1. Name Of The Medicinal Product
Myfortic ® 180 mg gastro-resistant tablets
Myfortic ® 360 mg gastro-resistant tablets
2. Qualitative And Quantitative Composition
Each gastro-resistant tablet contains 180mg or 360 mg mycophenolic acid (as mycophenolate sodium).
Excipients:
Lactose, anhydrous: 45 mg or 90 mg per tablet.
For a full list of excipients, see section 6.1.
3. Pharmaceutical Form
Gastro-resistant tablet
180mg: Lime green, film-coated round tablet, with bevelled edges and the imprint (debossing) “C” on one side.
360mg: Pale orange red film-coated ovaloid tablet, with imprint (debossing) “CT” on one side.
4. Clinical Particulars
4.1 Therapeutic Indications
Myfortic is indicated in combination with ciclosporin and corticosteroids for the prophylaxis of acute transplant rejection in adult patients receiving allogeneic renal transplants.
4.2 Posology And Method Of Administration
Treatment with Myfortic should be initiated and maintained by appropriately qualified transplant specialists.
The recommended dose is 720 mg administered twice daily (1,440 mg daily dose). This dose of mycophenolate sodium corresponds to 1 g mycophenolate mofetil administered twice daily (2 g daily dose) in terms of mycophenolic acid (MPA) content.
For additional information about the corresponding therapeutic doses of mycophenolate sodium and mycophenolate mofetil, see sections 4.4 and 5.2.
In de novo patients, Myfortic should be initiated within 72 hours following transplantation.
Myfortic can be taken with or without food. Patients may select either option but must adhere to their selected option (see section 5.2).
In order to retain the integrity of the enteric coating, Myfortic tablets should not be crushed.
Where crushing of Myfortic tablets is necessary, avoid inhalation of the powder or direct contact of the powder with skin or mucous membrane.
Children and adolescents
Insufficient data are available to support the efficacy and safety of Myfortic in children and adolescents. Limited pharmacokinetic data are available for paediatric renal transplant patients (see section 5.2).
Elderly
The recommended dose in elderly patients is 720 mg twice daily.
Patients with renal impairment
In patients experiencing delayed renal graft function post-operatively, no dose adjustments are needed (see section 5.2).
Patients with severe renal impairment (glomerular filtration rate <25 ml·min-1·1.73 m-2) should be carefully monitored and the daily dose of Myfortic should not exceed 1,440 mg.
Patients with hepatic impairment
No dose adjustments are needed for renal transplant patients with severe hepatic impairment.
Treatment during rejection episodes
Renal transplant rejection does not lead to changes in mycophenolic acid (MPA) pharmacokinetics; dosage modification or interruption of Myfortic is not required.
4.3 Contraindications
Hypersensitivity to mycophenolate sodium, mycophenolic acid or mycophenolate mofetil or to any of the excipients (see section 6.1).
Myfortic is contraindicated in women who are breastfeeding (see section 4.6).
For information on use in pregnancy and lactation and contraceptive requirements, see section 4.6.
4.4 Special Warnings And Precautions For Use
Patients receiving immunosuppressive regimens involving combinations of drugs, including Myfortic, are at increased risk of developing lymphomas and other malignancies, particularly of the skin (see section 4.8). The risk appears to be related to the intensity and duration of immunosuppression rather than to the use of any specific agent. As general advice to minimise the risk for skin cancer, exposure to sunlight and UV light should be limited by wearing protective clothing and using a sunscreen with a high protection factor.
Patients receiving Myfortic should be instructed to immediately report any evidence of infection, unexpected bruising, bleeding or any other manifestation of bone marrow depression.
Patients treated with immunosuppressants, including Myfortic, are at increased risk for opportunistic infections (bacterial, fungal, viral and protozoal), fatal infections and sepsis (see section 4.8). Among the opportunistic infections are BK virus associated nephropathy and JC virus associated progressive multifocal leukoencephalopathy (PML). These infections are often related to a high total immunosuppressive burden and may lead to serious or fatal conditions that physicians should consider in the differential diagnosis in immunosuppressed patients with deteriorating renal function or neurological symptoms.
Cases of pure red cell aplasia (PRCA) have been reported in patients treated with MPA derivatives (which include mycophenolate mofetil and mycophenolate sodium) in combination with other immunosuppressants. The mechanism for MPA derivatives induced PRCA is unknown. PRCA may resolve with dose reduction or cessation of therapy. Changes to Myfortic therapy should only be undertaken under appropriate supervision in transplant recipients in order to minimise the risk of graft rejection (see Section 4.8).
Patients receiving Myfortic should be monitored for blood disorders (e.g. neutropenia or anemia – see section 4.8), which may be related to MPA itself, concomitant medications, viral infections, or some combination of these causes. Patients taking Myfortic should have complete blood counts weekly during the first month, twice monthly for the second and third months of treatment, then monthly through the first year. If blood disorders occur (e.g. neutropenia with (absolute neutrophil count <1.5 x 103/µl or anemia) it may be appropriate to interrupt or discontinue Myfortic.
Patients should be advised that during treatment with MPA vaccinations may be less effective and the use of live attenuated vaccines should be avoided (see section 4.5).
Influenza vaccination may be of value. Prescribers should refer to national guidelines for influenza vaccination.
Because MPA derivatives have been associated with an increased incidence of digestive system adverse events, including infrequent cases of gastrointestinal tract ulceration and haemorrhage and perforation, Myfortic should be administered with caution in patients with active serious digestive system disease.
It is recommended that Myfortic not be administered concomitantly with azathioprine because concomitant administration of these drugs has not been evaluated.
Mycophenolic acid (as sodium salt) and mycophenolate mofetil should not be indiscriminately interchanged or substituted because of their different pharmacokinetic profiles.
Myfortic has been administered in combination with corticosteroids and ciclosporin.
There is limited experience with its concomitant use with induction therapies such as anti-lymphocyte globulin or basiliximab. The efficacy and safety of the use of Myfortic with other immunosuppressive agents (for example, tacrolimus) have not been studied.
Myfortic contains lactose. Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicine.
The concomitant administration of Myfortic and drugs which interfere with enterohepatic circulation, for example cholestyramine or activated charcoal, may result in sub-therapeutic systemic MPA exposure and reduced efficacy.
Myfortic is an IMPDH (inosine monophosphate dehydrogenase) inhibitor. Therefore, it should be avoided in patients with rare hereditary deficiency of hypoxanthine-guanine phosphoribosyl-transferase (HGPRT) such as Lesch-Nyhan and Kelley-Seegmiller syndrome.
Myfortic therapy should not be initiated until a negative pregnancy test has been obtained. Effective contraception must be used before beginning Myfortic therapy, during therapy and for six weeks following therapy discontinuation (see section 4.6).
4.5 Interaction With Other Medicinal Products And Other Forms Of Interaction
The following interactions have been reported between MPA and other medicinal products:
Aciclovir and ganciclovir
The potential for myelosuppression in patients receiving both Myfortic and aciclovir or ganciclovir has not been studied. Increased levels of mycophenolic acid glucuronide (MPAG) and aciclovir/ganciclovir may be expected when aciclovir/ganciclovir and Myfortic are administered concomitantly, possibly as a result of competition for the tubular secretion pathway.
The changes in MPAG pharmacokinetics are unlikely to be of clinical significance in patients with adequate renal function. In the presence of renal impairment, the potential exists for increases in plasma MPAG and aciclovir/ganciclovir concentrations; dose recommendations for aciclovir/ganciclovir should be followed and patients carefully observed.
Gastroprotective agents:
Magnesium-aluminium containing antacids:
MPA AUC and Cmax have been shown to decrease by approximately 37% and 25%, respectively, when a single dose of magnesium-aluminium containing antacids is given concomitantly with Myfortic. Magnesium aluminium-containing antacids may be used intermittently for the treatment of occasional dyspepsia. However the chronic, daily use of magnesium-aluminium containing antacids with Myfortic is not recommended due to the potential for decreased mycophenolic acid exposure and reduced efficacy.
Proton pump inhibitors:
In healthy volunteers, no changes in the pharmacokinetics of MPA were observed following concomitant administration of Myfortic and pantoprazole given at 40 mg twice daily during the four previous days. No data are available with other proton pump inhibitors given at high doses.
Oral contraceptives
Interaction studies between MMF and oral contraceptives indicate no interaction. Given the metabolic profile of MPA, no interactions would be expected for Myfortic and oral contraceptives.
Cholestyramine and drugs that bind bile acids
Caution should be used when co-administering drugs or therapies that may bind bile acids, for example bile acid sequestrates or oral activated charcoal, because of the potential to decrease MPA exposure and thus reduce the efficacy of Myfortic.
Ciclosporin
When studied in stable renal transplant patients, ciclosporin pharmacokinetics were unaffected by steady state dosing of Myfortic. When co-administered with mycophenolate mofetil, ciclosporin is known to decrease the exposure of MPA. When co-administered with Myfortic, ciclosporin may decrease the concentration of MPA as well (by approximately 20%, extrapolated from mycophenolate mofetil data), but the exact extent of this decrease is unknown because such an interaction has not been studied. However, as efficacy studies were conducted in combination with ciclosporin, this interaction does not modify the recommended posology of Myfortic. In case of interruption or discontinuation of ciclosporin, Myfortic dosage should be re-evaluated depending on the immunosuppressive regimen.
Tacrolimus
In a calcineurin cross-over study in stable renal transplant patients, steady-state Myfortic pharmacokinetics were measured during both Neoral and tacrolimus treatment. Mean MPA AUC was 19% higher (90% CI: -3, +47), whereas mean MPAG AUC was about 30% lower (90% CI: 16, 42) on tacrolimus compared to Neoral treatment. In addition, MPA AUC intra-subject variability was doubled when switching from Neoral to tacrolimus. Clinicians should note this increase both in MPA AUC and variability, and adjustments to Myfortic dosing should be dictated by the clinical situation. Close clinical monitoring should be performed when a switch from one calcineurin inhibitor to another is planned.
Live attenuated vaccines
Live vaccines should not be given to patients with an impaired immune response. The antibody response to other vaccines may be diminished.
4.6 Pregnancy And Lactation
Pregnancy
Myfortic therapy should not be initiated until a negative pregnancy test has been obtained. Effective contraception must be used before beginning Myfortic therapy, during Myfortic therapy and for six weeks after discontinuing therapy. Patients should be instructed to consult their physician immediately should pregnancy occur.
The use of Myfortic is not recommended during pregnancy and should be reserved for cases where no alternative treatment is available.
There is limited data from the use of Myfortic in pregnant women. However, congenital malformations including ear malformations, i.e. abnormally formed or absent external/middle ear, have been reported in children of patients exposed to mycophenolate in combination with other immunosuppressants during pregnancy. Cases of spontaneous abortions have been reported in patients exposed to mycophenolic acid compounds. Studies in animals have shown reproductive toxicity (see section 5.3).
Lactation
MPA is excreted in milk in lactating rats. It is unknown whether Myfortic is excreted in human breast milk. Because of the potential for serious adverse reactions to MPA in breast-fed infants, Myfortic is contra-indicated in women who are breast-feeding (see section 4.3).
4.7 Effects On Ability To Drive And Use Machines
No studies on the effects on the ability to drive and use machines have been performed. The mechanism of action and pharmacodynamic profile and the reported adverse reactions indicate that an effect is unlikely.
4.8 Undesirable Effects
The following undesirable effects cover adverse drug reactions from clinical trials:
Malignancies
Patients receiving immunosuppressive regimens involving combinations of drugs, including MPA, are at increased risk of developing lymphomas and other malignancies, particularly of the skin (see section 4.4). Lymphoproliferative disease or lymphoma developed in 2 de novo (0.9%) patients and in 2 maintenance patients (1.3%) receiving Myfortic for up to 1 year. Non-melanoma skin carcinomas occurred in 0.9% of de novo and 1.8% of maintenance patients receiving Myfortic for up to 1 year; other types of malignancy occurred in 0.5% of de novo and 0.6% of maintenance patients.
Opportunistic infections
All transplant patients are at increased risk of opportunistic infections; the risk increased with total immunosuppressive load (see section 4.4). The most common opportunistic infections in de novo renal transplant patients receiving Myfortic with other immunosuppressants in controlled clinical trials of renal transplant patients followed for 1 year were cytomegalovirus (CMV), candidiasis and herpes simplex. CMV infection (serology, viraemia or disease) was reported in 21.6% of de novo and in 1.9% of maintenance renal transplant patients.
Elderly patients
Elderly patients may generally be at increased risk of adverse drug reactions due to immunosuppression.
Other adverse drug reactions
Table 1 below contains adverse drug reactions possibly or probably related to Myfortic reported in the controlled clinical trials in renal transplant patients, in which Myfortic was administered together with ciclosporin microemulsion and corticosteroids at a dose of 1,440 mg/day for 12 months. It is compiled according to MedDRA system organ class.
Adverse reactions are listed according to the following categories:
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Table 1
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* event reported in a single patient (out of 372) only.
Note: renal transplant patients were treated with 1,440 mg Myfortic daily up to one year. A similar profile was seen in the de novo and maintenance transplant population although the incidence tended to be lower in the maintenance patients.
Rash has been identified as an adverse drug reaction from post marketing experience.
The following additional adverse reactions are attributed MPA derivatives as a class effect:
Gastrointestinal disorders:
colitis, CMV gastritis, intestinal perforation, gastric ulcers, duodenal ulcers.
Infections and infestations:
serious, life-threatening infections, including meningitis, infectious endocarditis, tuberculosis, and atypical mycobacterial infection. Cases of BK virus associated nephropathy, as well as cases of JC virus associated progressive multifocal leukoencephalopathy (PML), have been reported in patients treated with immunosuppressants, including Myfortic (see section 4.4).
Blood and lymphatic system disorders:
neutropenia, pancytopenia.
Cases of pure red cell aplasia (PRCA) have been reported in patients treated with MPA derivatives (see section 4.4).
Isolated cases of abnormal neutrophil morphology, including acquired Pelger-Huet anomaly, have been observed in patients treated with MPA derivatives. These changes are not associated with impaired neutrophil function. These changes may suggest a 'left shift' in maturity of neutrophils in haematological investigations, which may be mistakenly interpreted as a sign of infection in immunosuppressed patients such as those that received Myfortic.
4.9 Overdose
No case of overdose has been reported. Although dialysis may be used to remove the inactive metabolite MPAG, it would not be expected to remove clinically significant amounts of the active moiety MPA. This is in large part due to the very high plasma protein binding of MPA, 97%. By interfering with enterohepatic circulation of MPA, bile acid sequestrants, such as cholestyramine, may reduce the systemic MPA exposure.
5. Pharmacological Properties
5.1 Pharmacodynamic Properties
Pharmacotherapeutic group: immunosuppressant, ATC code: L04AA06
MPA is a potent, selective, uncompetitive and reversible inhibitor of inosine monophosphate dehydrogenase, and therefore inhibits the de novo pathway of guanosine nucleotide synthesis without incorporation into DNA. Because T- and B-lymphocytes are critically dependent for their proliferation on de novo synthesis of purines whereas other cell types can utilize salvage pathways, MPA has more potent cytostatic effects on lymphocytes than on other cells.
5.2 Pharmacokinetic Properties
Absorption
Following oral administration, mycophenolate sodium is extensively absorbed. Consistent with its enteric coated design, the time to maximal concentration (Tmax) of MPA was approximately 1.5-2 hours. Approximately 10% of all morning pharmacokinetic profiles showed a delayed Tmax, sometimes up to several hours, without any expected impact on 24 hour/daily MPA exposure.
In stable renal transplant patients on ciclosporin based immunosuppression, the gastrointestinal absorption of MPA was 93% and the absolute bioavailability was 72%. Myfortic pharmacokinetics are dose proportional and linear over the studied dose range of 180 to 2,160 mg.
Compared to the fasting state, administration of a single dose of Myfortic 720 mg with a high fat meal (55 g fat, 1,000 calories) had no effect on the systemic exposure of MPA (AUC), which is the most relevant pharmacokinetic parameter linked to efficacy. However there was a 33% decrease in the maximal concentration of MPA (Cmax). Moreover, Tlag and Tmax were on average 3-5 hours delayed, with several patients having a Tmax of>15 hours. The effect of food on Myfortic may lead to an absorption overlap from one dose interval to another. However, this effect was not shown to be clinically significant.
Distribution
The volume of distribution at steady state for MPA is 50 litres. Both mycophenolic acid and mycophenolic acid glucuronide are highly protein bound (97% and 82%, respectively). The free MPA concentration may increase under conditions of decreased protein binding sites (uraemia, hepatic failure, hypoalbuminaemia, concomitant use of drugs with high protein binding). This may put patients at increased risk of MPA-related adverse effects.
Elimination
The half life of MPA is approximately 12 hours and the clearance is 8.6 l/h.
Metabolism
MPA is metabolised principally by glucuronyl transferase to form the phenolic glucuronide of MPA, mycophenolic acid glucuronide (MPAG). MPAG is the predominant metabolite of MPA and does not manifest biological activity. In stable renal transplant patients on ciclosporin-based immunosuppression, approximately 28% of the oral Myfortic dose is converted to MPAG by presystemic metabolism. The half life of MPAG is longer than that of MPA, approximately 16 hours and its clearance is 0.45 l/h.
Excretion
Although negligible amounts of MPA are present in the urine (<1.0%), the majority of MPA is eliminated in the urine as MPAG. MPAG secreted in the bile is available for deconjugation by gut flora. The MPA resulting from this deconjugation may then be reabsorbed. Approximately 6-8 hours after Myfortic dosing a second peak of MPA concentration can be measured, consistent with reabsorption of the deconjugated MPA. There is large variability in the MPA trough levels inherent to MPA preparations, and high morning trough levels (C0> 10 µg/ml) have been observed in approximately 2% of patients treated with Myfortic. However, across studies, the AUC at steady state (0-12h) which is indicative of the overall exposure showed a lower variability than the one corresponding to Ctrough.
Pharmacokinetics in renal transplant patients on ciclosporin based immunosuppression
Shown in Table 2 are mean pharmacokinetic parameters for MPA following the administration of Myfortic. In the early post transplant period, mean MPA AUC and mean MPA Cmax were approximately one-half of the values measured six months post transplant.
Table 2 Mean (SD) pharmacokinetic parameters for MPA following oral administration of Myfortic to renal transplant patients on ciclosporin-based immunosuppression
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* median values
Renal impairment
MPA pharmacokinetics appeared to be unchanged over the range of normal to absent renal function. In contrast, MPAG exposure increased with decreased renal function; MPAG exposure being approximately 8 fold higher in the setting of anuria. Clearance of either MPA or MPAG was unaffected by haemodialysis. Free MPA may also significantly increase in the setting of renal failure. This may be due to decreased plasma protein binding of MPA in the presence of high blood urea concentration.
Hepatic impairment
In volunteers with alcoholic cirrhosis, hepatic MPA glucuronidation processes were relatively unaffected by hepatic parenchymal disease. Effects of hepatic disease on this process probably depend on the particular disease. However, hepatic disease with predominantly biliary damage, such as primary biliary cirrhosis, may show a different effect.
Children and adolescents
Limited data are available on the use of Myfortic in children and adolescents. In Table 2 above the mean (SD) MPA pharmacokinetics are shown for stable paediatric renal transplant patients (aged 5-16 years) on ciclosporin-based immunosuppression. Mean MPA AUC at a dose of 450 mg/m2 was similar to that measured in adults receiving 720 mg Myfortic. The mean apparent clearance of MPA was approximately 6.7 l/h/m2.
Gender
There are no clinically significant gender differences in Myfortic pharmacokinetics.
Elderly
Pharmacokinetics in the elderly have not formally been studied. MPA exposure does not appear to vary to a clinically significant degree by age.
5.3 Preclinical Safety Data
The haematopoetic and lymphoid system were the primary organs affected in repeated-dose toxicity studies conducted with mycophenolate sodium in rats and mice. These effects occurred at systemic exposure levels which are equivalent to or less than the clinical exposure at the recommended dose of 1.44 g/day of Myfortic in renal transplant patients.
Gastrointestinal effects were observed in the dog at systemic exposure levels equivalent to or less than the clinical exposure at the recommended doses.
The non-clinical toxicity profile of mycophenolic acid (as sodium salt) appears to be consistent with adverse events observed in human clinical trials which now provide safety data of more relevance to the patient population (see section 4.8).
Three genotoxicity assays (in vitro mouse lymphoma assay, micronucleus test in V79 Chinese hamster cells and in vivo mouse bone marrow micronucleus test) showed a potential of mycophenolic acid to cause chromosomal aberrations. These effects can be related to the pharmacodynamic mode of action, i.e. inhibition of nucleotide synthesis in sensitive cells. Other in vitro tests for detection of gene mutation did not demonstrate genotoxic activity.
Mycophenolic acid (as sodium salt) was not tumourigenic in rats and mice. The highest dose tested in the animal carcinogenicity studies resulted in approximately 0.6-5 times the systemic exposure (AUC or Cmax) observed in renal transplant patients at the recommended clinical dose of 1.44 g/day.
Mycophenolic acid (as sodium salt) had no effect on fertility of male or female rats up to dose levels at which general toxicity and embryotoxicity were observed.
In a teratology study performed with mycophenolic acid (as sodium salt) in rats, at a dose as low as 1 mg/kg, malformations in the offspring were observed, including anophthalmia, exencephaly and umbilical hernia. The systemic exposure at this dose represents 0.05 times the clinical exposure at the dose of 1.44 g/day of Myfortic (see section 4.6).
In a pre- and postnatal development study in rat, mycophenolic acid (as sodium salt) caused developmental delays (abnormal pupillary reflex in females and preputial separation in males) at the highest dose of 3 mg/kg that also induced malformations.
Mycophenolic acid (as sodium salt) showed a phototoxic potential in an in vitro 3T3 NRU phototoxicity assay.
6. Pharmaceutical Particulars
6.1 List Of Excipients
Core
Maize starch
Povidone
Crospovidone
Lactose, anhydrous
Silica, colloidal anhydrous
Magnesium stearate
Coating
Hypromellose phthalate
Titanium dioxide (E 171)
Iron oxide yellow (E 172)
Indigo Carmine (E 132) (180mg only)
Iron oxide red (E 172) (360mg only)
6.2 Incompatibilities
Not applicable.
6.3 Shelf Life
30 months.
6.4 Special Precautions For Storage
Do not store above 30°C.
Store in the original package in order to protect from moisture and light.
6.5 Nature And Contents Of Container
The tablets are packed in polyamide/aluminium/PVC/aluminium blister packs of 10 tablets per blister in quantities of 20, (180mg only), 50, 100, 120 and 250 tablets per carton.
Not all pack sizes may be marketed.
6.6 Special Precautions For Disposal And Other Handling
In order to retain the integrity of the enteric coating, Myfortic tablets should not be crushed (see section 4.2).
Mycophenolic acid has demonstrated teratogenic effects in rats and rabbits (see section 4.6). Where crushing of Myfortic tablets is necessary, avoid inhalation of the powder or direct contact of the powder with skin or mucous membrane.
Any unused product or waste material should be disposed of in accordance with local requirements.
7. Marketing Authorisation Holder
Novartis Pharmaceuticals UK Limited
Frimley Business Park
Frimley
Camberley
Surrey
GU16 7SR
United Kingdom
8. Marketing Authorisation Number(S)
Myfortic 180mg gastro-resistant tablets: PL 00101/0664
Myfortic 360mg gastro-resistant tablets: PL 00101/0665
9. Date Of First Authorisation/Renewal Of The Authorisation
10/10/2008
10. Date Of Revision Of The Text
28/10/2010
LEGAL CATEGORY:
POM
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