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Also known as:  Selegiline Hydrochloride.


Eldepryl is a medication which prevents the breakdown of a chemical in your brain.

Eldepryl is used to treat Parkinson's disease.

Eldepryl is also known as Selegiline.

Eldepryl prevents the breakdown of a chemical in your brain called dopamine, thereby prevents Parkinson's disease.

Brand names of Eldepryl are Eldepryl, Zelapar.


Take Eldepryl orally.

Take Eldepryl capsules twice a day, at breakfast and lunch.

Do not swallow the tablet whole. Allow it to dissolve in your mouth without chewing.

Do not drink or eat anything for at least 5 minutes after takink Eldepryl.

While using Eldepryl, you must not eat foods that are high in tyramine such as air dried meats, aged or fermented meats, sausage or salami (including cacciatore and mortadella), pickled herring, and any spoiled or improperly stored beef, poultry, fish, or liver; beer from a tap, beer that has not been pasteurized; aged cheeses, including blue, boursault, brick, brie, camembert, cheddar, emmenthaler, gruyere, parmesan, romano, roquefort, stilton, and swiss; sauerkraut, soy beans, soy sauce, tofu, miso soup, bean curd, fava beans; yeast extracts (such as Marmite).

Preferable food during Eldepryl usage are fresh meat, poultry, or fish (including lunch meat, hot dogs, breakfast sausage, and cooked sliced ham); any vegetables except broad bean pods (fava beans); processed cheese, mozzarella, ricotta, cottage cheese; pizza made with cheeses low in tyramine; soy milk, yogurt.

If you want to achieve most effective results do not stop taking Eldepryl suddenly.


If you overdose Eldepryl and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Eldepryl overdosage: severe headache, hallucinations, vision problems, sweating, cool or clammy skin, fast or uneven heart rate, feeling light-headed, fainting, seizure.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Eldepryl are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Eldepryl if you are allergic to Eldepryl components.

Do not take Eldepryl if you are pregnant, planning to become pregnant or breast-feeding.

Be careful using Eldepryl if you have kidney disease, liver disease, heart disease, high or low blood pressure, seizure disorder.

Be careful using Eldepryl if you take over-the-counter medications you use, including vitamins, minerals, and herbal products, carbamazepine (Tegretol), diet pills or cold medicines that contain ephedrine, pseudoephedrine or phenylephrine, nafcillin (Unipen), phenobarbital (Luminal, Solfoton), rifampin (Rifadin, Rifater, Rifamate, Rimactane), antidepressants such as amitriptyline (Elavil), amoxapine (Ascendin), bupropion (Wellbutrin, Zyban), citalopram (Celexa), clomipramine (Anafranil), desipramine (Norpramin), doxepin (Sinequan), duloxetine (Cymbalta), escitalopram (Lexapro), fluoxetine (Prozac), fluvoxamine (Luvox), imipramine (Tofranil), nortriptyline (Pamelor), paroxetine (Paxil), protriptyline (Vivactil), sertraline (Zoloft), venlafaxine (Effexor) or trimipramine (Surmontil).

While using Eldepryl, you must not eat foods that are high in tyraminesuch as air dried meats, aged or fermented meats, sausage or salami (including cacciatore and mortadella), pickled herring, and any spoiled or improperly stored beef, poultry, fish, or liver; beer from a tap, beer that has not been pasteurized; aged cheeses, including blue, boursault, brick, brie, camembert, cheddar, emmenthaler, gruyere, parmesan, romano, roquefort, stilton, and swiss; sauerkraut, soy beans, soy sauce, tofu, miso soup, bean curd, fava beans; yeast extracts (such as Marmite).

Do not take Eldepryl if you use over-the-counter supplements or cough and cold medicines that contain tyramine.

It can be dangerous to stop Eldepryl taking suddenly.

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The most frequently used drugs are levodopa, biperiden and selegiline. The total cost reached values of 116,346,589.30 euros during the study period. The CID was 4,14 euros. It was very high the daily treatment cost of pramipexol and entacapone. The prevalence of Parkinson's disease is considered in 1.7 per 1,000 inhabitants in Spain. There is an important geographical variability; regions as Castilla-Leon, Galicia and La Rioja have a higher prevalence than Andalucia or Murcia. The number of patients in Spain can be considered in 69,571 people.

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To test the impact of deprenyl on ischemia-induced changes in vitro, we followed the time course of propidium iodide (PI) uptake as an indicator of neuronal cell death as well as the expression of apoptotic factors in organotypic hippocampal slice cultures exposed to oxygen-glucose deprivation (OGD) for 45 min.

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Although basic research has revealed many mechanisms involved in the repair or elimination of damaged neurons, turning these mechanisms into clinically useful neuroprotective interventions is a slow process. Numerous neurotrophic factors seem to mediate neuronal repair and viability, but because the neurotrophic factors are proteins or polypeptides, they cannot be given orally and do not enter the brain if given intravenously. Tapping into the neuroprotective potential of the neurotrophic factor mechanisms must await further developments. Similarly, pharmacological agents that protect damaged neurons by reducing glutamate excitotoxicity, by scavenging free radicals, or by increasing adenosine inhibitory influences, are not ready yet for widespread clinical use. Also, appropriate therapeutic protocols for currently available neuroprotective agents such as vitamin E, selegiline, and NSAIDs remain to be determined. Given the rate of advance of research in this area, however, meaningful neuroprotection and neurorescue will be attainable in the very near future. In the meantime, neuron damaging oxidative stress can be kept in check by insuring adequate dietary sources of antioxidants. Although there is as yet little or no scientific evidence that dietary antioxidants are neuroprotective, the consumption of high antioxidant foods, such as blueberries and strawberries, is appealing to most people regardless of any neuroprotective potential.

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Greater improvement was observed after 6 weeks in patients treated with transdermal selegiline than in those given placebo according to all measures. A statistically significant difference between drug and placebo was seen in Hamilton depression scale and Montgomery-Asberg Depression Rating Scale scores as early as week 1 of treatment. There were no differences in the adverse event profile of the patients given selegiline and those given placebo with the exception of application-site reactions, which were more common with the selegiline transdermal system. No orthostatic hypotensive or hypertensive reactions were observed.

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In patients with moderately severe impairment from Alzheimer's disease, treatment with selegiline or alpha-tocopherol slows the progression of disease.

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The goal of this study was to examine the multiple-dose pharmacokinetics of selegiline and its metabolites desmethylselegiline, 1-methamphetamine, and 1-amphetamine after oral administration of selegiline HCl. Twelve healthy volunteers received 10 mg of selegiline HCl once daily for 8 days. The pharmacokinetic profiles of selegiline and the metabolites were examined from serum samples for 24 hours (i.e., the dosing interval, tau) on days 1, 4, and 8. The results indicated significant apparent accumulation of selegiline and desmethylselegiline during the 8-day period of selegiline administration. The AUC tau S of selegiline and desmethylselegiline were increased 2.7 fold (p < 0.001) and 1.5 fold (p < 0.001), respectively, from day 1 to day 8. However, the half-lives of selegiline (range, 1.5-3.5 h) and desmethylselegiline (range, 3.4-5.3 h) were found to be relatively short. Accordingly, the short half-lives of these compounds failed to predict the apparent accumulation. With both of the 1-amphetamine metabolites of selegiline, steady state was reached by day 4. We suggest that the most likely explanation for the apparent accumulation of selegiline and desmethylselegiline was the saturation of the MAO-B binding sites in tissues, although decreased first-pass metabolism of selegiline cannot be ruled out. The observed increase in selegiline and desmethylselegiline concentrations on multiple dosing is not likely to significantly increase the pharmacodynamic effect or adverse effects of selegiline compared with what has been found after a single 10-mg dose.

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Agents that are currently available in Canada to treat the cognitive deficits of AD include donepezil, ginkgo biloba, selegiline, and ergoloid mesylates. Donepezil and ginkgo biloba are associated with a statistically significant but clinically modest improvement in cognitive function in a substantial minority of patients with mild to moderate AD. Selegiline may have a mild beneficial effect on cognitive function in some patients with AD, but the data are inconclusive. Ergoloid mesylates have questionable efficacy in AD and can only be recommended as a last line of treatment. The results of a single trial suggest that vitamin E or selegiline (both have antioxidant properties) may slow the progression of AD. Antipsychotic medications can result in clinically significant improvement in agitation and psychosis. Carbamazepine also appears to be an effective treatment for agitation in AD, and there is preliminary evidence that the selective serotonin reuptake inhibitor citalopram reduces irritability in this disorder. There is no evidence that other nonneuroleptic medications are more efficacious than placebo in treating agitation in AD. Limited data indicate that depression in dementia responds to antidepressant medication.

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In order to investigate the conversion of selegiline (SG), a drug used in the treatment of Parkinson's disease, to selegiline N-oxide (SGO) as a major metabolic pathway for SG, rat liver microsomal incubations were carried out in vitro in the presence of NADPH. SG was transformed into SGO in vitro as described in our previous human in vivo experiment. In the kinetic studies, the Vmax/Km value of the N-oxidation at pH 8 was found to be approximately four times greater than that at pH 7.4. The N-oxidation was also found to be inhibited by methimazole, an inhibitor of the flavin-containing monooxigenase (FMO) rather than by SKF 525A, an inhibitor of cytochrome P450s, and stimulated approximately two times by n-octylamine, an stimulator of FMO. Moreover, the N-oxidation activity remained almost unchanged in the presence of NADPH even after heating at 50 degrees C for a few minutes. The present data demonstrate that the N-oxidation of SG to SGO is principally mediated by FMO.

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This study found a differential compliance and persistence across PD drug therapies. The compliance rate for rasagiline was significantly higher than that for all of the other PD medications. In addition, rasagiline and levodopa/carbidopa/entacapone were associated with significantly higher persistence rates than were the other PD medications.

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eldepryl generic 2015-12-29

The presence of VH is helpful in the differentiation of PD from other non-Lewy-body causes of parkinsonism. We propose that VH Cordarone 900 Mg be added, as a supportive criterion, to the operational clinical criteria for the diagnosis of PD.

eldepryl reviews 2015-07-13

A 48-h incubation of PC12 cells with rotenone caused an apoptotic cell death and elevated intracellular reactive oxygen species (ROS) and lactic acid accumulation. Intracellular DA depletion with reserpine significantly attenuated rotenone-induced ROS accumulation and apoptotic cell death. No change was found in rotenone-induced ROS accumulation when cells were co-treated with deprenyl. Brief treatment with reserpine at the end of rotenone treatment had no effect on rotenone-induced neurotoxicity. However, when cells were first incubated with deprenyl, a monoamine oxidase-B inhibitor for 30 min then co-incubated with rotenone plus deprenyl, a brief treatment with reserpine enhanced Bystolic Pill cell injury.

eldepryl and alcohol 2016-02-26

One hundred fifty-seven de novo PD patients were randomized in a double-blind, placebo-controlled study of 7 years' duration. In the monotherapy part, selegiline significantly delayed the initiation of levodopa therapy vs placebo. The authors now report the results from the combination part of the study, in which Cozaar Drug Interactions 140 patients received selegiline or placebo in addition to individually tailored levodopa therapy.

eldepryl drug 2015-12-06

1. We have studied the effect of (-)-deprenyl on the oxidative damage Lamictal Max Dose that the rat substantia nigra suffers during aging. 2. (-)-Deprenyl (2 mg kg-1, three times a week) administered for two months, beginning at 22 months of age, produced a significant increase in tyrosine hydroxylase (TH) activity (2.67 +/- 0.40 and 3.64 +/- 0.38 nmol mg-1 protein h-1 in untreated aged rats and treated aged rats respectively, P < 0.05) and in TH amount (0.072 +/- 0.012 and 0.128 +/- 0.38 absorbance 405 nm in untreated aged and treated aged rats respectively, P < 0.05). 3. The proteins of aged rat substantia nigra showed a significant decrease of carbonyl groups in treated animals compared with saline-injected control rats (136.2 +/- 21.8 and 71.5 +/- 13.2 c.p.m. microgram-1 protein in untreated aged and treated aged rats respectively, P < 0.05). 4. The carbonyl groups measured in TH enzyme showed a statistically significant decrease (42.3%) after (-)-deprenyl treatment (471.4 +/- 73.0 and 271.9 +/- 50.00 c.p.m. in untreated aged and treated aged rats respectively, P < 0.001). 5. All these results suggest that oxidative damage produced during aging is prevented by (-)-deprenyl treatment and could explain the effect of this drug in Parkinson's disease (PD) and other degenerative diseases such as Alzheimer's disease.

eldepryl dosing 2017-11-29

The deamination of some monoamines in human blood lymphocytes and granulocytes is dependent on the presence of two different enzymes: a mitochondrial (type B) monoamine oxidase and Luvox Depression Medication a "benzylamine oxidase" similar to the plasma BAO which is inhibited by semicarbazide and resistant to clorgyline.

eldepryl tablets 2015-03-30

The clinical pharmacology of the new reversible monoamine oxidase (MAO) inhibitor, moclobemide, was examined in three separate studies in healthy male volunteers. In a single oral dose study, moclobemide (25-150 mg) was rapidly absorbed from the gastrointestinal tract and had a relatively short plasma half-life (mean 1.3 h after 150 mg). A decrease in the plasma concentrations of the noradrenaline metabolite 4- hydroxy-3-methoxyphenylglycol (HMPG), however, indicated a longer time to peak pharmacodynamic effect and longer duration of activity. Assay of platelet MAO activity did not reveal any evidence of irreversible inhibition of the B form of the isoenzyme. Single oral doses of moclobemide (150 and 300 mg) significantly lowered the threshold to the cardiovascular effects ('cheese reaction') of intravenous tyramine. However, after repeated administration of 100 Lanoxin Dose Range mg three times daily for over 2 weeks, moclobemide caused significantly less potentiation than did phenelzine (15 mg three times per day) on the cardiovascular effects of oral tyramine, a clinically more relevant model. The MAO-B inhibitor, selegiline (5 mg once daily), also lowered the oral tyramine threshold significantly. Moclobemide was generally well tolerated by these healthy volunteers.

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Intranigral infusion of 1-Methyl-4-phenylpyridinium ion (MPP+, 2.1-16.8 nmol) dose-dependently injured nigral Anafranil 25mg Prices neurons as reflected by reduced dopamine levels in the ipsilateral striatum four days after the infusion of this toxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Coadministration of deprenyl (4.2 nmol) with MPP+ into the substantia nigra protected against MPP(+)-induced moderate (20-50%) but not severe (over 70%) nigral injury as reflected in striatal dopamine reductions. However, supplementary treatment with deprenyl (0.25 mg/kg, s.c., twice daily for 4 days) after intranigral infusion of MPP+ significantly rescued nigral neurons from more severe damage caused by a higher MPP+ does (8.4 nmol) manifested by a lesser striatal dopamine decrease (-31%) compared to the non-deprenyl treated group (-70%). Thus, in addition to the blockade of bioactivation of MPTP, deprenyl can protect and/or rescue nigral neurons from MPP(+)-induced dopaminergic neurotoxicity. These in vivo data add further evidence to suggest that deprenyl, a putative and clinically unproven neuroprotective agent, may be of value in slowing the progressive nigral degeneration in "early" Parkinson's disease, but may prove to be less so in its terminal stages.

buy eldepryl online 2015-07-18

Iron and monoamine oxidase activity are increased in brain of Parkinson's disease (PD). They are associated with autoxidation and oxidative deamination of dopamine by MAO resulting in the generation of reactive oxygen species and the onset of oxidative stress to induce neurodegeneration. Iron chelators (desferal, Vk-28 and clioquinol) but not copper chelators have been shown to be neuroprotective in the 6-hydroxydoapmine and MPTP models of Parkinson's disease (PD), as are monoamine oxidase B inhibitors such as selegiline and rasagiline. These findings prompted the development of multifunctional anti PD drugs possessing iron Vogel Menosan Reviews chelating phamacophore of VK-28 and the propargylamine MAO inhibitory activity of rasagiline. M30 is a potent iron chelator, radical scavenger and brain selective irreversible MAO-A and B inhibitor, with little inhibition of peripheral MAO. It has neuroprotective activity in in vitro and in vivo models of PD and unlike selective MAO-B inhibitors it increases brain dopamine, serotonin and noradrenaline. These findings indicate beside its anti PD action, it may also possess antidepressant activity, similar to selective MAO-A and nonselective MAO inhibitors. These properties make it an ideal anti PD drug for which it is being developed.

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Deprenyl (DPN) and its metabolites, desmethyl deprenyl (desmethyl DPN), methamphetamine (MA) and amphetamine (AP), in the hair of rats and humans dosed with DPN were analyzed by selected ion monitoring of gas chromatograph-mass spectrometry (GC-MS-SIM). After intraperitoneal administration of DPN-HCl to rats (10 mg/kg/d, 10d, n = 3), the area under the concentration versus time curves (AUCs) of DPN and its metabolites in the rat plasma were compared with the concentrations of drugs in rat hair newly grown for 4 weeks. The concentrations of DPN, desmethyl DPN, MA and AP in the rat hair were 0.97 +/- 0.06, 0.68 +/- 0.02, 14.04 +/- 0.54 and 13.20 +/- 1.09 ng/mg, and the ratios of the concentrations in the hair to AUCs in their plasma were 0.05: 0.02: 0.3: 0.2, respectively. This fact suggested that the incorporation rates of DPN and desmethyl DPN into hair from blood were relatively lower than those of MA and AP. The method was applied to determination of the metabolites in scalp hair, beard and urine of humans who orally ingested DPN (15 mg/d, 5 d, n = 3). DPN (trace level), desmethyl DPN (0.17-0.29 ng/mg), MA (1.30-2.25 ng/mg) and AP (0.42-0.99 ng/mg) were detected in the scalp hair collected three weeks after the first intake, while in beard or urine these drugs were detected only for Casodex Mg a few days.(ABSTRACT TRUNCATED AT 250 WORDS)

eldepryl dosage forms 2015-06-01

Poor peroral therapeutic efficiency of selegiline is primarily due to the extensive hepatic metabolism and hence the need for an alternative route of administration. The present study is based on evaluation of a buccal film which is impregnated with selegiline nanospheres to enhance the systemic bioavailability. Selegiline-loaded nanospheres prepared using poly(lactide-co-glycolide) was embedded into buccal films (F1-F4) with varying polymer composition [hydroxypropyl methylcellulose and eudragit]. The developed films were evaluated for their physicomechanical properties, hydration, mucoadhesive strength, in vitro drug release and ex vivo permeation in order to identify the ideal system suitable for further development. In vivo studies were carried out on rabbits to assess the comparative pharmacokinetics profile of the selected buccal film with oral solution. Preliminary studies indicated that the prepared films exhibited excellent physical properties, adequate mucoadhesive strength and moderate hydration. In vitro drug release data of the buccal films (F1, F2 and F3) showed distinct profiles. Permeation studies Xenical To Buy indicated higher steady-state flux from film F3 (p < 0.0001) when compared to film F2. In-vivo results of film (F3) demonstrated significant increase in absorption (p < 0.0001), Cmax (∼1.6-fold), Tmax, AUC0-α (∼3-fold, p < 0.0001) and improved bioavailability, when compared to control. This study concludes that the buccal delivery of selegiline using the developed buccal film (F3) would be a promising alternative approach for the treatment of Parkinson's disease.