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Fingolimod

BioIntegrator LLC
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2019-09-19
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Clinical Pharmacology

Fingolimod modulates sphingosine-1-phosphate receptors (SIP receptors). Fingolimod is metabolized by sphingosine kinase to the active metabolite of fingolymodiphosphate. At nanomolar concentrations, fingolymodophosphate binds to SIP receptors 1, 3 and 4 on the surface of lymphocytes and quickly enters the central nervous system (CNS) through the blood-brain barrier, binding to SIP receptors 1, 3 and 5 on the surface of neurons. By binding to SIP receptors of lymphocytes, fingolymodiphosphate blocks the ability of lymphocytes to leave the lymph nodes, which leads to a redistribution of lymphocytes in the body. At the same time, there is no decrease in the total number of lymphocytes in the body.
The redistribution of lymphocytes leads to a decrease in lymphocytic infiltration of the CNS, a decrease in the severity of inflammation and the degree of damage to the nervous tissue.
Within 4-6 hours after a single dose of 0.5 mg, the number of blood lymphocytes is reduced to approximately 75% of the initial value. With long-term daily intake of the drug, the number of lymphocytes continues to decline for 2 weeks, reaching a minimum of 500 cells / μl, or approximately 30% of the initial level. In 18% of patients, a decrease in the number of lymphocytes below 200 cells / mcl was noted (at least once). With regular use of the drug, a decrease in the number of lymphocytes was maintained. Since the majority of T-and B-lymphocytes constantly pass through the lymphoid organs, the effect of fingolimod on these cells is most pronounced. However, about 15-20% of T-lymphocytes, which are effector cells of the immune memory and play an important role in the peripheral immune control, do not pass through the lymphoid organs and are not affected by fingolimod.
Within a few days after stopping the drug in the blood, there is an increase in the number of lymphocytes. Normalization of the number of lymphocytes occurs 1-2 months after discontinuation of treatment. Constant intake of fingolimod leads to a slight decrease in the number of neutrophils to approximately 80% of the initial value. Monocytes are not affected by fingolimod.
When using the drug in patients with remittent multiple sclerosis (average score on the scale of disability by EDSS 2.0), fingolimod at a dose of 0.5 mg reduced the incidence of clinical manifestations of the disease by 54%. When taking the drug, 70% of patients had a stable remission for 2 years (compared with 45.6% in the placebo group). Fingolimod significantly reduced the risk of disability progression, significantly increased the time before the 3-month and 6-month period of confirmation of progression of disability (estimated as an increase in the EDSS score from baseline) compared with placebo. The results of magnetic resonance imaging (MRI) of the brain in patients with remitting multiple sclerosis during treatment with fingolimod confirm a significant decrease in the activity of the disease (intensity of the inflammatory process in the central nervous system, size and number of foci of demyelination).

Pharmacokinetics
The pharmacologically active metabolite is the (S) enantiomer of fingolimiodophosphate.
Absorption
When ingestion is absorbed> 85% of the dose. Fingolimod absorption is slow (time to reach maximum plasma concentration, tmax 12-16 h)
Absolute bioavailability when administered orally is 93%. Equilibrium plasma concentration is achieved within 1-2 months of regular use of the drug (1 time per day). Equilibrium concentration of fingolimod is approximately 10 times higher than its concentration after the first dose. After repeated administration of 0.5 mg once a day, the concentration of fingolimod and fingolimiodophosphate are increased, probably in proportion to the dose.
Food does not affect the maximum concentration (Cmax) or exposure (AUC - area under the curve "concentration-time") of fingolymod or fingolymodiphosphate.
Distribution
Fingolimod is significantly distributed in erythrocytes (fingolimod fraction in blood cells is 86%). Fingolimodimfosfat has a lower ability to enter the blood cells (fraction in blood cells is 99%). The association of fingolimod and fingolimodiphosphate with plasma proteins does not change in patients with impaired renal or hepatic function. Fingolimod is largely distributed in body tissues (volume of distribution is about (1200 ± 260) l). Fingolimod penetrates the brain, which was shown in a clinical study on healthy volunteers.
In a study of 13 volunteers with remitting multiple sclerosis, who received in the equilibrium state of fingolimod at a dose of 0.5 mg, the amount of fingolimod (or fingolimodimodophosphate) in seminal fluid was 10,000 times lower than the initial dose (0.5 mg).
Metabolism
In humans, biotransformation of fingolimod occurs by reverse stereoselective phosphorylation to the pharmacologically active groups of the creating elements of the fingolymodiphosphate, and by oxidative biotransformation through the cytochrome CYP4F isoenzyme, mainly CYP4F2, and subsequent decomposition, like fatty acids to inactive metabolites of the authors, to the inactive metabolites of the creators, mainly CYP4F2. fingolimod.
After a single dose of fingolimod orally, the main fingolimod-related components in the blood for 34 days after ingestion are fingolimod (23.3%), fingolimiodophosphate (10.3%) and inactive metabolites (carboxylic acid metabolite ME (8.3%) , a metabolite of ceramide M29 (8.9%) and a metabolite of ceramide M30 (7.3%)).
Removal
The rate of clearance of fingolimod from the blood is (6.3 ± 2.3) l / h, and the average expected final T½ is 6-9 days. Levels of fingolimod and fingolimodphosphate decrease similarly in the terminal phase, which leads to a similar T½. After oral administration, 81% of the dose is slowly excreted in the urine as inactive metabolites. Fingolimod and fingolimodphosphate are not excreted intact in the urine, but are the main components of the drug metabolites in the feces, where the number of each is Characteristics of individual groups of patients.
The pharmacokinetics of fingolimod and fingolimodimfosfat does not differ in men and women, in patients of different ethnic origin. In patients with impaired renal function, severe increases in AUC by 34 and 14% for fingolymod and fingolymodophosphate, respectively.
Fingolimod should be used with caution in patients with mild to moderate hepatic impairment: this increases the AUC of fingolimod by 12% and 44%, respectively. In patients with moderate and severe liver dysfunction (Child-Pugh classes B and C), the elimination half-life of the drug is increased by approximately 50%.
The mechanism of elimination and the results of studies of population pharmacokinetics indicate that dose adjustment is not required for elderly patients. It should be used with caution drug Nescler®® in patients over the age of 65 due to limited clinical experience.
Pharmacokinetics of the drug Nescler®® in children and adolescents under the age of 18 years has not been studied.

Indications

Nescler®® indicated for monotherapy in adult patients with highly active relapsing, remitting multiple sclerosis, for the following groups of patients:
Patients with a high disease activity, despite the treatment with at least one drug that modifies the course of the disease. These patients can be defined as “not responding” to a full, adequately prescribed course of therapy (in general - at least one year of treatment), with one type of therapy modifying the course of the disease. Patients should have at least 1 relapse during the previous year on therapy, and at least 9 T2 foci, as determined by brain MRI, or at least 1 lesion accumulating gadolinium.“Unanswered” can also be defined as patients with a constant or increasing recurrence rate, or continuing severe recurrences, compared with the previous year.
Patients with rapidly developing, severe remitting multiple sclerosis, defined as having 2 or more disabling relapses for one year, or having 1 or more gadolinium accumulating lesions, or a significant increase in T2 lesions according to MRI compared to previous MRI.
Fingolimod is prescribed to reduce the frequency of clinical exacerbations of the disease and reduce the risk of progression of disability.

Composition

1 capsule contains:

Active substances: fingolimod hydrochloride 0.56 mg (corresponding to 0.50 mg of fingolimod base)

Excipients: lactulose 47.45 mg; Povidone 1.04 mg; polyethylene glycol-6000 0.95 mg.

Fingolimod is marketed under different brands and generic names, and comes in different dosage forms:

Brand nameManufacturerCountryDosage form
Nescler® BioIntegrator LLC Russia capsules
Gilenya® Novartis Switzerland capsules

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Fingolimod

Dosage and Administration

The recommended dose of the drug is one capsule of 0.5 mg orally once a day, regardless of the meal time. In case of missing an appointment, the next day the drug Neskler® used at the usual time. The drug is intended for long-term use.
Patients who have previously received treatment with interferon-beta and Glatiramer acetate, with good endurance (no neutropenia), can be transferred to treatment with Neskler®
When using the drug Neskler® 2-3 months after discontinuation of treatment with natalizumab, the joint effect on the immune system may be enhanced due to the long half-life of natalizumab. Care must be taken when transferring a patient from natalizumab to fingolimod.
After taking the first dose of the drug Neskler® all patients should be monitored for 6 hours, including: measuring heart rate and blood pressure every hour, as well as electrocardiography before treatment with the drug and 6 hours after taking the first dose of the drug in order to diagnose possible manifestations of bradyarrhythmia as soon as possible.
With the development of bradyarrhythmias on the background of the beginning of drug therapy, if necessary, appropriate measures should be taken to correct this disorder, and the patient should be monitored until the condition is relieved. If it is necessary to conduct drug therapy during the monitoring period after the first dose has been applied, patient monitoring should be extended in the hospital at least until the next morning. After applying the second dose of the drug Neskler® in such patients, it is necessary to repeat all the measures, as well as after applying the first dose of the drug.
Additional observation until the resolution of the condition is also required in the following cases:

  • if the heart rate 6 hours after the first dose of the drug is
  • when a new AV block is detected for the first time, grade II or higher, according to the ECG data, 6 hours after the first dose of the drug;
  • if the QTc interval on the ECG is> 500 ms.

With the resumption of drug therapy Neskler®After a break in therapy, it is necessary to monitor the activity of the cardiovascular system, as well as after taking the first dose, in case of a break in therapy:

  • at least for 1 day during the first 2 weeks of therapy;
  • more than 7 days on the 3rd or 4th week of treatment;
  • more than 2 weeks after the treatment lasted more than a month.


Patients with impaired liver function
Dosage adjustment of the drug in patients with mild and moderately impaired liver function is not required. Neskler drug treatment® Patients with impaired liver function in history should be carried out with caution. It is recommended to control the activity of hepatic transaminases 6 months before the start of therapy with the drug. In the absence of clinical manifestations of liver damage, it is recommended to determine the level of hepatic transaminases in 1, 3, 6, 9, and 12 months of treatment, and then periodically. The increased activity of hepatic transaminases> 5 VGN requires more frequent biochemical examination of blood serum, including the determination of the level of bilirubin and alkaline phosphatase. If symptoms appear that suggest impaired liver function (vomiting and nausea of ​​unknown etiology, jaundice, abdominal pain, fatigue, anorexia, dark urine color), it is necessary to determine the activity of liver enzymes. At detection of damage to the liver drug treatment should be discontinued.
Use of the drug Neskler® in patients with severe liver function impairment (Child-Pugh class C) is contraindicated.
Elderly patients (over 65 years)
Dose adjustment of the drug in this category of patients is not required, but treatment should be carried out with caution due to the lack of clinical experience with the drug in patients over 65 years of age.
Patients with diabetes
Research on the use of the drug Neskler® in patients with diabetes mellitus was not performed. Care must be taken in appointing the drug in this category of patients because of the risk of macular edema, to prevent the development of which it is necessary to regularly carry out ophthalmological monitoring.
Patients with impaired renal function
Dose adjustment of the drug in patients with impaired renal function is not required.
Patients under 18 years old
Efficacy and safety of the drug Neskler® in children and adolescents under the age of 18 years have not been established.
Termination of drug treatment
Upon termination of drug treatment, it is necessary to consider that the normalization of the number of lymphocytes occurs 1-2 months after the last use of the drug Neskler®Since the use of immunosuppressants for 1-2 months after discontinuation of the drug Neskler® Perhaps an additional depressant effect on the immune system, care must be taken when using immunosuppressants shortly after stopping treatment with the drug.

Adverse reactions

Infections and invasions: very often - infections caused by the influenza virus, sinusitis;
often - bronchitis, infections caused by the herpes virus, shingles, pityriasis versicolor; rarely, pneumonia *.
Violations of the blood and lymphatic system:
often - lymphopenia, leukopenia.
Mental disorders: often - depression; infrequently - depressed mood.
Violations of the nervous system: very often - headache; often headache, migraine; rarely - reversible posterior encephalopathy syndrome.
Violations of the organ of vision: often - blurred vision; infrequently - macular edema.
Heart disorders: often - bradycardia, atrioventricular block.
Vascular abnormalities: increased blood pressure.
Disturbances of the respiratory system, organs of the chest and mediastinum: very often - cough, often - shortness of breath.
Disorders of the gastrointestinal tract: very often - diarrhea.
Violations of the skin and subcutaneous tissues: often - eczema, alopecia, itching.
Disorders of the musculoskeletal and connective tissues: very often - back pain.
General disorders: often - asthenia.

Contraindications

Efficacy and safety of the drug Neskler® in children and adolescents under the age of 18 have not been established.

Drug interactions

Pharmacodynamic interaction
Considering the possibility of an additional inhibitory effect on the immune system, caution should be exercised when using fingolimod along with anti-tumor immunosuppressants (including glucocorticosteroids) or immunomodulators. Since glucocorticosteroids have an immunosuppressive effect, the duration of treatment and their dose when applied simultaneously with fingolimod should be adjusted based on clinical data.
In clinical studies with the use of fingolimod in patients with RRS who received short courses of glucocorticosteroids (for five days), there was no increase in the frequency of infections.
Fingolimod should be used with caution in patients who have previously received drugs such as natalizumab or mitoxantrone for a long time.
Limited experience with fingolimod in patients receiving concomitant therapy with beta-blockers, calcium channel blockers that reduce heart rate (such as verapamil, diltiazem or ivabradine), or other drugs that can reduce the heart rate (such as digoxin)The use of these drugs in combination with the drug Neskler may be accompanied by the development of severe bradycardia and heart block. When taking fingolimod in combination with atenolol, the heart rate is further reduced by 15% (when taken with diltiazem, this effect is not observed). Due to the powerful combined effect on heart rate, the drug Neskler® not recommended for patients currently receiving these drugs.
If treatment with Neskler is intended®, consultation of the cardiologist is necessary regarding the possibility of switching to drugs that do not reduce the heart rate, as well as monitoring.
The use of fingolimod in patients receiving class IA antiarrhythmic drugs (for example, quinidine, procainamide) or class III (for example, amiodarone, sotalol) has not been studied. Since the use of antiarrhythmic drugs IA and III classes may develop bradyarrhythmia, the drug Neskler® should not be prescribed with these antiarrhythmic drugs.
Pharmacokinetic interaction
Fingolimod is primarily metabolized with the participation of cytochrome P450 4F2 and, possibly, other CYP4F isoenzymes. In vitro in hepatocytes in the event of significant induction, the CYP3A4 isoenzyme may also be involved in fingolimod metabolism. In connection with the foregoing, the effect of fingolimod and fingolimodiphosphate on the clearance of drugs metabolized by the main CYP isoenzymes is unlikely.
Effect of fingolimod and fingolimodphosphate on the metabolism of co-administered drugs:
In vitro studies have shown that fingolimod and fingolimodphosphate are almost or not able to suppress the activity of human cytochrome P450 isoenzymes (1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1, ZA4 / 5 or 4A9 / 11). Thus, a decrease in clearance of drugs metabolized mainly by the main isoenzymes of cytochrome P450 in the presence of fingolimod and fingolimodimo phosphate is clinically unlikely.
The ability of fingolimod and fingolimodphosphate to induce their own metabolism and / or metabolism of co-administered drugs:
In in vitro studies, fingolimod did not induce mRNA of cytochrome ZA4, 1A2, 4F2 and ABCB1 isoenzymes (P-glycoprotein), as well as the activity of the cytochrome ZA, 1A2, 2B6, 2C8, 2C9, 2C19, 4C2 isoenzymes; fingolimodimfosfat did not possess an inducing action against cytochrome isoenzymes. Thus, an increase in the activity of different isoenzymes of cytochrome P450 and ABCB1 in the presence of fingolimod is unlikely.
Transport proteins
The drug probably does not interfere with the absorption and elimination of drugs from the cell and other substances that are substrates of the main transport proteins.
Cyclosporine
The pharmacokinetics of fingolimod and cyclosporine in the case of single or repeated use did not change.
Oral contraceptives
The simultaneous use of fingolimod at a dose of 0.5 mg per day and oral contraceptives (ethinyl estradiol and levonorgestrel) does not alter the effects of oral contraceptives. Despite the lack of research, the effect of oral contraceptives containing progestogens on fingolimod is not expected.
Ketoconazole
In the case of simultaneous use of ketoconazole (at a dose of 200 mg 2 times a day until an equilibrium state was reached) and fingolimod (at a dose of 5 mg once), a moderate increase in AUC of fingolimod and fingolymodophosphate was observed (1.7 times).
Isoprenaline, atropine, atenolol and diltiazem
The exposure of fingolimod and fingolimodimfosfat was not affected by the simultaneous use with isoprenaline or atropine. Concurrent administration with atenolol, diltiazem or cyclosporine did not affect the pharmacokinetics of fingolimod or fingolimodimo phosphate.
Carbamazepine
The simultaneous use of carbamazepine in a dose of 600 mg 2 times a day and 2 mg of fingolimod once did not significantly affect the AUC of fingolimod and fingolimodophosphate, reducing them by about 40%. The simultaneous use of carbamazepine with fingolimod can reduce the effectiveness of the latter.
Potential drug interactions
In clinical studies in patients with XRD, no significant effect of fluoxetine and paroxetine (potent inhibitors of the CYP2D6 isoenzyme) on the concentration of fingolymod or fingolymodiphosphate was observed. Baclofen, gabapentin, oxybutynin, amantadine, modafinil, amitriptyline, pregabalin, glucocorticosteroids and oral contraceptives did not have a clinically significant effect on the concentration (Vaccination
Since the use of live attenuated vaccines may increase the risk of developing infections, the use of the drug should not be immunized with live attenuated vaccines. During drug therapy, as well as for 2 months after discontinuation of treatment with fingolimod, vaccination may be less effective.

Pregnancy and Lactation

Before the start of drug therapy Neskler®In women with fertile potential, a negative pregnancy test should be obtained. During drug therapy and for at least 2 months after the end of its use, you should use reliable methods of contraception. It is necessary to exclude pregnancy before treatment with fingolimod. If pregnancy occurs during treatment with fingolimod, therapy should be canceled. According to the results of experimental studies, the negative effect of fingolimod on fertility is unlikely.
When prescribing the drug Neskler® the doctor should inform women of childbearing age about the possible risk of a negative effect of the drug on the fetus during pregnancy. When using the drug in experimental studies, reproductive toxicity was detected, which included fetal death and organ malformations, especially non-clotting of the ductus arteriosus and ventricular septal defects. In addition, sphingosine-1-phosphate receptors, which are affected by fingolimod, are involved in the process of vascular formation during embryogenesis. Currently, it is not known about the effect of fingolimod on the formation of the cardiovascular system in humans, and there are very limited data on the use of the drug in pregnant women. In clinical studies, cases of 20 pregnancies were reported in patients who received fingolimod, but these data are insufficient to assess the safety of fingolimod in this category of patients.
Data on the effect of fingolimod on the contractile activity of the uterus and childbirth is not.
In experimental studies in animals treated with the drug, the release of the drug with milk was noted. The concentration of the drug in the milk of animals was 2-3 times higher than in the plasma of lactating animals. Given the theoretical possibility of the development of undesirable reactions in infants who are breastfed, it is necessary to stop breastfeeding or discontinue the drug.

Special instructions

Neskler drug treatment® should be appointed and conducted under the supervision of a physician with experience in the treatment of multiple sclerosis.
Since fingolimod reduces the number of lymphocytes in the blood (by redistributing them in secondary lymphoid organs), the number of lymphocytes in peripheral blood cannot be used to evaluate different lymphocyte populations in patients receiving treatment with the drug. Patients receiving fingolimod, to determine the number of mononuclear cells requires the collection of large volumes of blood (due to a decrease in the number of circulating lymphocytes). Before the start of therapy with fingolimod, a clinical analysis of blood with a leukocyte formula should be carried out regularly for 6 months.
Infections
Since the use of the drug may increase the risk of developing infections during the drug treatment Neskler® In patients with symptoms of the infectious process, effective diagnostic and therapeutic measures should be taken. Removal of fingolimod after cessation of treatment can occur within 2 months, so for this period it is necessary to remain wary of the development of infections. Patients receiving therapy with the drug should be instructed to immediately inform the doctor about all symptoms of infection.
With the development of severe infections on the background of drug therapy, drug treatment Neskler® need to stop. Resume Neskler drug treatment® follows only if the benefits of therapy outweigh the possible risk.
Patients who do not have a history of documented evidence of varicella or a complete course of vaccination against Varicella zoster virus (VZV) should be screened for antibodies to VZV before the start of therapy. If necessary, vaccination is carried out 1 month before the start of therapy for the prevention of post-vaccination complications.
Macular edema
Since, against the background of drug therapy, macular edema may develop in the first 3-4 months of taking the drug Neskler®, it is recommended to conduct an ophthalmologic examination. In patients with a history of uveitis, as well as in patients with concomitant diabetes, there is an increased risk of developing macular edema. Since the use of the drug in patients with XRD and concomitant diabetes mellitus has not been studied, patients with diabetes or a history of uveitis are recommended to conduct an ophthalmologic examination before and during the therapy with Neskler.®
In identifying patients with visual impairment during therapy with the drug, it is necessary to examine the fundus, especially the macular region. If macula edema develops, treatment with the drug should be discontinued. The risk of recurrent edema of the macula with the resumption of drug therapy Neskler® not studied Resume Neskler drug treatment® follows only if the benefits of therapy outweigh the potential risk to the patient.
Diabetes
Research on the use of the drug Neskler® in patients with diabetes mellitus was not performed. Care must be taken in appointing the drug in this category of patients because of the risk of macular edema, to prevent the development of which it is necessary to regularly carry out ophthalmological monitoring.
Bradyarrhythmia
Due to the risk of serious rhythm disturbances, the drug Neskler® should not be used in patients with AV-blockade grade II type Mobitz II or higher, sick sinus syndrome or sinoatrial blockade. Because severe bradycardia can be poorly tolerated by patients with ischemic heart disease, a history of myocardial infarction, chronic heart failure, a history of cardiac arrest, cerebrovascular disease, uncontrolled elevation of blood pressure or severe untreated sleep apnea, the drug Nesclear® should not be used in such patients. Since the use of the drug Neskler® leads to a decrease in heart rate and, thus, a prolongation of the QT interval, the drug Neskler® should not be used in patients with significant lengthening of the QT interval (QTc> 470 ms (women) or> 450 ms (men)). If it is necessary to use the drug in this category of patients, a cardiologist should be consulted before starting therapy to select the optimal monitoring of cardiac activity, possibly until the morning of the next day. Also, care should be taken in patients with low heart rate (HR) at rest, less than 55 beats per minute (low heart rate, not associated with impaired cardiac function), while using (ß-blockers, with a history of syncope).
After the first dose of the drug Neskler® It is recommended that patients be monitored for 6 hours, including measuring heart rate and blood pressure every hour to rule out bradyarrhythmias.All patients should undergo electrocardiography before taking the drug and during the 6-hour monitoring period. With the development of bradyarrhythmias on the background of drug therapy, if necessary, appropriate measures should be started, patient monitoring up to the relief of this disorder should be ensured. If necessary, drug therapy during the monitoring of the first dose should be extended to monitor at least until the next morning, and monitoring should be repeated after applying the second dose of the drug Neskler®. Additional observation is also required in the following cases:

  • if the heart rate after 6 hours of taking the drug is
  • for the first time AV blockade of the II degree or higher according to the ECG data 6 hours after taking the drug;
  • or if the QTc ECG interval is> 500 ms.

When drug therapy is resumed after a break for more than 2 weeks after the first month of treatment, it is necessary to monitor cardiovascular activity, as after taking the first dose. During the first 2 weeks of therapy after a break of 1 day or more, it is recommended to carry out procedures characteristic of the first dose. If a break in therapy was more than 7 days, then such procedures are recommended for 3-4 weeks after the resumption of therapy. It is advisable to avoid taking the drug Neskler® in patients with risk factors for prolongation of the QT interval, in particular hypokalemia, hypomagnesemia, or congenital prolongation of the QT interval. The decision on the use of the drug Neskler® in patients with recurrent syncopal conditions or symptomatic bradycardia, should be based on an assessment of the risk-benefit ratio.
All patients should have an ECG before starting therapy with Neskler and at the end of the 6-hour monitoring period.
QT Interval
When using fingolimod in doses of 1.25 mg or 2.5 mg at rest, the QTcI interval (corrected QT interval in terms of pulse frequency based on the data of an individual patient) was prolonged up to 90% (DI Increased blood pressure
In clinical studies, the use of the drug at a dose of 0.5 mg in patients with XRD showed a slight increase in blood pressure (BP) by an average of 3 mm Hg. Art. systolic, at 1 mm Hg. Art. - diastolic. Increased blood pressure was observed approximately 1 month after the start of treatment and persisted with continued therapy. An increase in blood pressure was observed in 6.1% of patients who received fingolimod at the recommended dose (3.8% in the placebo group). According to post-marketing observations, arterial hypertension was observed during the first month of treatment and may require the use of antihypertensive drugs or interruption of treatment.
Reversible posterior encephalopathy syndrome
In clinical and post-marketing studies, there were rare cases of reversible posterior encephalopathy when using fingolimod at a dose of 0.5 mg with the following symptoms: intense headache with sudden onset, accompanied by nausea and vomiting, impaired consciousness, visual disturbances and seizures. The condition is usually reversible, but can lead to ischemic or hemorrhagic stroke, so delaying diagnosis and delaying the start of correction of the condition can lead to neurological consequences. If suspected reversible encephalopathy syndrome is taking the drug Neskler® should stop.
Previously treated immunosuppressants
Patients who have previously received treatment with interferon-beta and Glatiramer acetate, with good tolerability (no cytopenia), can be transferred to treatment with Neskler®. When prescribing the drug Neskler® 2-3 months after discontinuation of treatment with natalizumab, the joint effect on the immune system may be enhanced due to the long half-life of natalizumab.Care must be taken when transferring a patient from natalizumab to fingolimod.
Discontinuation of treatment with fingolimod
After the abolition of fingolimod, a 6-week interval without treatment is necessary to remove fingolimod from the bloodstream. When you stop taking the drug should be borne in mind that the normalization of the number of lymphocytes occurs 1-2 months after the last use of fingolimod. Since the appointment of immunosuppressants for 1 -2 months after discontinuation of the drug Neskler® Perhaps an additional depressant effect on the immune system, care must be taken when using immunosuppressants shortly after stopping treatment with the drug.
Liver function disorders

Not earlier than 6 months before the start of therapy with Neskler® It is necessary to conduct a study of the activity of hepatic transaminases. In the absence of clinical manifestations of liver damage, it is recommended to determine the level of hepatic transaminases in 1, 3, 6, 9, and 12 months of treatment, and then periodically. The increased activity of hepatic transaminases> 5 VGN requires more frequent biochemical examination of blood serum, including the determination of the level of bilirubin and alkaline phosphatase.
If symptoms appear that suggest impaired liver function (vomiting and nausea of ​​unknown etiology, jaundice, abdominal pain, fatigue, anorexia, dark urine color), it is necessary to conduct a study of the activity of liver enzymes and stop taking the drug.
Respiratory system
Spirometry is recommended for patients with suspected respiratory disorders.

Influence on ability to drive vehicles and mechanisms
Patients who, on the background of the use of the drug Neskler, have such undesirable phenomena as dizziness or visual impairment, should not drive a car or work with mechanisms until these side effects disappear completely.
It is necessary to monitor the patient's condition within the first 6 hours after the first dose of the drug before starting to drive.

  • Brand name: Nescler®
  • Active ingredient: Fingolimod
  • Dosage form: Capsules
  • Manufacturer: BioIntegrator LLC
  • Country of Origin: Russia

Studies and clinical trials of Fingolimod (Click to expand)

  1. Fingolimod provides long-term protection in rodent models of cerebral ischemia
  2. Mechanisms of fingolimod's efficacy and adverse effects in multiple sclerosis
  3. Fingolimod treatment for multiple sclerosis Patients What Do We Do with Varicella?
  4. Synthesis and Immunomodulating Activity of New Analogues of Fingolimod
  5. Oral-intravenous crossover study of fingolimod pharmacokinetics, lymphocyte responses and cardiac effects
  6. ChemInform Abstract: Synthesis of the Key Intermediate, Diethyl 2-Acetylamino-2-(2-(4-octanoylphenyl)ethyl)propane-1,3-dioate, of the Immunomodulatory Agent FTY720 (Fingolimod).
  7. ChemInform Abstract: A New Therapeutic Approach for Autoimmune Diseases by the Sphingosine 1-Phosphate Receptor Modulator, Fingolimod (FTY720)
  8. Efficient chromatography-free synthesis of the oxy-analogue of fingolimod
  9. The Immunosuppressant FTY720 (Fingolimod) enhances Glycosaminoglycan depletion in articular cartilage
  10. Fingolimod modulates microglial activation to augment markers of remyelination
  11. FTY720 (Fingolimod) als neue Therapiemöglichkeit der Multiplen Sklerose
  12. Orales Fingolimod bei Multipler Sklerose
  13. Therapie der Multiplen Sklerose mit Fingolimod
  14. The effect on heart rate of combining single-dose fingolimod with steady-state atenolol or diltiazem in healthy subjects
  15. Does fingolimod in multiple sclerosis patients cause macular edema?
  16. Fingolimod for Multiple Sclerosis: Mechanism of Action, Clinical Outcomes, and Future Directions
  17. Neurological S1P signaling as an emerging mechanism of action of oral FTY720 (Fingolimod) in multiple sclerosis
  18. Fingolimod: an oral disease-modifying therapy for relapsing multiple sclerosis
  19. The ability of atropine to prevent and reverse the negative chronotropic effect of fingolimod in healthy subjects
  20. Pharmacokinetics, pharmacodynamics, safety, and tolerability of single-dose fingolimod (FTY720) in adolescents with stable renal transplants
  21. FTY720 (fingolimod) in Multiple Sclerosis: therapeutic effects in the immune and the central nervous system
  22. Oral fingolimod rescues the functional deficits of synapses in experimental autoimmune encephalomyelitis
  23. Targeting synaptic pathology in multiple sclerosis: fingolimod to the rescue?
  24. Oral fingolimod for the treatment of patients with relapsing forms of multiple sclerosis

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