Thursday, October 6, 2016

Xagrid 0.5mg hard capsule





1. Name Of The Medicinal Product



Xagrid


2. Qualitative And Quantitative Composition



Each hard capsule contains 0.5 mg anagrelide (as anagrelide hydrochloride)



Excipients



Each hard capsule contains lactose monohydrate (53.7 mg) and anhydrous lactose (65.8 mg).



For a full list of excipients, see section 6.1



3. Pharmaceutical Form



Hard capsule.



An opaque white hard capsule imprinted with S 063.



4. Clinical Particulars



4.1 Therapeutic Indications



Xagrid is indicated for the reduction of elevated platelet counts in at risk essential thrombocythaemia (ET) patients who are intolerant to their current therapy or whose elevated platelet counts are not reduced to an acceptable level by their current therapy.



An at risk patient



An at risk essential thrombocythaemia patient is defined by one or more of the following features:



• > 60 years of age or



• a platelet count> 1000 x 109/l or



• a history of thrombo-haemorrhagic events.



4.2 Posology And Method Of Administration



Treatment with Xagrid should be initiated by a clinician with experience in the management of essential thrombocythaemia.



The recommended starting dose of anagrelide is 1 mg/day, which should be administered orally in two divided doses (0.5 mg/dose).



The starting dose should be maintained for at least one week. After one week the dose may be titrated, on an individual basis, to achieve the lowest effective dose required to reduce and/or maintain a platelet count below 600 x 109/l and ideally at levels between 150 x 109/l and 400 x 109/l. The dose increment must not exceed more than 0.5 mg/day in any one-week and the recommended maximum single dose should not exceed 2.5 mg (see section 4.9). During clinical development doses of 10 mg/day have been used.



The effects of treatment with anagrelide must be monitored on a regular basis (see section 4.4). If the starting dose is> 1 mg/day platelet counts should be performed every two days during the first week of treatment and at least weekly thereafter until a stable maintenance dose is reached. Typically, a fall in the platelet count will be observed within 14 to 21 days of starting treatment and in most patients an adequate therapeutic response will be observed and maintained at a dose of 1 to 3 mg/day (for further information on the clinical effects refer to section 5.1).



Elderly



The observed pharmacokinetic differences between elderly and young patients with ET (see section 5.2) do not warrant using a different starting regimen or different dose titration step to achieve an individual patient-optimised anagrelide regimen.



During clinical development approximately 50% of the patients treated with anagrelide were over 60 years of age and no age specific alterations in dose were required in these patients. However, as expected, patients in this age group had twice the incidence of serious adverse events (mainly cardiac).



Renal impairment



Currently, there are no specific pharmacokinetic data for this patient population and the potential risks and benefits of anagrelide therapy in a patient with impairment of renal function should be assessed before treatment is commenced.



Hepatic impairment



Currently, there are no specific pharmacokinetic data for this patient population. However, hepatic metabolism represents the major route of drug clearance and liver function may therefore be expected to influence this process. Therefore it is recommended that patients with moderate or severe hepatic impairment are not treated with anagrelide. The potential risks and benefits of anagrelide therapy in a patient with mild impairment of hepatic function should be assessed before treatment is commenced (see sections 4.3 and 4.4).



Paediatric patients



The experience in children is limited; anagrelide should be used in this patient group with caution (see sections 5.1 and 5.2).



4.3 Contraindications



Hypersensitivity to anagrelide or to any of the excipients.



Patients with moderate or severe hepatic impairment.



Patients with moderate or severe renal impairment (creatinine clearance < 50 ml/min).



4.4 Special Warnings And Precautions For Use



Hepatic impairment



The potential risks and benefits of anagrelide therapy in a patient with mild impairment of hepatic function should be assessed before treatment is commenced. It is not recommended in patients with elevated transaminases (> 5 times the upper limit of normal) (see sections 4.2 and 4.3).



Renal impairment



The potential risks and benefits of anagrelide therapy in a patient with impairment of renal function should be assessed before treatment is commenced (see sections 4.2 and 4.3).



Monitoring



Therapy requires close clinical supervision of the patient which will include a full blood count (haemoglobin and white blood cell and platelet counts), and assessment of liver function (ALT and AST) and renal function (serum creatinine and urea) tests.



Platelets



The platelet count will increase within 4 days of stopping treatment with Xagrid capsules and will return to pre-treatment levels within 10 to 14 days.



Cardiovascular



Cases of cardiomegaly and congestive heart failure have been reported (see section 4.8). Anagrelide should be used with caution in patients of any age with known or suspected heart disease, and only if the potential benefits of therapy outweigh the potential risks. Anagrelide is an inhibitor of cyclic AMP phosphodiesterase III and because of its positive inotropic effects, a pre-treatment cardiovascular examination (including further investigation such as echocardiography, electrocardiogram) is recommended. Patients should be monitored during treatment for evidence of cardiovascular effects that may require further cardiovascular examination and investigation.



Paediatric patients



Limited data are available on the use of anagrelide in the paediatric population and anagrelide should be used in this patient group with caution (see sections 5.1 and 5.2).



Clinically relevant interactions



Anagrelide is an inhibitor of cyclic AMP phosphodiesterase III (PDE III). Concomitant use of anagrelide with other PDE III inhibitors such as milrinone, amrinone, enoximone, olprinone and cilostazol is not recommended.



Excipients



Xagrid contains lactose. Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicinal product.



4.5 Interaction With Other Medicinal Products And Other Forms Of Interaction



Limited pharmacokinetic and/or pharmacodynamic studies investigating possible interactions between anagrelide and other medicinal products have been conducted.



Drug interactions: effects of other substances on anagrelide



• Anagrelide is primarily metabolised by CYP1A2. It is known that CYP1A2 is inhibited by several medicinal products, including fluvoxamine and omeprazole, and such medicinal products could theoretically adversely influence the clearance of anagrelide.



In vivo interaction studies in humans have demonstrated that digoxin and warfarin do not affect the pharmacokinetic properties of anagrelide.



Drug interactions: effects of anagrelide on other substances



• Anagrelide demonstrates some limited inhibitory activity towards CYP1A2 which may present a theoretical potential for interaction with other co-administered medicinal products sharing that clearance mechanism e.g. theophylline.



• Anagrelide is an inhibitor of PDE III. The effects of medicinal products with similar properties such as the inotropes milrinone, enoximone, amrinone, olprinone and cilostazol may be exacerbated by anagrelide.



In vivo interaction studies in humans have demonstrated that anagrelide does not affect the pharmacokinetic properties of digoxin or warfarin.



• At the doses recommended for use in the treatment of essential thrombocythaemia, anagrelide may theoretically potentiate the effects of other medicinal products that inhibit or modify platelet function e.g. acetylsalicylic acid.



• A clinical interaction study performed in healthy subjects showed that co-administration of repeat-dose anagrelide 1 mg once daily and acetylsalicylic acid 75 mg once daily may enhance the anti-platelet aggregation effects of each drug compared with administration of acetylsalicylic acid alone. Therefore, due to the lack of data in ET patients, the potential risks of the concomitant use of anagrelide with acetylsalicylic acid should be assessed, particularly in patients with a high risk profile for haemorrhage before treatment is initiated.



• Anagrelide may cause intestinal disturbance in some patients and compromise the absorption of hormonal oral contraceptives.



Food interactions



• Food delays the absorption of anagrelide, but does not significantly alter systemic exposure.



• The effects of food on bioavailability are not considered clinically relevant to the use of anagrelide.



4.6 Pregnancy And Lactation



Pregnancy



There are no adequate data from the use of anagrelide in pregnant women.



Studies in animals have shown reproductive toxicity (see section 5.3). The potential risk for humans is unknown.



Use of Xagrid during pregnancy is not recommended. If Xagrid is used during pregnancy, or if the patient becomes pregnant while using the medicinal product, she should be advised of the potential risk to the foetus.



Women of child-bearing potential should use adequate birth-control measures during treatment with anagrelide.



Lactation



It is not known whether anagrelide hydrochloride is excreted in milk. Since many medicinal products are excreted in human milk and because of the potential for adverse reactions in breast-feeding infants, mothers should discontinue breast-feeding when taking Xagrid.



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.



In clinical development, dizziness was commonly reported. Patients are advised not to drive or operate machinery while taking Xagrid if dizziness is experienced.



4.8 Undesirable Effects



The safety of anagrelide has been examined in 4 open label clinical studies. In 3 of the studies 942 patients who received anagrelide at a mean dose of approximately 2 mg/day were assessed for safety. In these studies 22 patients received anagrelide for up to 4 years.



In the later study 3660 patients who received anagrelide at a mean dose of approximately 2 mg/day were assessed for safety. In this study 34 patients received anagrelide for up to 5 years. The most commonly reported drug related adverse reactions were headache occurring at approximately 14%, palpitations occurring at approximately 9%, fluid retention and nausea both occurring at approximately 6%, and diarrhoea occurring at 5%. These adverse drug reactions are expected based on the pharmacology of anagrelide (inhibition of PDE III). Gradual dose titration may help diminish these effects (see section 4.2).



The following convention was used for frequency of adverse drug reactions: Very common (



Blood and lymphatic system disorders








Common:




Anaemia




Uncommon:




Thrombocytopenia, pancytopenia, ecchymosis, haemorrhage



Metabolism and nutrition disorders










Common:




Fluid retention




Uncommon:




Oedema, weight loss




Rare:




Weight gain



Nervous system disorders












Very common:




Headache




Common:




Dizziness




Uncommon:




Paraesthesia, insomnia, depression, confusion, hypoaesthesia, nervousness, dry mouth, amnesia




Rare:




Somnolence, abnormal coordination, dysarthria, migraine



Eye disorders






Rare:




Vision abnormal, diplopia



Ear and labyrinth disorders






Rare:




Tinnitus



Cardiac disorders










Common:




Palpitations, tachycardia




Uncommon:




Congestive heart failure, hypertension, arrhythmia, atrial fibrillation, supraventricular tachycardia, ventricular tachycardia, syncope




Rare:




Angina pectoris, myocardial infarction, cardiomegaly, cardiomyopathy, pericardial effusion, vasodilatation, postural hypotension



Respiratory and thoracic mediastinal disorders










Uncommon:




Dyspnoea, epistaxis, pleural effusion, pneumonia




Rare:




Pulmonary hypertension, pulmonary infiltrates




Not known:




Allergic alveolitis



Gastrointestinal disorders










Common:




Nausea, diarrhoea, abdominal pain, flatulence, vomiting




Uncommon:




Dyspepsia, anorexia, pancreatitis, constipation, gastrointestinal haemorrhage, gastrointestinal disorder




Rare:




Colitis, gastritis, gingival bleeding



Hepatobiliary disorders








Uncommon:




Hepatic enzymes increased




Not known:




Hepatitis



Skin and subcutaneous tissue disorders










Common:




Rash




Uncommon:




Alopecia, skin discoloration, pruritus




Rare:




Dry skin



Musculoskeletal and connective tissue disorders






Uncommon:




Myalgia, arthralgia, back pain



Renal and urinary disorders








Uncommon:




Impotence




Rare:




Nocturia, renal failure



General disorders and administration site conditions










Common:




Fatigue




Uncommon:




Chest pain, weakness, chills, malaise, fever




Rare:




Asthenia, pain, flu-like syndrome



Investigations






Rare:




Blood creatinine increased



4.9 Overdose



There have been a small number of post-marketing case reports of intentional overdose with anagrelide. Reported symptoms include sinus tachycardia and vomiting. Symptoms resolved with conservative management.



A specific antidote for anagrelide has not been identified. In case of overdose, close clinical supervision of the patient is required; this includes monitoring of the platelet count for thrombocytopenia. Dose should be decreased or stopped, as appropriate, until the platelet count returns to within the normal range.



Xagrid, at higher than recommended doses, has been shown to produce reductions in blood pressure with occasional instances of hypotension. A single 5 mg dose of anagrelide can lead to a fall in blood pressure usually accompanied by dizziness.



5. Pharmacological Properties



5.1 Pharmacodynamic Properties



Pharmacotherapeutic group: Other antineoplastic agents, ATC Code: L01XX35



The specific mechanism of action by which anagrelide reduces platelet count is not yet fully understood although it has been confirmed that anagrelide is platelet selective from in vitro and in vivo study information.



In vitro studies of human megakaryocytopoiesis established that anagrelide's inhibitory actions on platelet formation in man are mediated via retardation of maturation of megakaryocytes, and reducing their size and ploidy. Evidence of similar in vivo actions was observed in bone marrow biopsy samples from treated patients.



Anagrelide is an inhibitor of cyclic AMP phosphodiesterase III.



The safety and efficacy of anagrelide as a platelet lowering agent have been evaluated in four open-label, non-controlled clinical trials (study numbers 700-012, 700-014, 700-999 and 13970-301) including more than 4000 patients with myeloproliferative disorders (MPDs). In patients with essential thrombocythaemia complete response was defined as a decrease in platelet count to 9/l or a



Paediatric patients



An open label clinical study with a 3 month treatment period did not raise any safety concerns for anagrelide in 17 children/adolescent patients with ET (age range 7-14 years) compared to 18 adult patients. Earlier during clinical development a limited number (12) of children (age range 5 - 17 years) with essential thrombocythaemia were treated with anagrelide.



This medicine has been authorised under “Exceptional Circumstances”.



This means that because of the rarity of this disease it has been impossible to get complete information on this medicine.



The European Medicines Agency (EMEA) will review any new information which may become available every year and this SPC will be updated as necessary.



5.2 Pharmacokinetic Properties



Following oral administration of anagrelide in man, at least 70% is absorbed from the gastrointestinal tract. In fasted subjects, peak plasma levels occur about 1 hour after a 0.5 mg dose; the plasma half-life is short, approximately 1.3 hours. Dose proportionality has been found in the dose range 0.5 mg to 2 mg.



Anagrelide is primarily metabolised by CYP1A2; less than 1% is recovered in the urine as anagrelide. Two major urinary metabolites, 2-amino-5, 6-dichloro-3, 4-dihydroquinazoline and 3-hydroxy anagrelide have been identified. The mean recovery of 2-amino-5, 6-dichloro-3, 4-dihydroquinazoline in urine is approximately 18-35% of the administered dose.



Pharmacokinetic data from healthy subjects established that food decreases the Cmax of anagrelide by 14%, but increases the AUC by 20%. Food had a more significant effect on the active metabolite and decreased the Cmax by 29%, although it had no effect on the AUC.



As expected from its half-life, there is no evidence for anagrelide accumulation in the plasma. Additionally these results show no evidence of auto-induction of the anagrelide clearance.



Special populations



Paediatric patients



Pharmacokinetic data from fasting children and adolescents (age range 7 - 14 years) with essential thrombocythaemia indicate that dose and body weight normalised exposure, Cmax and AUC, of anagrelide were lower in children/adolescents compared to adults. There was also a trend to lower exposure to the active metabolite. These observations may be a reflection of more efficient metabolic clearance in younger subjects.



Elderly



Pharmacokinetic data from fasting elderly patients with ET (age range 65-75 years) compared to fasting adult patients (age range 22-50 years) indicate that the Cmax and AUC of anagrelide were 36% and 61% higher respectively in elderly patients, but that the Cmax and AUC of the active metabolite, 3-hydroxy anagrelide, were 42% and 37% lower respectively in the elderly patients. These differences were likely to be caused by lower presystemic metabolism of anagrelide to 3-hydroxy anagrelide in the elderly patients.



5.3 Preclinical Safety Data



Repeated dose toxicity



Following repeated administration of anagrelide, at doses of 1 mg/kg/day or higher, subendocardial haemorrhage and focal myocardial necrosis occurred in dogs.



Reproductive toxicology



Maternally toxic doses of anagrelide (60 mg/kg/day and above) in rats and rabbits were associated with increased embryo resorption and foetal mortality.



Mutagenic and carcinogenic potential



Studies on the genotoxic potential of anagrelide did not identify any mutagenic or clastogenic effects.



In a two-year rat carcinogenicity study, non-neoplastic and neoplastic findings were observed and related or attributed to an exaggerated pharmacological effect. Among them, the incidence of adrenal phaeochromocytomas was increased relative to control in males at all dose levels (



Currently, there is no clinical evidence that these findings are of relevance to human use.



6. Pharmaceutical Particulars



6.1 List Of Excipients



Capsule contents



Povidone (E1201)



Anhydrous lactose



Lactose monohydrate



Microcrystalline cellulose (E460)



Crospovidone



Magnesium stearate



Capsule shell



Gelatin



Titanium dioxide (E171)



Printing ink



Shellac



Strong ammonium solution



Potassium hydroxide (E525)



Black iron oxide (E172)



6.2 Incompatibilities



Not applicable



6.3 Shelf Life



4 years



6.4 Special Precautions For Storage



This medicinal product does not require any special storage conditions.



6.5 Nature And Contents Of Container



High-density polyethylene (HDPE) bottles with child-resistant closures and desiccant containing 100 capsules.



6.6 Special Precautions For Disposal And Other Handling



No special requirements.



7. Marketing Authorisation Holder



Shire Pharmaceutical Contracts Ltd



Hampshire International Business Park



Chineham



Basingstoke



Hampshire RG24 8EP



United Kingdom



8. Marketing Authorisation Number(S)



EU/1/04/295/001



9. Date Of First Authorisation/Renewal Of The Authorisation



Date of first authorisation: 16/11/2004



Date of latest renewal: 16/11/2009



10. Date Of Revision Of The Text



05/2010



Detailed information on this product is available on the website of the European Medicines Agency (EMEA) http://www.ema.europa.eu




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