(fin GOL i mod)
- Fingolimod HCl
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Gilenya: 0.5 mg
Brand Names: U.S.
- Sphingosine 1-Phosphate (S1P) Receptor Modulator
Fingolimod-phosphate, active metabolite of fingolimod, binds to sphingosine 1-phosphate receptors 1, 3, 4, and 5. Fingolimod-phosphate blocks the lymphocytes' ability to emerge from lymph nodes; therefore, the amount of lymphocytes available to the central nervous system is decreased, which reduces central inflammation.
Vd: ~1,200 L: distributes into red blood cells (86%)
Hepatic via CYP4F2 to fingolimod-phosphate (active) and other metabolites (inactive); CYP2D6, 2E1, 3A4, and 4F12 also contribute to metabolism
Urine (~81% as inactive metabolites); feces (fingolimod and fingolimod phosphate: <2.5% of dose)
Time to Peak
Plasma: 12 to 16 hours
6 to 9 days; prolonged by approximately 50% in patients with moderate or severe hepatic impairment
>99.7% (fingolimod and fingolimod-phosphate)
Special Populations: Renal Function Impairment
Fingolimod Cmax and AUC are increased by 32% and 43%, respectively, and by 25% and 14%, respectively, for fingolimod-phosphate in patients with severe renal impairment.
Special Populations: Hepatic Function Impairment
Fingolimod area under the curve (AUC) increased by 12%, 44%, and 103% in patients with mild, moderate, or severe hepatic impairment, respectively. Fingolimod-phosphate maximal drug concentration (Cmax) was decreased by 22% in patients with severe hepatic impairment.
Use: Labeled Indications
Multiple sclerosis: Treatment of relapsing forms of multiple sclerosis (MS) to reduce the frequency of clinical exacerbations and to delay the accumulation of physical disability.
US labeling: Hypersensitivity to fingolimod (including rash, urticaria, and angioedema) or any component of the formulation; MI, unstable angina, stroke, transient ischemic attack, decompensated heart failure requiring hospitalization, or New York Heart Association (NYHA) class III/IV heart failure in the past 6 months; Mobitz Type II second- or third-degree atrioventricular (AV) block or sick sinus syndrome (unless patient has a functioning pacemaker); baseline QTc interval ≥500 msec; concurrent use of a class Ia or III antiarrhythmic.
Canadian labeling: Hypersensitivity to fingolimod or any component of the formulation; patients at increased risk for opportunistic infections, including those who are immunocompromised due to treatment (eg, antineoplastic, immunosuppressive or immunomodulating therapies, total lymphoid irradiation or bone marrow transplantation) or disease (eg, immunodeficiency syndrome); severe active infections including active chronic bacterial, fungal or viral infections (eg, hepatitis, tuberculosis); known active malignancy (excluding basal cell carcinoma); severe hepatic impairment (Child-Pugh class C)
Multiple sclerosis: Oral: 0.5 mg once daily; doses >0.5 mg daily are associated with increased adverse events and no additional benefit. Note: The first dose and doses following therapy interruption (longer than 14 days) should be administered in a setting in which resources to appropriately manage symptomatic bradycardia are available.
Refer to adult dosing.
Dosing: Renal Impairment
There are no dosage adjustments provided in the manufacturer’s labeling; use with caution in severe renal impairment (exposure is increased). A small pharmacokinetic study in patients with stable severe impairment (CrCl <30 mL/minute) and not on dialysis suggests that increases in exposure to fingolimod and the active metabolite (fingolimod-P) are not clinically meaningful and dosage adjustment may not be necessary (David 2015).
Dosing: Hepatic Impairment
Mild to moderate impairment (Child-Pugh classes A and B): No dosage adjustment necessary.
Severe impairment (Child-Pugh class C):
US labeling: There are no dosage adjustments provided in the manufacturer's labeling; use with caution and closely monitor; exposure is doubled in severe hepatic impairment.
Canadian labeling: Use is contraindicated
Administer with or without food.
Hazardous agent; use appropriate precautions for handling and disposal (NIOSH 2014 [group 2]). NISOH recommends single gloving for administration of intact capsules (NIOSH 2014).
Store at 25°C (77°F); excursions are permitted between 15°C and 30°C (59°F and 86°F). Protect from moisture.
Antiarrhythmic Agents (Class Ia): Fingolimod may enhance the arrhythmogenic effect of Antiarrhythmic Agents (Class Ia). Avoid combination
Antiarrhythmic Agents (Class III): Fingolimod may enhance the arrhythmogenic effect of Antiarrhythmic Agents (Class III). Avoid combination
BCG (Intravesical): Immunosuppressants may diminish the therapeutic effect of BCG (Intravesical). Avoid combination
Beta-Blockers: May enhance the bradycardic effect of Fingolimod. Management: Avoid the concomitant use of fingolimod and beta-blockers if possible. If coadministration is necessary, patients should have overnight continuous ECG monitoring conducted after the first dose of fingolimod. Monitor patients for bradycardia. Consider therapy modification
Bradycardia-Causing Agents: May enhance the bradycardic effect of other Bradycardia-Causing Agents. Monitor therapy
Bretylium: May enhance the bradycardic effect of Bradycardia-Causing Agents. Bretylium may also enhance atrioventricular (AV) blockade in patients receiving AV blocking agents. Monitor therapy
CarBAMazepine: May decrease the serum concentration of Fingolimod. Monitor therapy
Ceritinib: Bradycardia-Causing Agents may enhance the bradycardic effect of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Avoid combination
Coccidioides immitis Skin Test: Immunosuppressants may diminish the diagnostic effect of Coccidioides immitis Skin Test. Monitor therapy
Denosumab: May enhance the adverse/toxic effect of Immunosuppressants. Specifically, the risk for serious infections may be increased. Monitor therapy
DiltiaZEM: May enhance the bradycardic effect of Fingolimod. Monitor therapy
Echinacea: May diminish the therapeutic effect of Immunosuppressants. Consider therapy modification
Esmolol: May enhance the bradycardic effect of Fingolimod. Avoid combination
Highest Risk QTc-Prolonging Agents: QTc-Prolonging Agents (Indeterminate Risk and Risk Modifying) may enhance the QTc-prolonging effect of Highest Risk QTc-Prolonging Agents. Management: Avoid such combinations when possible. Use should be accompanied by close monitoring for evidence of QT prolongation or other alterations of cardiac rhythm. Consider therapy modification
Immunosuppressants: May enhance the immunosuppressive effect of Fingolimod. Management: Avoid the concomitant use of fingolimod and other immunosuppressants when possible. If combined, monitor patients closely for additive immunosuppressant effects (eg, infections). Consider therapy modification
Ivabradine: Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. Monitor therapy
Ketoconazole (Systemic): May increase serum concentrations of the active metabolite(s) of Fingolimod. Ketoconazole (Systemic) may increase the serum concentration of Fingolimod. Monitor therapy
Lacosamide: Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. Monitor therapy
Leflunomide: Immunosuppressants may enhance the adverse/toxic effect of Leflunomide. Specifically, the risk for hematologic toxicity such as pancytopenia, agranulocytosis, and/or thrombocytopenia may be increased. Management: Consider not using a leflunomide loading dose in patients receiving other immunosuppressants. Patients receiving both leflunomide and another immunosuppressant should be monitored for bone marrow suppression at least monthly. Consider therapy modification
MiFEPRIStone: May enhance the QTc-prolonging effect of QTc-Prolonging Agents (Indeterminate Risk and Risk Modifying). Management: Though the drugs listed here have uncertain QT-prolonging effects, they all have some possible association with QT prolongation and should generally be avoided when possible. Consider therapy modification
Moderate Risk QTc-Prolonging Agents: QTc-Prolonging Agents (Indeterminate Risk and Risk Modifying) may enhance the QTc-prolonging effect of Moderate Risk QTc-Prolonging Agents. Monitor therapy
Natalizumab: Immunosuppressants may enhance the adverse/toxic effect of Natalizumab. Specifically, the risk of concurrent infection may be increased. Avoid combination
Nivolumab: Immunosuppressants may diminish the therapeutic effect of Nivolumab. Consider therapy modification
Pimecrolimus: May enhance the adverse/toxic effect of Immunosuppressants. Avoid combination
Roflumilast: May enhance the immunosuppressive effect of Immunosuppressants. Consider therapy modification
Sipuleucel-T: Immunosuppressants may diminish the therapeutic effect of Sipuleucel-T. Monitor therapy
Tacrolimus (Topical): May enhance the adverse/toxic effect of Immunosuppressants. Avoid combination
Tofacitinib: Immunosuppressants may enhance the immunosuppressive effect of Tofacitinib. Management: Concurrent use with antirheumatic doses of methotrexate or nonbiologic disease modifying antirheumatic drugs (DMARDs) is permitted, and this warning seems particularly focused on more potent immunosuppressants. Avoid combination
Trastuzumab: May enhance the neutropenic effect of Immunosuppressants. Monitor therapy
Vaccines (Inactivated): Fingolimod may diminish the therapeutic effect of Vaccines (Inactivated). Management: Vaccine efficacy may be reduced. Complete all age-appropriate vaccinations at least 2 weeks prior to starting fingolimod. If vaccinated during fingolimod therapy, revaccinate 2 to 3 months after fingolimod discontinuation. Consider therapy modification
Vaccines (Live): Fingolimod may enhance the adverse/toxic effect of Vaccines (Live). Vaccinal infections may develop. Fingolimod may diminish the therapeutic effect of Vaccines (Live). Avoid combination
Verapamil: May enhance the bradycardic effect of Fingolimod. Monitor therapy
Zoster Vaccine: Fingolimod may enhance the adverse/toxic effect of Zoster Vaccine. The risk of herpes zoster infection may be increased. Fingolimod may diminish the therapeutic effect of Zoster Vaccine. Management: Wait 1 month after zoster vaccine administration to initiate fingolimod therapy. Avoid the use of the zoster vaccine during fingolimod treatment, and for 2 months following treatment discontinuation. Consider therapy modification
Central nervous system: Headache (25%)
Endocrine & metabolic: Increased gamma-glutamyl transfer (5% to ≤15%)
Gastrointestinal: Nausea (13%), diarrhea (12% to 13%), abdominal pain (11%)
Hepatic: Increased serum ALT (14% to ≤15%), increased serum AST (14% to ≤15%)
Infection: Influenza (11% to 13%)
Neuromuscular & skeletal: Back pain (10% to 12%)
Respiratory: Cough (10% to 12%), sinusitis (7% to 11%)
1% to 10%:
Cardiovascular: Hypertension (6% to 8%), atrioventricular block (first degree: 5%; second degree: 4%; third degree: ≤1%), bradycardia (≤4%)
Central nervous system: Depression (8%), dizziness (7%), migraine (5% to 6%), paresthesia (5%)
Dermatologic: Alopecia (3% to 4%), tinea (2% to 4%), eczema (3%), pruritus (3%), actinic keratosis (2%)
Endocrine & metabolic: Weight loss (5%), increased serum triglycerides (3%)
Gastrointestinal: Gastroenteritis (5%)
Hematologic & oncologic: Lymphocytopenia (4% to 7%), cutaneous papilloma (3%), leukopenia (2% to 3%), basal cell carcinoma (2%)
Neuromuscular & skeletal: Leg pain (≤10%), upper extremity pain (≤10%), weakness (2% to 3%)
Ophthalmic: Blurred vision (4%), eye pain (3%)
Respiratory: Dyspnea (8% to 9%), bronchitis (8%)
Miscellaneous: Herpes virus infection (9%), herpes zoster (2%)
<1% (Limited to important or life-threatening): Angiodema, asystole, cerebrovascular accident (ischemic and hemorrhagic), cholestatic hepatitis, hepatocellular hepatitis, macular edema, malignant lymphoma (including B-cell and T-cell), multiorgan failure, non-Hodgkin's lymphoma, peripheral arterial disease, pneumonia, progressive multifocal leukoencephalopathy (FDA Safety Alert, Aug 4, 2015), prolonged Q-T interval on ECG, reversible posterior leukoencephalopathy syndrome, skin rash, syncope
Concerns related to adverse reactions:
• Atrioventricular (AV) block: May result in transient and asymptomatic AV conduction delays, which typically resolve within 24 hours of treatment initiation; recurrence may be observed following discontinuation and subsequent reinitiation of therapy. Third-degree AV block and AV block with junctional escape occurred within the first 6 hours of the initial dose, and transient asystole and unexplained death have occurred within the first 24 hours; syncope has also occurred.
• Bradycardia: Initiation must occur in a setting with resources and personnel capable of appropriately managing symptomatic bradycardia. Following the first dose, heart rate may decrease as soon as 1 hour postdose, with the maximal decrease usually occurring ~6 hours postdose with recovery (but not to baseline levels) 8 to 10 hours postdose. A second heart rate decrease occurs within 24 hours after the first dose and may be more pronounced than the first 6-hour rate decrease. Most patients are asymptomatic; however, hypotension, dizziness, fatigue, palpitations, and/or chest pain may occur; symptoms usually resolve within 24 hours. With the second dose, heart rate may also decrease, but to a lesser magnitude than observed with the first dose. Heart rate typically returns to baseline after 1 month of chronic therapy.
• Cryptococcal infections: Cases of cryptococcal meningitis and disseminated cryptococcal infections have been reported. Cryptococcal infections have generally occurred after ~2 years of treatment, although may occur earlier (relationship between risk and duration of treatment is unknown). Patients with signs and symptoms of cryptococcal infections should undergo prompt diagnostic evaluation and treatment.
• Hepatic effects: Elevated liver enzymes may occur; most elevations occurred within 6 to 9 months. Recurrence of liver transaminase elevations may occur with rechallenge. Liver injury with hepatocellular and/or cholestatic hepatitis has been reported. Obtain baseline liver enzymes and bilirubin in all patients prior to therapy initiation (within 6 months); monitor liver enzymes in patients who develop symptoms of hepatic dysfunction (eg, nausea, vomiting, abdominal pain, fatigue, anorexia, jaundice, dark urine). Discontinue treatment with confirmation of liver injury; transaminases tend to return to normal within 2 months of discontinuation.
• Herpes infection: Serious, life-threatening herpes infections, including fatalities (eg, disseminated primary herpes zoster and herpes simplex encephalitis) have occurred. Consider disseminated herpes infections as an etiology if an atypical MS relapse or multiorgan failure occurs. Consider varicella zoster virus vaccination prior to initiation of treatment in patients without a health care professional–confirmed history of chickenpox, without a documented full course of varicella zoster vaccination, and patients who are VZV antibody negative; postpone fingolimod treatment for 1 month after varicella zoster vaccination. Cases of Kaposi sarcoma (associated with human herpes virus-8) have been reported; if suspected, prompt diagnostic evaluation and management is required.
• Hypersensitivity reaction: Hypersensitivity reactions, including rash, urticaria, and angioedema upon treatment initiation, have been reported.
• Hypertension: Increased blood pressure may occur ~1 month after initiation of therapy; monitor blood pressure throughout treatment.
• Immune suppression: May increase risk of infection (including serious infections) with opportunistic pathogens including viruses (eg, John Cunningham virus [JCV], herpes simplex virus 1 and 2, varicella-zoster virus), fungi (eg, cryptococci), and bacteria (eg, atypical mycobacteria), due to reversible dose-dependent reduction of lymphocytes. Lymphocyte counts may be decreased for up to 2 months following discontinuation of therapy. Obtain a complete blood cell count (CBC) (within 6 months or after discontinuation of prior therapy) before starting therapy. Monitor for signs and symptoms of infection; consider therapy interruption in patients who develop a serious infection; reassess benefits and risks prior to reinitiation of therapy. Do not initiate treatment in patients with acute or chronic infections until the infection has resolved. Use with caution in patients receiving concomitant immunosuppressant, immune modulating, or antineoplastic medications, or when switching from other immunosuppressants (consider the duration and mode of action for each substance to avoid additive effects). The Canadian labeling contraindicates use in patients who are immunocompromised due to concomitant treatment or disease. Patients with low lymphocyte counts at baseline and underweight females (BMI <18.5 kg/m2) are at higher risk for developing severe lymphopenia and should be monitored more closely (Warnke 2014).
• Macular edema: Macular edema may occur, typically within the first 6 months of treatment. Patients may present with blurred vision, decreased visual acuity, or without symptoms. Signs and symptoms generally improve or resolve with discontinuation of treatment; however, residual decreased visual acuity has occurred in some patients. Patients with a history of diabetes mellitus or uveitis are at increased risk; use with caution. Ophthalmologic exams (including the fundus and macula) should be performed prior to therapy, 3 to 4 months after treatment initiation, and anytime visual disturbances are reported; more frequent examination is warranted in patients with diabetes or a history of uveitis.
• Malignancy: Cases of lymphoma and skin cancers have been reported. Basal cell carcinoma is associated with fingolimod use; monitor for suspicious skin lesions. Promptly evaluate any suspicious skin lesion.
• Neurotoxicity: Posterior reversible encephalopathy syndrome (PRES) has been observed. Monitor for signs/symptoms of PRES (eg, sudden onset of severe headache, altered mental status, visual disturbances, seizure); symptoms are usually reversible, but may evolve into ischemic stroke or cerebral hemorrhage. Delayed diagnosis and treatment may result in permanent neurological sequelae. Discontinue use if PRES is suspected.
• Progressive multifocal leukoencephalopathy: Cases of progressive multifocal leukoencephalopathy (PML) due to the JC virus have been reported, including cases in patients who were not immunocompromised and had no prior exposure to immunosuppressant drugs, including natalizumab. PML cases occurred in patient treated with fingolimod for at least 2 years (relationship between risk and duration of treatment is unknown). At the first sign or symptom suggestive of PML, perform a diagnostic evaluation (MRI findings may appear before clinical signs/symptoms) and withhold therapy; symptoms progress over days to weeks and may include progressive weakness on one side of the body or clumsiness of limbs; vision disturbances; mental status changes.
• Respiratory effects: Reductions of forced expiratory volume in the first second of expiration (FEV1) and diffusion lung capacity for carbon monoxide (DLCO) are dose dependent and may occur within the first month of therapy. FEV1 changes may be reversible with drug discontinuation. Use in multiple sclerosis (MS) patients with compromised respiratory function has not been evaluated. If clinically necessary, spirometric evaluation of respiratory function and evaluation of DLCO should be performed during therapy.
• QT prolongation: May cause QT prolongation; patients with a prolonged QT interval at baseline (males: >450 msec; females: >470 msec) or during the first 6 hours of treatment initiation, or are at an increased risk of QT prolongation (eg, hypokalemia, hypomagnesemia, concomitant QT-prolonging drugs, congenital long-QT syndrome) require continuous overnight electrocardiogram (ECG) monitoring in a medical facility after the initial dose. Unless deemed clinically necessary, the Canadian labeling does not recommend use in patients with QT prolongation >470 msec (females) or >450 msec (men)] or risk factors for QT prolongation (eg, hypokalemia, hypomagnesemia, congenital QT prolongation).
• Cardiovascular: Due to the risk of bradycardia and AV conduction delays, an ECG is required prior to initiation of therapy and after the initial observation period (6 hours) in all patients. Patients receiving concomitant therapy with drugs that slow heart rate or AV conduction (eg, beta-blockers, heart rate–lowering calcium channel blockers, digoxin) or with other cardiac risk factors (eg, AV block, sick sinus syndrome, prolonged QT interval, ischemic cardiac disease, history of myocardial infarction [MI], symptomatic bradycardia and/or cardiac arrest, heart failure, cerebrovascular disease, uncontrolled hypertension, recurrent syncope, severe sleep apnea [untreated]) require continuous overnight ECG monitoring in a medical facility after the first dose. Unless deemed clinically necessary, the Canadian labeling does not recommend use in patients with Mobitz type II or higher AV block, sino-atrial heart block, sick sinus syndrome, history of MI or cardiac arrest, ischemic heart disease (including angina), heart failure, cerebrovascular disease, uncontrolled hypertension, severe untreated sleep apnea or receiving concomitant Class Ia or Class III anti-arrhythmic agents.
• Hepatic impairment: Use with caution and closely monitor patients with severe hepatic impairment (contraindicated in the Canadian labeling). Use caution in patients with preexisting liver disease; may be at increased risk of increased liver enzymes.
Concurrent drug therapy issues:
• Drug-drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult drug interactions database for more detailed information.
• Hazardous agent: Use appropriate precautions for handling and disposal (NIOSH 2014 [group 2]).
Complete blood cell count (CBC) including lymphocyte count (baseline [within 6 months of initiation] and periodically thereafter).
US labeling: Baseline bilirubin and transaminase levels in all patients prior to therapy initiation (within 6 months); monitor transaminases in patients who develop symptoms of hepatic dysfunction.
Canadian labeling: Baseline transaminase and bilirubin levels prior to therapy initiation (within 6 months), every 3 months during the first year of therapy and periodically thereafter (asymptomatic patients); monitor transaminases in patients who develop symptoms of hepatic dysfunction.
ECG (baseline; repeat after initial dose observation period); heart rate, blood pressure, and signs and symptoms of bradycardia (hourly for 6 hours following first dose; continued observation (until resolved) required if 6-hour postdose heart rate is <45 bpm, is lowest postbaseline measurement, or new-onset second degree or higher AV block occurs on repeat ECG); continuous (until symptoms resolved) ECG monitoring if postdose symptomatic bradycardia occurs (overnight continuous ECG in a medical facility and repeat observation period for second dose if pharmacologic intervention for bradycardia necessary); overnight continuous ECG monitoring in a medical facility if baseline or 6-hour post dose QT interval is prolonged [>450 msec (men), >470 msec (females)] or additional risks for QT prolongation (eg, hypokalemia, hypomagnesemia, congenital long-QT syndrome) or concurrent therapy with QT prolonging agents with a known risk of torsades de pointes.
Initial monitoring procedures (ECG, heart rate, blood pressure) must be repeated for
- treatment interruption of ≥1 day during the first 2 weeks after treatment initiation, or
- treatment interruption of >7 days during weeks 3 to 4 after treatment initiation, or
- treatment interruption of >14 days after ≥1 month of treatment initiation
Ophthalmologic exam at baseline and 3 to 4 months after initiation of treatment (continue periodic examinations for duration of therapy in patients with diabetes, history of uveitis, or visual complaints); respiratory function (FEV1, DLCO) if clinically indicated; VZV antibodies (patients with no health care professional–confirmed history of chickenpox or without documented previous full series VZV vaccination); signs and symptoms of infection (during treatment and at least 2 months after discontinuation), progressive multifocal leukoencephalopathy, and/or posterior reversible encephalopathy syndrome; monitor for suspicious skin lesions
Pregnancy Risk Factor
Adverse events have been observed in animal reproduction studies. Elimination of fingolimod takes approximately 2 months; to avoid potential fetal harm, women of childbearing potential should use effective contraception to avoid pregnancy during and for 2 months after discontinuing treatment. Health care providers are encouraged to enroll pregnant women, or pregnant women may enroll themselves, in the Gilenya Pregnancy Registry (1-877-598-7237 or https://www.gilenyapregnancyregistry.com).
• Discuss specific use of drug and side effects with patient as it relates to treatment. (HCAHPS: During this hospital stay, were you given any medicine that you had not taken before? Before giving you any new medicine, how often did hospital staff tell you what the medicine was for? How often did hospital staff describe possible side effects in a way you could understand?)
• Patient may experience headache, flu-like symptoms, painful extremities, sinusitis, abdominal pain, diarrhea, or back pain. Have patient report immediately to prescriber signs of infection, signs of meningitis (headache with fever, stiff neck, nausea, confusion, or if lights bother eyes), signs of liver problems (dark urine, feeling tired, lack of appetite, nausea, abdominal pain, light-colored stools, vomiting, or yellow skin or eyes), dizziness, bradycardia, arrhythmia, fatigue, angina, mole changes, skin growth, passing out, wound healing impairment, excessive weight loss, night sweats, enlarged lymph nodes, shortness of breath, difficulty breathing, vision changes, eye pain, severe eye irritation, burning or numbness feeling, signs of posterior reversible encephalopathy syndrome (illogical thinking, not alert, vision changes, seizures, or severe headache), or signs of progressive multifocal leukoencephalopathy (confusion, depression, trouble with memory, behavioral changes, change in strength on one side, trouble speaking, change in balance, or vision changes) (HCAHPS).
• Educate patient about signs of a significant reaction (eg, wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat). Note: This is not a comprehensive list of all side effects. Patient should consult prescriber for additional questions.
Intended Use and Disclaimer: Should not be printed and given to patients. This information is intended to serve as a concise initial reference for health care professionals to use when discussing medications with a patient. You must ultimately rely on your own discretion, experience, and judgment in diagnosing, treating, and advising patients.
More about fingolimod
- Other brands: Gilenya