Selegiline Hydrochloride

(BANM, USAN, rINNM)
Selegiline Hydrochloride Chemical formula
Synonyms: (BANM, USAN, rINNM) Deprenyl; L-Deprenyl; Hidrocloruro de selegilina; Selegiliinihydrokloridi; Selegilin Hidroklorür; Selegilin hydrochlorid; Sélégiline, chlorhydrate de; Selegilinhydroklorid; Selegilini hydrochloridum; Selegilino hidrochloridas; Szelegilin-hidroklorid. (−)-(R)N, DimethylN-(prop-2-ynyl)phenethylamine hydrochloride; (R)Methyl(
Cyrillic synonym: Селегилина Гидрохлорид.

💊 Chemical information

Chemical formula: C13H17N,HCl = 223.7.
CAS — 14611-51-9 (selegiline); 2079-54-1 (selegiline hydrochloride); 14611-52-0 (selegiline hydrochloride). ATC — N04BD01.
ATC Vet — QN04BD01.

Pharmacopoeias.

In Eur. and US.

Ph. Eur. 6.2

(Selegiline Hydrochloride). A white or almost white, crystalline powder. Freely soluble in water and in methyl alcohol; slightly soluble in acetone. A 2% solution in water has a pH of 3.5 to 4.5. Protect from light.

USP 31

(Selegiline Hydrochloride). A white, odourless crystalline powder. Freely soluble in water, in chloroform, and in methyl alcohol. Store in airtight containers. Protect from light.

💊 Adverse Effects

Selegiline is often given as an adjunct to levodopa therapy and many of the adverse effects reported may be attributed to enhanced levodopa activity; dosage of levodopa may have to be reduced. However, most reported adverse effects, with the possible exception of increased dyskinesias and cardiac arrhythmias, have also been seen with selegiline monotherapy. Adverse effects have included orthostatic hypotension, chest pain, nausea, vomiting, constipation, diarrhoea, confusion, headache, tremor, vertigo, dizziness, psychosis, depression, hallucinations, agitation, dry mouth, sore throat, difficulty in micturition, skin reactions, back pain, muscle cramps, joint pain, and myopathy. The amfetamine metabolites of selegiline may cause insomnia and abnormal dreams; evening doses should be avoided. Transient increases in liver enzymes have been reported. Mouth ulcers and stomatitis may occur with the oral lyophilisate. Since the selectivity of selegiline is lost at higher doses, signs and symptoms of overdosage may resemble those of non-selective MAOIs such as phenelzine.

Effects on carbohydrate metabolism.

Profound hypoglycaemia developed in a 70-year-old man after selegiline was added to his existing medication for Parkinson’s disease.1 Hypoglycaemia was accompanied by hyperinsulinaemia and resolved 1 week after stopping selegiline.
1. Rowland MJ, et al. Hypoglycemia caused by selegiline, an antiparkinsonian drug: can such side effects be predicted? J Clin Pharmacol 1994; 34: 80–5.

Effects on mortality.

For reference to a study which observed an increased mortality rate in patients with Parkinson’s disease taking selegiline and levodopa compared with those taking levodopa alone, see Parkinsonism under Uses and Administration, below.

💊 Precautions

Selegiline should be used with caution in patients with a history of peptic ulceration and avoided in those with active ulceration. It should also be used with caution in uncontrolled hypertension, arrhythmias, angina, severe liver or kidney dysfunction, or psychosis.

Cardiovascular disorders.

An investigation1 of the autonomic effects of selegiline as a potential cause of the unexpected mortality observed in a study2 in patients with Parkinson’s disease receiving selegiline and levodopa (see Parkinsonism, below) suggested that the risk of orthostatic hypotension with this combination may have been underestimated. It was considered prudent to withdraw selegiline from those with symptomatic orthostatic hypotension or cardiovascular or cerebrovascular disease. For those without symptomatic morbidity, but a greater than 20 mmHg fall in blood pressure on standing for 2 minutes, gradual withdrawal of selegiline with adjustment of levodopa dosage should be considered.
1. Churchyard A, et al. Autonomic effects of selegiline: possible cardiovascular toxicity in Parkinson’s disease. J Neurol Neurosurg Psychiatry 1997; 63: 228–34
2. Parkinson’s Disease Research Group of the United Kingdom. Comparison of therapeutic effects and mortality data of levodopa and levodopa combined with selegiline in patients with early, mild Parkinson’s disease. BMJ 1995; 311: 1602–7.

💊 Interactions

Selegiline is less likely than non-selective MAOIs, such as phenelzine, to interact with tyramine in food; such hypertensive reactions have been reported rarely at usual doses but UK licensed product information for oral formulations states that its selectivity is lost at higher doses and it must be assumed that selegiline can usually only be used safely without dietary restrictions at doses of up to 10 mg daily. US licensed information for the transdermal preparation states that dietary restrictions are necessary at doses of 9 mg daily and above. For dietary restrictions applicable to patients taking MAOIs. Even when given in therapeutic doses life-threatening interactions can occur between selegiline and pethidine. Serious reactions, sometimes fatal, have also been reported when selegiline was used with tricyclic antidepressants or serotonin reuptake inhibitors including the SSRIs and venlafaxine. Licensed drug information states that 14 days should elapse between stopping selegiline and starting treatment with tricyclic or serotonergic antidepressants. Conversely, selegiline should not be given to patients who have recently received these antidepressants; at least 5 weeks should elapse between stopping fluoxetine and starting treatment with selegiline. Use of selegiline with non-selective MAOIs may cause severe hypotension and such use is not recommended.

Antidepressants.

Although there have been studies in which patients with parkinsonism have received selegiline with SSRIs such as fluoxetine1 or paroxetine2 (apparently without any problems) there have been reports of reactions3-5 such as shivering and sweating, hypertension, hyperactivity, and ataxia occurring when selegiline and fluoxetine have been used together. The FDA noted6 that reactions similar to those between SSRIs and non-selective MAOIs had also been reported in patients taking selegiline with paroxetine or sertraline. Severe reactions, sometimes fatal, have also occurred in patients taking selegiline and tricyclic antidepressants.6 For a report of serotonin syndrome developing when venlafaxine was given after selegiline (despite a drug-free period). There has been a report7 of a patient receiving the non-selective MAOI iproniazid who experienced severe orthostatic hypotension when given selegiline. Selegiline given with the reversible MAOI moclobemide to healthy subjects markedly increased the pressor response to tyramine compared with the effects of each drug used alone.8 The authors concluded that dietary restriction of tyramine-containing foods would be necessary if these drugs were to be used together. One UK manufacturer (Cephalon, UK) states that oral selegiline should not be given with any type of antidepressant, while another (Orion, UK) advises that use with SSRIs or venlafaxine be avoided and recommends caution when used with the tricyclics. The US manufacturer of transdermal selegiline (Bristol-Myers Squibb, USA), used for depression, states that use with other antidepressants such as bupropion, mirtazapine, serotonin reuptake inhibitors, St John’s wort, and tricyclics is contra-indicated.
1. Waters CH. Fluoxetine and selegiline—lack of significant interaction. Can J Neurol Sci 1994; 21: 259–61
2. Toyama SC, Iacono RP. Is it safe to combine a selective serotonin reuptake inhibitor with selegiline? Ann Pharmacother 1994; 28: 405–6
3. Suchowersky O, de Vries JD. Interaction of fluoxetine and selegiline. Can J Psychiatry 1990; 35: 571–2
4. Jermain DM, et al. Potential fluoxetine-selegiline interaction. Ann Pharmacother 1992; 26: 1300
5. Montastruc JL, et al. Pseudophaeochromocytoma in parkinsonian patient treated with fluoxetine plus selegiline. Lancet 1993; 341: 555
6. Anonymous. Eldepryl and antidepressant interaction. FDA Med Bull 1995; 25 (Feb.): 6
7. Pare CMB, et al. Attempts to attenuate the ‘cheese effect’: combined drug therapy in depressive illness. J Affect Disord 1985; 9: 137–41
8. Korn A, et al. Tyramine pressor sensitivity in healthy subjects during combined treatment with moclobemide and selegiline. Eur J Clin Pharmacol 1996; 49: 273–8.

Antimigraine drugs.

Some serotonin agonists including rizatriptan, sumatriptan, and zolmitriptan are metabolised via monoamine oxidase type A and therefore it is considered unlikely that selegiline, a monoamine oxidase type B inhibitor, would interact with these drugs. Nevertheless, one manufacturer (Cephalon, UK) of oral selegiline contra-indicates its use in patients also receiving serotonin agonists; it is also recommended that at least 24 hours should elapse between stopping selegiline and starting treatment with these drugs.

Opioid analgesics.

Selegiline can produce life-threatening reactions when given with pethidine.1 Some manufacturers contra-indicate use of selegiline with pethidine and other opioid analgesics such as dextropropoxyphene, methadone, and tramadol.
1. Zornberg GL, et al. Severe adverse interaction between pethidine and selegiline. Lancet 1991; 337: 246. Correction. ibid.; 440.

Oral contraceptives.

The total area under the concentrationtime curve for selegiline given in single doses of 5 to 40 mg was raised ten- to twentyfold in 4 women who were using oral hormonal contraceptives when compared with 4 women receiving no other medication.1 It was suggested that use of selegiline and oral hormonal contraceptives should be avoided or the dosage of selegiline reduced.
1. Laine K, et al. Dose linearity study of selegiline pharmacokinetics after oral administration: evidence for strong drug interaction with female sex steroids. Br J Clin Pharmacol 1999; 47: 249–54.

Sympathomimetics.

Licensed information for a US product (Eldepryl; Somerset, USA) states that there has been a report of hypertensive crisis in a patient taking recommended doses of selegiline and ephedrine. A hypertensive reaction after low-dose dopamine infusion has been reported1 in a 75-year-old patient taking selegiline 10 mg daily for Parkinson’s disease. The authors suggest that this may indicate a non-specific action of selegiline at usual doses on peripheral monoamine oxidase type-A. UK licensed product information states that dopamine should be used with caution in patients taking selegiline.
1. Rose LM, et al. A hypertensive reaction induced by concurrent use of selegiline and dopamine. Ann Pharmacother 2000; 34: 1020–4.

💊 Pharmacokinetics

Selegiline is readily absorbed from the gastrointestinal tract and peak plasma concentrations are achieved in 30 minutes after oral doses of conventional preparations. Although subject to large interindividual variation, bioavailability is about 10% and is increased when given with food. Selegiline is rapidly distributed throughout the body and crosses the blood-brain barrier. It undergoes extensive first-pass metabolism in the liver to produce at least 5 metabolites, including l-(−)desmethylselegiline (norselegiline), l-(−)-N-methylamfetamine, and l-(−)-amfetamine. Plasma concentrations of selegiline metabolites are greatly reduced after doses of the oral lyophilisate preparation, the majority of which undergoes absorption through the buccal mucosa. Selegiline is excreted as metabolites mainly in the urine and about 15% appears in the faeces. At steady state the elimination half-life is reported to be 10 hours.
1. Heinonen EH, et al. Pharmacokinetic aspects of l-deprenyl (selegiline) and its metabolites. Clin Pharmacol Ther 1994; 56: 742–9
2. Mahmood I, et al. Clinical pharmacokinetics and pharmacodynamics of selegiline: an update. Clin Pharmacokinet 1997; 33: 91–102
3. Anttila M, et al. Marked effect of liver and kidney function on the pharmacokinetics of selegiline. Clin Pharmacol Ther 2005; 77: 54–62
4. Azzaro AJ, et al. Pharmacokinetics and absolute bioavailability of selegiline following treatment of healthy subjects with the selegiline transdermal system (6 mg/24 h): a comparison with oral selegiline capsules. J Clin Pharmacol 2007; 47: 1256–67.

💊 Uses and Administration

Selegiline is an irreversible selective inhibitor of monoamine oxidase type B, an enzyme involved in the metabolic degradation of dopamine in the brain. It enhances the effects of levodopa and is used in the treatment of Parkinson’s disease mainly as an adjunct to levodopa therapy to reduce ‘end-of-dose’ or ‘on-off’ fluctuations in response, but see Parkinsonism, below. Addition of selegiline to levodopa therapy may enable the dosage of levodopa to be reduced by about 10 to 30%. Selegiline may be given alone in early Parkinson’s disease in an attempt to delay the need for levodopa therapy. It is also used in the treatment of depression (see also below). In the treatment of Parkinson’s disease, selegiline hydrochloride is given by mouth as conventional preparations such as capsules, tablets, or liquid, or as lyophilisate tablets. The dose of the conventional preparations is 10 mg daily, either as a single dose in the morning or in 2 divided doses of 5 mg at breakfast and lunchtime. The initial dose of the oral lyophilisate tablets is 1.25 mg daily at least 5 minutes before breakfast; patients already receiving 10 mg of conventional preparations can be transferred to 1.25 mg of the oral lyophilisate. In the USA, the initial oral lyophilisate dose of 1.25 mg daily may be increased, after at least 6 weeks, to 2.5 mg given once daily, if necessary. To avoid initial confusion and agitation, particularly in the elderly, the BNF suggests it may be appropriate when using conventional preparations to start treatment with a dose of 2.5 mg daily. In the USA, transdermal patches delivering 6, 9, or 12 mg of selegiline over 24 hours are available for the treatment of depression. The initial dose is 6 mg daily, increased in steps of 3 mg every 2 weeks if necessary, to a maximum of 12 mg daily. Patches are applied once daily and should be replaced every 24 hours with the new patch being applied to a different site. Dose increases should be made with caution in the elderly and patients should be closely observed for postural changes in blood pressure during treatment. Dietary restrictions are necessary at doses of 9 mg daily and above. Other conditions in which selegiline has been tried include dementia.
1. Youdim MBH, Finberg JPM. Pharmacological actions of l-deprenyl (selegiline) and other selective monoamine oxidase B inhibitors. Clin Pharmacol Ther 1994; 56: 725–33
2. Lange KW, et al. Biochemical actions of l-deprenyl (selegiline). Clin Pharmacol Ther 1994; 56: 734–41.

Cocaine dependence.

Cocaine use may affect the dopaminergic modulation of CNS function; selegiline is one of several drugs that interact with dopaminergic systems and have been tried in treatment of cocaine abuse and dependence.
1. Houtsmuller EJ, et al. Transdermal selegiline and intravenous cocaine: safety and interactions. Psychopharmacology (Berl) 2004; 172: 31–40.

Dementia.

The hypothesis that neurodegeneration in Alzheimer’s disease might be due to free radical formation has led to drugs such as selegiline being tried as antoxidant therapy. Early double-blind studies1,2 indicated that oral selegiline 10 mg daily might produce beneficial effects in patients with Alzheimer’s disease but it was suggested that improvements in mood and cognitive function may have been due to a reduction in tension and depression.3 A 15-month study in Alzheimers’s patients with mild cognitive impairment showed oral selegiline 10 mg daily to have little effect,4 although the authors pointed out that those with more severe dementia have shown more response in other studies. The conclusion of a later study5 that oral selegiline 10 mg daily slowed progression in patients with moderate disease has been criticised6 on the grounds that any effect was only evident after statistical adjustment to the original analysis. In addition a systematic review7 examining the effects of selegiline concluded that there was no meaningful evidence of a beneficial effect of oral selegiline in patients with Alzheimer’s disease. They also considered that there was no longer any justification for its use in patients with Alzheimer’s disease.
1. Piccinin GL, et al. Neuropsychological effects of -deprenyl in Alzheimer’s type dementia. Clin Neuropharmacol 1990; 13: 147–63
2. Mangoni A, et al. Effects of a MAO-B inhibitor in the treatment of Alzheimer disease. Eur Neurol 1991; 31: 100–107
3. Anonymous. Drugs for Alzheimer’s disease. Drug Ther Bull 1990; 28: 42–4
4. Burke WJ, et al. L-Deprenyl in the treatment of mild dementia of the Alzheimer type: results of a 15-month trial. J Am Geriatr Soc 1993; 41: 1219–25
5. Sano M, et al. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer’s disease. N Engl J Med 1997; 336: 1216–22
6. Pincus MM. Alpha-tocopherol and Alzheimer’s disease. N Engl J Med 1997; 337: 572
7. Birks J, Flicker L. Selegiline for Alzheimer’s disease. Available in The Cochrane Database of Systematic Reviews; Issu
1. Chichester: John Wiley; 2003 (accessed 16/02/06).

Depression.

Selegiline is a selective inhibitor of monoamine oxidase type B and there are reports1-3 of it producing improvement in depression. However, at the doses usually required to produce an antidepressant effect the specificity of oral selegiline is reported to be lost and it has been suggested that the efficacy of selegiline as an antidepressant might depend on inhibition of monoamine oxidase A rather than inhibition of monoamine oxidase B alone. Such a loss of specificity would mean that patients taking selegiline for depression would need to observe the dietary restrictions applicable to non-selective MAOIs. To overcome the problems associated with the oral route, transdermal selegiline has also been tried and may be more effective than placebo in the treatment of depression.4 The use of the transdermal route allows sustained blood levels of selegiline to be delivered without extensive inhibition of peripheral monoamine oxidase A. Transdermal patches of selegiline are licensed for the treatment of depression in the USA.
1. Mendlewicz J, Youdim MBH. L-Deprenil, a selective monoamine oxidase type B inhibitor, in the treatment of depression: a double-blind evaluation. Br J Psychiatry 1983; 142: 508–11
2. Mann JJ, et al. A controlled study of the antidepressant efficacy and side-effects of (−)-deprenyl. Arch Gen Psychiatry 1989; 46: 45–50
3. Sunderland T, et al. High-dose selegiline in treatment-resistant older depressive patients. Arch Gen Psychiatry 1994; 51: 607–15
4. Frampton JE, Plosker GL. Selegiline transdermal system: in the treatment of major depressive disorder. Drugs 2007; 67: 257–65.

Narcoleptic syndrome.

Small controlled studies1,2 have suggested that oral selegiline 20 to 40 mg daily has a beneficial effect on symptoms of narcolepsy and cataplexy; at such a dosage a low-tyramine diet is considered necessary.
1. Hublin C, et al. Selegiline in the treatment of narcolepsy. Neurology 1994; 44: 2095–2101
2. Mayer G, et al. Selegeline [sic] hydrochloride treatment in narcolepsy: a double-blind, placebo-controlled study. Clin Neuropharmacol 1995; 18: 306–19.

Parkinsonism.

As a selective monoamine oxidase type B inhibitor, selegiline reduces the metabolism of dopamine and thereby enhances its actions. It reduces levodopa’s ‘end-of-dose’ effect and has a dose-sparing effect. Some have used it as monotherapy in an attempt to delay the need for levodopa. If progression of Parkinson’s disease were due to a cytotoxic effect of free radicals, generated during the metabolism of dopamine, on dopaminergic neurones in the substantia nigra, selegiline might slow the process by reducing their formation. In a large early study,1 the DATATOP study, selegiline monotherapy delayed the need to start levodopa in patients with early Parkinson’s disease. These findings were corroborated by other smaller studies.2,3 There has been much debate over whether the benefit was due to a neuroprotective or symptomatic effect. Re-analysis of the DATATOP data by independent workers4,5 and findings of other studies6 supported a symptomatic effect. Subsequent studies involving DATATOP patients were also consistent with a symptomatic effect; any benefit produced by selegiline appeared to be less pronounced as the duration of treatment increased7 and was lost completely long term.8,9 However, a later study10designed to minimise any symptomatic effect cast doubt on whether the delay in progression of the signs and symptoms of Parkinson’s disease obtained with selegiline was entirely due to a symptomatic effect. Studies of the use of selegiline as an adjunct to levodopa therapy6,11,12 indicate that selegiline permits a modest reduction in the dosage requirements of levodopa. An interim analysis of a study of the early addition of selegiline to levodopa has also suggested that selegiline might stabilise the long-term daily levodopa dosage.13 As with monotherapy, combined therapy has been reported to slow symptom progression.14 The use of selegiline in Parkinson’s disease has been questioned after a UK study11 found an unexpected increase in mortality in patients taking levodopa with selegiline compared with those taking levodopa alone. No difference in mortality had been detected at the 3-year follow-up15 but after an average follow-up time of 5.6 years11 mortality was 60% higher in the group also receiving selegiline. The study has been criticised on many grounds including the fact that mortality was very high in both arms of the study16 and has been the subject of much debate.17,18The authors of the study11 had stated that they would advise the study patients to withdraw selegiline therapy. Analysis of followup data19 until the selegiline arm of the study was terminated (average 6.8 years) found an excess mortality of about 35%, a figure calculated20 to be no longer significant. However, because of the premature termination of the study such results were considered21 to be biased. Whether any excess in mortality is causally related to selegiline is still unclear. Some consider that changes in prescribing practice based on this study are not warranted.17 Others21 have made a cautious recommendation not to start combination treatment in patients with newly diagnosed Parkinson’s disease but consider that there is little evidence to advise patients who have been using selegiline with levodopa for years without problem to change their treatment. An evaluation of mortality among patients taking antiparkinsonian drugs (using the UK General Practice Research Database) provided evidence against there being substantial excess mortality associated with the use of selegiline.22 These results are supported by a systematic review23 and meta-analyses24,25 of randomised, double-blind studies which found no increase in mortality associated with selegiline treatment regardless of concurrent levodopa. Furthermore, increased mortality was not seen in patients in the original DATATOP trial1 after an average follow-up time of 8.2 years. However, it was noted that the delay of disability observed in the early phase of selegiline therapy1,7 was not associated with longer life during follow-up.26 A recent systematic review23 has also found no convincing evidence that selective monoamine oxidase type B inhibitors (selegiline and lazabemide) significantly delay disease progression in early Parkinson’s disease and routine use is not recommended.
1. The Parkinson Study Group. Effect of deprenyl on the progression of disability in early Parkinson’s disease. N Engl J Med 1989; 321: 1364–71
2. Tetrud JW, Langston JW. The effect of deprenyl (selegiline) on the natural history of Parkinson’s disease. Science 1989; 245: 519–22
3. Allain H, et al. Selegiline in de novo parkinsonian patients: the French selegiline multicenter trial (FSMT). Acta Neurol Scand 1991; 84 (suppl 136): 73–8
4. Schulzer M, et al. The antiparkinson efficacy of deprenyl derives from transient improvement that is likely to be symptomatic. Ann Neurol 1992; 32: 795–8.
5. Ward CD. Does selegiline delay progression of Parkinson’s disease? A critical re-evaluation of the DATATOP study. J Neurol Neurosurg Psychiatry 1994; 57: 217–20
6. Brannan T, Yahr MD. Comparative study of selegiline plus dopa–carbidopa versus -dopa–carbidopa alone in the treatment of Parkinson’s disease. Ann Neurol 1995; 37: 95–8
7. The Parkinson Study Group. Effects of tocopherol and deprenyl on the progression of disability in early Parkinson’s disease. N Engl J Med 1993; 328: 176–83
8. Parkinson Study Group. Impact of deprenyl and tocopherol treatment on Parkinson’s disease in DATATOP subjects not requiring levodopa. Ann Neurol 1996; 39: 29–36
9. Parkinson Study Group. Impact of deprenyl and tocopherol treatment on Parkinson’s disease in DATATOP patients requiring levodopa. Ann Neurol 1996; 39: 37–45
10. Olanow CW, et al. The effect of deprenyl and levodopa on the progression of Parkinson’s disease. Ann Neurol 1996; 38: 771–7
11. Parkinson’s Disease Research Group of the United Kingdom. Comparison of therapeutic effects and mortality data of levodopa and levodopa combined with selegiline in patients with early, mild Parkinson’s disease. BMJ 1995; 311: 1602–7
12. Myllylä VV, et al. Early selegiline therapy reduces levodopa dose requirement in Parkinson’s disease. Acta Neurol Scand 1995; 91: 177–82
13. Larsen JP, Boas J. Norwegian-Danish Study Group. The effects of early selegiline therapy on long-term treatment and parkinsonian disability: an interim analysis of a Norwegian-Danish 5year study. Mov Disord 1997; 12: 175–82
14. Pålhagen S, et al. Selegiline slows the progression of the symptoms of Parkinson disease. Neurology 2006; 66: 1200–6
15. Parkinson’s Disease Research Group in the United Kingdom. Comparisons of the therapeutic effects of levodopa, levodopa and selegiline, and bromocriptine in patients with early, mild Parkinson’s disease: three year interim report. BMJ 1993; 307: 467–72
16. Olanow CW, et al. Patients taking selegiline may have received more levodopa than necessary. BMJ 1996; 312: 702–3
17. Ahlskog JE. Treatment of early Parkinson’s disease: are complicated strategies justified? Mayo Clin Proc 1996; 71: 659–70
18. Mizuno Y, Kondo T. Mortality associated with selegiline in Parkinson’s disease: what do the available data mean? Drug Safety 1997; 16: 289–94
19. Ben-Shlomo Y, et al. Investigation by Parkinson’s Disease Research Group of United Kingdom into excess mortality seen with combined levodopa and selegiline treatment in patients with early, mild Parkinson’s disease: further results of randomised trial and confidential inquiry. BMJ 1998; 316: 1191–6
20. Abrams KR. Monitoring randomised controlled trials. BMJ 1998; 316: 1183–4
21. Breteler MMB. Selegiline, or the problem of early termination of clinical trials. BMJ 1998; 316: 1182–3
22. Thorogood M, et al. Mortality in people taking selegiline: observational study. BMJ 1998; 317: 252–4
23. Macleod AD, et al. Monoamine oxidase B inhibitors for early Parkinson’s disease. Available in The Cochrane Database of Systematic Reviews; Issu
3. Chichester: John Wiley; 2005 (accessed 16/02/06)
24. Olanow CW, et al. Effect of selegiline on mortality in patients with Parkinson’s disease: a meta-analysis. Neurology 1998; 51: 825–30
25. Ives NJ, et al. Monoamine oxidase type B inhibitors in early Parkinson’s disease: meta-analysis of 17 randomised trials involving 3525 patients. BMJ 2004; 329: 593–6
26. The Parkinson Study Group. Mortality in DATATOP: A multicenter trial in early Parkinson’s disease. Ann Neurol 1998; 43: 318–25.

Smoking cessation.

Selegiline has been investigated as an aid to smoking cessation.
1. George TP, et al. A preliminary placebo-controlled trial of selegiline hydrochloride for smoking cessation. Biol Psychiatry 2003; 53: 136–43
2. Biberman R, et al. A randomized controlled trial of oral selegiline plus nicotine skin patch compared with placebo plus nicotine skin patch for smoking cessation. Addiction 2003; 98: 1403–7.

💊 Preparations

BP 2008: Selegiline Oral Solution; Selegiline Tablets; USP 31: Selegiline Hydrochloride Tablets.

Proprietary Preparations

Arg.: Brintenal; Jumex; Kinabide†; Zelapar; Austral.: Eldepryl; Selgene; Austria: Amboneural; Cognitiv; Jumex; Regepar; Xilopar; Belg.: Eldepryl; Braz.: Deprilan; Elepril; Jumexil; Niar; Parkexin; Canad.: Eldepryl†; Chile: Selgina; Cz.: Apo-Seleg; Cognitiv; Jumex; Niar; Segalin†; Sepatrem†; Denm.: Eldepryl; Fin.: Eldepryl; Fr.: Deprenyl; Otrasel; Ger.: Amindan†; Antiparkin; Jutagilin; MAOtil†; Movergan; Selegam†; Selemerck; Selepark; Selgimed; Xilopar; Gr.: Cosmopril; Ermolax; Feliselin; Krautin; Legil; Procythol; Resostyl; Hong Kong: Julab; Jumex; Sefmex; Selegos; Hung.: Cognitiv; Jumex; Primulex†; India: Selerin; Selgin; Indon.: Jumex; Irl.: Eldepryl; Israel: Jumex; Ital.: Egibren; Jumex; Selecom; Seledat; Xilopar; Jpn: FP Tab; Malaysia: Ginex†; Jumex; Sefmex; Selegos†; Mex.: Niar; Neth.: Eldepryl; Norw.: Eldepryl; NZ: Eldepryl; Selgene†; Philipp.: Jumex; Pol.: Apo-Selin; Jumex; Parkinil†; Segan; Selerin; Selgin; Selgres; Port.: Jumex; Niponeurin; Xilopar; Rus.: Cognitiv (Когнитив); Segan (Сеган); Selegos (Селегос); S.Afr.: Eldepryl; Parkilyne; Singapore: Jumex; Selegos; Spain: Plurimen; Swed.: Eldepryl; Switz.: Jumexal; Selecim†; Thai.: Elegelin†; Julab; Jumex; Kinline†; Sefmex; Seline†; Turk.: Moverdin; Seldepar; UK: Eldepryl; Zelapar; USA: Atapryl; Carbex; Eldepryl; Emsam; Zelapar; Venez.: Jumex.
Published November 27, 2018.