Rasagiline - Indications, Dosages, side effects

Rasagiline is a potent, selective, and irreversible inhibitor of MAO type B. It confers neuroprotective, anti-apoptotic, and anti-oxidant effects that delay the progression of neuronal degeneration.

It is used for the treatment of Parkinson disease

Rasagiline Dose in Adults

Dosage in the treatment of Parkinson disease:

Monotherapy or adjunctive therapy (not including levodopa):
- 1 mg once daily is given
- the maximum dose is 1 mg once daily
Adjunctive therapy with levodopa:
- The initial dose is 0.5 mg once daily
- It can be increased to 1 mg once daily based on response and tolerability
- The maximum dose is 1 mg once daily
When added to existing levodopa therapy, a dose reduction of levodopa might be required to avoid exacerbation of dyskinesias
Dose reduction with concomitant ciprofloxacin or other CYP1A2 inhibitors:
- The maximum dose is 0.5 mg once daily

Rasagiline Dose in Childrens

Not recommended for use in Children.

Rasagiline pregnancy Risk Factor: C

Animal reproduction studies have shown adverse effects.
Limited data are available on rasagiline usage during pregnancy.

Use of Rasagiline during lactation

It is unknown if rasagiline can be found in breast milk.
According to the manufacturer the decision to breastfeed while on therapy should consider the risks to infants, the benefits to breastfeeding to infants, and the benefits to mother during treatment.

Rasagiline Dose in Kidney Disease:

US Labeling
- Mild to moderate impairment
  - There is no need to adjust the dosage.
- Severe impairment
  - The manufacturer's labeling does not include any dosage adjustments.
Canadian labeling
- Mild impairment
  - There is no need to adjust the dosage.
- Moderate to severe impairment
  - It is not recommended to use

Rasagiline Dose in Liver Disease:

Mild impairment (Child–Pugh score 5-6:
- Maximum daily dose is 0.5mg
Moderate to severe impairment (Child Puugh score 7-15)
- It is not recommended.

Common Side Effects of Rasagiline Include:

Cardiovascular:
- Orthostatic Hypotension
- Hypotension
Central Nervous System:
- Headache
Gastrointestinal:
- Nausea
Neuromuscular & Skeletal:
- Dyskinesia
Miscellaneous:
- Trauma

Less Common Side Effects of Rasagiline Include:

Cardiovascular:
- Peripheral Edema
- Increased Blood Pressure
- Angina
- Bundle Branch Block
- Chest Pain
Central Nervous System:
- Dizziness
- Drowsiness
- Ataxia
- Depression
- Falling
- Abnormal Dreams
- Dystonia
- Malaise
- Paresthesia
- Insomnia
- Hallucinations
- Myasthenia
- Vertigo
- Anxiety
Dermatologic:
- Skin Rash
- Ecchymosis
- Diaphoresis
- Alopecia
- Skin Carcinoma
- Vesiculobullous Rash
Endocrine & Metabolic:
- Weight Loss
- Impotence
- Libido Decreased
Gastrointestinal:
- Constipation
- Dyspepsia
- Diarrhea
- Vomiting
- Xerostomia
- Abdominal Pain
- Anorexia
- Gastroenteritis
- Gingivitis
- Hernia
- Gastrointestinal Hemorrhage
Genitourinary:
- Hematuria
- Urinary Incontinence
Hematologic And Oncologic:
- Hemorrhage
- Leukopenia
Hepatic:
- Liver Function Tests Increased
Infection:
- Infection
Neuromuscular & Skeletal:
- Arthralgia
- Back Pain
- Neck Pain
- Tenosynovitis
- Arthritis
- Abnormal gait
- Hyperkinesias
- Hypertonia
- Neuropathy
- Weakness
Ophthalmic:
- Conjunctivitis
Renal:
- Albuminuria
Respiratory:
- Flu-Like Symptoms
- Dyspnea
- Cough
- Upper Respiratory Tract Infection
- Rhinitis
- Asthma
Miscellaneous:
- Fever
- Allergic Reaction

Contraindication to Rasagiline Include:

Use of an MAO inhibitor, including selective MAO-B inhibitors, in conjunction with MAO.
meperidine
Methadone
propoxyphene
Tramadol within 14 Days of rasagiline
Concomitant use of cyclobenzaprine or dextromethorphan with St John's wort

Warnings and precautions

CNS effects
- You may experience a change in your mental state or behavior.
- There have been instances of intense urges to gamble, spend money, binge-eating, increased sexual urges and/or inability to control such urges.
- These signs should be monitored.
- Consider reducing or stopping therapy if symptoms develop.
Dyskinesia
- When used in conjunction with levodopa, dysskinesia can occur.
- Side effects may be lessened by decreasing the dosage of levodopa.
Hypertension
- It can lead to hypertension exacerbation. Monitor for hypertension new-onset or not properly controlled after taking the drug.
- If blood pressure is high, medication adjustment may be necessary.
Melanoma
- Rasagaline can increase the risk of melanoma, but this has also been linked to Parkinson's disease.
- Patients should undergo regular, frequent skin examinations.
Orthostatic hypotension
- Orthostatic hypotension can be caused by it, especially when combined with levodopa.
- Orthostatic hypotension is most common in the first two months of therapy, but it decreases as time goes by.
Serotonin syndrome/neuroleptic malignant Syndrome-like Reactions:
- Serotonin syndrome (SS), can be caused by concurrent antidepressant use (eg, SSRI/SNRI/TCA, tetracyclic, triazolopyridine antidepressants).
- Concomitant use of rasagiline is not recommended within two weeks (within five weeks for antidepressants such as fluoxetine).
- Concomitant MAO inhibitors, including selective MAO-B inhibitors, meperidine, methadone and propoxyphene have been linked to SS. However, concomitant rasagiline administration within two weeks is contraindicated.
- In association with rapid dose reductions, withdrawals, or modifications to drugs that could increase central dopaminergic tone, a symptom complex similar to neuroleptic malignant (NMS), has been observed.
- It is difficult to distinguish between SS (eg. tremors, myoclonus and agitation) as well as more severe NMS-like reactions such hyperthermia and muscle rigidity. Patients should be closely monitored for either of these syndromes.
- The Hunter Serotonin Toxicity Criteria can be used to diagnose SS.
- If you notice any signs or symptoms, stop taking antidepressants and all concomitant medications immediately.
Somnolence
- It has happened to me that I have experienced somnolence or fallen asleep while doing daily activities (including driving motor vehicles).
- Sometimes symptoms can appear as soon as treatment is initiated. Some events may occur up to one year after rasagiline was started.
- Prior to treatment, consider factors that could increase these risks, such as concomitant use of sedating drugs, sleep disorders, or concomitant medication that increases rasagiline plasma levels (eg ciprofloxacin).
- You should monitor for sleepiness and drowsiness.
- If you experience significant sleepiness during the day or fall asleep episodes, especially while driving or eating, it should be stopped.
- Continue therapy if necessary. Tell the patient not to drive or engage in any other dangerous activity.
Hepatic impairment
- Patients with mild hepatic impairment should be cautious; a reduction in dose is recommended.
- Patients with severe impairments or moderate-to-severe impairment should not use this product.
Psychotic disorders
- Patients with severe psychotic disorders should not use this medication. It can worsen psychosis by increasing central dopaminergic tone.
- Rasagaline's effectiveness can be affected by many psychosis treatments that reduce central dopaminergic tone.

Rasagilinesv: Drug Interaction

Risk Factor C (Monitor therapy)
Abiraterone Acetate	May increase the serum concentration of CYP1A2 Substrates (High risk with Inhibitors).
Alfuzosin	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Altretamine	May enhance the orthostatic hypotensive effect of Monoamine Oxidase Inhibitors.
Amifampridine	Agents With Seizure Threshold Lowering Potential may enhance the neuroexcitatory and/or seizure-potentiating effect of Amifampridine.
Antiemetics (5HT3 Antagonists)	May enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
Antipsychotic Agents	Serotonin 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.
Antipsychotic Agents (Second Generation [Atypical])	Blood Pressure Lowering Agents may enhance the hypotensive effect of Antipsychotic Agents (Second Generation [Atypical]).
Barbiturates	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Benperidol	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Beta2-Agonists	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Beta2Agonists.
Betahistine	Monoamine Oxidase Inhibitors may increase the serum concentration of Betahistine.
Blood Glucose Lowering Agents	Monoamine Oxidase Inhibitors may enhance the hypoglycemic effect of Blood Glucose Lowering Agents.
Blood Pressure Lowering Agents	May enhance the hypotensive effect of HypotensionAssociated Agents.
Brimonidine (Ophthalmic)	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Brimonidine (Ophthalmic). Monoamine Oxidase Inhibitors may increase the serum concentration of Brimonidine (Ophthalmic).
Brimonidine (Topical)	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Brimonidine (Topical). Monoamine Oxidase Inhibitors may increase the serum concentration of Brimonidine (Topical).
Brimonidine (Topical)	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Broccoli	May decrease the serum concentration of CYP1A2 Substrates (High risk with Inducers).
Cannabis	May decrease the serum concentration of CYP1A2 Substrates (High risk with Inducers).
Cerebrolysin	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors.
Chlorphenesin Carbamate	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors.
Codeine	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Codeine.
CYP1A2 Inducers (Moderate)	May decrease the serum concentration of CYP1A2 Substrates (High risk with Inducers).
Cyproterone	May decrease the serum concentration of CYP1A2 Substrates (High risk with Inducers).
Diazoxide	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Dihydrocodeine	May enhance the serotonergic effect of Monoamine Oxidase Inhibitors. This could result in serotonin syndrome.
Domperidone	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Domperidone. Monoamine Oxidase Inhibitors may diminish the therapeutic effect of Domperidone. Domperidone may diminish the therapeutic effect of Monoamine Oxidase Inhibitors.
Doxapram	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of Doxapram.
EPINEPHrine (Nasal)	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of EPINEPHrine (Nasal).
Epinephrine (Racemic)	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of Epinephrine (Racemic).
EPINEPHrine (Systemic)	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of EPINEPHrine (Systemic).
Esketamine	May enhance the hypertensive effect of Monoamine Oxidase Inhibitors.
Herbs (Hypotensive Properties)	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Hypotension-Associated Agents	Blood Pressure Lowering Agents may enhance the hypotensive effect of Hypotension-Associated Agents.
Lormetazepam	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Metaraminol	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of Metaraminol.
Metaxalone	May enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
Metoclopramide	Serotonin Modulators may enhance the adverse/toxic effect of Metoclopramide. This may be manifest as symptoms consistent with serotonin syndrome or neuroleptic malignant syndrome.
Molsidomine	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Naftopidil	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Nicergoline	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Nicorandil	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Nitroprusside	Blood Pressure Lowering Agents may enhance the hypotensive effect of Nitroprusside.
Norepinephrine	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of Norepinephrine.
Obeticholic Acid	May increase the serum concentration of CYP1A2 Substrates (High risk with Inhibitors).
Opioid Agonists	May enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
Peginterferon Alfa-2b	May increase the serum concentration of CYP1A2 Substrates (High risk with Inhibitors).
Pentoxifylline	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Phosphodiesterase 5 Inhibitors	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Pipamperone [INT]	May diminish the therapeutic effect of Anti-Parkinson Agents (Monoamine Oxidase Inhibitor). Anti-Parkinson Agents (Monoamine Oxidase Inhibitor) may diminish the therapeutic effect of Pipamperone [INT].
Prostacyclin Analogues	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Quinagolide	May enhance the hypotensive effect of Blood Pressure Lowering Agents.
Teriflunomide	May decrease the serum concentration of CYP1A2 Substrates (High risk with Inducers).
Risk Factor D (Consider therapy modification)
Amifostine	Blood Pressure Lowering Agents may enhance the hypotensive effect of Amifostine. Management: When amifostine is used at chemotherapy doses, blood pressure lowering medications should be withheld for 24 hours prior to amifostine administration. If blood pressure lowering therapy cannot be withheld, amifostine should not be administered.
Benzhydrocodone	May enhance the serotonergic effect of Monoamine Oxidase Inhibitors. This could result in serotonin syndrome. Management: The use of benzhydrocodone is not recommended for patients taking monoamine oxidase inhibitors (MAOIs) or within 14 days of MAOI discontinuation.
COMT Inhibitors	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors.
CYP1A2 Inhibitors (Moderate)	May increase the serum concentration of Rasagiline. Management: Limit rasagiline dose to 0.5 mg once daily in patients taking moderate CYP1A2 inhibitors.
DOPamine	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of DOPamine. Management: Initiate dopamine at no greater than one-tenth (1/10) of the usual dose in patients who are taking (or have taken within the last 2 to 3 weeks) monoamine oxidase inhibitors. Monitor for an exaggerated hypertensive response to dopamine.
HYDROcodone	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of HYDROcodone. Management: Consider alternatives to this combination when possible.
Iohexol	Agents With Seizure Threshold Lowering Potential may enhance the adverse/toxic effect of Iohexol. Specifically, the risk for seizures may be increased. Management: Discontinue agents that may lower the seizure threshold 48 hours prior to intrathecal use of iohexol. Wait at least 24 hours after the procedure to resume such agents. In nonelective procedures, consider use of prophylactic anticonvulsants.
Iomeprol	Agents With Seizure Threshold Lowering Potential may enhance the adverse/toxic effect of Iomeprol. Specifically, the risk for seizures may be increased. Management: Discontinue agents that may lower the seizure threshold 48 hours prior to intrathecal use of iomeprol. Wait at least 24 hours after the procedure to resume such agents. In nonelective procedures, consider use of prophylactic anticonvulsants.
Iopamidol	Agents With Seizure Threshold Lowering Potential may enhance the adverse/toxic effect of Iopamidol. Specifically, the risk for seizures may be increased. Management: Discontinue agents that may lower the seizure threshold 48 hours prior to intrathecal use of iopamidol. Wait at least 24 hours after the procedure to resume such agents. In nonelective procedures, consider use of prophylactic anticonvulsants.
Levodopa-Containing Products	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors. Of particular concern is the development of hypertensive reactions when levodopa is used with nonselective MAOI. Management: The concomitant use of nonselective monoamine oxidase inhibitors (MAOIs) and levodopa is contraindicated. Discontinue the nonselective MAOI at least two weeks prior to initiating levodopa. Monitor patients taking a selective MAOIs and levodopa.
Lithium	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Lithium. Management: This combination should be undertaken with great caution. When combined treatment is clinically indicated, monitor closely for signs of serotonin toxicity/serotonin syndrome.
Obinutuzumab	May enhance the hypotensive effect of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion.
OxyCODONE	May enhance the serotonergic effect of Monoamine Oxidase Inhibitors. This could result in serotonin syndrome. Management: Seek alternatives when possible. Avoid use of oxycodone/naltrexone during and within 14 days after monoamine oxidase inhibitor treatment. Non-US labeling for some oxycodone products states that such use is contraindicated.
Pindolol	Monoamine Oxidase Inhibitors may enhance the hypotensive effect of Pindolol. Management: Canadian labeling for pindolol states that concurrent use with a monoamine oxidase inhibitor is not recommended.
Reserpine	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Reserpine. Existing MAOI therapy can result in paradoxical effects of added reserpine (e.g., excitation, hypertension). Management: Monoamine oxidase inhibitors (MAOIs) should be avoided or used with great caution in patients who are also receiving reserpine.
Serotonin Modulators	Anti-Parkinson Agents (Monoamine Oxidase Inhibitor) may enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome. Management: Monitor for signs and symptoms of serotonin syndrome/serotonin toxicity if selegiline, rasagiline, or safinamide is combined with a serotonin modulator. Use of transdermal selegiline with serotonin modulators is contraindicated. Exceptions: Nicergoline.
Vemurafenib	May increase the serum concentration of CYP1A2 Substrates (High risk with Inhibitors). Management: Consider alternatives to such combinations whenever possible, particularly if the CYP1A2 substrate has a relatively narrow therapeutic index. Drugs listed as exceptions to this monograph are discussed in separate drug interaction monographs.
Risk Factor X (Avoid combination)
Alcohol (Ethyl)	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors.
Alpha-/Beta-Agonists (Indirect-Acting)	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of Alpha-/Beta-Agonists (Indirect-Acting). While linezolid is expected to interact via this mechanism, management recommendations differ from other monoamine oxidase inhibitors. Refer to linezolid specific monographs for details.
Alpha1-Agonists	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of Alpha1Agonists. While linezolid is expected to interact via this mechanism, management recommendations differ from other monoamine oxidase inhibitors. Refer to linezolid specific monographs for details.
Amphetamines	Monoamine Oxidase 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.
Apraclonidine	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Apraclonidine. Monoamine Oxidase Inhibitors may increase the serum concentration of Apraclonidine.
AtoMOXetine	Monoamine Oxidase Inhibitors may enhance the neurotoxic (central) effect of AtoMOXetine.
Atropine (Ophthalmic)	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of Atropine (Ophthalmic).
Bezafibrate	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Bezafibrate.
Bromperidol	Blood Pressure Lowering Agents may enhance the hypotensive effect of Bromperidol. Bromperidol may diminish the hypotensive effect of Blood Pressure Lowering Agents.
Buprenorphine	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors.
BuPROPion	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of BuPROPion.
BusPIRone	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors. Specifically, blood pressure elevations been reported.
CarBAMazepine	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors. Management: Avoid concurrent use of carbamazepine during, or within 14 days of discontinuing, treatment with a monoamine oxidase inhibitor.
Cyclobenzaprine	May enhance the serotonergic effect of Monoamine Oxidase Inhibitors. This could result in serotonin syndrome.
Cyproheptadine	Monoamine Oxidase Inhibitors may enhance the anticholinergic effect of Cyproheptadine. Cyproheptadine may diminish the serotonergic effect of Monoamine Oxidase Inhibitors.
Dapoxetine	May enhance the adverse/toxic effect of Serotonin Modulators.
Deutetrabenazine	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Deutetrabenazine.
Dexmethylphenidate	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of Dexmethylphenidate.
Dextromethorphan	Monoamine Oxidase Inhibitors may enhance the serotonergic effect of Dextromethorphan. This may cause serotonin syndrome.
Diethylpropion	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of Diethylpropion.
Diphenoxylate	May enhance the hypertensive effect of Monoamine Oxidase Inhibitors.
EPINEPHrine (Oral Inhalation)	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of EPINEPHrine (Oral Inhalation).
FentaNYL	May enhance the serotonergic effect of Monoamine Oxidase Inhibitors. This could result in serotonin syndrome.
Guanethidine	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors.
Heroin	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Heroin.
HYDROmorphone	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of HYDROmorphone.
Indoramin	Monoamine Oxidase Inhibitors may enhance the hypotensive effect of Indoramin.
Iobenguane Radiopharmaceutical Products	Monoamine Oxidase Inhibitors may diminish the therapeutic effect of Iobenguane Radiopharmaceutical Products. Management: Discontinue all drugs that may inhibit or interfere with catecholamine transport or uptake for at least 5 biological half-lives before iobenguane administration. Do not administer these drugs until at least 7 days after each iobenguane dose.
Isometheptene	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Isometheptene.
Levomethadone	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors.
Levonordefrin	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of Levonordefrin.
Linezolid	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Linezolid.
Maprotiline	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors.
Meperidine	Monoamine Oxidase Inhibitors may enhance the serotonergic effect of Meperidine. This may cause serotonin syndrome.
Meptazinol	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Meptazinol.
Mequitazine	Monoamine Oxidase Inhibitors may enhance the anticholinergic effect of Mequitazine.
Methyldopa	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Methyldopa.
Methylene Blue	Monoamine Oxidase Inhibitors may enhance the serotonergic effect of Methylene Blue. This could result in serotonin syndrome.
Methylene Blue	May enhance the serotonergic effect of Serotonin Modulators. This could result in serotonin syndrome.
Methylphenidate	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of Methylphenidate.
Mianserin	Monoamine Oxidase Inhibitors may enhance the neurotoxic effect of Mianserin.
Mirtazapine	Monoamine Oxidase 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.
Moclobemide	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Moclobemide.
Monoamine Oxidase Inhibitors	May enhance the hypertensive effect of other Monoamine Oxidase Inhibitors. Monoamine Oxidase Inhibitors may enhance the serotonergic effect of other Monoamine Oxidase Inhibitors. This could result in serotonin syndrome.
Morphine (Systemic)	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Morphine (Systemic).
Nefopam	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Nefopam.
Opium	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Opium.
OxyMORphone	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors.
Pheniramine	May enhance the anticholinergic effect of Monoamine Oxidase Inhibitors.
Pholcodine	May enhance the serotonergic effect of Monoamine Oxidase Inhibitors. This could result in serotonin syndrome.
Pizotifen	Monoamine Oxidase Inhibitors may enhance the anticholinergic effect of Pizotifen.
Reboxetine	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Reboxetine.
Selective Serotonin Reuptake Inhibitors	Monoamine Oxidase Inhibitors may enhance the serotonergic effect of Selective Serotonin Reuptake Inhibitors. This may cause serotonin syndrome. While methylene blue and linezolid are expected to interact via this mechanism, management recommendations differ from other monoamine oxidase inhibitors. Refer to monographs specific to those agents for details.
Serotonin 5-HT1D Receptor Agonists	Monoamine Oxidase Inhibitors may decrease the metabolism of Serotonin 5-HT1D Receptor Agonists. Management: If MAO inhibitor therapy is required, naratriptan, eletriptan or frovatriptan may be a suitable 5-HT1D agonist to employ. Exceptions: Eletriptan; Frovatriptan; Naratriptan.
Serotonin Reuptake Inhibitor/Antagonists	Monoamine Oxidase Inhibitors may enhance the adverse/toxic effect of Serotonin Reuptake Inhibitor/Antagonists. 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.
Serotonin/Norepinephrine Reuptake Inhibitors	Monoamine Oxidase Inhibitors may enhance the serotonergic effect of Serotonin/Norepinephrine Reuptake Inhibitors. This may cause serotonin syndrome. While methylene blue and linezolid are expected to interact via this mechanism, management recommendations differ from other monoamine oxidase inhibitors. Refer to monographs specific to those agents for details.
Solriamfetol: Monoamine Oxidas	Inhibitors may enhance the hypertensive effect of Solriamfetol.
SUFentanil	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors. Specifically, the risk for serotonin syndrome or opioid toxicities (eg, respiratory depression, coma) may be increased. Management: Sufentanil should not be used with monoamine oxidase (MAO) inhibitors (or within 14 days of stopping an MAO inhibitor) due to the potential for serotonin syndrome and/or excessive CNS depression.
Tapentadol	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors. Specifically, the additive effects of norepinephrine may lead to adverse cardiovascular effects. Tapentadol may enhance the serotonergic effect of Monoamine Oxidase Inhibitors. This could result in serotonin syndrome.
Tetrabenazine	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors.
Tetrahydrozoline (Nasal)	Monoamine Oxidase Inhibitors may enhance the hypertensive effect of Tetrahydrozoline (Nasal).
Tricyclic Antidepressants	Monoamine Oxidase Inhibitors may enhance the serotonergic effect of Tricyclic Antidepressants. This may cause serotonin syndrome. While methylene blue and linezolid are expected to interact via this mechanism, management recommendations differ from other monoamine oxidase inhibitors. Refer to monographs specific to those agents for details.
Tryptophan	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors.
Valbenazine	May enhance the adverse/toxic effect of Monoamine Oxidase Inhibitors.

Monitor:

Blood pressure
Parkinsonism symptoms
New or worsening mental state and behavioral changes
Excessive somnolence or falling asleep while performing daily activities
Skin examination to determine if there is melanoma.

How to administer Rasagiline?

Give without regard to meals.

Mechanism of action of Rasagiline:

It is a powerful, irreversible inhibitor of brain monoamine oxygenase (MAO type B), which plays an important role in the catabolism and metabolism of dopamine.
The primary effect of inhibiting dopamine depletion at the striatal brain region is to reduce the symptoms of Parkinson's disease.
There is evidence that rasagiline may have neuroprotective properties (antioxidant, neuroapoptotic), which may delay the onset and progression of neuronal degeneration.

Time: Almost 1 week (irreversible inhibition)

AbsorptionRapid

Protein binding: 88%-94%, primarily due to albumin

Metabolism: Hepatic N-dealkylation and/or hydroxylation via CYP1A2 for multiple inactive metabolites

DistributionV : 87 L

Bioavailability: Almost 36%

Eliminating half-life: Almost 3 hours (no correlation to biologic effect due irreversible inhibition).

Plasma peak time- Almost 1 hour

Excretion: By Urine (62%; 1% total dose as unchanged drug); & Feces (7%)