Components:
Medically reviewed by Kovalenko Svetlana Olegovna, PharmD. Last updated on 11.05.2022
Attention! Information on this page is intended only for medical professionals! Information is collected in open sources and may contain significant errors! Be careful and double-check all the information on this page!
Top 20 medicines with the same components:
Fingya is indicated as single disease modifying therapy in highly active relapsing-remitting multiple sclerosis for the following adult patient groups: Patients with high disease activity despite treatment with at least 1 disease-modifying therapy (for exceptions and information about washout periods see
Pharmacology: Pharmacodynamics under Action and Precautions). These patients may be defined as those who have failed to respond to a full and adequate course (normally at least one year of treatment) of at least one disease-modifying therapy. Patients should have had at least 1 relapse in the previous year while on therapy, and have at least 9 T2-hyperintense lesions in cranial MRI or at least 1 Gadolinium-enhancing lesion. A "non-responder" could also be defined as a patient with an unchanged or increased relapse rate or ongoing severe relapses, as compared to the previous year.
Patients with rapidly evolving severe relapsing-remitting multiple sclerosis defined by ≥2 disabling relapses in 1 year, and with ≥1 Gadolinium-enhancing lesions on brain MRI or a significant increase in T2 lesion load as compared to a previous recent MRI.
Fingya (Fingya) is an immunosuppressant. It works by keeping immune cells trapped in your lymph nodes so they can't reach the central nervous system (brain and spinal cord).
Fingya is used to treat relapsing multiple sclerosis (MS) in adults.
Fingya will not cure MS, it will only decrease the frequency of relapse symptoms.
Recommended Dose: 0.5 mg once daily. Fingya doses >0.5 mg are associated with a greater incidence of adverse reactions without additional benefit.
First Dose Monitoring: Initiation of Fingya treatment results in a decrease in heart rate. After the 1st dose of Fingya, the heart rate decrease starts within an hr and the day 1 nadir generally occurs within approximately 6 hrs, although the nadir can be observed up to 24 hrs after the 1st dose in some patients.
The 1st dose of Fingya should be administered in a setting in which resources to appropriately manage symptomatic bradycardia are available. In order to assess patient response to the 1st dose of Fingya, observe all patients for 6 hrs for signs and symptoms of bradycardia with hourly pulse and blood pressure measurement. Obtain in all patients an electrocardiogram (ECG) prior to dosing, and at the end of the observation period.
Additional observation should be instituted until the finding has resolved in the following situations: The heart rate 6 hrs post-dose is <45 bpm. The heart rate 6 hrs post-dose is at the lowest value post-dose (suggesting that the maximum pharmacodynamic effect on the heart may not have occurred). The ECG 6 hrs post-dose shows new onset 2nd degree or higher AV block.
Should post-dose symptomatic bradycardia occur, initiate appropriate management, begin continuous ECG monitoring and continue observation until the symptoms have resolved.
Should a patient require pharmacologic intervention for symptomatic bradycardia, continuous overnight ECG monitoring in a medical facility should be instituted and the 1st dose monitoring strategy should be repeated after the 2nd dose of Fingya.
Patients with some preexisting conditions (eg, ischemic heart disease, history of myocardial infarction (MI), congestive heart failure, history of cardiac arrest, cerebrovascular disease, uncontrolled hypertension, history of symptomatic bradycardia, history of recurrent syncope, severe untreated sleep apnea, AV block, sino-atrial heart block) may poorly tolerate the Fingya-induced bradycardia, or experience serious rhythm disturbances after the 1st dose of Fingya. Prior to treatment with Fingya, these patients should have a cardiac evaluation by a physician appropriately trained to conduct such evaluation and, if treated with Fingya, should be monitored overnight with continuous ECG in a medical facility after the 1st dose. Fingya is contraindicated in patients who in the last 6 months experienced MI, unstable angina, stroke, transient ischemic attack (TIA), decompensated heart failure requiring hospitalization or class III/IV heart failure).
Since initiation of Fingya treatment results in decreased heart rate and may prolong the QT interval, patients with a prolonged QT interval (>450 msec males, >470 msec females) before dosing or during 6-hr observation, or at additional risk for QT prolongation (eg, hypokalemia, hypomagnesemia, congenital long-QT syndrome), or on concurrent therapy with QT prolonging drugs with a known risk of Torsades de pointes (eg, citalopram, chlorpromazine, haloperidol, methadone, erythromycin) should be monitored overnight with continuous ECG in a medical facility.
Experience with Fingya is limited in patients receiving concurrent therapy with drugs that slow heart rate or AV conduction (eg, β-blockers, heart-rate lowering calcium channel blockers eg, diltiazem or verapamil or digoxin). Because the initiation of Fingya treatment is also associated with slowing of the heart rate, concomitant use of these drugs during Fingya initiation may be associated with severe bradycardia or heart block. The possibility to switch to drugs that do not slow the heart rate or AV conduction should be evaluated by the physician prescribing these drugs before initiating Fingya. Patients who cannot switch should have overnight continuous ECG monitoring after the first dose.
Clinical data indicate effects of Fingya on heart rate are maximal after the 1st dose although milder effects on heart rate may persist for, on average, 2-4 weeks after initiation of therapy at which time heart rate generally returns to baseline. Physicians should continue to be alert to patient reports of cardiac symptoms.
Re-initiation of Therapy Following Discontinuation: If Fingya therapy is discontinued for >14 days, after the 1st month of treatment, the effects on heart rate and AV conduction may recur on reintroduction of Fingya treatment and the same precautions (1st dose monitoring) as for initial dosing should apply. Within the first 2 weeks of treatment, 1st dose procedures are recommended after interruption of ≥1 day, during weeks 3 and 4 of treatment, 1st dose procedures are recommended after treatment interruption of >7 days.
Children: The safety and effectiveness of Fingya in pediatric patients <18 years with MS have not been established.
Elderly: Clinical MS studies of Fingya did not include sufficient numbers of patients ≥65 years to determine whether they respond differently than younger patients. Fingya should be used with caution in patients ≥65 years, reflecting the greater frequency of decreased hepatic, or renal, function and of concomitant disease or other drug therapy.
Renal Impairment: The blood level of some Fingya metabolites is increased (up to 13-fold) in patients with severe renal impairment. The toxicity of these metabolites has not been fully explored. The blood level of these metabolites has not been assessed in patients with mild or moderate renal impairment.
Hepatic Impairment: Because Fingya, but not Fingya-phosphate, exposure is doubled in patients with severe hepatic impairment, patients with severe hepatic impairment should be closely monitored, as the risk of adverse reactions may be greater.
No dose adjustment is needed in patients with mild or moderate hepatic impairment.
Administration: Fingya can be taken with or without food.
See also:
What is the most important information I should know about Fingya?
You should not use Fingya if you are allergic to it, or if you have certain serious heart conditions, especially severe heart failure, "AV block," sick sinus syndrome (unless you have a pacemaker), if you take certain heart rhythm medicines, or if you have recently had a heart attack, stroke (including "mini-stroke"), chest pain (unstable angina), or other serious heart problem.
Before you take Fingya, tell your doctor if you have an infection, a very slow heart rate, low blood pressure or a history of fainting, high blood pressure, diabetes, liver or kidney disease, asthma or other breathing disorder, congestive heart failure, heart rhythm disorder, a serious heart condition, or if you have ever had an eye condition called uveitis.
Also tell your doctor if you have never had chickenpox or if you have never received a varicella vaccine (Varivax).
You will receive your first dose of Fingya in a hospital setting where your heart rhythm can be monitored, in case the medication causes serious side effects. Your blood pressure and heart rate will be constantly monitored for at least 6 hours after your first dose of Fingya.
To be sure this medication is not causing harmful effects, your blood cells, blood pressure, liver function, and lung function will need to be tested often. You may also need to eye exams. Fingya can have long lasting effects on your body. Do not miss any follow up visits to your doctor for blood tests or eye exams.
Tell your doctor if you use any heart or blood pressure medications. Do not receive a "live" vaccine while using Fingya.
Do not stop taking Fingya without first talking to your doctor. Stopping suddenly may make your condition worse. If you stop taking Fingya for 2 weeks or longer, do not start taking it again without asking your doctor. You will need to restart the medication in a hospital setting under observation.
Use Fingya as directed by your doctor. Check the label on the medicine for exact dosing instructions.
- Fingya comes with an extra patient information sheet called a Medication Guide. Read it carefully. Read it again each time you get Fingya refilled.
- Take Fingya by mouth with or without food.
- Your first dose of Fingya will be given in a doctor's office, hospital, or clinic. You will be observed for at least 6 hours following your first dose.
- Take Fingya on a regular schedule to get the most benefit from it. Taking Fingya at the same time each day will help you remember to take it.
- Continue to take Fingya even if you feel well. Do not miss any doses.
- If you miss a dose of Fingya, call your doctor to find out what to do.
Ask your health care provider any questions you may have about how to use Fingya.
There are specific as well as general uses of a drug or medicine. A medicine can be used to prevent a disease, treat a disease over a period or cure a disease. It can also be used to treat the particular symptom of the disease. The drug use depends on the form the patient takes it. It may be more useful in injection form or sometimes in tablet form. The drug can be used for a single troubling symptom or a life-threatening condition. While some medications can be stopped after few days, some drugs need to be continued for prolonged period to get the benefit from it.Use: Labeled Indications
Multiple sclerosis, relapsing: Treatment of relapsing forms of multiple sclerosis (MS), including clinically isolated syndrome, relapsing-remitting disease, and active secondary progressive disease, in patients ≥10 years.
See also:
What other drugs will affect Fingya?
Pharmacodynamic Interactions: Anti-neoplastic, immune-modulating or immunosuppressive therapies (including corticosteroids) should be co-administered with caution due to the risk of additive immune system effects. Specific decisions as to the dosage and duration of concomitant treatment with corticosteroids should be based on clinical judgment. Co-administration of a short course of corticosteroids (up to 5 days as per study protocols) did not increase the overall rate of infection in patients treated with Fingya in the Phase III clinical trials, compared to placebo.
Caution should also be applied when switching patients from long-acting therapies with immune effects such as natalizumab, teriflunomide or mitoxantrone.
When Fingya is used with atenolol, there is an additional 15% reduction in heart rate upon Fingya initiation, an effect not seen with diltiazem. Treatment with Fingya should not be initiated in patients receiving beta blockers, heart rate lowering calcium channel blockers (such as verapamil, diltiazem or ivabradine), or other substances which may decrease heart rate (e.g. digoxin) because of the potential additive effects on heart rate. If treatment with Fingya is considered, advice from a cardiologist should be sought regarding the switch to non-heart-rate lowering medicinal products or appropriate monitoring for treatment initiation (should last overnight).
During and for up to two months after treatment with Fingya vaccination may be less effective. The use of live attenuated vaccines may carry the risk of infection and should therefore be avoided.
Pharmacokinetic Interactions: Fingya is primarily cleared via cytochrome P450 4F2 (CYP4F2) and possibly other CYP4F isoenzymes. In vitro studies in hepatocytes indicated that CYP3A4 may contribute to Fingya metabolism in the case of strong induction of CYP3A4.
Potential of Fingya and Fingya-Phosphate to Inhibit the Metabolism of Co-Medications: In vitro inhibition studies using pooled human liver microsomes and specific metabolic probe substrates demonstrated that Fingya and Fingya-phosphate have little or no capacity to inhibit the activity of CYP enzymes [CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4/5, or CYP4A9/11 (Fingya only)]. Therefore, Fingya and Fingya-phosphate are unlikely to reduce the clearance of drugs that are mainly cleared through metabolism by the major CYP isoenzymes.
Potential of Fingya and Fingya-Phosphate to Induce Its Own and/or the Metabolism of Co-Medications: Fingya was examined for its potential to induce human CYP3A4, CYP1A2, CYP4F2, and ABCB1 (P-gp) mRNA and CYP3A, CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, and CYP4F2 activity in primary human hepatocytes. Fingya did not induce mRNA or activity of the different CYP enzymes and ABCB1 with respect to the vehicle control. Therefore, no clinically relevant induction of the tested CYP enzymes or ABCB1 (P-gp) by Fingya is expected at therapeutic concentrations. In vitro experiments did not provide an indication of CYP induction by Fingya-phosphate.
Potential of Fingya and Fingya-Phosphate to Inhibit the Active Transport of Co-Medications: Based on in vitro data, Fingya as well as Fingya-phosphate are not expected to inhibit the uptake of co-medications and/or biologics transported by the organic anion transporting polypeptides 1B1 and 1B3 (OATP1B1, OATP1B3) or the sodium taurocholate co-transporting polypeptide (NTCP). Similarly, they are not expected to inhibit the efflux of co-medications and/or biologics transported by the breast cancer resistance protein (BCRP), the bile salt export pump (BSEP), the multidrug resistance-associated protein 2 (MRP2) or P-glycoprotein (P-gp) at therapeutic concentrations.
Oral Contraceptives:
Cyclosporine: The pharmacokinetics of single-dose Fingya were not altered during co-administration with cyclosporine at steady-state, nor were cyclosporine steady-state pharmacokinetics altered by single-dose, or multi-dose (28 days) Fingya administration. These data indicate that Fingya is unlikely to reduce, or increase the clearance of drugs mainly cleared by CYP3A4 and that inhibition of CYP3A4 is unlikely to reduce the clearance of Fingya. Potent inhibition of transporters P-gp, MRP2 and OATP1B1 does not influence Fingya disposition.
Ketoconazole: The co-administration of ketoconazole 200 mg twice daily at steady-state and a single dose of Fingya 5 mg led to a modest increase in the AUC of Fingya and Fingya-phosphate (1.7-fold increase) by inhibition of CYP4F2.
Isoproterenol, Atropine, Atenolol and Diltiazem: Single-dose Fingya and Fingya-phosphate exposure was not altered by co-administered isoproterenol, or atropine. Likewise, the single-dose pharmacokinetics of Fingya and Fingya-phosphate and the steady-state pharmacokinetics of both atenolol and diltiazem were unchanged during the co-administration of the latter two drugs with Fingya.
Carbamazepine: The co-administration of carbamazepine 600 mg twice daily at steady-state and a single dose of Fingya 2 mg had a weak effect on the AUC of Fingya and Fingya-phosphate, decreasing both by approximately 40%. The clinical relevance of this decrease is unknown.
Population Pharmacokinetics Analysis of Potential Drug-Drug Interactions: A population pharmacokinetics evaluation, performed in multiple sclerosis patients did not provide evidence for a significant effect of fluoxetine and paroxetine (strong CYP2D6 inhibitors) on Fingya or Fingya-phosphate concentrations. In addition, the following, commonly prescribed substances had no clinically relevant effect (≤20%) on Fingya or Fingya-phosphate concentrations: Baclofen, gabapentin, oxybutynin, amantadine, modafinil, amitriptyline, pregabalin, corticosteroids and oral contraceptives.
Laboratory Tests: Since Fingya reduces blood lymphocyte counts via re-distribution in secondary lymphoid organs, peripheral blood lymphocyte counts cannot be utilized to evaluate the lymphocyte subset status of a patient treated with Fingya.
Laboratory tests requiring the use of circulating mononuclear cells require larger blood volumes due to reduction in the number of circulating lymphocytes.
See also:
What are the possible side effects of Fingya?
The following serious adverse reactions are described elsewhere in labeling: Bradyarrhythmia and atrioventricular blocks; infections; progressive multifocal leukoencephalopathy; macular edema; Posterior Reversible Encephalopathy Syndrome; respiratory effects; liver injury; fetal risk; increased blood pressure; basal cell carcinoma; immune system effects following Fingya discontinuation; hypersensitivity reactions.
Clinical Trials Experience: Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
In clinical trials (Studies 1, 2, and 3), a total of 1,212 patients with relapsing forms of multiple sclerosis received Fingya 0.5 mg. This included 783 patients who received Fingya 0.5 mg in the 2-year placebo-controlled trials (Studies 1 and 3) and 429 patients who received Fingya 0.5 mg in the 1 year active-controlled trial (Study 2). The overall exposure in the controlled trials was equivalent to 1,716 person-years. Approximately 1,000 patients received at least 2 years of treatment with Fingya 0.5 mg. In all clinical studies, including uncontrolled extension studies, the exposure to Fingya 0.5 mg was approximately 4,119 person-years.
In placebo-controlled trials, the most frequent adverse reactions (incidence ≥10% and > placebo) for Fingya 0.5 mg were headache, liver transaminase elevation, diarrhea, cough, influenza, sinusitis, back pain, abdominal pain, and pain in extremity. Adverse events that led to treatment discontinuation and occurred in more than 1% of patients taking Fingya 0.5 mg were serum transaminase elevations (4.7% compared to 1% on placebo) and basal cell carcinoma (1% compared to 0.5% on placebo).
Table 3 lists adverse reactions that occurred in ≥ 1% of Fingya-treated patients and ≥ 1% higher rate than for placebo.
Adverse reactions of dizziness, pneumonia, eczema and pruritus were also reported in Studies 1 and 3 but did not meet the reporting rate criteria for inclusion in Table 1 (difference was less than 1%).
Adverse reactions with Fingya 0.5mg in Study 2, the 1-year active-controlled (versus interferon beta-1a) study were generally similar to those in Studies 1 and 3.
Vascular Events: Vascular events, including ischemic and hemorrhagic strokes and peripheral arterial occlusive disease were reported in premarketing clinical trials in patients who received Fingya doses (1.25-5 mg) higher than recommended for use in MS. Similar events have been reported with Fingya in the post-marketing setting although a causal relationship has not been established.
Lymphoma: Cases of lymphoma, including both T-cell and B-cell types and CNS lymphoma, have occurred in patients receiving Fingya. The reporting rate of non-Hodgkin lymphoma with Fingya is greater than that expected in the general population adjusted by age, gender, and region. The relationship of lymphoma to Fingya remains uncertain.
Each capsule contains 0.5 mg Fingya (as hydrochloride).
Fingya hydrochloride is a synthetic analogue of sphingosine. The chemical designation is 2-amino-2[2-(4-octylphenyl)ethyl]propane1,3-diol hydrochloride. Its molecular formula is C19H33NO2·HCl and it has a molecular weight of 343.93.
Fingya hydrochloride is a white to almost white crystalline powder which is freely soluble in water.
Excipients/Inactive Ingredients: Mannitol, magnesium stearate, titanium dioxide and gelatin.
However, we will provide data for each active ingredient