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Therapeutic indications:
Treatment of secondary hyperparathyrodism (HPT) in patients with end-dtage renal disease (ESRD) on maintenance dialysis therapy. Mimpara may be used as part of a therapeutic regimen including phosphate binders and/or Vitamin D sterols, as appropriate. Reduction of hypercalcaemia in patients with parathyroid carcinoma.
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Patient Information leaflet Patient Information leaflet - Arabic


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1813 ABR0475


The format of this leaflet was determined by the Ministry of Health and its content was checked and

approved by it inJune 2013.


Mimpara 30 mg film-coated tablets.

Mimpara 60 mg film-coated tablets.

Mimpara 90 mg film-coated tablets.


Each tablet contains 30 mg cinacalcet (as hydrochloride).

Each tablet contains 60 mg cinacalcet (as hydrochloride).

Each tablet contains 90 mg cinacalcet (as hydrochloride).

Excipientwith known effect

Each 30 mg tablet contains 2.74 mg of lactose

Each 60 mg tablet contains 5.47 mg of lactose

Each 90 mg tablet contains 8.21 mg of lactose

Forthefull list ofexcipients, see section 6.1.


Film-coated tablet (tablet).

Light green, oval, film-coated tablet marked “AMG” on one side and “30” on the other.

Light green, oval, film-coated tablet marked “AMG” on one side and “60” on the other.

Light green, oval, film-coated tablet marked “AMG” on one side and “90” on the other.


4.1 Therapeutic indications

Treatment of secondary hyperparathyroidism (HPT) in patients with end-stage renal disease (ESRD)

on maintenance dialysis therapy.

Mimpara may be used as part of a therapeutic regimen includingphosphate binders and/or Vitamin D

sterols, as appropriate (see section 5.1).

Reduction of hypercalcaemia in patients with parathyroid carcinoma.

4.2Posology and method of administration


Adults and elderly (> 65 years)

The recommended starting dose for adults is 30 mg once per day. Mimpara should be titrated every 2

to 4 weeks to a maximum dose of 180 mg once daily to achieve a target parathyroid hormone (PTH)

in dialysis patients of between 150-300 pg/ml (15.9-31.8 pmol/l) in the intact PTH (iPTH) assay. PTH

levels should be assessed at least 12 hours after dosing with Mimpara.Reference should be made to

current treatment guidelines.

PTH should be measured 1 to 4 weeks after initiation or dose adjustment of Mimpara.PTH should be

monitored approximately every 1-3 months during maintenance. Either the intact PTH (iPTH) or bio-

intact PTH (biPTH) may be used to measure PTH levels; treatment with Mimpara does not alter the

relationship between iPTH and biPTH.

During dose titration, serum calcium levels should be monitored frequently, and within 1 week of

initiation or dose adjustment of Mimpara. Once the maintenance dose has been established, serum

calcium should be measured approximately monthly. If serum calcium levels decrease below the

normal range, appropriate steps should be taken, including adjustment of concomitant therapy(see

section 4.4).

Children and adolescents

Mimpara is not indicated for use in children and adolescents due to a lack of data on safety and

efficacy (see section 5.2).


Adults and elderly (>65 years)

The recommended starting dose of Mimpara for adults is 30 mg twice per day. The dose of Mimpara

should be titrated every 2 to 4 weeks through sequential doses of 30 mg twice daily, 60 mg twice

daily, 90 mg twice daily, and 90 mg three or four times daily as necessary to reduce serum calcium

concentration to or below the upper limit of normal. The maximum dose used in clinical trials was 90

mg four times daily.

Serum calcium should be measured within 1 week after initiation or dose adjustment of Mimpara.

Once maintenance dose levels have been established, serum calcium should be measured every 2 to 3

months. After titration to the maximum dose of Mimpara, serum calcium should beperiodically

monitored; if clinically relevant reductions in serum calcium are not maintained, discontinuation of

Mimpara therapy should be considered (see section 5.1).

Children and adolescents

Mimpara is not indicated for use in children and adolescents due to a lack of data on safety and

efficacy (see section 5.2).

Hepatic impairment

No change in starting dose is necessary.Mimpara should be used with caution inpatients with

moderate to severe hepatic impairment and treatment should be closely monitored during dose

titration and continued treatment (see sections 4.4 and 5.2).

Method of administration

For oral use. It is recommended that Mimpara be taken with food or shortly after a meal, as studies

have shown that bioavailability of cinacalcet isincreased when taken with food (see section 5.2).

Tablets should be taken whole and not divided.

4.3 Contraindications

Hypersensitivity to the active substance or to any of the excipientslisted in section 6.1.

4.4Special warnings and precautions foruse


In clinical studies seizures were observed in 1.4% of Mimpara treated patients and 0.7% of placebo-

treated patients. While the basis for the reported difference in seizure rate is not clear, the threshold

for seizures is lowered by significant reductions in serum calcium levels.

Hypotension and/or worsening heart failure

In post-marketing safety surveillance, isolated, idiosyncratic cases of hypotension and/or worsening

heart failure have been reported in patients with impaired cardiac function, in which a causal

relationship to cinacalcet could not be completely excluded and may be mediated by reductions in

serum calcium levels. Clinical trial data showed hypotension occurred in 7% of cinacalcet-treated

patients, 12% of placebo-treated patients, and heart failure occurred in 2% of patients receiving

cinacalcet or placebo.


Mimpara treatment should not be initiated in patients with a serum calcium (corrected for albumin)

below the lower limit of the normal range.Potential manifestations of hypocalcaemia may include

paraesthesias, myalgias, cramping, tetany and convulsions. Decreases in serum calcium can also

prolong the QT interval, potentially resulting in ventricular arrhythmia.Cases of QT prolongation

and ventricular arrhythmia have been reported in patients treated with cinacalcet (see section 4.8).

Caution is advised in patients with other risk factors for QT prolongation such as patients with known

congenital long QT syndrome or patients receiving medicinal products known to cause QT


Since cinacalcet lowers serum calcium, patients should be monitored carefully for the occurrence of

hypocalcaemia (see section 4.2). In CKD patients receiving dialysis who were administered Mimpara,

4% of serum calcium values were less than 7.5mg/dl (1.875mmol/l). In the event of hypocalcaemia,

calcium-containing phosphate binders, vitamin D sterols and/or adjustment of dialysis fluid calcium

concentrations can be used to raise serum calcium. If hypocalcaemia persists, reduce the dose or

discontinue administration of Mimpara.

Cinacalcet is not indicated for CKD patients not on dialysis. Investigational studies have shown that

CKD patients not on dialysis treated with cinacalcet have an increased risk for hypocalcaemia (serum

calcium levels < 8.4mg/dl [2.1mmol/l]) compared with cinacalcet-treated CKD patients on dialysis,

which may be due to lower baseline calcium levels and/or the presence of residual kidney function.


Adynamic bone disease may develop if PTH levels are chronically suppressed below approximately

1.5 times the upper limit of normal with the iPTH assay. If PTH levels decrease below the

recommended target range in patients treated with Mimpara, the dose of Mimpara and/or vitamin D

sterols should be reduced or therapy discontinued.


Testosterone levels are often below the normal range in patients with end-stage renal disease. In a

clinical study of ESRD patients on dialysis, free testosterone levels decreased by a median of 31.3%

in the Mimpara-treated patients and by 16.3% in the placebo-treated patients after 6 months of

treatment.An open-label extension of this study showed no further reductions in free and total

testosterone concentrations over a period of 3 years in Mimpara-treated patients.The clinical

significance of these reductions in serum testosterone is unknown.


Due to the potential for 2 to 4 fold higher plasma levels of cinacalcet in patients with moderate to

severe hepatic impairment (Child-Pughclassification), Mimpara should be used with caution in these

patients and treatment should be closely monitored (see sections 4.2 and 5.2).


Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or

glucose-galactose malabsorption should not take this medicine.

4.5 Interaction with other medicinal products and other forms of interaction

Effect of other medications on cinacalcet

Cinacalcet is metabolised in part by the enzyme CYP3A4. Co-administration of 200mg bid

ketoconazole, a strong inhibitor of CYP3A4, caused an approximate 2-fold increase in cinacalcet

levels. Dose adjustment of Mimpara may be required if a patient receiving Mimpara initiates or

discontinues therapy with a strong inhibitor (e.g. ketoconazole, itraconazole, telithromycin,

voriconazole, ritonavir) or inducer (eg rifampicin) of this enzyme (seesection 4.4).

In vitrodata indicate that cinacalcet is in part metabolised by CYP1A2.Smoking induces CYP1A2;

the clearance of cinacalcet was observed to be 36-38% higher in smokers than non-smokers.The

effect of CYP1A2 inhibitors (e.g. fluvoxamine, ciprofloxacin) on cinacalcet plasma levels has not

been studied.Dose adjustment may be necessary if a patient starts or stops smoking or when

concomitant treatment with strong CYP1A2 inhibitors is initiated or discontinued.

Calcium carbonate: Co-administration of calcium carbonate (single 1500 mg dose) did not alter the

pharmacokinetics of cinacalcet.

Sevelamer: Co-administration of sevelamer (2400mg tid) did not affect the pharmacokinetics of


Pantoprazole: Co-administration of pantoprazole (80 mg od) did not alter the pharmacokinetics of


Effect of cinacalcet on other medications

Medicinal products metabolised by the enzyme P450 2D6 (CYP2D6): Cinacalcet is a strong inhibitor

of CYP2D6. Dose adjustments of concomitant medicinal products may be required when Mimpara is

administered with individually titrated, narrow therapeutic index substances that are predominantly

metabolised by CYP2D6 (e.g., flecainide, propafenone, metoprolol, desipramine, nortriptyline,

clomipramine) (see section 4.4).

Desipramine: Concurrent administration of 90 mg cinacalcet once daily with 50 mg desipramine, a

tricyclic antidepressant metabolised primarily by CYP2D6, significantly increased desipramine

exposure 3.6-fold (90 % CI 3.0, 4.4) in CYP2D6 extensive metabolisers.

Warfarin: Multiple oral doses ofcinacalcetdid not affect the pharmacokinetics or pharmacodynamics

(as measured by prothrombintime and clotting factor VII) of warfarin.

The lack of effect of cinacalcet on the pharmacokinetics of R-and S-warfarin and the absence of auto-

induction upon multiple dosing in patients indicates that cinacalcet is not an inducer of CYP3A4,

CYP1A2 or CYP2C9 in humans.

Midazolam: Co-administration of cinacalcet (90 mg) with orally administered midazolam (2 mg), a

CYP3A4 and CYP3A5 substrate, did not alter the pharmacokinetics of midazolam. These data suggest

that cinacalcet would not affect the pharmacokinetics of those classes ofmedicinesthat are

metabolized by CYP3A4 and CYP3A5, such as certain immunosuppressants, including cyclosporine

and tacrolimus.

4.6 Fertility, pregnancy and lactation


There are no clinical data from the use of cinacalcet in pregnant women. Animal studies do not

indicate direct harmful effects with respect to pregnancy, parturition or postnatal development. No

embryonal/foetal toxicities were seen in studies in pregnant rats and rabbits with the exception of

decreased foetal body weights in rats at doses associated with maternal toxicities (see section 5.3).

Mimpara should be used during pregnancy only if the potential benefit justifies the potential risk to

the foetus.


Itis not known whether cinacalcet is excreted in human milk. Cinacalcet is excreted in the milk of

lactating rats with a high milk to plasma ratio. Following careful benefit/risk assessment, a decision

should be made to discontinue either breast-feeding or treatment with Mimpara.


There are no clinical data relating to the effect of cinacalcet on fertility. There were no effects on

fertility in animal studies.

4.7 Effects on ability to drive and use machines

No studies on the effects on the ability to drive and use machineshave been performed.However,

certain adverse reactions may affect the ability to drive and use machines (see section 4.8).

4.8 Undesirable effects


Data presented from controlled studies include 656 patients who received Mimpara and 470 patients

who received placebo for up to 6 months. The most commonly reportedadverse reactionswere nausea

and vomiting, occurring in 31% Mimpara and 19% placebo treated patients, and 27% Mimpara and

15% placebo treated patients, respectively. Nausea and vomiting were mild to moderate in severity

and transient in nature in the majority of patients. Discontinuation of therapy as a result of undesirable

effects was mainly due to nausea (1% placebo; 5% cinacalcet) and vomiting (< 1% placebo;4%


Adverse reactions, considered at least possibly attributable to cinacalcet treatment based on best-

evidence assessment of causality and reported in excess of placebo in double-blind clinical studies are

listed below using the following convention: very common (>1/10); common (>1/100to<1/10);

uncommon (>1/1,000to<1/100); rare (>1/10,000to<1/1,000); very rare (<1/10,000).

Immune system disorders

Uncommon: hypersensitivity reactions

Metabolism and nutrition disorders

Common: anorexia

Nervous system disorders

Common: dizziness, paraesthesia

Uncommon: seizures

Gastrointestinal disorders

Very common:nausea, vomiting

Uncommon: dyspepsia, diarrhoea

Skin and subcutaneous tissue disorders

Common: rash

Musculoskeletal, connective tissueand bone disorders

Common: myalgia

General disorders and administration site conditions

Common: asthenia


Common: hypocalcaemia (see section 4.4), reduced testosterone levels (see section 4.4)


The safety profile ofMimpara in this patient population is generally consistent with that seen in

patients with Chronic Kidney Disease. The mostcommonADRs in this patient population were

nausea and vomiting.Seizures were reported uncommonly.


Thefollowing adverse reactions have been identified during postmarketing use of Mimpara, the

frequencies of whichcannot be estimated from available data:

There have been reports of isolated, idiosyncratic cases of hypotension and/or worsening

heart failure in cinacalcet-treated patients with impaired cardiac function in post marketing

safety surveillance.

Allergic reactions, including angioedema and urticaria.

QT prolongation and ventricular arrhythmia secondary to hypocalcaemia (see section 4.4).

4.9 Overdose

Doses titrated up to 300 mg once daily have been safely administered to patients receiving dialysis.

Overdose of Mimpara may lead to hypocalcaemia. In the event of overdose, patients should be

monitored for signs and symptoms of hypocalcaemia, and treatment should be symptomatic and

supportive. Since cinacalcet is highly protein-bound, haemodialysis is not an effective treatment for



5.1Pharmacodynamic properties

Pharmacotherapeutic group:Calcium homeostasis,anti-parathyroid agents.ATC code: H05BX01.

Mechanism of action

The calcium sensing receptor on the surface of the chief cell of the parathyroid gland is the principal

regulator of PTH secretion. Cinacalcet is a calcimimetic agent which directly lowers PTH levels by

increasing the sensitivity of the calcium sensing receptor to extracellular calcium. The reduction in

PTH is associated with a concomitant decrease in serum calcium levels.

Reductions in PTH levels correlate with cinacalcet concentration.

After steady state is reached, serum calcium concentrations remain constant over the dosing interval.

Secondary Hyperparathyroidism

Three, 6-month, double-blind, placebo-controlled clinical studies were conducted in ESRD patients

with uncontrolled secondary HPT receiving dialysis (n=1136). Demographic and baseline

characteristics were representative of the dialysis patient population with secondary HPT. Mean

baseline iPTH concentrations across the 3 studies were 733 and 683pg/ml (77.8 and 72.4 pmol/l)for

the cinacalcet and placebo groups, respectively. 66% of patients werereceiving vitaminD sterols at

study entry, and > 90% were receiving phosphate binders. Significant reductions in iPTH, serum

calcium-phosphorus product (Ca x P), calcium, and phosphorus were observed in the cinacalcet

treated patients compared with placebo-treated patients receiving standard of care, and the results

were consistent across the 3 studies. In each of the studies, the primary endpoint (proportion of

patients with an iPTH 250 pg/ml (26.5 pmol/l)) was achieved by 41%, 46%, and 35% of patients

receiving cinacalcet, compared with 4%, 7%, and 6% of patients receiving placebo. Approximately

60% of cinacalcet-treated patients achieved a 30% reduction in iPTH levels, and this effect was

consistent across the spectrum of baseline iPTH levels. The mean reductions in serum Ca x P,

calcium, and phosphorus were 14%, 7% and 8%, respectively.

Reductions in iPTH and Ca x P were maintained for up to 12 months of treatment. Cinacalcet

decreased iPTH and Ca x P,calcium and phosphorus levels regardless of baseline iPTH or Ca x P

level, dialysis modality (PD versus HD), duration of dialysis, and whether or not vitamin D sterols

were administered.

Reductions in PTH were associated withnon-significant reductions of bone metabolism markers

(bone specific alkaline phosphatase, N-telopeptide, bone turnover and bone fibrosis). In post-hoc

analyses ofpooled data from 6 and 12 months clinical studies, Kaplan-Meier estimates of bone

fractureand parathyroidectomy were lower in the cinacalcet group compared with the control group.

Investigational studiesin patients with CKD and secondary HPT not undergoing dialysisindicated

that cinacalcet reduced PTH levels to a similar extent as in patients with ESRD andsecondary HPT

receiving dialysis. However, efficacy, safety, optimal doses and treatment targets have not been

established in treatment of predialytic renal failure patients. These studies show that CKD patients not

undergoing dialysis treated with cinacalcet have an increased risk for hypocalcaemia compared with

cinacalcet-treated ESRDpatients receiving dialysis, which may be due to lower baseline calcium

levelsand/or the presence of residual kidney function.

Parathyroid carcinoma

In akey study, 29 patients (21 with parathyroid carcinoma, 8 with intractable primary HPT (failed or

contraindicated to surgery)), received cinacalcet for up to 2 years (mean of 188 days). Cinacalcet was

administered at doses ranging from 30 mg twice daily to90 mg four times daily. The primary

endpoint of the study was a reduction of serum calcium of 1 mg/dL (0.25 mmol/l).In patients with

parathyroid carcinoma, mean serum calcium declined from 14.5 mg/dl to 12.4 mg/dl (3.6 mmol/l to

3.1 mmol/l). Fifteen out of 21 patients with parathyroid carcinoma achieved a reduction in serum

calcium of 1 mg/dl (0.25 mmol/l). Similar reductions of serum calcium levels were observed in

patients with intractable primary HPT but data are too limited to allow conclusionsregarding the

usefulness of cinacalcet in this condition.

5.2 Pharmacokinetic properties


After oral administration of Mimpara, maximum plasma cinacalcet concentration is achieved in

approximately 2to 6 hours.

Based on between-study comparisons, the absolute bioavailability of cinacalcet in fasted subjects has

been estimated to be about 20-25%. Administration of Mimpara with food results in an approximate

50–80% increase in cinacalcet bioavailability.Increases in plasma cinacalcet concentration are

similar, regardless of the fat content of the meal.

At doses above 200mg, the absorption was saturated probably due to poor solubility.


The volume of distribution is high (approximately 1000litres), indicating extensive distribution.

Cinacalcet is approximately 97% bound to plasma proteins and distributes minimally into red blood


After absorption, cinacalcet concentrations decline in a biphasic fashion with an initial half-life of

approximately 6hours and a terminal half-life of 30 to 40hours. Steady state levels of cinacalcet are

achieved within 7days with minimal accumulation. The pharmacokinetics of cinacalcet does not

change over time.


Cinacalcet is metabolised by multiple enzymes, predominantlyCYP3A4 and CYP1A2 (the

contribution of CYP1A2 has not been characterised clinically). The major circulating metabolites are


Based onin vitrodata, cinacalcet is a strong inhibitor of CYP2D6, but is neither an inhibitor of other

CYP enzymes atconcentrations achieved clinically, including CYP1A2, CYP2C8, CYP2C9,

CYP2C19, and CYP3A4 nor an inducer of CYP1A2, CYP2C19 and CYP3A4.


After administration of a 75mg radiolabelled dose to healthy volunteers, cinacalcet was rapidly and

extensively metabolised by oxidation followed by conjugation. Renal excretion of metabolites was the

prevalent route of elimination of radioactivity. Approximately 80% of the dose was recovered in the

urine and 15% in the faeces.


The AUC and C

of cinacalcet increase approximately linearly over the dose range of 30 to 180mg

once daily.

Pharmacokinetic/pharmacodynamic relationship(s)

Soon after dosing, PTH begins to decrease until a nadir at approximately 2 to 6hours postdose,

corresponding with cinacalcet C

. Thereafter, as cinacalcet levels begin to decline, PTH levels

increase until 12hours post-dose, and then PTH suppression remains approximately constant to the

end of the once-daily dosing interval. PTH levels in Mimpara clinical trials were measured at the end

of the dosing interval.

Elderly:There are no clinically relevant differences due to age in the pharmacokinetics of cinacalcet.

Renal Insufficiency:The pharmacokinetic profile of cinacalcet in patients with mild,moderate, and

severe renal insufficiency, and those on haemodialysis or peritoneal dialysis is comparable to that in

healthy volunteers.

Hepatic Insufficiency:Mild hepatic impairment did not notably affect the pharmacokinetics of

cinacalcet. Compared tosubjects with normal liver function, average AUC of cinacalcet was

approximately 2-fold higher in subjects with moderate impairment and approximately 4-fold higher in

subjects with severe impairment. The mean half-life of cinacalcet is prolonged by 33% and 70% in

patients with moderate and severe hepatic impairment, respectively. Protein binding of cinacalcet is

not affected by impaired hepatic function.Because doses are titrated for each subject based on safety

and efficacy parameters, no additional doseadjustment is necessary for subjects with hepatic

impairment.(see sections 4.2 and 4.4).

Gender:Clearance of cinacalcet may be lower in women than in men. Because doses are titrated for

each subject, no additional dose adjustment is necessary based ongender.

Paediatric Population:The pharmacokinetics of cinacalcet have been studied in 12 paediatric patients

(6-17 years) with CKD receiving dialysis following a single, oral, 15 mg dose.Mean AUC and C


values (23.5 (range 7.22 to 77.2) ng*hr/ml and7.26 (range 1.80 to 17.4) ng/ml, respectively) were

within approximately 30% of the means for AUC and C

max values observed in a single study in healthy

adults following a single 30 mg dose (33.6 (range 4.75 to 66.9) ng*hr/ml and 5.42 (range 1.41 to 12.7)

ng/ml, respectively).Due to the limited data in paediatric subjects, the potential for higher exposures

in the lighter/younger relative to heavier/older paediatric subjects for a given dose of cinacalcet

cannot be excluded.The pharmacokinetics in paediatric subjects after multiple doses has not been


Smoking:Clearance of cinacalcet is higher in smokers than in non-smokers, likely due to induction of

CYP1A2-mediated metabolism. If a patient stops or starts smoking, cinacalcet plasma levels may

change and dose adjustment may be necessary.

5.3 Preclinical safety data

Cinacalcet was not teratogenic in rabbits when given at a dose of 0.4 times, on an AUC basis, the

maximum human dose for secondary HPT (180 mg daily). The non-teratogenic dose in rats was4.4

times, on an AUC basis, the maximum dose for secondary HPT.There were no effects on fertility in

males or females at exposures up to 4 times a human dose of 180 mg/day (safety margins in the small

population of patients administered a maximum clinical dose of 360 mg daily would be approximately

half those given above).

In pregnant rats, there were slight decreases in body weight and food consumption at the highest dose.

Decreased foetal weights were seen in rats at doses where dams had severe hypocalcaemia. Cinacalcet

has been shown to cross the placental barrier in rabbits.

Cinacalcet did not show any genotoxic or carcinogenic potential. Safety margins from the toxicology

studies are small due to the dose-limiting hypocalcaemia observed in theanimal models. Cataracts

and lens opacities were observed in the repeat dose rodent toxicology and carcinogenicity studies, but

were not observed in dogs or monkeys or in clinical studies where cataract formation was monitored.

Cataracts are known to occur in rodents as a result of hypocalcaemia.

Inin vitrostudies, IC

values for the serotonin transporter and K

channels were found to be 7 and

12 fold greater, respectively, than the EC

for the calcium-sensing receptor obtained under the same

experimental conditions. The clinical relevance is unknown, however, the potential for cinacalcet to

act on these secondary targets cannot be fully excluded.


6.1 List of excipients


Pre-gelatinised starch




Magnesium stearate

Colloidal anhydrous silica



OpadryIIgreen: (Lactose monohydrate, hypromellose, titanium dioxide (E171),

glycerol triacetate, FD&C Blue (E132), iron oxide yellow (E172))

Opadry clear: (Hypromellose, macrogol)

6.2 Incompatibilities

Not applicable.

6.3 Shelf life

Blister: 4 years.

6.4 Special precautions for storage

Store in a cool and dry place.

6.5 Nature and contents of container

Aclar/PVC/PVAc/Aluminium blister containing 14 tablets. Pack sizes of 1 blister (14 tablets), 2

blisters (28 tablets), 6 blisters (84 tablets) per carton.

Not all pack sizes may be marketed.

6.6 Special precautions for disposal

No special requirementsfor disposal.




Amgen Europe B.V.

Minervum 7061

4817 ZK Breda

The Netherlands


AmgenEurope B.V.

P.O. BOX 53313 Maoz Aviv

Tel-Aviv 61532


Mimpara 30 137-29-31506-00

Mimpara 60 137-30-31507-00

Mimpara 90 137-31-31508-00

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