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SUMMARY OF PRODUCT CHARACTERISTICS
NAME OF THE MEDICINAL PRODUCT
Mimpara® 30 mg film-coated tablets.
Mimpara® 60 mg film-coated tablets.
Mimpara® 90 mg film-coated tablets. 2.
QUALITATIVE AND QUANTITATIVE COMPOSITION
Each tablet contains 30 mg cinacalcet (as hydrochloride).
Each tablet contains 60 mg cinacalcet (as hydrochloride).
Each tablet contains 90 mg cinacalcet (as hydrochloride).
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.
For a full list of excipients, see section 6.1. 3. PHARMACEUTICAL
Film-coated tablet (tablet).
30 mg: Light green, oval, film-coated tablets marked “AMG” on one side and “30” on the other.
60 mg: Light green, oval, film-coated tablets marked “AMG” on one side and “60” on the other.
90 mg: Light green, oval, film-coated tablets marked “AMG” on one side and “90” on the other. 4. CLINICAL
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 including phosphate binders and/or Vitamin D
sterols, as appropriate (see section 5.1).
Reduction of hypercalcaemia in patients with:
• parathyroid carcinoma.
• primary HPT for whom parathyroidectomy would be indicated on the basis of serum calcium
levels (as defined by relevant treatment guidelines), but in whom parathyroidectomy is not clinically appropriate or is contraindicated.
4.2 Posology and method of administration
Secondary hyperparathyroidism 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).
Parathyroid carcinoma and primary hyperparathyroidism 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 be periodically
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).
No change in starting dose is necessary. Mimpara should be used with caution in
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 is increased when taken with food (see section 5.2).
Tablets should be taken whole and not divided.
Hypersensitivity to the active substance or to any of the excipients. 4.4 Special warnings and precautions for use
In three clinical studies of Chronic Kidney Disease (CKD) patients on dialysis, 5% of the patients in
both the Mimpara and placebo groups reported a history of seizure disorder at baseline. In these
studies, seizures were observed in 1.4% of Mimpara treated patients and 0.4% 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. 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 7.5 mg/dl
(1.875 mmol/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. Potential
manifestations of hypocalcaemia may include paraesthesias, myalgias, cramping, tetany and
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 < 8.4 mg/dl [2.1 mmol/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-Pugh classification), 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 200 mg 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 (e.g. rifampicin) of this enzyme (see section 4.4). In vitro
data 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 1,500 mg dose) did not alter the pharmacokinetics of cinacalcet. Sevelamer
: Co-administration of sevelamer (2400 mg tid) did not affect the pharmacokinetics of cinacalcet. Pantoprazole
: Co-administration of pantoprazole (80 mg od) did not alter the pharmacokinetics of cinacalcet. 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 given in heart failure, 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 of cinacalcet did not affect the pharmacokinetics or pharmacodynamics (as measured by prothrombin time 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 of drugs that are
metabolized by CYP3A4 and CYP3A5, such as certain immunosuppressants, including cyclosporine
and tacrolimus. 4.6
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
It is 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. 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. However,
certain adverse reactions may affect the ability to drive and use machines (see section 4.8).
Secondary hyperparathyroidism 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 reported adverse reactions were 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% cinacalcet). 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 (> 1/100 to < 1/10); uncommon (> 1/1,000 to < 1/100); rare (> 1/10,000 to < 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
Uncommon: dyspepsia, diarrhoea Skin and subcutaneous tissue disorders
Musculoskeletal, connective tissue and bone disorders
Common: myalgia General disorders and administration site conditions
Common: asthenia Investigations
Common: hypocalcaemia (see section 4.4), reduced testosterone levels (see section 4.4)
Parathyroid carcinoma and primary hyperparathyroidism
The safety profile of Mimpara in these patient populations is generally consistent with that seen in
patients with Chronic Kidney Disease. The most frequent ADRs in these patient populations were
nausea and vomiting.
The following adverse reactions have been identified during postmarketing use of Mimpara, the
frequencies of which
cannot 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.
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
5.1 Pharmacodynamic properties
Pharmacotherapeutic group: 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. Soon after dosing, PTH begins to
decrease until a nadir at approximately 2 to 6 hours post dose, corresponding with cinacalcet Cmax.
Thereafter, as cinacalcet levels begin to decline, PTH levels increase until 12 hours 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.
After steady state is reached, serum calcium concentrations remain constant over the dosing interval.
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 683 pg/ml (77.8 and 72.4 pmol/l) for
the cinacalcet and placebo groups, respectively. 66% of patients were
receiving vitamin D 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
Reductions in PTH were associated with non-significant reductions of bone metabolism markers (bone
specific alkaline phosphatase, N-telopeptide, bone turnover and bone fibrosis). In post-hoc analyses
pooled data from 6 and 12 months clinical studies, Kaplan-Meier estimates of bone fracture and
parathyroidectomy were lower in the cinacalcet group compared with the control group.
Investigational studies in patients with CKD and secondary HPT not undergoing dialysis indicated that
cinacalcet reduced PTH levels to a similar extent as in patients with ESRD and
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
patients receiving dialysis, which may be due to lower baseline calcium
levels and/or the presence of residual kidney function.
Parathyroid carcinoma and Primary Hyperparathyroidism
In a key study, 46 patients (29 with parathyroid carcinoma and 17 with primary HPT (who had failed
or had contraindications to parathyroidectomy) received cinacalcet for up to 3 years (mean of 328 days
for patients with parathyroid carcinoma and mean of 347 days for patients with primary HPT).
Cinacalcet was administered at doses ranging from 30 mg twice daily to 90 mg four times daily. The
primary endpoint of the study was a reduction of serum calcium of ≥ 1 mg/dl (≥ 0.25 mmol/l).
patients with parathyroid carcinoma, mean serum calcium declined from 14.1 mg/dl to 12.4 mg/dl
(3.5 mmol/l to 3.1 mmol/l), while in patients with primary HPT, serum calcium levels declined from
12.7 mg/dl to 10.4 mg/dl (3.2 mmol/l to 2.6 mmol/l). Eighteen of 29 patients (62 %) with parathyroid
carcinoma and 15 of 17 subjects (88 %) with primary HPT achieved a reduction in serum calcium of ≥
1 mg/dl (≥ 0.25 mmol/l).
5.2 Pharmacokinetic properties
After oral administration of Mimpara, maximum plasma cinacalcet concentration is achieved in
approximately 2 to 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.
After absorption, cinacalcet concentrations decline in a biphasic fashion with an initial half-life of
approximately 6 hours and a terminal half-life of 30 to 40 hours. Steady state drug levels are achieved
within 7 days with minimal accumulation. The AUC and Cmax of cinacalcet increase approximately
linearly over the dose range of 30 to 180 mg once daily. At doses above 200 mg, the absorption was
saturated probably due to poor solubility. The pharmacokinetics of cinacalcet does not change over
time. The volume of distribution is high (approximately 1000 litres), indicating extensive distribution.
Cinacalcet is approximately 97% bound to plasma proteins and distributes minimally into red blood
Cinacalcet is metabolised by multiple enzymes, predominantly CYP3A4 and CYP1A2 (the
contribution of CYP1A2 has not been characterised clinically). The major circulating metabolites are
Based on in vitro
data, cinacalcet is a strong inhibitor of CYP2D6, but is neither an inhibitor of other
CYP enzymes at concentrations achieved clinically, including CYP1A2, CYP2C8, CYP2C9,
CYP2C19, and CYP3A4 nor an inducer of CYP1A2, CYP2C19 and CYP3A4.
After administration of a 75 mg 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. Elderly:
There are no clinically relevant differences due to age in the pharmacokinetics of cinacalcet.
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
Mild hepatic impairment did not notably affect the pharmacokinetics of
cinacalcet. Compared to subjects 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 dose adjustment 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 on gender.
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 Cmax
values (23.5 (range 7.22 to 77.2) ng*hr/ml and 7.26 (range 1.80 to 17.4) ng/ml, respectively) were
within approximately 30% of the means for AUC and Cmax 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 studied.
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.
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 was 4.4
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 the animal 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.
In in vitro
studies, IC50 values for the serotonin transporter and KATP channels were found to be 7 and
12 fold greater, respectively, than the EC50 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. PHARMACEUTICAL
List of excipients
Tablet Core Pre-gelatinised starch (maize) Microcrystalline cellulose Povidone Crospovidone Magnesium stearate Colloidal anhydrous silica Tablet Coat Carnauba wax Opadry II green:
(Lactose monohydrate, hypromellose, titanium dioxide (E171), glycerol triacetate, FD&C Blue (E132), iron oxide yellow (E172)
Blister: 4 years.
Bottle: 4 years.
Special precautions for storage
This medicinal product does not require any special storage conditions.
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.
High Density Polyethylene (HDPE) bottle with a cotton coil, and a child-resistant polypropylene cap
with an induction seal, packed into a carton. Each bottle contains 30 tablets.
Not all pack sizes may be marketed.
Special Precautions for disposal
No special requirements.
MARKETING AUTHORISATION HOLDER
Amgen Europe B.V.
4817 ZK Breda
MARKETING AUTHORISATION NUMBER(S)
DATE OF FIRST AUTHORISATION/RENEWAL OF THE AUTHORISATION
Date of first authorisation: 22 October 2004
Date of renewal of the authorisation: 23 September 2009 10.
DATE OF REVISION OF THE TEXT
31 August 2009
Detailed information on this product is available on the website of the European Medicines Agency
Propranolol and the risk of hospitalized myopathy:Translating chemical genomics findings intopopulation-level hypothesesSoko Setoguchi, MD, DrPH, a ,d John M. Higgins, MD, b,d,e Helen Mogun, MS, a Vamsi K. Mootha, MD, c andJerry Avorn, MD a Boston, MABackground A recent large-scale, chemical screening study raised the hypothesis that propranolol may increase the riskof myopathy. We tested this hy
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