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CAS 136236-51-6 manufacturers and suppliers on PharmaCompass

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  • Chemistry
003N66TS6T
Also known as: 136236-51-6, (r)-n-(2-propynyl)-2,3-dihydroinden-1-amine, Azilect, (r)-n-2-propynyl-1-indanamine, (r)-2,3-dihydro-n-2-propynyl-1h-inden-1-amine, 1-indanamine, n-2-propynyl-, (r)-
Molecular Formula
C12H13N
Molecular Weight
171.24  g/mol
InChI Key
RUOKEQAAGRXIBM-GFCCVEGCSA-N
FDA UNII
003N66TS6T

Rasagiline is an irreversible inhibitor of monoamine oxidase and is used as a monotherapy in early Parkinson's disease or as an adjunct therapy in more advanced cases.
Rasagiline is a Monoamine Oxidase Inhibitor. The mechanism of action of rasagiline is as a Monoamine Oxidase Inhibitor.
1 2D Structure

003N66TS6T

2 Identification
2.1 Computed Descriptors
2.1.1 IUPAC Name
(1R)-N-prop-2-ynyl-2,3-dihydro-1H-inden-1-amine
2.1.2 InChI
InChI=1S/C12H13N/c1-2-9-13-12-8-7-10-5-3-4-6-11(10)12/h1,3-6,12-13H,7-9H2/t12-/m1/s1
2.1.3 InChI Key
RUOKEQAAGRXIBM-GFCCVEGCSA-N
2.1.4 Canonical SMILES
C#CCNC1CCC2=CC=CC=C12
2.1.5 Isomeric SMILES
C#CCN[C@@H]1CCC2=CC=CC=C12
2.2 Other Identifiers
2.2.1 UNII
003N66TS6T
2.3 Synonyms
2.3.1 MeSH Synonyms

1. 2,3-dihydro-n-2-propynyl-1h-inden-1-amine-(1r)-hydrochloride

2. Agn 1135

3. Agn-1135

4. Azilect

5. N-2-propynyl-1-indanamine

6. N-propargyl-1-aminoindan Mesylate

7. Rasagiline Hydrochloride

8. Tvp 101

9. Tvp 1022

10. Tvp-101

11. Tvp-1022

12. Tvp1022

2.3.2 Depositor-Supplied Synonyms

1. 136236-51-6

2. (r)-n-(2-propynyl)-2,3-dihydroinden-1-amine

3. Azilect

4. (r)-n-2-propynyl-1-indanamine

5. (r)-2,3-dihydro-n-2-propynyl-1h-inden-1-amine

6. 1-indanamine, N-2-propynyl-, (r)-

7. Tv-1030

8. (1r)-n-(prop-2-yn-1-yl)-2,3-dihydro-1h-inden-1-amine

9. Azilect (tn)

10. Ras

11. Chembl887

12. Nsc-759639

13. (1r)-n-prop-2-ynyl-2,3-dihydro-1h-inden-1-amine

14. 1h-inden-1-amine, 2,3-dihydro-n-2-propynyl-, (1r)-

15. (1r)-n-propargylindan-1-amine

16. Chebi:63620

17. 003n66ts6t

18. (r)-indan-1-yl-prop-2-ynyl-amine

19. Rasagiline [inn]

20. Tvp1012

21. Rasagiline [usan]

22. (r)-(+)-rasagiline

23. Rasagiline [usan:inn]

24. Unii-003n66ts6t

25. Mfcd00866571

26. Hsdb 7699

27. (1r)-n-prop-2-ynylindan-1-amine

28. 1h-inden-1-amine, 2,3-dihydro-n-2-propynyl-, (1r)

29. Tv 1030

30. Rasagiline [mi]

31. Rasagiline (usan/inn)

32. Rasagiline [hsdb]

33. Rasagiline [vandf]

34. Rasagiline [who-dd]

35. Schembl74699

36. Mls006012042

37. N-propargyl-1-(r)aminoindan

38. Rasagiline [ema Epar]

39. Gtpl6641

40. Schembl2029054

41. Dtxsid3041112

42. Rasagiline [orange Book]

43. Bdbm10989

44. Hms3264k12

45. Hms3715l12

46. Hms3886n03

47. Pharmakon1600-01502333

48. Ac-723

49. Hy-14605a

50. Nsc759639

51. Nsc789038

52. S5795

53. Zinc19875504

54. Akos006271452

55. Akos015837675

56. Am84542

57. Ccg-213034

58. Db01367

59. Fs-3130

60. Nsc 759639

61. Nsc-789038

62. Smr002533187

63. (1r)-n-(prop-2-yn-1-yl)indan-1-amine

64. Db-001111

65. A2916

66. D08469

67. Ab01562963_01

68. Ab01562963_02

69. Q420685

70. Sr-00000006359

71. Sr-00000006359-3

72. (r)-n-(prop-2-ynyl)-2,3-dihydro-1h-inden-1-amine

73. (1r)-2,3-dihydro-n-2-propyn-1-yl-1h-inden-1-amine

74. 1h-inden-1-amine, 2,3-dihydro-n-2-propynyl-, (r)-

75. 1h-inden-1-amine, 2,3-dihydro-n-2-propyn-1-yl-, (1r)-

76. (r)-n-(prop-2-ynyl)-2,3-dihydro-1h-inden-1-amine;(r)-n-(2-propynyl)-2,3-dihydroinden-1-amine

77. 1204184-69-9

2.4 Create Date
2005-08-09
3 Chemical and Physical Properties
Molecular Weight 171.24 g/mol
Molecular Formula C12H13N
XLogP31.8
Hydrogen Bond Donor Count1
Hydrogen Bond Acceptor Count1
Rotatable Bond Count2
Exact Mass171.104799419 g/mol
Monoisotopic Mass171.104799419 g/mol
Topological Polar Surface Area12 Ų
Heavy Atom Count13
Formal Charge0
Complexity212
Isotope Atom Count0
Defined Atom Stereocenter Count1
Undefined Atom Stereocenter Count0
Defined Bond Stereocenter Count0
Undefined Bond Stereocenter Count0
Covalently Bonded Unit Count1
4 Drug and Medication Information
4.1 Therapeutic Uses

Rasagiline is used as initial monotherapy or as adjunctive therapy to levodopa for the symptomatic treatment of idiopathic parkinsonian syndrome.

American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 2696


Azilect (rasagiline mesylate) is indicated for the treatment of the signs and symptoms of idiopathic Parkinson's disease as initial monotherapy and as adjunct therapy to levodopa. The effectiveness of Azilect was demonstrated in patients with early Parkinson's disease who were receiving Azilect as monotherapy and who were not receiving any concomitant dopaminergic therapy. The effectiveness of Azilect as adjunct therapy was demonstrated in patients with Parkinson's disease who were treated with levodopa.

FDA; Center for Drug Evaluation and Research; Label Information for Azilect (Rasagiline) (Last updated May 2006). Available from, as of February 20, 2009: https://www.fda.gov/cder/foi/label/2006/021641lbl.pdf


4.2 Drug Warning

When used as monotherapy, postural hypotension was reported in approximately 3% of patients treated with 1 mg rasagiline and 5% of patients treated with placebo. In the monotherapy trial, postural hypotension did not lead to drug discontinuation and premature withdrawal in the rasagiline or placebo treated patients. When used as an adjunct to levodopa, postural hypotension was reported in approximately 6% of patients treated with 0.5 mg rasagiline, 9% of patients treated with 1 mg rasagiline and 3% of patients treated with placebo. Postural hypotension led to drug discontinuation and premature withdrawal from clinical trials in one (0.7%) patient treated with rasagiline 1 mg/day, no patients treated with rasagiline 0.5 mg/day and no placebo-treated patients. Clinical trial data suggest that postural hypotension occurs most frequently in the first two months of rasagiline treatment and tends to decrease over time.

FDA; Center for Drug Evaluation and Research; Label Information for Azilect (Rasagiline) (Last updated May 2006). Available from, as of February 20, 2009: https://www.fda.gov/cder/foi/label/2006/021641lbl.pdf


Data from epidemiologic studies indicate that patients with Parkinson's disease have an approximately twofold to fourfold greater risk of developing melanoma than the general population; however, it is unclear whether the observed increased risk is related to the underlying disease or to antiparkinsonian drug therapy. The risk of developing melanoma in patients receiving rasagiline appears to be greater than that in the general population but comparable to that in patients with Parkinson's disease. Because of these findings, patients and clinicians should monitor for melanomas frequently. The manufacturer recommends that dermatologic examinations be performed by qualified clinicians (e.g., dermatologists) periodically; the frequency of dermatologic examinations should be determined by the patient's dermatologist.

American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 2697


In the monotherapy study, hallucinations were reported as an adverse event in 1.3% of patients treated with 1 mg rasagiline and in 0.7% of patients treated with placebo. In the monotherapy trial, hallucinations led to drug discontinuation and premature withdrawal from clinical trials in 1.3% of the 1 mg rasagiline treated patients and in none of the placebo treated patients. When used as an adjunct to levodopa, hallucinations were reported as an adverse event in approximately 5% of patients treated with 0.5 mg/day, 4% of patients treated with 1 mg/day rasagiline and 3% of patients treated with placebo. Hallucinations led to drug discontinuation and premature withdrawal from clinical trials in about 1% of patients treated with 0.5 mg/day or 1 mg/day and none of the placebo treated patients. Patients should be cautioned of the possibility of developing hallucinations and instructed to report them to their health care provider promptly should they develop.

FDA; Center for Drug Evaluation and Research; Label Information for Azilect (Rasagiline) (Last updated May 2006). Available from, as of February 20, 2009: https://www.fda.gov/cder/foi/label/2006/021641lbl.pdf


Safety and efficacy of rasagiline have not been established in pediatric patients younger than 18 years of age.

American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 2697


For more Drug Warnings (Complete) data for RASAGILINE (10 total), please visit the HSDB record page.


4.3 Drug Indication

For the treatment of the signs and symptoms of idiopathic Parkinsons disease as initial monotherapy and as adjunct therapy to levodopa.


FDA Label


Azilect is indicated for the treatment of idiopathic Parkinson's disease (PD) as monotherapy (without levodopa) or as adjunct therapy (with levodopa) in patients with end-of-dose fluctuations.


5 Pharmacology and Biochemistry
5.1 Pharmacology

Rasagiline is a propargylamine and an irreversible inhibitor of monoamine oxidase (MAO). MAO, a flavin-containing enzyme, regulates the metabolic degradation of catecholamines and serotonin in the CNS and peripheral tissues. It is classified into two major molecular species, A and B, and is localized in mitochondrial membranes throughout the body in nerve terminals, brain, liver and intestinal mucosa. MAO-A is found predominantly in the GI tract and liver, and regulates the metabolic degradation of circulating catecholamines and dietary amines. MAO-B is the major form in the human brain and is responsible for the regulation of the metabolic degradation of dopamine and phenylethylamine. In ex vivo animal studies in brain, liver and intestinal tissues rasagiline was shown to be a potent,selective, and irreversible monoamine oxidase type B (MAO-B) inhibitor. At the recommended therapeutic doses, Rasagiline was also shown to be a potent and irreversible inhibitor of MAO-B in platelets. The selectivity of rasagiline for inhibiting only MAO-B (and not MAO-A) in humans and the sensitivity to tyramine during rasagiline treatment at any dose has not been sufficiently characterized to avoid restriction of dietary tyramine and amines contained in medications.


5.2 MeSH Pharmacological Classification

Monoamine Oxidase Inhibitors

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) (See all compounds classified as Monoamine Oxidase Inhibitors.)


Neuroprotective Agents

Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids. (See all compounds classified as Neuroprotective Agents.)


5.3 FDA Pharmacological Classification
5.3.1 Active Moiety
RASAGILINE
5.3.2 FDA UNII
003N66TS6T
5.3.3 Pharmacological Classes
Monoamine Oxidase Inhibitors [MoA]; Monoamine Oxidase Inhibitor [EPC]
5.4 ATC Code

N04BD02


N04BD02

S76 | LUXPHARMA | Pharmaceuticals Marketed in Luxembourg | Pharmaceuticals marketed in Luxembourg, as published by d'Gesondheetskeess (CNS, la caisse nationale de sante, www.cns.lu), mapped by name to structures using CompTox by R. Singh et al. (in prep.). List downloaded from https://cns.public.lu/en/legislations/textes-coordonnes/liste-med-comm.html. Dataset DOI:10.5281/zenodo.4587355


N - Nervous system

N04 - Anti-parkinson drugs

N04B - Dopaminergic agents

N04BD - Monoamine oxidase b inhibitors

N04BD02 - Rasagiline


5.5 Absorption, Distribution and Excretion

Absorption

Rasagiline is rapidly absorbed following oral administration. The absolute bioavailability of rasagiline is about 36%.


Route of Elimination

Rasagiline undergoes almost complete biotransformation in the liver prior to excretion. Glucuronide conjugation of rasagiline and its metabolites, with subsequent urinary excretion, is the major elimination pathway. After oral administration of 14C-labeled rasagiline, elimination occurred primarily via urine and secondarily via feces (62% of total dose in urine and 7% of total dose in feces over 7 days), with a total calculated recovery of 84% of the dose over a period of 38 days. Less than 1% of rasagiline was excreted as unchanged drug in urine.


Volume of Distribution

87 L


After oral administration of (14)C-labeled rasagiline, elimination occurred primarily via urine and secondarily via feces (62% of total dose in urine and 7% of total dose in feces over 7 days), with a total calculated recovery of 84% of the dose over a period of 38 days. Less than 1% of rasagiline was excreted as unchanged drug in urine.

FDA; Center for Drug Evaluation and Research; Label Information for Azilect (Rasagiline) (Last updated May 2006). Available from, as of February 20, 2009: https://www.fda.gov/cder/foi/label/2006/021641lbl.pdf


Rasagiline is rapidly absorbed; following oral administration, peak plasma concentrations are achieved in approximately 1 hour. The absolute bioavailability of rasagiline is about 36%. Following administration with a high-fat meal, peak plasma rasagiline concentrations and area under the plasma concentration-time curve (AUC) decreased by approximately 60 and 20%, respectively; because AUC is not substantially affected, rasagiline may be administered with or without food. Rasagiline readily crosses the blood-brain barrier. The mean steady-state or terminal half-life of rasagiline is 31 or 1.342 hours, respectively; however, there is no correlation between rasagiline's pharmacokinetic profile and its pharmacologic effects because the drug irreversibly inhibits MAO-B, and restoration of normal enzyme activity depends on the rate of de novo enzyme synthesis. Rasagiline is approximately 88-94% bound to plasma proteins, with 61-63% bound to albumin.

American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 2698


IV studies in rats and dogs show that the volume of distribution (Vd) of rasagiline is several times that of total body water, indicating extensive tissue distribution. Tissue distribution of (14)C-rasagiline was studied in albino and pigmented rats, revealing peaks of tissue radioactivity between 0.25 and 0.5 hours. Distribution to large intestine, urinary bladder and lacrimal glands takes longer, whilst persistence (up to 24 hrs) was seen in eyes, skin and arterial walls of pigmented animals. In-vitro protein binding in plasma of animals is in the range of 70 to 90% and in human plasma in the range of 88 to 94%.

European Medicines Agency (EMEA), The European Agency for the Evaluation of Medicinal Products, European Public Assessment Report (EPAR) for Authorized Medicinal Products for Human Use; Azilect, Scientific Discussion (2005). Available from, as of February 25, 2009: https://www.emea.europa.eu/humandocs/PDFs/EPAR/Azilect/5289705en6.pdf


Oral studies with (14)C-rasagiline show that absorption is rapid in all species, with Cmax attained in less than 2 hours. Absolute bioavailability has been estimated as 53-69% in rats, 13-22% in dogs, and 36% in humans. Toxicokinetic analyses during the toxicology studies showed that exposure was linear at doses higher than the pharmacological selectivity for inhibition of MOA-B and was maintained up to about 5 mg/kg/day. However, kinetics became non-linear at higher doses, possibly indicating saturation of the elimination processes for both rasagiline and its metabolite aminoindan. Accumulation was seen only at the highest doses in the mouse and dog studies (60 and 21 mg/kg/day respectively).

European Medicines Agency (EMEA), The European Agency for the Evaluation of Medicinal Products, European Public Assessment Report (EPAR) for Authorized Medicinal Products for Human Use; Azilect, Scientific Discussion (2005). Available from, as of February 25, 2009: https://www.emea.europa.eu/humandocs/PDFs/EPAR/Azilect/5289705en6.pdf


For more Absorption, Distribution and Excretion (Complete) data for RASAGILINE (6 total), please visit the HSDB record page.


5.6 Metabolism/Metabolites

Rasagiline undergoes almost complete biotransformation in the liver prior to excretion. In vitro experiments indicate that both routes of rasagiline metabolism are dependent on the cytochrome P450 (CYP) system, with CYP 1A2 being the major isoenzyme involved in rasagiline metabolism.


Rasagiline is extensively metabolized in the liver following oral administration. In vitro studies have shown that CYP1A2 is the predominant P450 isoform involved in the metabolic elimination of rasagiline. The primary human plasma metabolite formed following biotransformation of rasagiline is aminoindan. The proposed principal biotransformation pathways of rasagiline in human are N-dealkylation, hydroxylation of the indan ring, along with Phase II N or O-conjugation, including N-glucuronidation of the parent drug and of its metabolites. There was no bioconversion of rasagiline mesylate (R enantiomer) to its S enantiomer within the human body, as determined in plasma samples for healthy volunteers dosed with rasagiline. Rasagiline is not metabolized to amphetamine or methamphetamine.

European Medicines Agency (EMEA), The European Agency for the Evaluation of Medicinal Products, European Public Assessment Report (EPAR) for Authorized Medicinal Products for Human Use; Azilect, Scientific Discussion (2005). Available from, as of February 25, 2009: https://www.emea.europa.eu/humandocs/PDFs/EPAR/Azilect/5289705en6.pdf


An extensive first pass metabolism effect is evident, likely due to rasagiline binding to MAO sites in the intestine prior to passing the liver. Metabolism is rapid and extensive, with a similar profile in all tested species. The primary route of biotransformation is via N-dealkylation to form aminoindan and by hydroxylation to form 3-hydroxy-N-propargyl-1-aminoindan. Conjugation by sulfide or glucuronic acid occurs. Microsomal studies indicate CYP1A2 as the primary metabolising isotype, but rasagiline is neither an inducer nor inhibitor of cytochrome p450. The metabolism of rasagiline under inhibition, induction of CYP1A2 or in presence of concomitant substrate to the enzyme has been addressed clinically.

European Medicines Agency (EMEA), The European Agency for the Evaluation of Medicinal Products, European Public Assessment Report (EPAR) for Authorized Medicinal Products for Human Use; Azilect, Scientific Discussion (2005). Available from, as of February 25, 2009: https://www.emea.europa.eu/humandocs/PDFs/EPAR/Azilect/5289705en6.pdf


Rasagiline undergoes almost complete biotransformation in the liver prior to excretion. The metabolism of rasagiline proceeds through two main pathways: N-dealkylation and/or hydroxylation to yield 1-aminoindan (AI), 3-hydroxy-N-propargyl-1 aminoindan (3-OH-PAI) and 3-hydroxy-1-aminoindan (3-OH-AI). In vitro experiments indicate that both routes of rasagiline metabolism are dependent on the cytochrome P450 (CYP) system, with CYP 1A2 being the major isoenzyme involved in rasagiline metabolism. Glucuronide conjugation of rasagiline and its metabolites, with subsequent urinary excretion, is the major elimination pathway.

FDA; Center for Drug Evaluation and Research; Label Information for Azilect (Rasagiline) (Last updated May 2006). Available from, as of February 20, 2009: https://www.fda.gov/cder/foi/label/2006/021641lbl.pdf


5.7 Biological Half-Life

Rasagiline has a mean steady-state half life of 3 hours but there is no correlation of pharmacokinetics with its pharmacological effect because of its irreversible inhibition of MAO-B.


Rasagiline's mean steady-state half life is 3 hours ... .

FDA; Center for Drug Evaluation and Research; Label Information for Azilect (Rasagiline) (Last updated May 2006). Available from, as of February 20, 2009: https://www.fda.gov/cder/foi/label/2006/021641lbl.pdf


Rasagiline is eliminated with a half life of about 0.6 - 2 hours and ranging from 0.3 to 3.5 hours across the 0.5 to 20 mg dose range examined following oral administration.

European Medicines Agency (EMEA), The European Agency for the Evaluation of Medicinal Products, European Public Assessment Report (EPAR) for Authorized Medicinal Products for Human Use; Azilect, Scientific Discussion (2005). Available from, as of February 25, 2009: https://www.emea.europa.eu/humandocs/PDFs/EPAR/Azilect/5289705en6.pdf


5.8 Mechanism of Action

The precise mechanisms of action of rasagiline is unknown. One mechanism is believed to be related to its MAO-B inhibitory activity, which causes an increase in extracellular levels of dopamine in the striatum. The elevated dopamine level and subsequent increased dopaminergic activity are likely to mediate rasagiline's beneficial effects seen in models of dopaminergic motor dysfunction.


The anti-Parkinson drug rasagiline (Azilect), an irreversible and selective monoamine oxidase (MAO)-B inhibitor, was shown to possess neuroprotective activities, involving multiple survival pathways among them the up-regulation of protein kinase C (PKC)alpha, PKCepsilon, the anti-apoptotic Bcl-2, Bcl-xL, and Bcl-w and the induction of brain-derived- and glial cell line-derived neurotrophic factors (BDNF, GDNF). More recently, employing conventional neurochemical techniques, as well as transcriptomic and proteomic screening tools, combined with a biology-based clustering method, it was shown that rasagiline also possesses neurorescue/neurogenesis activity in mice midbrain dopaminergic neurons when given chronically, post-MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). This action was attributed to the activation of cell signaling mediators associated with neurotrophic factors responsive-tyrosine kinase receptor (Trk) pathway, including ShcC, SOS, AF6, Rin1, and Ras and the increase in the Trk-downstream effecter phosphatidylinositol 3 kinase (PI3K) protein and its substrate, Akt/PKB. ...

PMID:17701352 Mandel SA et al; Neurochem Res 32 (10): 1694-9 (2007)


The anti-Parkinson's disease drug rasagiline, the anti-Alzheimer's disease drug ladostigil, and their propargyl moiety, propargylamine, enhanced the expression levels of brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor, endogenous neurotrophic factors associated with activation of phosphatidylinositol 3-kinase, protein kinase, and mitogen-activated protein kinase cell signaling/survival pathways. ...

PMID:18077571 Weinreb O et al; Ann N Y Acad Sci 1122: 155-68 (2007)


Rasagiline mesylate, a propargylamine, is an irreversible monoamine oxidase-B (MAO-B) inhibitor. MAO is a mitochondrial enzyme that regulates the metabolic degradation of catecholamines and serotonin in the CNS and peripheral tissues. There appear to be at least 2 isoforms of MAO, MAO-A and MAO-B, which differ in localization and substrate specificity. MAO-A, predominantly found in the GI tract and liver, regulates the metabolic degradation of circulating catecholamines and dietary amines (e.g., tyramine). MAO-B, predominantly found in the brain, regulates the metabolic degradation of dopamine and phenylethylamine. Inhibition of MAO-A in the periphery results in systemic absorption of dietary amines (e.g., tyramine), which, in substantial amounts, can cause release of norepinephrine and subsequent substantial increases in blood pressure. Inhibition of MAO-B results in increased extracellular concentrations of dopamine and, therefore, enhanced dopaminergic activity in the striatum. While the precise mechanisms of activity of rasagiline have not been fully characterized, data from ex vivo animal studies indicate that the drug potently and irreversibly inhibits MAO-B in brain, liver, and intestinal tissues; the selectivity of rasagiline in inhibiting MAO-B (and not MAO-A) in humans has not been fully elucidated to avoid restriction of dietary tyramine and sympathomimetic amines.

American Society of Health System Pharmacists; AHFS Drug Information 2009. Bethesda, MD. (2009), p. 2698


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