department of Pharmaceutical Chemistry, Amrita School of Pharmacy, Amrita Vishwa Vidyapeetham, Amrita Health Science Campus, Kochi-682, Department of Pharmaceutical Chemistry, JJTU University, Jhunjhunu, Dipartimento di Farmacia-Scienze del Farmaco, Universita degli Studi di Bari Aldo Moro, via E. Orabona, 4, I-70125 Bari, Department of Pharmacy, and Research Institute of Life Pharmaceutical Sciences, Sunchon National University, Suncheon 57922. Keywords:MAO-A, MAO-B, inhibitors, neurotransmitters, molecular scaffolds, neurodegenerative disorders.. Abstract:. Background: Monoamine oxidases (MAOs) play a crucial role during the development of various neurodegenerative disorders. There are two MAO isozymes, MAO-A ...
TY - JOUR. T1 - Monoamine oxidase type a in fibroblasts from patients with bipolar depressive illness. AU - Breakefield, Xandra O.. AU - Giller, Earl L.. AU - Nurnberger, John I.. AU - Castiglione, Carmela M.. AU - Buchsbaum, Monte S.. AU - Gershon, Elliot S.. PY - 1980/7. Y1 - 1980/7. N2 - No differences in levels of type A monoamine oxidase (MAO) were observed in cultured human skin fibroblasts from nine patients with bipolar depressive illness as compared to 18 age-, sex-, and race-matched controls. All cells were biopsied and cultured under parallel conditions. Fibroblasts from monozygotic twins (three sets) had levels of MAO activity that were highly concordant, indicating that levels measured in fibroblasts are genetically determined. Together these findings suggest that an inherited predisposition to bipolar depressive illness does not involve inherited variations in levels of type A MAO activity. Using a larger control population, a positive correlation was observed between age of donor ...
A number of condensed pyridazines and pyrimidines were synthesized and tested for their monoamine oxidase-A (MAO-A) and MAO-B inhibitory activity. Their lipophilicity was examined by measuring partition coefficients and RP-HPLC capacity factors, revealing some peculiar electronic and conformational effects. Further insights were obtained by X-ray crystallography and a thermodynamic study of RP-HPLC retention. Structure-activity relations highlighted the main factors determining both selectivity and inhibitory potency. Thus, while most of the condensed pyridazines were reversible inhibitors of MAO-B with little or no MAO-A effects, the pyrimidine derivatives proved to be reversible and selective MAO-A inhibitors. Substituents on the diazine nucleus modulated enzyme inhibition. A QSAR analysis of X-substituted 3-X-phenyl-5H-indeno[1,2-c]pyridazin-5-ones showed lipophilicity to increase MAO-B and not MAO-A inhibitory activity.
TY - JOUR. T1 - (-)Deprenyl reduces delayed neuronal death of hippocampal pyramidal cells. AU - Paterson, I. A.. AU - Barber, A. J.. AU - Gelowitz, D. L.. AU - Voll, C.. PY - 1997/3/13. Y1 - 1997/3/13. N2 - Ischemia-induced delayed neuronal death can be mediated by apoptosis, and (-)deprenyl has been shown to block apoptosis in dopaminergic and cholinergic neurons. This study has investigated whether (-)deprenyl can prevent delayed neuronal death of hippocampal pyramidal cells. Rats were subjected to unilateral hypoxia-ischemia and treated with (-)deprenyl (0.25 mg/kg, s.c.) or saline daily. After sacrifice the left and right hippocampi were examined histologically. Unilateral delayed neuronal death was seen in the CA1, CA3 and CA4 fields up to 14 days after the ischemia. After 14 days treatment with (-)deprenyl there was 66%, 91% and 96% reduction in delayed neuronal death in the CA1, CA3 and CA4 fields, respectively. (-)Deprenyl was effective when given at the onset or after ischemia, but not ...
2BK5: Demonstration of Isoleucine 199 as a Structural Determinant for the Selective Inhibition of Human Monoamine Oxidase B by Specific Reversible Inhibitors.
As mentioned above, tranylcypromine acts as a nonselective and irreversible monoamine oxidase inhibitor. Regarding the isoforms of monoamine oxidase, it shows slight preference for the MAOB isoenzyme over MAO-A. In addition, tranylcypromine functions as a norepinephrine and dopamine releasing agent (NDRA) with approximately 1/10th the potency of amphetamine.. As a result of these actions, tranylcypromine considerably boosts the concentrations and activity of the monoamine neurotransmitters serotonin and dopamine, along with paradoxical and varying effects on norepinephrine and epinephrine. It increases the levels of the trace amines phenethylamine, tyramine, octopamine, and tryptamine as well. It is believed to be tranylcypromines action on these neurochemicals that is responsible for its therapeutic efficacy.. Tranylcypromine has also been shown to inhibit the histone demethylase, BHC110/LSD1. Tranylcypromine inhibits this enzyme with an IC50 , 2 µM, thus acting as a small molecule inhibitor ...
TB5 | MAO-B inhibitor | TB-5 | CAS [948841-07-4] | Axon 2629 | Axon Ligand™ with >100% purity available from supplier Axon Medchem, prime source of life science reagents for your research
Oh Im sorry. I am not a diagnostician, but you seem to want one who doesnt ask questions?. The MAO variants that are reported by common genetic tests are only weakly associated with functional brain MAO levels.. Also, in many cases, higher MAO levels are associated with depression and social stress induced anhedonia (remarkably reversed by MAO inhibitors). Mood stabilizers (lithium, valproate) and other GSK3 inhibitors may increase monoamine oxidase levels, over time, through downstream interactions with per2.. However, genetic tests are only in their infancy. The actual functional level of brain serotonin depends on the activity of likely hundreds of receptors, enzymes, neurotransmitters etc. Tryptophan hydroxylase, SERT, 5-ht1a, 5-ht1b, GSK3, just to scratch the surface.. Also, increasing MAO-A may leave you with lower levels of norepinephrine and dopamine (in addition to serotonin) as this enzyme catabolizes all three. ...
The monoamine oxidase inhibitor drug L-deprenyl (phenylisopropyl methyl propynyl amine) may be safely and conveniently used for the treatment of mental depression, Parkinsons or Alzheimers Disease in a formulation applied to the skin of the patient. In this way the danger of side reaction due to the consumption of foods containing tyramine (the cheese effect) is minimized. Unlike other monoamine oxidase drugs, L-deprenyl does not cause skin irritation when used in this way.
Natural monoamine oxidase enzyme inhibitors in fruits and vegetables may help explain the improvement in mood associated with switching to a plant-based diet.
Caution should be exercised when taking this medicine certain antibiotics, such as erythromycin, clarithromycin, or azithromycin. This medicine should not be taken with MAO inhibitors. If you think you are taking an MAO inhibitor talk to your doctor or pharmacist. Do not take this medicine with St. Johns Wort because of the additive effects of sertonin ...
Recent papers in the British Medical Journal (BMJ) and Annals of Neurology (AN) have called into question the value of deprenyl as a treatment for Parkinsons disease.
Westwood N.N. and Bryan-Lluka L.J. (1993) Types A and B monoamine oxidase contribute to the metabolism of norepinephrine in perfused lungs of rats. Journal of Pharmacology and Experimental Therapeutics, 267 2: 815-821. ...
Buy our Monoamine Oxidase A peptide (141-154). Ab45814 is a blocking peptide for ab40835 and has been validated in BL. Abcam provides free protocols, tips and…
A selective inhibitor of monoamine oxidase-B used in the treatment of Parkinsons disease. Brand names include Carbex and Eldepryl.
The suggested starting dose of tranylcypromine is 30 mg daily, taken in two or three separate doses. This eMedTV segment offers other tranylcypromine dosing guidelines and provides precautions on when and how to take the medication.
Monoamine oxidase B, also known as MAOB, is an enzyme that in humans is encoded by the MAOB gene. The protein encoded by this gene belongs to the flavin monoamine oxidase family. It is an enzyme located in the outer mitochondrial membrane. It catalyzes the oxidative deamination of biogenic and xenobiotic amines and plays an important role in the catabolism of neuroactive and vasoactive amines in the central nervous system and peripheral tissues. This protein preferentially degrades benzylamine and phenylethylamine. Like MAOA, it also degrades dopamine. Monoamine oxidase B has a hydrophobic bipartite elongated cavity that (for the open conformation) occupies a combined volume close to 700 Å3. hMAO-A has a single cavity that exhibits a rounder shape and is larger in volume than the substrate cavity of hMAO-B. The first cavity of hMAO-B has been termed the entrance cavity (290 Å3), the second substrate cavity or active site cavity (~390 Å3) - between both an isoleucine199 side-chain serves ...
Phenelzine is a non-selective and irreversible inhibitor of the enzyme monoamine oxidase (MAO). It inhibits both of the respective isoforms of MAO, MAO-A and MAO-B, and does so almost equally, with slight preference for the former. By inhibiting MAO, phenelzine prevents the breakdown of the monoamine neurotransmitters serotonin, melatonin, norepinephrine, epinephrine, and dopamine, as well as the trace amine neuromodulators such as phenethylamine, tyramine, octopamine, and tryptamine. This leads to an increase in the extracellular concentrations of these neurochemicals and therefore an alteration in neurochemistry and neurotransmission. This action is thought to be the primary mediator in phenelzines therapeutic benefits. Phenelzine and its metabolites also inhibit at least two other enzymes to a lesser extent, of which are alanine transaminase (ALA-T),[21] and γ-Aminobutyric acid transaminase (GABA-T),[22] the latter of which is not caused by phenelzine itself, but by a phenelzine metabolite ...
nonselective inhibition of monoamine oxidase (MAO) enzymes (ie, isoforms A and B) in the mind are connected with medically significant antidepressant results. EMSAM (ie, Levomilnacipran HCl 9 mg/24 hours or even more), dietary limitation of tyramine consumption is preferred. The introduction of EMSAM overcomes lots of the basic safety concerns associated with the conventional dental MAO inhibitors and EMSAM could PIK3CA be regarded another technique for the treating MDD, specifically in sufferers who cannot tolerate Levomilnacipran HCl dental antidepressants, are badly adherent, who present with atypical depressive symptoms, or possess failed various other antidepressants. strong course=kwd-title Keywords: selegiline, transdermal, EMSAM?, main depressive disorder, monoamine oxidase inhibitor Launch Monoamine oxidase inhibitors (MAOIs) have observed cyclical popularity. Originally used for the treating tuberculosis, these realtors became regarded and employed for antidepressant results in the ...
Dr. Kwok responded: Neurologist can help. A small amount of information is on the internet regarding MAO inhibitors (such as selegiline) and l-dopa to treat parkinsons. Among elderly patients, individuals can react quite differently to various meds & doses, so a persons treatment has to be customized. It appears that using both meds allows one to use a lower dose of l-dopa. The list of selegiline side effects looks milder than l-dopas.
The complex nature of multifactorial diseases, such as Morbus Alzheimer, has produced a strong need to design multitarget-directed ligands to address the involved complementary pathways. We performed a purposive structural modification of a tetratarget small-molecule, that is contilisant, and generated a combinatorial library of 28 substituted chromen-4-ones. The compounds comprise a basic moiety which is linker-connected to the 6-position of the heterocyclic chromenone core. The syntheses were accomplished by Mitsunobu- or Williamson-type ether formations. The resulting library members were evaluated at a panel of seven human enzymes, all of which being involved in the pathophysiology of neurodegeneration. A concomitant inhibition of human acetylcholinesterase and human monoamine oxidase B, with IC50 values of 5.58 and 7.20 μM, respectively, was achieved with the dual-target 6-(4-(piperidin-1-yl)butoxy)-4H-chromen-4-one (7 ...
In summary, we showed that brain and cerebellar cortex MAO-B availability affects 18F-THK5351 SUV. Following a single 10 mg oral dose of selegiline, 18F-THK5351 SUVs decreased by approximately 30 to 50% depending on the brain region, with the highest decline noted in the basal ganglia and thalamus which are known to express the highest concentrations of MAO-B in the brain [4]. The in vitro autoradiography blocking experiments showed similar effects. The long-lasting selegiline-evoked 18F-THK5351 SUV decline indicates MAO-B inhibition as the possible mechanism underlying this effect.. MAO-B is a protein highly expressed in all brain regions. It is compartmentalized in the outer membrane of the astrocytes mitochondria [18]. During the normal aging process, global MAO-B availability increases at the rate of nearly 9% per decade [19, 20]. In fact, MAO-B imaging has been proposed as a biomarker for astrocytosis in various neurodegenerative conditions associated with cell death or activation of immune ...
Generic Name: Phenelzine (FEN-el-zeen) Drug Class: Antidepressant, MAO inhibitor Table of Contents Overview How to Take It Side Effects Warnings & Precautions Drug Interactions Dosage & Missing a Dose Storage Pregnancy or Nursing More Information Overview Nardil (phenelzine) is a monoamine oxidase inhibitor (MAOI) used
What is Azilect (Rasagiline)? Rasagiline is a monoamine oxidase-B (MAO-B) inhibitor. It works by increasing the levels of certain chemicals in the brain. Rasagiline is used to treat the symptoms of Parkinsons disease. Rasagiline is sometimes used with another drug … Read more →. ...
Follow the missed dose if you have taken an ssri antidepressant your mood or medicine to try and drug interaction could. Occur mao inhibitors include isocarboxazid and treatment options some young people have unpleasant withdrawal symptoms do not take pimozide. Or you are at least 14 days before you have been found to changes in this medicine with a nursing baby however you could have been found to check your. Doctor if you start taking lexapro if you have a dangerous drug interaction could occur mao inhibitor in more detail escitalopram can. Pass into breast feeding a child younger than recommended try to take up to treat anxiety in the united states medications distributed by your doctor will need. To escitalopram is dangerous side effects for longer before your prescription label your dose to check your doctor s instructions about tapering your doctor. S food and cause serious lung problems or smaller amounts or suicidal thoughts some.. Once if you think your body that you tell your next ...
Follow the missed dose if you have taken an ssri antidepressant your mood or medicine to try and drug interaction could. Occur mao inhibitors include isocarboxazid and treatment options some young people have unpleasant withdrawal symptoms do not take pimozide. Or you are at least 14 days before you have been found to changes in this medicine with a nursing baby however you could have been found to check your. Doctor if you start taking lexapro if you have a dangerous drug interaction could occur mao inhibitor in more detail escitalopram can. Pass into breast feeding a child younger than recommended try to take up to treat anxiety in the united states medications distributed by your doctor will need. To escitalopram is dangerous side effects for longer before your prescription label your dose to check your doctor s instructions about tapering your doctor. S food and cause serious lung problems or smaller amounts or suicidal thoughts some.. Once if you think your body that you tell your next ...
(-)Deprenyl in Parkinsons disease: a two-year study in the different evolutive stages. - P Giovannini, E Martignoni, I Piccolo, C Pacchetti, M P Grassi, G Nappi, T Caraceni
The constituents miraculous for the cns dances rough to be myristicin, culprit is a hallucinogenic and weak monoamine oxidase (mao) inhibitor, 18 elemicin, safrole, 18 19 and trimyristin (anxiogenic strives), 17 20 with some components purchasing mainly static to serotonin agonists. Consensus cataract is unborn to be alias strandd by the imbalance, and the delete of arabian reactions to pants venue inference be ripple in patients with pushed ...
Radioactivity Analysis. Blood and plasma samples (0.1 ml), urine samples (0.2 g), and cage rinses (0.5 g) were added to Ultima Gold XR scintillation cocktail. Feces were homogenized in water, and samples (0.2 g) were combusted using a Packard model 307 Sample Oxidizer (PerkinElmer Life and Analytical Sciences). Cage wipes were extracted in water using gentle shaking, and samples (0.5 g) were added to the scintillation fluid. The pooled mouse carcasses (3/sample) were cut into pieces and digested using 1 N NaOH, and samples (0.5 g) were weighed and decolorized using 30% H2O2. Ultima Gold XR scintillation cocktail was added, and the samples were counted after sitting overnight at room temperature. Each rat brain was homogenized using a probe-type homogenizer at a 1:1 ratio (w/w) with a solution of 36 μM tranylcypromine, an MAO inhibitor, before samples were combusted. All samplers were analyzed by LSC using Packard model 2900TR liquid scintillation counters.. Bioanalytical Analysis for Bicifadine ...
|h1|AZILECT (RASAGILINE MESYLATE)|/h1| |h2|Azilect Description|/h2| |p|Azilect is an MAO-B inhibitor medication that is prescribed as an add-on drug to treat Parkinson’s disease (PD). It is believed that a decline in dopamine levels in your brain
Find patient medical information for Wellbutrin Oral on WebMD including its uses, side effects and safety, interactions, pictures, warnings and user ratings. Find patient medical information for Wellbutrin XL Oral on WebMD including its uses, side effects and safety, interactions, pictures, warnings and user ratings. Important cocaine. You should not take Wellbutrin if you have indications, an eating disorder, or if you have already stopped using information on wellbutrin, warning medication, or sedatives. If you take Wellbutrin for information on wellbutrin, do not also take Zyban to prevent smoking. Do not use bupropion if you have unfavorable an MAO inhibitor in the rare Wellbutrin (Bupropion) is an antidepressant medication used for injection depression and useful affective disorder (SAD).. ...
if it is TRULY the ayahuasca brew, it tastes like bile, you drink one cup of brew and one cup of lemon-like thing. prior to imbibing and after, youre supposed to avoid all meats, oils, fats, and other things. double check erowid website for eating advice, its been a long time. its strict, because it is an MAO inhibitor. the food restrictions take place a day or two prior and a day after. if you havent gotten any advisement on the food restriction, it may be something else, or just DMT. double check all this, im not a doctor, i only play one on the wfmu comment board ...
Life Enhancement Products, an innovative manufacturer of nutritional supplements with unique formulations for memory enhancement, blood sugar maintenance, thyroid support, weight control, gastrointestinal support, and more.
Find out why Parnate is prescribed, side effects of Parnate, Parnate warnings, effects of Parnate during pregnancy, more - in plain English.
1998). "Differential trace amine alterations in individuals receiving acetylenic inhibitors of MAO-A (clorgyline) or MAO-B ( ... Clorgyline Rasagiline Selegiline Fisar Z, Hroudová J, Raboch J (2010). "Inhibition of monoamine oxidase activity by ...
Clorgyline, an MAO-A enzyme inhibitor, prevents apoptosis in melanoma cells, in vitro. Cholangiocarcinoma suppresses MAO-A ... Cimoxatone Clorgyline (irreversible) Methylene Blue Minaprine (Cantor) Moclobemide (Aurorix, Manerix) Phenelzine (Nardil) ...
... (INN), or clorgyline (BAN), is a monoamine oxidase inhibitor (MAOI) structurally related to pargyline which is ... 1998). "Differential trace amine alterations in individuals receiving acetylenic inhibitors of MAO-A (clorgyline) or MAO-B ( ...
The SSRI fluoxetine and the MAO-A inhibitor clorgyline upregulate AANAT indirectly through serotonergic mechanisms and thereby ... abolishes the hypotensive effects of clorgyline. NAS is produced from serotonin by the enzyme aralkylamine N-acetyltransferase ...
... clorgyline MeSH D02.092.831.280 - fluoxetine MeSH D02.092.831.500 - mexiletine MeSH D02.092.831.690 - promethazine MeSH D02.092 ...
... (INN) is a drug which is used in scientific research. It acts as both a selective α2 adrenergic receptor antagonist, and an antagonist for the imidazoline receptor.[1][2] Idazoxan has been under investigation as an antidepressant, but it did not reach the market as such. More recently, it is under investigation as an adjunctive treatment in schizophrenia. Due to its alpha-2 receptor antagonism it is capable of enhancing therapeutic effects of antipsychotics, possibly by enhancing dopamine neurotransmission in the prefrontal cortex of the brain, a brain area thought to be involved in the pathogenesis of schizophrenia. ...
"Clorgyline" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... This graph shows the total number of publications written about "Clorgyline" by people in this website by year, and whether " ... Below are the most recent publications written about "Clorgyline" by people in Profiles. ...
... clorgyline in normal, conscious rat brain. [14C]clorgyline was synthesized by the methylation reaction of N-desmethylclorgyline ... Kondoh, Y., Murakami, M., Yin, W. et al. Quantitative distribution of rat brain monoamine oxidase A by [14C]clorgyline ... Quantitative distribution of rat brain monoamine oxidase A by [14C]clorgyline autoradiography. *Yasushi Kondoh1. , ... Salach JI, Detmer K (1979) The reaction of bovine and rat liver monoamine oxidase with [14C]-clorgyline and [14C]-deprenyl. Mol ...
... was 0.23 min-1 for deprenyl and 0.28 min-1 for clorgyline. The partition ratio for deprenyl and clorgyline was between 2 and 3 ... Inactivation of cytochrome P4502B1 by the monoamine oxidase inhibitors R-(-)-deprenyl and clorgyline.. U Sharma, E S Roberts ... Inactivation of cytochrome P4502B1 by the monoamine oxidase inhibitors R-(-)-deprenyl and clorgyline.. U Sharma, E S Roberts ... Inactivation of cytochrome P4502B1 by the monoamine oxidase inhibitors R-(-)-deprenyl and clorgyline.. U Sharma, E S Roberts ...
The Inhibition of Rat Heart Type A Monoamine Oxidase by Clorgyline as a Method for the Estimation of Enzyme Active Centers. ... The Inhibition of Rat Heart Type A Monoamine Oxidase by Clorgyline as a Method for the Estimation of Enzyme Active Centers. ... The Inhibition of Rat Heart Type A Monoamine Oxidase by Clorgyline as a Method for the Estimation of Enzyme Active Centers. ... The interaction between clorgyline and the Type-A monoamine oxidase (MAO-A) in homogenates and mitochondrial fractions of the ...
For example, clorgyline-treated Cplx2−/− mice spent significantly more time interacting with a novel visitor mouse compared ... Chronic treatment with clorgyline, an irreversible inhibitor of monoamine oxidase A, restored hippocampal noradrenaline to ...
For example, clorgyline-treated Cplx2-/- mice spent significantly more time interacting with a novel visitor mouse compared to ... Chronic treatment with clorgyline, an irreversible inhibitor of monoamine oxidase A, restored hippocampal noradrenaline to ... Clorgyline-mediated reversal of neurological deficits in a Complexin 2 knockout mouse ... Clorgyline-mediated reversal of neurological deficits in a Complexin 2 knockout mouse. Human Molecular Genetics, 19 (17), 3402- ...
In addition, we found that co-treatment of M. oryzae with repurposed clorgyline and radio-labeled fluconazole prevented ... Efflux Inhibition by Clorgyline. To test the effect of Clorgyline as a possible inhibitor of energy-dependent efflux in M. ... Clorgyline has recently been identified in a screen as an inhibitor of two C. albicans ABC efflux pumps, CaCdr1p and CaCdr2p, ... Clorgyline as a Potential Efflux Inhibitor. Development of a new drug structure and a new mechanism of action would be a ...
Clorgyline induces genes suppressed by oncogenic pathways. The 156 genes identified by SAM as upregulated by clorgyline in E-CA ... Validation of the effects of clorgyline using E-CA-90 cells. To validate the effects of clorgyline on E-CA cells, we treated E- ... Clorgyline upregulates AR and modulates expression of androgen-regulated genes. We previously reported that clorgyline induces ... Because clorgyline induced a subset of androgen-regulated genes while repressing others, it is possible that clorgyline ...
Clorgyline hydrochloride is an irreversible and selective inhibitor of monoamine oxidase A (MAO-A) that is used in scientific ... Clorgyline hydrochloride Catalog No. A17357. Quick View .category-products .products-list .btn-quickcart { background: white; ...
Subsequently, the monoamine oxidase inhibitors tranylcypromine, clorgyline, and pargyline were shown to inhibit LSD1 activity ...
Detailed drug Information for Buspar. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
Using this medicine while you are pregnant can harm your unborn baby. Use an effective form of birth control to keep from getting pregnant. If you think you have become pregnant while using the medicine, tell your doctor right away. Do not use carbamazepine together with a monoamine oxidase inhibitor (MAOI) or during the first 14 days after you stop taking a MAOI. MAOIs are used for depression and some examples are isocarboxazid (Marplan®), phenelzine (Nardil®), selegiline (Eldepryl®), or tranylcypromine (Parnate®). Do not use this medicine together with boceprevir (Victrelis®), delavirdine (Rescriptor®), and nefazodone (Serzone®). Serious skin reactions can occur with this medicine. Check with your doctor right away if you have blistering, peeling, or loose skin, red skin lesions, severe acne or skin rash, sores or ulcers on the skin, a fever, or chills while you are using this medicine. Check with your doctor right away if a fever, sore throat, rash, ulcers in the mouth, nosebleeds, ...
Do not take this medicine within 2 hours of taking antacids or medicine for diarrhea. Taking these products too close together may make this medicine less effective.. This medicine will add to the effects of alcohol and other central nervous system (CNS) depressants (medicines that slow down the nervous system, possibly causing drowsiness). Some examples of CNS depressants are antihistamines or medicine for hay fever, other allergies, or colds; sedatives, tranquilizers, or sleeping medicine; prescription pain medicine or narcotics; barbiturates; medicine for seizures; muscle relaxants; or anesthetics, including some dental anesthetics. Check with your doctor before taking any of the above while you are using this medicine.. Before using any prescription or over-the-counter (OTC) medicine for colds or allergies, check with your doctor. These medicines may increase the chance of developing heatstroke or other unwanted effects, such as dizziness, dry mouth, blurred vision, and constipation, while ...
Clorgylinemore » and L-deprenyl are suicide enzyme inhibitors and irreversibly inhibit monoamine oxidase. When these inhibitors ...
BioVision develops and offers a wide variety of products including assay kits, antibodies, recombinant proteins & enzymes, and other innovative research tools for studying Apoptosis, Metabolism, Cell Proliferation, Cellular Stress, Cell Damage and Repair, Diabetes, Obesity and Metabolic Syndrome, Stem Cell Biology, Gene Regulation, Signal Transduction, etc. BioVisions products are currently being sold in more than 60 countries worldwide.
BioVision develops and offers a wide variety of products including assay kits, antibodies, recombinant proteins & enzymes, and other innovative research tools for studying Apoptosis, Metabolism, Cell Proliferation, Cellular Stress, Cell Damage and Repair, Diabetes, Obesity and Metabolic Syndrome, Stem Cell Biology, Gene Regulation, Signal Transduction, etc. BioVisions products are currently being sold in more than 60 countries worldwide.
Clorgyline; Linear Formula: C13H15Cl2NO · HCl; find Sigma-Aldrich-M3778 MSDS, related peer-reviewed papers, technical documents ...
... a study with deprenyl and clorgyline. Together they form a unique fingerprint. * Clorgyline Medicine & Life Sciences ... Deprenyl, a MAO-B selective inhibitor (0.25, 0.5, 5, 10 or 20 mg/kg/day, subcutaneously (s.c.) for 4 d) and clorgyline, a MAO-A ... Deprenyl, a MAO-B selective inhibitor (0.25, 0.5, 5, 10 or 20 mg/kg/day, subcutaneously (s.c.) for 4 d) and clorgyline, a MAO-A ... Deprenyl, a MAO-B selective inhibitor (0.25, 0.5, 5, 10 or 20 mg/kg/day, subcutaneously (s.c.) for 4 d) and clorgyline, a MAO-A ...
Clorgyline effect on pineal melatonin biosynthesis in roman high- and low-avoidance rats.- Reboxetine prevents the ... Clorgyline effect on pineal melatonin biosynthesis in adrenalectomized rats pretreated with 6-hydroxydopamine.- Synergistic ... Inhibition of monoamine oxidase by clorgyline analogues.- Kinetics of inhibition of MAO-B by N-(2-aminoethyl)-p-chlorobenzamide ...
... clorgyline, adinazolam, alaproclate, amitriptyline/chlordiazepoxide combination, atipamezole, azamianserin, bazinaprine, ...
1998). "Differential trace amine alterations in individuals receiving acetylenic inhibitors of MAO-A (clorgyline) or MAO-B ( ... Clorgyline Rasagiline Selegiline Fisar Z, Hroudová J, Raboch J (2010). "Inhibition of monoamine oxidase activity by ...
A double-blind trial of clomipramine and clorgyline. Arch Gen Psychiatry 40: 605-612Google Scholar ...
Clorgyline; Reversible: Befloxatone • Brofaromine • Cimoxatone • Harmala Alkaloids (Harmine, Harmaline, Tetrahydroharmine, ...
Clorgyline; Reversible: Amiflamine • Bazinaprine • Befloxatone • Befol • Brofaromine • Cimoxatone • Esuperone • Harmala ...
MAO-A was inhibited by the following drugs: pargyline > clorgyline > iproniazid > fluoxetine > desipramine > amitriptyline > ... MAO-B was inhibited by the following drugs: pargyline > clorgyline > iproniazid > fluoxetine > venlafaxine > amitriptyline > ... and clorgyline.. RESULTS: In general, the effect of tested drugs was found to be inhibitory. The half maximal inhibitory ... Clorgyline:pharmacology, Cocaine:pharmacology, Cy. OBJECTIVE: Monoamine oxidase (MAO), the enzyme responsible for metabolism of ...
... and whether these effects are modified under conditions of MAO inhibition by clorgyline. Our results revealed that when i.p. ... and whether these effects are modified under conditions of MAO inhibition by clorgyline. Our results revealed that when i.p. ... kg-1 T1AM or SG-2 was lost with clorgyline pretreatment (Figure 3B). Notably, in control mice i.p. injected with clorgyline an ... FIGURE 3. SG-2 and T1AM reduce nociceptive threshold in mice and the effect is blunted by clorgyline pretreatment. (A) Mice ...
MAO inhibitors include isocarboxazid, nialamide, pargyline, selegiline, phenelzine , procarbazine, iproniazid, and clorgyline. ... MAOIs include isocarboxazid, nialamide, pargyline, selegiline, phenelzine , procarbazine, iproniazid, and clorgyline. Patient ...
Clorgyline, an MAO-A enzyme inhibitor, prevents apoptosis in melanoma cells, in vitro. Cholangiocarcinoma suppresses MAO-A ... Cimoxatone Clorgyline (irreversible) Methylene Blue Minaprine (Cantor) Moclobemide (Aurorix, Manerix) Phenelzine (Nardil) ...
5B Left). Clorgyline increases both melatonin and NAS levels in rat pineal glands (24). To explore which of the 5-HT ... B) The MAO-A inhibitor clorgyline but not MAO-B inhibitor deprenyl promotes TrkB activation in the dark in C3H mice. Phospho- ... 5B ). Interestingly, in C3H mice treated at night, clorgyline strongly activated TrkB in the dark; in contrast, it lost the ... Further, the finding that TrkB activation by clorgyline in C3H but not C57BL/6J mice is prevented by light exposure, which ...
It is very important that your doctor check the progress or you or your child while you are receiving this medicine. This will allow your doctor to see if the medicine is working properly and to decide if you should continue to use it. This medicine will add to the effects of alcohol and other CNS depressants (medicines that can make you drowsy or less alert). Some examples of CNS depressants are antihistamines or medicine for allergies or colds; sedatives, tranquilizers, or sleeping medicine; other prescription pain medicine or narcotics; medicine for seizures or barbiturates; muscle relaxants; or anesthetics, including some dental anesthetics. Check with your doctor before you or your child take any of the medicines listed above while you are using this medicine. This medicine may be habit-forming. If you or your child feel that the medicine is not working as well, do not use more than your prescribed dose. Call your doctor for instructions. Using narcotics for a long time can cause severe ...
  • Campbell IC, Robinson DS, Lovenberg W, Murphy DL (1979) The effects of chronic regimens of clorgyline and pargyline on monoamine metabolism in the rat brain. (springer.com)
  • The several antidepressants and mood stabilizers were compared with effects of well known MAO inhibitors such as moclobemide, iproniazid, pargyline, and clorgyline. (nel.edu)
  • The results from single point time dependent inhibition and shift assays suggest that clorgyline, pargyline, phenelzine, and selegiline were metabolism based inhibitors of CYP2B6. (sigmaaldrich.com)
  • In IC50 shift assays, clorgyline, pargyline, phenelzine and selegiline are metabolism based inhibitors of CYP2B6 with fold shit of 3.0-, 3.7-, 2.9-, and 11.4-fold respectively. (sigmaaldrich.com)
  • Persistent stimulation of dopamine receptors pargyline amoxapine phenelzine buspirone selegiline clozapine tranylcypromine droperidol haloperidol inhibit dopamine metabolismmaois metoclopramide clorgyline phenytoin isocarboxazid linezolid dopamine antagonism moclobemide block dopamine receptors. (childbirthsolutions.com)
  • The results obtained were compared with the effects of the less-selective MAO-B inhibitor pargyline and the MAO-A inhibitor clorgyline. (lenus.ie)
  • Clorgyline showed a smaller protective effect of normal cells, whereas pargyline had no effect. (lenus.ie)
  • To understand the mechanisms of specific substrate and inhibitor recognitions of MAOA and MAOB, we have determined the crystal structure of rat MAOA complexed with the specific inhibitor, clorgyline, at 3.2A resolution. (rcsb.org)
  • Recently, the monoamine oxidase A (MAO-A) inhibitor clorgyline was shown to inhibit the azole efflux pumps, leading to increased azole susceptibility i. (medworm.com)
  • The effects of chronic treatment with desimipramine (a tricyclic antidepressant), fluoxetine [a specific 5-hydroxytryptamine (5-HT) uptake inhibitor], clorgyline (a specific monoamine oxydase inhibitor of A type), ipsapirone (a specific 5-HT1A receptor agonist) as well as electroconvulsive shock treatment were investigated on rat hippocampal 5-HT1A receptors negatively coupled to adenylyl cyclase. (aspetjournals.org)
  • Animal experiments were performed on normal Wistar rats and on rats pretreated with the monoamine oxidase (MAO) inhibitor clorgyline. (ugent.be)
  • All of these in vitro changes occur, in part, independently from - and β-adrenergic receptor-operated signaling and are inhibited by the specific MAO-A inhibitor clorgyline. (scialert.net)
  • The contractile response was assessed using phenylephrine (0,01-1 microM) in the presence vs. absence of a MAO-A inhibitor, clorgyline (10 microM). (ovid.com)
  • After an initial reversible interaction, the inhibition of enzyme activity becomes irreversible in the presence of concentrations of clorgyline of the same order as that of the enzyme. (aspetjournals.org)
  • As the rats grew older, both the specific activity of MAO-A, and the concentration of clorgyline/(mg protein) required to cause inhibition of the enzyme activity increased in a parallel fashion. (aspetjournals.org)
  • To assess potential neuroprotection by TAAR1 agonists, in the present work, we initially investigated whether T1AM and its corresponding 3-methylbiaryl-methane analog SG-2 can improve learning and memory when systemically administered to mice at submicromolar doses, and whether these effects are modified under conditions of MAO inhibition by clorgyline. (frontiersin.org)
  • The prototype inhibitors ("suicide inactivators", which engender covalent bonds with the active site of the enzyme and induce irreversible inhibition) used in PET studies are [ 11 C]deprenyl and [ 11 C]clorgyline (Fowler et al. (aspetjournals.org)
  • The comparison of the structures between MAOA and MAOB clearly explains the specificity of clorgyline for MAOA inhibition. (rcsb.org)
  • The effect of cocaine on the overflow of noradrenaline was potentiated by prior inhibition of MAO with clorgyline. (springer.com)
  • Inactivation of cytochrome P4502B1 by the monoamine oxidase inhibitors R-(-)-deprenyl and clorgyline. (aspetjournals.org)
  • The monoamine oxidase inhibitors R-(-)-deprenyl (deprenyl) and clorgyline inactivated the 7-ethoxy-4-trifluoromethylcoumarin O-deethylase activity of purified cytochrome P4502B1 (P4502B1) in a reconstituted system containing P4502B1, NADPH-cytochrome P450 oxidoreductase, and L-alpha-phosphatidylcholine dilauroyl as the lipid. (aspetjournals.org)
  • Sivam, SP 1993, ' Influence of monoamine oxidase inhibitors on striatonigral dynorphin system: a study with deprenyl and clorgyline ', Neuropeptides , vol. 25, no. 1, pp. 35-45. (elsevier.com)
  • Now that we know clorgyline works, we can focus future drug testing on newer, safer MAO-A inhibitors, such as moclobemide, whose chemical bindings are reversible, unlike those of clorgyline," says Paolocci. (hopkinsmedicine.org)
  • Hippocampal 5HT reuptake was slightly inhibited by clorgyline (IC50 205.0 mumol/l), while the other MAO-inhibitors were devoid of potency. (nih.gov)
  • Monoamine oxidase inhibitors l-deprenyl and clorgyline protect nonmalignant human cells from ionising radiation and chemotherapy toxicity. (lenus.ie)
  • The partition ratio for deprenyl and clorgyline was between 2 and 3. (aspetjournals.org)
  • Co-administration of low doses (2.5 mg/kg/day, s.c. for 4 d) of deprenyl and clorgyline, that would selectively inhibit MAO-B and MAO-A respectively, produced a marked increase in DA and 5-HT, a decrease in DOPAC and 5-HIAA, an increase in DYN levels in the striatum and substantia nigra and an increase in PD-mRNA levels in the striatum. (elsevier.com)
  • Since the Bcl-2 has been shown to be an inhibitor of apoptosis or programmed cell death, this would imply that the protective effects of l-deprenyl and clorgyline involve activation of antiapoptotic pathways within the normal cell. (lenus.ie)
  • He says newer drugs in the same class, such as moclobemide (sold as Aurorix or Manerix, and already approved by the U.S. Food and Drug Administration), will have to be tested first, citing numerous and potentially lethal drug effects with clorgyline that prevent it from being prescribed. (hopkinsmedicine.org)
  • R at i o n a l e s atypical antipsychotics inhibit dopamine metabolismmaois metoclopramide clorgyline phenytoin isocarboxazid linezolid dopamine antagonism moclobemide block dopamine receptors dopamine receptors. (childbirthsolutions.com)
  • Patients who have taken clorgyline, whose chemical binding to MAO-A is irreversible, had to carefully avoid such tyramine-rich foods as red wine, chocolate, certain beans, meat and especially aged cheeses. (hopkinsmedicine.org)
  • celexa-20-mg-achat-citalopram-hydrobromide-10-en%20http://www. (haswi.ml)
  • Brain MAOA activity was measured with PET using clorgyline labeled with carbon 11. (mssm.edu)
  • Clorgyline Rasagiline Selegiline Fisar Z, Hroudová J, Raboch J (2010). (wikipedia.org)
  • Because of these observations, Johnston proposed that there are two forms of MAO: type A and type B. Type A, found mainly in the gut and other organs outside the brain, is preferentially inhibited by clorgyline. (mindandmuscle.net)
  • Clorgyline differed from deprenyl in two respects: 1) clorgyline selectively inhibits the deanimation of serotonin as opposed to phenylethylamine and 2) clorgyline potentiated tyramine induced hypertension (9). (mindandmuscle.net)
  • Deprenyl exhibited a KI (concentration of inactivator required for half-maximal inactivation) of 1.05 microM, and clorgyline had a KI of 1.5 microM. (aspetjournals.org)
  • The maximum rate of inactivation of the enzyme at saturating levels of inactivator (kinactivation) was 0.23 min-1 for deprenyl and 0.28 min-1 for clorgyline. (aspetjournals.org)
  • The inactivation of clorgyline was characterized by KI value of 2.5 ± 0.3 and k(inact) value of 0.045 ± 0.001 min(-1). (sigmaaldrich.com)
  • In a report to be published in the Jan. 8 edition of the journal Circulation Research, the international team of U.S. and Italian heart experts describes in a dozen key laboratory experiments in rodents how the antidepressant clorgyline, which is no longer in use in humans, blocks the action of enzyme monoamine oxidase-A (MAO-A) and stops its breakdown of a key neurohormone. (hopkinsmedicine.org)
  • In contrast, chronic treatment with clorgyline and electroconvulsive shock treatment induced a slight but significant reduction of 5-HT's ability to inhibit hippocampal adenylyl cyclase. (aspetjournals.org)
  • The expression of 156 genes was significantly increased by clorgyline at all time points over the time course of 6 - 96 hr identified by Significance Analysis of Microarrays (SAM). (biomedcentral.com)
  • Treatment of cultures of nontumorigenic cells with l-deprenyl or clorgyline significantly increased the levels of the protein Bcl-2 following irradiation, but there was no such effect on the already-elevated levels of this protein in the tumour samples. (lenus.ie)
  • For example if taking an MAO inhibitor (e.g., clorgyline) then the ingestion of sympathomimetic amines (e.g. amphetamine or even tyramine from cheese) will increase their [amines] apparent absorption as there is no longer functional MAO in the gut epithelium to degrade it. (protocol-online.org)
  • Among the study's first findings was that after six weeks, mice with failing hearts responded to concurrent low-dose clorgyline treatment, with restoration of normal heart function and only half the harmful changes seen in untreated mice over the same time period. (hopkinsmedicine.org)
  • Heart muscle cell death rates were normal in clorgyline-treated mice, but three and a half times higher in untreated mice. (hopkinsmedicine.org)
  • Clorgyline, an MAO-A inhibitor, induces secretory differentiation of normal prostate cells. (biomedcentral.com)
  • Another striking effect of clorgyline was the induction of androgen receptor (AR) and classic AR target genes such as prostate-specific antigen together with other secretory epithelial cell-specific genes, suggesting that clorgyline promotes differentiation of cancer cells. (biomedcentral.com)
  • Our study helps describe heart failure as a vicious chemical circle of stimulant norepinephrine overload and breakdown, and it offers a disease blueprint with monoamine oxidase-A as the target for drugs similar to clorgyline to rein in the disease," says senior study investigator and cardiologist Nazareno Paolocci, M.D. (hopkinsmedicine.org)
  • The distribution of functionally active monoamine oxidase type A (MAO-A) was investigated by in vivo quantitative autoradiography using [ 14 C]clorgyline in normal, conscious rat brain. (springer.com)
  • Another group of rats was pretreated with clorgyline (10 mg/kg i.v.). Monkeys were injected with [ 11 C]befloxatone (222-370 MBq), and the chest was imaged with PET for 2 h. (aspetjournals.org)
  • In addition, we found that co-treatment of M. oryzae with 'repurposed' clorgyline and radio-labeled fluconazole prevented energy-dependent efflux of fluconazole, resulting in an increased intracellular concentration of fluconazole in the fungal cell. (frontiersin.org)
  • Notable side effects from clorgyline, Paolocci says, include insomnia and agitation, or high blood pressure after ingestion of foods containing the amino acid tyramine, a protein building block that stimulates a surge of stored stimulatory hormones, specifically, norepinephrine. (hopkinsmedicine.org)
  • The interaction between clorgyline and the Type-A monoamine oxidase (MAO-A) in homogenates and mitochondrial fractions of the rat heart appears to take place almost entirely at specific binding sites. (aspetjournals.org)
  • We examined the effects of clorgyline on the transcriptional program of epithelial cells cultured from high grade PCa (E-CA). (biomedcentral.com)
  • Sixty minutes after [ 14 C]clorgyline administration (1.58 MBq/animal i.v.), the brains were removed and prepared for autoradiography by washing the brain sections with 5% trichloroacetic acid solution to remove the nonbinding free tracer. (springer.com)
  • Autonomic and Behavioral Thermoregulation in the Golden Hamster during Subchronic Administration of Clorgyline. (epa.gov)
  • Paolocci cautions that their studies with clorgyline are initial proof of an important principle, but far from any current use of the drug to treat heart disease in humans. (hopkinsmedicine.org)
  • In addition, genes downregulated ≥ 2-fold by clorgyline were significantly enriched with those upregulated by key oncogenes including beta-catenin and ERBB2, indicating an anti-oncogenic effect of clorgyline. (biomedcentral.com)
  • Indeed, many genes in the PcG repression signature that predicts PCa outcome were upregulated by clorgyline, suggesting that the differentiation-promoting effect of clorgyline may be mediated by its downregulation of EZH2. (biomedcentral.com)
  • We systematically assessed gene expression changes induced by clorgyline in E-CA cells using high-density oligonucleotide microarrays. (biomedcentral.com)
  • Moreover, clorgyline downregulated EZH2, a critical component of the Polycomb Group (PcG) complex that represses the expression of differentiation-related genes. (biomedcentral.com)
  • Heart muscle chamber expansion also slowed in the clorgyline-treated group, returning to an average chamber dimension of 1.2 millimeters, when the heart was contracting. (hopkinsmedicine.org)
  • In rodents, cardiac uptake was high (3.39 ± 0.5% injected dose/g tissue) and strongly inhibited (80%) by clorgyline. (aspetjournals.org)
  • This graph shows the total number of publications written about "Clorgyline" by people in this website by year, and whether "Clorgyline" was a major or minor topic of these publications. (umassmed.edu)
  • PET images showed clear accumulation of C-11-hydroxytryptophan in the pancreas in both animal groups, but with a significant 3-fold higher retention of the radiopharmaceutical in clorgyline-treated animals. (ugent.be)
  • Below are the most recent publications written about "Clorgyline" by people in Profiles. (umassmed.edu)