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Fesoterodine fumarate 4 mg Prolonged-Release Tablets

Active Ingredient:
fesoterodine fumarate
Company:  
Dr. Reddy's Laboratories (UK) Ltd See contact details
ATC code: 
G04BD11
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About Medicine
{healthcare_pro_orange} This information is for use by healthcare professionals
Last updated on emc: 12 May 2022
1. Name of the medicinal product

Fesoterodine fumarate Dr. Reddy's 4 mg Prolonged-Release Tablets

TERALEVE 4 mg Prolonged-Release Tablets

2. Qualitative and quantitative composition

Each prolonged-release tablet contains fesoterodine fumarate 4 mg corresponding to 3.1 mg of fesoterodine.

Excipients with known effect:

Each prolonged-release tablet contains glycerol, lactose and sodium.

For the full list of excipients , see section 6.1.

3. Pharmaceutical form

Prolonged-release tablet.

The tablets are light blue, oval, biconvex, film-coated, with dimension of approximately 13 mm x 6 mm, and engraved on one side with the number '4'.

4. Clinical particulars
4.1 Therapeutic indications

Fesoterodine is indicated in adults for treatment of the symptoms (increased urinary frequency and/or urgency and/or urgency incontinence) that may occur with overactive bladder syndrome.

4.2 Posology and method of administration

Posology

Adults (including elderly)

The recommended starting dose is 4 mg once daily. Based upon individual response, the dose may be increased to 8 mg once daily. The maximum daily dose is 8 mg. Full treatment effect was observed between 2 and 8 weeks. Hence, it is recommended to reevaluate the efficacy for the individual patient after 8 weeks of treatment. In subjects with normal renal and hepatic function receiving concomitant administration of potent CYP3A4 inhibitors, the maximum daily dose of fesoterodine should be 4 mg once daily (see section 4.5).

Special population

Renal and hepatic impairment

The following table provides the daily dosing recommendations for subjects with renal or hepatic impairment in the absence and presence of moderate and potent CYP3A4 inhibitors (see sections 4.3, 4.4, 4.5 and 5.2).

Moderate(3) or potent(4) CYP3A4 inhibitors

None

Moderate

Potent

Renal impairment(1)

Mild

4→8 mg(2)

4 mg

Should be avoided

Moderate

4→8 mg(2)

4 mg

Contraindicated

Severe

4 mg

Should be avoided

Contraindicated

Hepatic impairment

Mild

4→8 mg(2)

4 mg

Should be avoided

Moderate

4 mg

Should be avoided

Contraindicated

(1) Mild GFR = 50-80 ml/min; Moderate GFR = 30-50 ml/min; Severe GFR = <30 ml/min

(2) Cautious dose increase. See sections 4.4, 4.5 and 5.2

(3) Moderate CYP3A4 inhibitors. See section 4.5

(4) Potent CYP3A4 inhibitors. See sections 4.3, 4.4 and 4.5

Fesoterodine is contraindicated in subjects w ith severe hepatic impairment (see section 4.3).

Paediatric population

The safety and efficacy of fesoterodine in children below 18 years of age have not yet been established. No data are available.

Method of administration

Tablets are to be taken once daily w ith liquid and sw allow ed w hole. Fesoterodine can be administered w ith or w ithout food.

4.3 Contraindications

• hypersensitivity to the active substance or to peanut or to any of the excipients listed in section 6.1

• urinary retention

• gastric retention

• uncontrolled narrow angle glaucoma

• myasthenia gravis

• severe hepatic impairment (Child Pugh C)

• concomitant use of potent CYP3A4 inhibitors in subjects w ith moderate to severe hepatic or renal impairment

• severe ulcerative colitis

• toxic megacolon.

4.4 Special warnings and precautions for use

Fesoterodine should be used w ith caution in patients w ith:

• clinically significant bladder outflow obstruction at risk of urinary retention ( e.g. clinically significant prostate enlargement due to benign prostatic hyper plasia, see section 4.3)

• gastrointestinal obstructive disorders (e.g. pyloric stenosis)

• gastro-oesophageal reflux and/or w ho are concurrently taking medicinal products (such as oral bisphosphonates) that can cause or exacerbate oesophagitis

• decreased gastrointestinal motility

• autonomic neuropathy

• controlled narrow -angle glaucoma.

Caution should be exercised w hen prescribing or uptitrating fesoterodine to patients in w hom an increased exposure to the active metabolite (see section 5.1) is expected:

• hepatic impairment (see sections 4.2, 4.3 and 5.2)

• renal impairment (see sections 4.2, 4.3 and 5.2)

• concomitant administration of potent or moderate CYP3A4 inhibitors (see sections 4.2 and 4.5)

• concomitant administration of a potent CYP2D6 inhibitor (see sections 4.5 and 5.2).

Dose inc reases

In patients w ith a combination of these factors, additional exposure increases are expected. Dose dependent antimuscarinic adverse reactions are likely to occur. In populations w here the dose may be increased to 8 mg once daily, the dose increase should be preceded by an evaluation of the individual response and tolerability.

Organic causes must be excluded before any treatment w ith antimuscarinics is considered. Safety and efficacy have not yet been established in patients w ith a neurogenic cause for detrusor overactivity.

Other causes of frequent urination (treatment of heart failure or renal disease) should be assessed before treatment w ith fesoterodine. If urinary tract infection is present, an appropriate medical approach should be taken/antibacterial therapy should be started.

Angioedema

Angioedema has been reported w ith fesoterodine and has occurred after the first dose in some cases. If angioedema occurs, fesoterodine should be discontinued and appropriate therapy sh ould be promptly provided.

Potent CYP3A4 induc ers

The concomitant use of fesoterodine w ith a potent CYP3A4 inducer (i.e. carbamazepine, rifampicin, phenobarbital, phenytoin, St John's Wort) is not recommended (see section 4.5).

QT prolongation

Fesoterodine should be used w ith caution in patients w ith risk for QT prolongation (e.g. hypokalaemia, bradycardia and concomitant administration of medicines know n to prolong QT interval) and relevant pre-existing cardiac diseases (e.g. myocardial ischaemia, arrhythmia, congestive heart failure), (see section 4.8). This especially holds true w hen taking potent CYP3A4 inhibitors (see sections 4.2, 4.5 and 5.1).

Lac tose

fesoterodine prolonged-release tablets contain lactose. Patients w ith rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicine.

Sodium

This product contains less then 1mmol sodium (23 mg) per tablet, that is to say essentially 'sodium-free'.

Glycerol

May cause headach, stomach upset and diarrhea.

4.5 Interaction with other medicinal products and other forms of interaction

Pharmacological interactions

Caution should be exercised in coadministration of fesoterodine w ith other antimuscarinic s and medicinal products w ith anticholinergic properties (e.g. amantadine, tri-cyclic antidepressants, certain neuroleptics) as this may lead to more pronounced therapeutic - and side-effects (e.g. constipation, dry mouth, drow siness, urinary retention).

Fesoterodine may reduce the effect of medicinal products that stimulate the motility of the gastro-intestinal tract, such as metoclopramide.

Pharmacokinetic interactions

In vitro data demonstrate that the active metabolite of fesoterodine does not inhibit CYP1A2, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1, or 3A4, or induce CYP1A2, 2B6, 2C9, 2C19, or 3A4 at clinically relevant plasma concentrations. Thus fesoterodine is unlikely to alter the clearance of medicinal products that are metabolised by these enzymes.

CYP3A4 inhibitors

Potent CYP3A4 inhibitors

Follow ing inhibition of CYP3A4 by co-administration of ketoconazole 200 mg twice daily, Cmax and AUC of the active metabolite of fesoterodine increased 2.0 and 2.3-fold in CYP2D6 extensive metabolisers and 2.1 and 2.5-fold in CYP2D6 poor metabolisers, respectively. Therefore, the maximum dose of fesoterodine should be restricted to 4 mg w hen used concomitantly w ith potent CYP3A4 inhibitors (e.g. atazanavir, clarithromycin, indinavir, itraconazole, ketoconazole, nefazodone, nelfinavir, ritonavir (and all ritonavir boosted PI -regimens), saquinavir and telithromycin (see sections 4.2 and 4.4)).

Moderate CYP3A4 inhibitors

Follow ing blockade of CYP3A4 by coadministration of the moderate CYP3A4 inhibitor fluconazole 200 mg tw ice a day for 2 days, Cmax and AUC of the active metabolite of fesoterodine increased approximately 19% and 27%, respectively. No dosing adjustments are recommended in the presence of moderate CYP3A4 inhibitors (e.g., erythromycin, fluconazole, diltiazem, verapamil and grapefruit juice).

Weak CYP3A4 inhibitors

The effect of w eak CYP3A4 inhibitors (e.g. cimetidine), w as not examined; it is not expected to be in excess of the effect of moderate inhibitor.

CYP3A4 inducers

Follow ing induction of CYP3A4 by coadministration of rifampicin 600 mg once a day, Cmax and AUC of the active metabolite of fesoterodine decreased by approximately 70% and 75%, respectively, after oral administration of fesoterodine 8 mg.

Induction of CYP3A4 may lead to subtherapeutic plasma levels. Concomitant use w ith CYP3A4 inducers (e.g. carbamazepine, rifampicin, phenobarbital, phenytoin, St John's Wort) is not recommended (see section 4.4).

CYP2D6 inhibitors

The interaction w ith CYP2D6 inhibitors w as not tested clinically. Mean Cmax and AUC of the active metabolite are 1.7 and 2-fold higher, respectively, in CYP2D6 poor metabolisers as compared to extensive metabolisers. Co-administration of a potent CYP2D6 inhibitor may result in increased exposure and adverse events. A dose reduction to 4 mg may be needed (see section 4.4).

Oral contraceptives

Fesoterodine does not impair the suppression of ovulation by oral hormonal contraception. In the presence of fesoterodine there are no changes in the plasma concentrations of combined oral contraceptives containing ethinylestradiol and levonorgestrel.

Warfarin

A clinical study in healthy volunteers has show n that fesoterodine 8 mg once daily has no significant effect on the pharmacokinetics or the anticoagulant activity of a single dose of warfarin.

Paediatric population

Interaction studies have only been performed in adults.

4.6 Fertility, pregnancy and lactation

Pregnanc y

There are no adequate data from the use of fesoterodine in pregnant w omen. Reproductive toxicity studies w ith fesoterodine in animals show minor embryotoxicity. In animal reproduction studies, oral administration of fesoterodine to pregnant mice and rabbits during organogenesis resulted in fetotoxicity at maternal exposures that w ere 6 and 3 times the maximum recommended human dose (MRHD), respectively, based on AUC (see section 5.3). The potential risk for humans is unknow n. Fesoterodine is not recommended during pregnancy.

Breast-feeding

It is unknow n w hether fesoterodine/metabolites are excreted into human milk; therefore, breast-feeding is not recommended during treatment w ith fesoterodine.

Fertility

No clinical trials have been conducted to assess the effect of fesoterodine on human fertility. Findings in mice at exposures approximately 5 to 19 times those at the MRHD show an effect on female fertility, how ever, the clinical implications of these animal findings are not know n (see section 5.3). Women of child bearing potential should be made aw are of the lack of human fertility data, and fesoterodine should only be given after consideration of individual risks and benefits.

4.7 Effects on ability to drive and use machines

Fesoterodine has minor influence on the ability to drive and use machines.

Caution should be exercised w hen driving or using machines due to possible occurrence of side effects such as blurred vision, dizziness, and somnolence (see section 4.8).

4.8 Undesirable effects

Summary of the safety profile

The safety of fesoterodine w as evaluated in placebo-controlled clinical studies in a total of 2859 patients w ith overactive bladder, of w hich 780 received placebo.

Due to the pharmacological properties of fesoterodine, treatment may cause mild to moderate antimuscarinic effects like dry mouth, dry eye, dyspepsia and constipation. Urinary retention may occur uncommonly.

Dry mouth, the only very common adverse reactions, occurred w ith a frequency of 28.8% in the fesoterodine group compared to 8.5% in the placebo group. The majority of adverse reactions occurred during the first month of treatment w ith the exception of cases classified as urinary retention or post void residual urine greater than 200 ml, w hich could occur after long term treatment and w as more common in male than female subjects.

Tabulated list of adverse reac tions

The table below gives the frequency of treatment emergent adverse reactions from placebo - controlled clinical trials and from post-marketing experience. The adverse reactions are reported in this table w ith the follow ing frequency 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).

Within each frequency grouping, adverse reactions are presented in order of decreasing seriousness.

System organ class

Very common

Common

Uncommon

Rare

Infections and infestations

Urinary tract infection

Psychiatric disorders

Insomnia

Confusional state

Nervous system disorders

Dizziness; Headache

Dysgeusia; Somnolence

Eye disorders

Dry eye

Blurred vision

Ear and labyrinth disorders

Vertigo

Cardiac disorders

Tachycardia; Palpitations

Respiratory, thoracic and mediastinal disorders

Dry throat

Pharyngolaryng eal pain; Cough; Nasal dryness

Gastrointestinal disorders

Dry mouth

Abdominal pain; Diarrhoea; Dyspepsia; Constipation; Nausea

Abdominal discomfort; Flatulence, Gastroesophage al reflux

Hepatobiliary disorders

ALT increased; GGT increased

Skin and subcutaneous tissue disorders

Rash; Dry skin; Pruritus

Angioedema; Urticaria

Renal and urinary disorders

Dysuria

Urinary retention (including feeling of residual urine; micturition disorder); Urinary hesitation

General disorders and administration site conditions

Fatigue

Desc ription of selec ted adverse reac tions

In clinical trials of fesoterodine, cases of markedly elevated liver enzymes w ere reported w ith the occurrence frequency no different from the placebo group. The relation to fesoterodine treatment is unclear.

Electrocardiograms w ere obtained from 782 patients treated w ith 4 mg, 785 treated w ith 8 mg, 222 treated w ith 12 mg fesoterodine and 780 w ith placebo. The heart rate corrected QT interval in fesoterodine treated patients did not differ from that seen in placebo treated patients. The incidence rates of QTc ≥500 ms post baseline or QTc increase of ≥60 ms is 1.9%, 1.3%, 1.4% and 1.5%, for fesoterodine 4 mg, 8 mg, 12 mg and placebo, respectively. The clinical relevance of these findings w ill depend on individual patient risk factors and susceptibilities present (see section 4.4).

Post-marketing cases of urinary retention requiring catheterisation have been described, generally w ithin the first w eek of treatment w ith fesoterodine. They have mainly involved elderly (≥ 65 years) male patients w ith a history consistent w ith benign prostatic hyper plasia (see section 4.4).

Reporting of suspec ted adverse reac tions

Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allow s continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme website www.mhra.gov.uk/yellowcard or search for MHRA Yellow Card in the Google Play or Apple App Store.

4.9 Overdose

Overdose w ith antimuscarinic s, including fesoterodine can result in severe anticholinergic effects. Treatment should be symptomatic and supportive. In the event of overdose, ECG monitoring is recommended; standard supportive measures for managing QT prolongation should be adopted. Fesoterodine has been safely administered in clinical studies at doses up to 28 mg/day.

In the event of fesoterodine overdose, treat w ith gastric lavage and give activated charcoal. Treat symptoms as follow s:

• Severe central anticholinergic effects (e.g. hallucinations, severe excitation): treat w ith physostigmine

• Convulsions or pronounced excitation: treat w ith benzodiazepines

• Respiratory insufficiency: treat w ith artificial respiration

• Tachycardia: treat w ith beta-blockers

• Urinary retention: treat w ith catheterisation

• Mydriasis: treat w ith pilocarpine eye drops and/or place patient in dark room.

5. Pharmacological properties
5.1 Pharmacodynamic properties

Pharmacotherapeutic group: Urologicals, Urinary antispasmodics, ATC code: G04BD11.

Mec hanism of ac tion

Fesoterodine is a competitive, specific muscarinic receptor antagonist. It is rapidly and extensively hydrolysed by non-specific plasma esterases to the 5-hydroxymethyl derivative, its primary active metabolite, w hich is the main active pharmacological principle of fesoterodine.

Clinic al effic ac y and s afety

The efficacy of fixed doses of fesoterodine 4 mg and 8 mg w as evaluated in tw o Phase 3 randomised, double-blind, placebo-controlled, 12-w eek studies. Female (79%) and male (21%) patients w ith a mean age of 58 years (range 19-91 years) w ere included. A total of 33% of patients w ere ≥65 years of age and 11% w ere ≥75 years of age.

Fesoterodine treated patients had statistically significant mean reductions in the number of micturitions per 24 hours and in the number of urge incontinence episodes per 24 hours at the end of treatment compared to placebo. Likew ise, the response rate (% of patients reporting that their condition has been “greatly improved” or “improved” using a 4-point Treatment Benefit Scale) w as significantly greater w ith fesoterodine compared to placebo. Furthermore, fesoterodine improved the mean change in the voided volume per micturition, and the mean change in the number of continent days per w eek (see Table 1 below ).

Table 1: Mean changes from Baseline to end of treatment for primary and selected secondary endpoints

Study 1

Study 2

Parameter

Placebo

Fes oterodine

4 mg

Fes oterodine

8 mg

Active comparator

Placebo

Fes oterodine

4 mg

Fes oterodine

8 mg

Number of micturitions per 24 hours#

N=279

N=265

N=276

N=283

N=266

N=267

N=267

Bas eline

12.0

11.6

11.9

11.5

12.2

12.9

12.0

Change from bas eline

-1.02

-1.74

-1.94

-1.69

-1.02

-1.86

-1.94

p-value

<0.001

<0.001

0.032

<0.001

Responder rate (treatment response)#

N=279

N=265

N=276

N=283

N=266

N=267

N=267

Res ponder rate

53.4%

74.7%

79.0%

72.4%

45.1%

63.7%

74.2%

p-value

<0.001

<0.001

<0.001

<0.001

Number of urge incontinence episodes per 24 hours

N=211

N=199

N=223

N=223

N=205

N=228

N=218

Bas eline

3.7

3.8

3.7

3.8

3.7

3.9

3.9

Change from bas eline

-1.20

-2.06

-2.27

-1.83

-1.00

-1.77

-2.42

p-value

0.001

<0.001

0.003

<0.001

Number of continent days per week

N=211

N=199

N=223

N=223

N=205

N=228

N=218

Bas eline

0.8

0.8

0.6

0.6

0.6

0.7

0.7

Change from bas eline

2.1

2.8

3.4

2.5

1.4

2.4

2.8

p-value

0.007

<0.001

<0.001

<0.001

Voided volume per micturition (ml)

N=279

N=265

N=276

N=283

N=266

N=267

N=267

Bas eline

150

160

154

154

159

152

156

Change from bas eline

10

27

33

24

8

17

33

p-value

<0.001

<0.001

0.150

<0.001

# primary end points

Cardiac elec trophysiology

The effect of fesoterodine 4 mg and 28 mg on the QT interval w as thoroughly evaluated in a double-blind, randomised, placebo- and positive-controlled (moxifloxacin 400 mg) parallel group study w ith once-daily treatment over a period of 3 days in 261 male and female s ubjects aged 45 to 65 years. Change from baseline in QTc based on the Fridericia correction method did not show any differences betw een the active treatment and placebo group.

5.2 Pharmacokinetic properties

Absorption

After oral administration, due to rapid and extensive hydrolysis by non-specific plasma esterases, fesoterodine w as not detected in plasma.

Bioavailability of the active metabolite is 52%. After single or multiple-dose oral administration of fesoterodine in doses from 4 mg to 28 mg, plasma concentrations of the active metabolite are proportional to the dose. Maximum plasma levels are reached after approximately 5 hours. Therapeutic plasma levels are achieved after the first administration of fesoterodine. No accumulation occurs after multiple-dose administration.

Distribution

Plasma protein binding of the active metabolite is low w ith approximately 50% bound to albumin and alpha-1-acid glycoprotein. The mean steady-state volume of distribution follow ing intravenous infusion of the active metabolite is 169 l.

Biotransformation

After oral administration, fesoterodine is rapidly and extensively hydrolysed to its active metabolite. The active metabolite is further metabolised in the liver to its carboxy, carboxy -N-desisopropyl, and N-desisopropyl metabolite w ith involvement of CYP2D6 and CYP3A4. None of these metabolites contribute significantly to the antimuscarinic activity of fesoterodine. Mean Cmax and AUC of the active metabolite are 1.7 and 2-fold higher, respectively, in CYP2D6 poor metabolisers as compared to extensive metabolisers.

Elimination

Hepatic metabolism and renal excretion contribute significantly to the elimination of the active metabolite. After oral administration of fesoterodine, approximately 70% of the administered dose w as recovered in urine as the active metabolite (16%), carboxy metabolite (34%), carboxy-N-desisopropyl metabolite (18%), or N-desisopropyl metabolite (1%), and a smaller amount (7%) w as recovered in faeces. The terminal half -life of the active metabolite follow ing oral administration is approximately 7 hours and is absorption rate-limited.

Age and gender

No dose adjustment is recommended in these subpopulations. The pharmacokinetics of fesoterodine are not significantly influenced by age and gender.

Paediatric population

The pharmacokinetics of fesoterodine have not been evaluated in paediatric patients.

Renal impairment

In patients w ith mild or moderate renal impairment (GFR 30 – 80 ml/min), Cmax and AUC of the active metabolite increased up to 1.5 and 1.8-fold, respectively, as compared to healthy subjects. In patients w ith severe renal impairment (GFR < 30 ml/min), Cmax and AUC are increased 2.0 and 2.3-fold, respectively.

Hepatic impairment

In patients w ith moderate hepatic impairment (Child Pugh B), Cmax and AUC of the active metabolite increased 1.4 and 2.1-fold, respectively, as compared to healthy subjects. Pharmacokinetics of fesoterodine in patients w ith severe hepatic impairment have not been studied.

5.3 Preclinical safety data

In non-clinical safety pharmacology, general toxicity, genotoxicity and carcinogenicity studies no clinically relevant effects have been observed, except those related to the pharmacological effect of the active substance.

Reproduction studies have show n minor embryotoxicity at doses close to maternally toxic ones (increased number of resorptions, pre-implantation and post-implantation losses).

Supratherapeutic concentrations of the active metabolite of fesoterodine, have been show n to inhibit K+ current in cloned human ether-à-go-go-related gene (hERG) channels and prolong action potential duration (70% and 90% repolarisation) in canine isolated Purkinje fibres. How ever in conscious dogs, the active metabolite had no effect on the QT interval and QTc interval at plas ma exposures at least 33-fold higher than mean peak free plasma concentration in human subjects w ho are extensive metabolisers and 21-fold higher than measured in subjects w ho are poor CYP2D6 metabolisers after fesoterodine 8 mg once daily.

In a study of fertility and early embryonic development in mice, fesoterodine had no effect on male reproductive function or fertility at doses up to 45 mg/kg/day. At 45 mg/kg/day, a low er number of corpora lutea, implantation sites and viable foetuses w as observed in female mice administered fesoterodine for 2 w eeks prior to mating and continuing through day 7 of gestation . The maternal No-Observed-Effect Level (NOEL) and the NOEL for effects on reproduction and early embryonic development w ere both 15 mg/kg/day. Based on AUC, the systemic exposure w as 0.6 to 1.5 times higher in mice than in humans at the MRHD, w hereas based on peak plasma concentrations, the exposure in mice w as 5 to 9 times higher.

6. Pharmaceutical particulars
6.1 List of excipients

Tablet c ore

Lactose monohydrate

Microcrystalline cellulose

Hypromellose

Glycerol dibehenate

Talc

Film-c oating

Poly(vinyl alcohol)

Titanium dioxide

Talc

Glycerol monocaprylocaprate

Sodium laurilsulfate

Indigo carmine aluminium lake

6.2 Incompatibilities

Not applicable.

6.3 Shelf life

2 years

6.4 Special precautions for storage

Do not store above 30°C.

Store in the original package in order to protect from moisture.

6.5 Nature and contents of container

Aluminium-aluminium blisters in cartons containing 7, 14, 28, 30, 56, 84, 98 or 100 tablets.

Not all pack sizes may be marketed.

6.6 Special precautions for disposal and other handling

Any unused medicinal product or w aste material should be disposed of in accordance w ith local requirements.

7. Marketing authorisation holder

Dr. Reddy's Laboratories (UK) Ltd.

6 Riverview Road

Beverley

East Yorkshire

HU17 0LD

United Kingdom

8. Marketing authorisation number(s)

PL 08553/0708

9. Date of first authorisation/renewal of the authorisation

10/12/2021

10. Date of revision of the text

10/12/2021

Dr. Reddy's Laboratories (UK) Ltd
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