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Identification
NameRasagiline
Accession NumberDB01367  (EXPT02758)
TypeSmall Molecule
GroupsApproved
Description

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.

Structure
Thumb
Synonyms
SynonymLanguageCode
(1R)-N-Propargylindan-1-amineNot AvailableNot Available
(R)-Indan-1-yl-prop-2-ynyl-amineNot AvailableNot Available
(R)-N-2-Propynyl-1-indanamineNot AvailableNot Available
RASNot AvailableNot Available
Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Azilecttablet1 mgoralPhysicians Total Care, Inc.2010-12-03Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Azilecttablet.5 mgoralTeva Neuroscience, Inc.2006-07-10Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Azilecttablet1 mgoralTeva Neuroscience, Inc.2006-07-10Not AvailableUs 0a2ef1ad1c84951dc1392a8bbe1f3cb241c91ed59e44ad8268635315440d978c
Azilecttablet0.5 mgoralTeva Pharmaceutical Industries LtdNot AvailableNot AvailableCanada 5f16b84899037e23705f146ff57e3794121879cb055f0954756d94bc690476b4
Azilecttablet1.0 mgoralTeva Pharmaceutical Industries LtdNot AvailableNot AvailableCanada 5f16b84899037e23705f146ff57e3794121879cb055f0954756d94bc690476b4
Generic Prescription ProductsNot Available
Over the Counter ProductsNot Available
International BrandsNot Available
Brand mixturesNot Available
SaltsNot Available
Categories
CAS number136236-51-6
WeightAverage: 171.2383
Monoisotopic: 171.104799421
Chemical FormulaC12H13N
InChI KeyRUOKEQAAGRXIBM-GFCCVEGCSA-N
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
IUPAC Name
(1R)-N-(prop-2-yn-1-yl)-2,3-dihydro-1H-inden-1-amine
SMILES
C#CCN[C@@H]1CCC2=CC=CC=C12
Taxonomy
DescriptionThis compound belongs to the class of organic compounds known as indanes. These are compounds containing an indane moiety, which consists of a cyclopentane fused to a benzene ring.
KingdomOrganic compounds
Super ClassBenzenoids
ClassIndanes
Sub ClassNot Available
Direct ParentIndanes
Alternative Parents
Substituents
  • Indane
  • Aralkylamine
  • Secondary amine
  • Secondary aliphatic amine
  • Hydrocarbon derivative
  • Organonitrogen compound
  • Amine
  • Aromatic homopolycyclic compound
Molecular FrameworkAromatic homopolycyclic compounds
External Descriptors
Pharmacology
IndicationFor the treatment of the signs and symptoms of idiopathic Parkinsons disease as initial monotherapy and as adjunct therapy to levodopa.
PharmacodynamicsRasagiline 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.
Mechanism of actionThe 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.
AbsorptionRasagiline is rapidly absorbed following oral administration. The absolute bioavailability of rasagiline is about 36%.
Volume of distribution
  • 87 L
Protein bindingPlasma protein binding ranges from 88-94% with mean extent of binding of 61-63% to human albumin over the concentration range of 1-100 ng/ml.
Metabolism

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.

Route of eliminationRasagiline 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.
Half lifeRasagiline 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.
ClearanceNot Available
ToxicitySigns and symptoms of overdosage may include, alone or in combination, any of the following: drowsiness, dizziness, faintness, irritability, hyperactivity, agitation, severe headache, hallucinations, trismus, opisthotonos, convulsions, and coma; rapid and irregular pulse, hypertension, hypotension and vascular collapse; precordial pain, respiratory depression and failure, hyperpyrexia, diaphoresis, and cool, clammy skin.
Affected organisms
  • Humans and other mammals
PathwaysNot Available
SNP Mediated EffectsNot Available
SNP Mediated Adverse Drug ReactionsNot Available
ADMET
Predicted ADMET features
PropertyValueProbability
Human Intestinal Absorption+0.9901
Blood Brain Barrier+0.9782
Caco-2 permeable+0.5585
P-glycoprotein substrateNon-substrate0.661
P-glycoprotein inhibitor INon-inhibitor0.7409
P-glycoprotein inhibitor IINon-inhibitor0.7116
Renal organic cation transporterNon-inhibitor0.5584
CYP450 2C9 substrateNon-substrate0.8037
CYP450 2D6 substrateSubstrate0.5724
CYP450 3A4 substrateNon-substrate0.6928
CYP450 1A2 substrateInhibitor0.9037
CYP450 2C9 substrateNon-inhibitor0.8259
CYP450 2D6 substrateInhibitor0.6769
CYP450 2C19 substrateInhibitor0.5689
CYP450 3A4 substrateNon-inhibitor0.8542
CYP450 inhibitory promiscuityHigh CYP Inhibitory Promiscuity0.534
Ames testNon AMES toxic0.6468
CarcinogenicityNon-carcinogens0.8959
BiodegradationNot ready biodegradable0.6073
Rat acute toxicity2.8164 LD50, mol/kg Not applicable
hERG inhibition (predictor I)Weak inhibitor0.7804
hERG inhibition (predictor II)Non-inhibitor0.7137
Pharmacoeconomics
ManufacturersNot Available
Packagers
Dosage forms
FormRouteStrength
Tabletoral.5 mg
Tabletoral0.5 mg
Tabletoral1 mg
Tabletoral1.0 mg
Prices
Unit descriptionCostUnit
Azilect 0.5 mg tablet12.11USD tablet
Azilect 1 mg tablet12.11USD tablet
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
Patents
CountryPatent NumberApprovedExpires (estimated)
Canada20317141998-08-252010-12-06
Canada22323102008-01-082016-09-18
United States53876121995-02-072012-02-07
United States75728342006-12-052026-12-05
Properties
StateSolid
Experimental PropertiesNot Available
Predicted Properties
PropertyValueSource
Water Solubility0.0249 mg/mLALOGPS
logP2.26ALOGPS
logP2.3ChemAxon
logS-3.8ALOGPS
pKa (Strongest Basic)8.69ChemAxon
Physiological Charge1ChemAxon
Hydrogen Acceptor Count1ChemAxon
Hydrogen Donor Count1ChemAxon
Polar Surface Area12.03 Å2ChemAxon
Rotatable Bond Count2ChemAxon
Refractivity54.47 m3·mol-1ChemAxon
Polarizability20.25 Å3ChemAxon
Number of Rings2ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Mass Spec (NIST)Not Available
SpectraNot Available
References
Synthesis Reference

Jeffrey Sterling, David Lerner, Harel Rosen, Leonid Bronov, Dalia Medini-Green, Berta Iosefzon, Tirtsah Berger-Peskin, Ramy Lidor-Hadas, Eliezer Bahar, “Rasagiline formulations and processes for their preparation.” U.S. Patent US07598420, issued October 06, 2009.

US07598420
General Reference
  1. Weinreb O, Amit T, Bar-Am O, Youdim MB: RASAGILINE; A NOVEL ANTI-PARKINSONIAN MONOAMINE OXIDASE-B INHIBITOR WITH NEUROPROTECTIVE ACTIVITY. Prog Neurobiol. 2010 Jun 19. Pubmed
  2. Leegwater-Kim J, Bortan E: The role of rasagiline in the treatment of Parkinson’s disease. Clin Interv Aging. 2010 May 25;5:149-56. Pubmed
  3. Chen JJ, Swope DM, Dashtipour K: Comprehensive review of rasagiline, a second-generation monoamine oxidase inhibitor, for the treatment of Parkinson’s disease. Clin Ther. 2007 Sep;29(9):1825-49. Pubmed
External Links
ATC CodesN04BD02
AHFS Codes
  • 28:92.00
PDB Entries
FDA labelDownload (200 KB)
MSDSNot Available
Interactions
Drug Interactions
Drug
AcepromazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
AcetophenazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
AltretamineMay enhance the orthostatic hypotensive effect of MAO Inhibitors.
AmisulprideSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
AmphetamineMAO Inhibitors may enhance the hypertensive effect of Amphetamines. While linezolid and tedizolid may interact via this mechanism, management recommendations differ from other monoamine oxidase inhibitors. Refer to monographs specific to those agents for details.
ApraclonidineMAO Inhibitors may enhance the adverse/toxic effect of Apraclonidine. MAO Inhibitors may increase the serum concentration of Apraclonidine.
AripiprazoleSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
AtomoxetineMAO Inhibitors may enhance the neurotoxic (central) effect of AtoMOXetine.
BenzquinamideSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
BetahistineMAO Inhibitors may increase the serum concentration of Betahistine.
BezafibrateMAO Inhibitors may enhance the adverse/toxic effect of Bezafibrate.
BuprenorphineMay enhance the adverse/toxic effect of MAO Inhibitors.
BupropionMAO Inhibitors may enhance the hypertensive effect of BuPROPion.
BuspironeMay enhance the adverse/toxic effect of MAO Inhibitors. Specifically, blood pressure elevations been reported.
CarbamazepineMay enhance the adverse/toxic effect of MAO Inhibitors.
CarphenazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
CathinoneMAO Inhibitors may enhance the hypertensive effect of Amphetamines. While linezolid and tedizolid may interact via this mechanism, management recommendations differ from other monoamine oxidase inhibitors. Refer to monographs specific to those agents for details.
ChlormezanoneSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
ChlorpromazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
ChlorprothixeneSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
ClozapineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
CyclobenzaprineMay enhance the serotonergic effect of MAO Inhibitors. This could result in serotonin syndrome.
CyproheptadineMAO Inhibitors may enhance the anticholinergic effect of Cyproheptadine. Cyproheptadine may diminish the serotonergic effect of MAO Inhibitors.
DapoxetineMay enhance the adverse/toxic effect of Serotonin Modulators.
DeferasiroxMay increase the serum concentration of CYP1A2 Substrates.
DexmethylphenidateMAO Inhibitors may enhance the hypertensive effect of Dexmethylphenidate.
DextromethorphanMAO Inhibitors may enhance the serotonergic effect of Dextromethorphan. This may cause serotonin syndrome.
DiethylpropionMAO Inhibitors may enhance the hypertensive effect of Diethylpropion.
DomperidoneMAO Inhibitors may enhance the adverse/toxic effect of Domperidone. MAO Inhibitors may diminish the therapeutic effect of Domperidone. Domperidone may diminish the therapeutic effect of MAO Inhibitors.
DoxapramMAO Inhibitors may enhance the hypertensive effect of Doxapram.
DoxylamineMAO Inhibitors may enhance the anticholinergic effect of Doxylamine.
DroperidolSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
FencamfamineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
FlupentixolSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
FluphenazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
FluspirileneSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
HaloperidolSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
HydrocodoneMAO Inhibitors may enhance the adverse/toxic effect of Hydrocodone.
HydromorphoneMAO Inhibitors may enhance the adverse/toxic effect of HYDROmorphone.
IsomethepteneMAO Inhibitors may enhance the adverse/toxic effect of Isometheptene.
LevonordefrinMAO Inhibitors may enhance the hypertensive effect of Levonordefrin.
LinezolidMAO Inhibitors may enhance the adverse/toxic effect of Linezolid.
LithiumMAO Inhibitors may enhance the adverse/toxic effect of Lithium.
LoxapineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
MaprotilineMay enhance the adverse/toxic effect of MAO Inhibitors.
MequitazineMAO Inhibitors may enhance the anticholinergic effect of Mequitazine.
MesoridazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
MethadoneMAO Inhibitors may enhance the adverse/toxic effect of Methadone.
MethotrimeprazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
MethyldopaMAO Inhibitors may enhance the adverse/toxic effect of Methyldopa.
MethylphenidateMAO Inhibitors may enhance the hypertensive effect of Methylphenidate.
MetoclopramideSerotonin Modulators may enhance the adverse/toxic effect of Metoclopramide. This may be manifest as symptoms consistent with serotonin syndrome or neuroleptic malignant syndrome.
MexiletineCYP1A2 Inhibitors (Strong) may increase the serum concentration of Rasagiline.
MianserinMAO Inhibitors may enhance the neurotoxic effect of Mianserin.
MirtazapineMAO Inhibitors may enhance the neurotoxic (central) effect of Mirtazapine. While methylene blue and linezolid are expected to interact, specific recommendations for their use differ from other monoamine oxidase inhibitors. Refer to monographs specific to those agents for details.
MolindoneSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
NorepinephrineMAO Inhibitors may enhance the hypertensive effect of Norepinephrine.
OlanzapineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
OndansetronSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
OxycodoneMAO Inhibitors may enhance the adverse/toxic effect of OxyCODONE.
OxymorphoneMay enhance the adverse/toxic effect of MAO Inhibitors.
PaliperidoneSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
Peginterferon alfa-2bMay increase the serum concentration of CYP1A2 Substrates.
PerphenazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
PimozideSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
PiperacetazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
PizotifenMAO Inhibitors may enhance the anticholinergic effect of Pizotifen.
PrimaquineCYP1A2 Inhibitors (Strong) may increase the serum concentration of Rasagiline.
ProchlorperazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
PromazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
QuetiapineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
RemoxiprideSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
ReserpineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
RisperidoneSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
SertindoleSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
SulpirideSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
TapentadolMay enhance the adverse/toxic effect of MAO Inhibitors.
TeriflunomideMay decrease the serum concentration of CYP1A2 Substrates.
TetrabenazineMay enhance the adverse/toxic effect of MAO Inhibitors.
ThioridazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
ThiothixeneSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
TramadolMay enhance the neuroexcitatory and/or seizure-potentiating effect of MAO Inhibitors. TraMADol may enhance the serotonergic effect of MAO Inhibitors.
TrifluoperazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
TriflupromazineSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
VemurafenibMay increase the serum concentration of CYP1A2 Substrates.
ZiprasidoneSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
ZuclopenthixolSerotonin Modulators may enhance the adverse/toxic effect of Antipsychotic Agents. Specifically, serotonin modulators may enhance dopamine blockade, possibly increasing the risk for neuroleptic malignant syndrome. Antipsychotic Agents may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
Food Interactions
  • Avoid alcohol and caffeine.

Targets

1. Amine oxidase [flavin-containing] B

Kind: protein

Organism: Human

Pharmacological action: yes

Actions: inhibitor

Components

Name UniProt ID Details
Amine oxidase [flavin-containing] B P27338 Details

References:

  1. Naoi M, Maruyama W: Functional mechanism of neuroprotection by inhibitors of type B monoamine oxidase in Parkinson’s disease. Expert Rev Neurother. 2009 Aug;9(8):1233-50. Pubmed
  2. Uzun M, Alp R, Uzlu E, Alp S, Citil M, Topcu B, Erdogan HM: Investigation of oral selegiline and rasagiline administration on QT interval in conscious rabbits. Eur Rev Med Pharmacol Sci. 2009 Mar-Apr;13(2):95-8. Pubmed
  3. Youdim MB, Weinstock M: Molecular basis of neuroprotective activities of rasagiline and the anti-Alzheimer drug TV3326 [(N-propargyl-(3R)aminoindan-5-YL)-ethyl methyl carbamate]. Cell Mol Neurobiol. 2001 Dec;21(6):555-73. Pubmed
  4. Chau KY, Cooper JM, Schapira AH: Rasagiline protects against alpha-synuclein induced sensitivity to oxidative stress in dopaminergic cells. Neurochem Int. 2010 Jul 17. Pubmed
  5. Weinreb O, Amit T, Bar-Am O, Youdim MB: RASAGILINE; A NOVEL ANTI-PARKINSONIAN MONOAMINE OXIDASE-B INHIBITOR WITH NEUROPROTECTIVE ACTIVITY. Prog Neurobiol. 2010 Jun 19. Pubmed
  6. Youdim MB, Bar Am O, Yogev-Falach M, Weinreb O, Maruyama W, Naoi M, Amit T: Rasagiline: neurodegeneration, neuroprotection, and mitochondrial permeability transition. J Neurosci Res. 2005 Jan 1-15;79(1-2):172-9. Pubmed
  7. Leegwater-Kim J, Bortan E: The role of rasagiline in the treatment of Parkinson’s disease. Clin Interv Aging. 2010 May 25;5:149-56. Pubmed
  8. Chen JJ, Swope DM, Dashtipour K: Comprehensive review of rasagiline, a second-generation monoamine oxidase inhibitor, for the treatment of Parkinson’s disease. Clin Ther. 2007 Sep;29(9):1825-49. Pubmed
  9. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed

2. Apoptosis regulator Bcl-2

Kind: protein

Organism: Human

Pharmacological action: yes

Actions: activator

Components

Name UniProt ID Details
Apoptosis regulator Bcl-2 P10415 Details

References:

  1. Youdim MB, Weinstock M: Molecular basis of neuroprotective activities of rasagiline and the anti-Alzheimer drug TV3326 [(N-propargyl-(3R)aminoindan-5-YL)-ethyl methyl carbamate]. Cell Mol Neurobiol. 2001 Dec;21(6):555-73. Pubmed
  2. Akao Y, Maruyama W, Yi H, Shamoto-Nagai M, Youdim MB, Naoi M: An anti-Parkinson’s disease drug, N-propargyl-1®-aminoindan (rasagiline), enhances expression of anti-apoptotic bcl-2 in human dopaminergic SH-SY5Y cells. Neurosci Lett. 2002 Jun 28;326(2):105-8. Pubmed
  3. Maruyama W, Akao Y, Carrillo MC, Kitani K, Youdium MB, Naoi M: Neuroprotection by propargylamines in Parkinson’s disease: suppression of apoptosis and induction of prosurvival genes. Neurotoxicol Teratol. 2002 Sep-Oct;24(5):675-82. Pubmed
  4. Youdim MB, Amit T, Falach-Yogev M, Am OB, Maruyama W, Naoi M: The essentiality of Bcl-2, PKC and proteasome-ubiquitin complex activations in the neuroprotective-antiapoptotic action of the anti-Parkinson drug, rasagiline. Biochem Pharmacol. 2003 Oct 15;66(8):1635-41. Pubmed
  5. Bar-Am O, Weinreb O, Amit T, Youdim MB: Regulation of Bcl-2 family proteins, neurotrophic factors, and APP processing in the neurorescue activity of propargylamine. FASEB J. 2005 Nov;19(13):1899-901. Epub 2005 Sep 7. Pubmed

Enzymes

1. Cytochrome P450 1A2

Kind: protein

Organism: Human

Pharmacological action: unknown

Actions: substrate

Components

Name UniProt ID Details
Cytochrome P450 1A2 P05177 Details

References:

  1. Lecht S, Haroutiunian S, Hoffman A, Lazarovici P: Rasagiline – a novel MAO B inhibitor in Parkinson’s disease therapy. Ther Clin Risk Manag. 2007 Jun;3(3):467-74. Pubmed
  2. Leegwater-Kim J, Bortan E: The role of rasagiline in the treatment of Parkinson’s disease. Clin Interv Aging. 2010 May 25;5:149-56. Pubmed
  3. Chen JJ, Swope DM, Dashtipour K: Comprehensive review of rasagiline, a second-generation monoamine oxidase inhibitor, for the treatment of Parkinson’s disease. Clin Ther. 2007 Sep;29(9):1825-49. Pubmed
  4. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. Epub 2009 Nov 24. Pubmed

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Drug created on June 13, 2005 07:24 / Updated on September 16, 2013 17:14