Rivastigmine Hexal

1. NAME OF THE MEDICINAL PRODUCT

Rivastigmine HEXAL 1.5 mg hard capsules

2. QUALITATIVE AND QUANTITATIVE COMPOSITION

Each capsule contains rivastigmine hydrogen tartrate corresponding to rivastigmine 1.5 mg.

For a full list of excipients, see section 6.1.

3. PHARMACEUTICAL FORM

Hard capsule

Off-white to slightly yellow powder in a capsule with yellow cap and yellow body, with red imprint

“RIV 1.5 mg” on the body.

4. CLINICAL PARTICULARS

4.1 Therapeutic indications

Symptomatic treatment of mild to moderately severe Alzheimer’s dementia.

Symptomatic treatment of mild to moderately severe dementia in patients with idiopathic Parkinson’s

disease.

4.2 Posology and method of administration

Treatment should be initiated and supervised by a physician experienced in the diagnosis and

treatment of Alzheimer’s dementia or dementia associated with Parkinson’s disease. Diagnosis should

be made according to current guidelines. Therapy with rivastigmine should only be started if a

caregiver is available who will regularly monitor intake of the medicinal product by the patient.

Rivastigmine should be administered twice a day, with morning and evening meals. The capsules

should be swallowed whole.

Initial dose

1.5 mg twice a day.

Dose titration

The starting dose is 1.5 mg twice a day. If this dose is well tolerated after a minimum of two weeks of

treatment, the dose may be increased to 3 mg twice a day. Subsequent increases to 4.5 mg and then

6 mg twice a day should also be based on good tolerability of the current dose and may be considered

after a minimum of two weeks of treatment at that dose level.

If adverse reactions (e.g. nausea, vomiting, abdominal pain or loss of appetite), weight decrease or

worsening of extrapyramidal symptoms (e.g. tremor) in patients with dementia associated with

Parkinson’s disease are observed during treatment, these may respond to omitting one or more doses.

If adverse reactions persist, the daily dose should be temporarily reduced to the previous well-tolerated

dose or the treatment may be discontinued.

Maintenance dose

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The effective dose is 3 to 6 mg twice a day; to achieve maximum therapeutic benefit patients should

be maintained on their highest well tolerated dose. The recommended maximum daily dose is 6 mg

twice a day.

Maintenance treatment can be continued for as long as a therapeutic benefit for the patient exists.

Therefore, the clinical benefit of rivastigmine should be reassessed on a regular basis, especially for

patients treated at doses less than 3 mg twice a day. If after 3 months of maintenance dose treatment

the patient’s rate of decline in dementia symptoms is not altered favourably, the treatment should be

discontinued. Discontinuation should also be considered when evidence of a therapeutic effect is no

longer present.

Individual response to rivastigmine cannot be predicted. However, a greater treatment effect was seen

in Parkinson’s disease patients with moderate dementia. Similarly a larger effect was observed in

Parkinson’s disease patients with visual hallucinations (see section 5.1).

Treatment effect has not been studied in placebo-controlled trials beyond 6 months.

Re-initiation of therapy

If treatment is interrupted for more than several days, it should be re-initiated at 1.5 mg twice daily.

Dose titration should then be carried out as described above.

Renal and hepatic impairment

Due to increased exposure in moderate renal and mild to moderate hepatic impairment, dosing

recommendations to titrate according to individual tolerability should be closely followed (see section

5.2).

Patients with severe liver impairment have not been studied (see section 4.3).

Children

Rivastigmine is not recommended for use in children.

4.3 Contraindications

The use of this medicinal product is contraindicated in patients with

-

hypersensitivity to the active substance, other carbamate derivatives or to any of the excipients

used in the formulation,

-

severe liver impairment, as it has not been studied in this population.

4.4 Special warnings and precautions for use

The incidence and severity of adverse reactions generally increase with higher doses. If treatment is

interrupted for more than several days, it should be re-initiated at 1.5 mg twice daily to reduce the

possibility of adverse reactions (e.g. vomiting).

Dose titration: Adverse reactions (e.g. hypertension and hallucinations in patients with Alzheimer’s

dementia and worsening of extrapyramidal symptoms, in particular tremor, in patients with dementia

associated with Parkinson’s disease) have been observed shortly after dose increase. They may

respond to a dose reduction. In other cases, rivastigmine has been discontinued (see section 4.8).

Gastrointestinal disorders such as nausea and vomiting may occur particularly when initiating

treatment and/or increasing the dose. These adverse reactions occur more commonly in women.

Patients with Alzheimer’s disease may lose weight. Cholinesterase inhibitors, including rivastigmine,

have been associated with weight loss in these patients. During therapy patient’s weight should be

monitored.

In case of severe vomiting associated with rivastigmine treatment, appropriate dose adjustments as

recommended in section 4.2 must be made. Some cases of severe vomiting were associated with

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oesophageal rupture (see section 4.8). Such events appeared to occur particularly after dose increments

or high doses of rivastigmine.

Care must be taken when using rivastigmine in patients with sick sinus syndrome or conduction

defects (sino-atrial block, atrio-ventricular block) (see section 4.8).

Rivastigmine may cause increased gastric acid secretions. Care should be exercised in treating patients

with active gastric or duodenal ulcers or patients predisposed to these conditions.

Cholinesterase inhibitors should be prescribed with care to patients with a history of asthma or

obstructive pulmonary disease.

Cholinomimetics may induce or exacerbate urinary obstruction and seizures. Caution is recommended

in treating patients predisposed to such diseases.

The use of rivastigmine in patients with severe dementia of Alzheimer’s disease or associated with

Parkinson’s disease, other types of dementia or other types of memory impairment (e.g. age-related

cognitive decline) has not been investigated and therefore use in these patient populations is not

recommended.

Like other cholinomimetics, rivastigmine may exacerbate or induce extrapyramidal symptoms.

Worsening (including bradykinesia, dyskinesia, gait abnormality) and an increased incidence or

severity of tremor have been observed in patients with dementia associated with Parkinson’s disease

(see section 4.8). These events led to the discontinuation of rivastigmine in some cases (e.g.

discontinuations due to tremor 1.7% on rivastigmine vs 0% on placebo). Clinical monitoring is

recommended for these adverse reactions.

4.5 Interaction with other medicinal products and other forms of interaction

As a cholinesterase inhibitor, rivastigmine may exaggerate the effects of succinylcholine-type muscle

relaxants during anaesthesia. Caution is recommended when selecting anaesthetic agents. Possible

dose adjustments or temporarily stopping treatment can be considered if needed.

In view of its pharmacodynamic effects, rivastigmine should not be given concomitantly with other

cholinomimetic substances and might interfere with the activity of anticholinergic medicinal products.

No pharmacokinetic interaction was observed between rivastigmine and digoxin, warfarin, diazepam

or fluoxetine in studies in healthy volunteers. The increase in prothrombin time induced by warfarin is

not affected by administration of rivastigmine. No untoward effects on cardiac conduction were

observed following concomitant administration of digoxin and rivastigmine.

According to its metabolism, metabolic interactions with other medicinal products appear unlikely,

although rivastigmine may inhibit the butyrylcholinesterase mediated metabolism of other substances.

4.6 Fertility, pregnancy and lactation

For rivastigmine no clinical data on exposed pregnancies are available. No effects on fertility or

embryofoetal development were observed in rats and rabbits, except at doses related to maternal

toxicity. In peri/postnatal studies in rats, an increased gestation time was observed. Rivastigmine

should not be used during pregnancy unless clearly necessary.

In animals, rivastigmine is excreted into milk. It is not known if rivastigmine is excreted into human

milk. Therefore, women on rivastigmine should not breast-feed.

4.7 Effects on ability to drive and use machines

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Alzheimer’s disease may cause gradual impairment of driving performance or compromise the ability

to use machinery. Furthermore, rivastigmine can induce dizziness and somnolence, mainly when

initiating treatment or increasing the dose. As a consequence, rivastigmine has minor or moderate

influence on the

ability to drive and use machines. Therefore, the ability of patients with dementia on rivastigmine to

continue driving or operating complex machines should be routinely evaluated by the treating

physician.

4.8 Undesirable effects

The most commonly reported adverse reactions are gastrointestinal, including nausea (38%) and

vomiting (23%), especially during titration. Female patients in clinical studies were found to be more

susceptible than male patients to gastrointestinal adverse reactions and weight loss.

The following adverse reactions, listed below in Table 1, have been accumulated in patients with

Alzheimer’s dementia treated with rivastigmine.

Adverse reactions in Table 1 are listed according to MedDRA system organ class and frequency

category. Frequency categories are defined 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); not known (cannot be estimated from the available data).

Table 1

Infections and infestations

Very rare

Urinary infection

Metabolism and nutritional disorders

Very common

Anorexia

Psychiatric disorders

Common

Uncommon

Very rare

Agitation

Confusion

Insomnia

Depression

Hallucinations

Nervous system disorders

Very common

Common

Uncommon

Rare

Very rare

Dizziness

Headache

Somnolence

Tremor

Syncope

Seizures

Extrapyramidal symptoms (including

worsening of Parkinson’s disease)

Cardiac disorders

Rare

Very rare

Angina pectoris

Cardiac arrhythmia (e.g. bradycardia, atrio-

ventricular block, atrial fibrillation and

tachycardia)

Vascular disorders

Very rare

Hypertension

Gastrointestinal disorders

Very common

Nausea

Vomiting

Diarrhoea

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Common

Rare

Very rare

Not known

Abdominal pain and dyspepsia

Gastric and duodenal ulcers

Gastrointestinal haemorrhage

Pancreatitis

Some cases of severe vomiting were

associated with oesophageal rupture (see

section 4.4).

Hepatobiliary disorders

Uncommon

Elevated liver function tests

Skin and subcutaneous tissue disorders

Common

Rare

Not known

Sweating increased

Rash

Pruritus

General disorders and administration site

conditions

Common

Uncommon

Fatigue and asthenia

Malaise

Accidental fall

Investigations

Common

Weight loss

The following additional adverse reactions have been observed with rivastigmine transdermal patches:

anxiety, delirium, pyrexia (common).

Table 2 shows the adverse reactions reported in patients with dementia associated with Parkinson’s

disease treated with rivastigmine.

Table 2

Metabolism and nutritional disorders

Common

Anorexia

Dehydration

Psychiatric disorders

Common

Insomnia

Anxiety

Restlessness

Nervous system disorders

Very common

Common

Uncommon

Tremor

Dizziness

Somnolence

Headache

Worsening of Parkinson’s disease

Bradykinesia

Dyskinesia

Dystonia

Cardiac disorders

Common

Uncommon

Bradycardia

Arial fibrillation

Atrioventricular block

Gastrointestinal disorders

Very common

Common

Nausea

Vomiting

Diarrhoea

Abdominal pain and dyspepsia

Salivary hypersecretion

Skin and subcutaneous tissue disorders

Common

Sweating increased

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Musculoskeletal and connective tissue disorders

Common

Muscle rigidity

General disorders and administration site

conditions

Common

Fatigue and asthenia

Gait abnormality

Table 3 lists the number and percentage of patients from the specific 24-week clinical study conducted

with rivastigmine in patients with dementia associated with Parkinson’s disease with pre-defined

adverse events that may reflect worsening of parkinsonian symptoms.

Table 3

Pre-defined adverse events that may reflect

worsening of parkinsonian symptoms in

patients with dementia associated with

Parkinson’s disease

Rivastigmine

n (%)

Placebo

n (%)

Total patients studied

Total patients with pre-defined AE(s)

362 (100)

99 (27.3)

179 (100)

28 (15.6)

Tremor

Fall

Parkinson’s disease (worsening)

Salivary hypersecretion

Dyskinesia

Parkinsonism

Hypokinesia

Movement disorder

Bradykinesia

Dystonia

Gait abnormality

Muscle rigidity

Balance disorder

Musculoskeletal stiffness

Rigors

Motor dysfunction

37 (10.2)

21 (5.8)

12 (3.3)

5 (1.4)

8 (2.2)

1 (0.3)

9 (2.5)

3 (0.8)

5 (1.4)

1 (0.3)

3 (0.8)

1 (0.3)

7 (3.9)

11 (6.1)

2 (1.1)

0

1 (0.6)

0

3 (1.7)

1 (0.6)

0

2 (1.1)

0

4.9 Overdose

Symptoms

Most cases of accidental overdose have not been associated with any clinical signs or symptoms and

almost all of the patients concerned continued rivastigmine treatment. Where symptoms have

occurred, they have included nausea, vomiting and diarrhoea, hypertension or hallucinations. Due to

the known vagotonic effect of cholinesterase inhibitors on heart rate, bradycardia and/or syncope may

also occur. Ingestion of 46 mg occurred in one case; following conservative management the patient

fully recovered within 24 hours.

Treatment

As rivastigmine has a plasma half-life of about 1 hour and a duration of acetylcholinesterase inhibition

of about 9 hours, it is recommended that in cases of asymptomatic overdose no further dose of

rivastigmine should be administered for the next 24 hours. In overdose accompanied by severe nausea

and vomiting, the use of antiemetics should be considered. Symptomatic treatment for other adverse

reactions should be given as necessary.

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In massive overdose, atropine can be used. An initial dose of 0.03 mg/kg intravenous atropine sulphate

is recommended, with subsequent doses based on clinical response. Use of scopolamine as an antidote

is not recommended.

5. PHARMACOLOGICAL PROPERTIES

5.1 Pharmacodynamic properties

Pharmacotherapeutic group: anticholinesterases, ATC code: N06DA03

Rivastigmine is an acetyl- and butyrylcholinesterase inhibitor of the carbamate type, thought to

facilitate cholinergic neurotransmission by slowing the degradation of acetylcholine released by

functionally intact cholinergic neurones. Thus, rivastigmine may have an ameliorative effect on

cholinergic-mediated cognitive deficits in dementia associated with Alzheimer’s disease and

Parkinson’s disease.

Rivastigmine interacts with its target enzymes by forming a covalently bound complex that

temporarily inactivates the enzymes. In healthy young men, an oral 3 mg dose decreases

acetylcholinesterase (AChE) activity in CSF by approximately 40% within the first 1.5 hours after

administration. Activity of the enzyme returns to baseline levels about 9 hours after the maximum

inhibitory effect has been achieved. In patients with Alzheimer’s disease, inhibition of AChE in CSF

by rivastigmine was dose-dependent up to 6 mg given twice daily, the highest dose tested. Inhibition

of butyrylcholinesterase activity in CSF of 14 Alzheimer patients treated by rivastigmine was similar

to that of AChE.

Clinical studies in Alzheimer’s dementia

The efficacy of rivastigmine has been established through the use of three independent, domain

specific, assessment tools which were assessed at periodic intervals during 6 month treatment periods.

These include the ADAS-Cog (a performance based measure of cognition), the CIBIC-Plus (a

comprehensive global assessment of the patient by the physician incorporating caregiver input), and

the PDS (a caregiver-rated assessment of the activities of daily living including personal hygiene,

feeding, dressing, household chores such as shopping, retention of ability to orient oneself to

surroundings as well as involvement in activities relating to finances, etc.).

The patients studied had an MMSE (Mini-Mental State Examination) score of 10–24.

The results for clinically relevant responders pooled from two flexible dose studies out of the three

pivotal 26-week multicentre studies in patients with mild-to-moderately severe Alzheimer’s Dementia,

are provided in Table 4 below. Clinically relevant improvement in these studies was defined a priori as

at least 4-point improvement on the ADAS-Cog, improvement on the CIBIC-Plus, or at least a 10%

improvement on the PDS.

In addition, a post-hoc definition of response is provided in the same table. The secondary definition

of response required a 4-point or greater improvement on the ADAS-Cog, no worsening on the

CIBIC-Plus, and no worsening on the PDS. The mean actual daily dose for responders in the 6-12 mg

group, corresponding to this definition, was 9.3 mg. It is important to note that the scales used in this

indication vary and direct comparisons of results for different therapeutic agents are not valid.

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Table 4

Patients with Clinically Significant Response (%)

Intent to Treat

Last Observation Carried

Forward

Response Measure

Rivastigmine

6–12 mg

N=473

Placebo

N=472

Rivastigmine

6–12 mg

N=379

Placebo

N=444

ADAS-Cog: improvement

of at least 4 points

21***

12

25***

12

CIBIC-Plus: improvement

29***

18

32***

19

PDS: improvement of at

least 10%

26***

17

30***

18

At least 4 points

improvement on ADAS-Cog

with no worsening on

CIBIC-Plus and PDS

10*

6

12**

6

*p<0.05, **p<0.01, ***p<0.001

Clinical studies in dementia associated with Parkinson’s disease

The efficacy of rivastigmine in dementia associated with Parkinson’s disease has been demonstrated in

a 24-week multicentre, double-blind, placebo-controlled core study and its 24-week open-label

extension phase. Patients involved in this study had an MMSE (Mini-Mental State Examination) score

of 10–24. Efficacy has been established by the use of two independent scales which were assessed at

regular intervals during a 6-month treatment period as shown in Table 5 below: the ADAS-Cog, a

measure of cognition, and the global measure ADCS-CGIC (Alzheimer’s Disease Cooperative

Study-Clinician’s Global Impression of Change).

Table 5

Dementia associated with

Parkinson’s Disease

ADAS-Cog

Rivastigmine

ADAS-Cog

Placebo

ADCS-CGIC

Rivastigmine

ADCS-CGIC

Placebo

ITT + RDO population

Mean baseline ± SD

Mean change at

24 weeks ± SD

(n=329)

23.8 ± 10.2

2.1 ± 8.2

(n=161)

24.3 ± 10.5

-0.7 ± 7.5

(n=329)

n/a

3.8 ± 1.4

(n=165)

n/a

4.3 ± 1.5

Adjusted treatment

difference

p-value versus placebo

2.88 1

<0.001 1

n/a

0.007 2

ITT - LOCF population

Mean baseline ± SD

Mean change at

24 weeks ± SD

(n=287)

24.0 ± 10.3

2.5 ± 8.4

(n=154)

24.5 ± 10.6

-0.8 ± 7.5

(n=289)

n/a

3.7 ± 1.4

(n=158)

n/a

4.3 ± 1.5

n/a

<0.001 2

1 Based on ANCOVA with treatment and country as factors and baseline ADAS-Cog as a covariate. A

positive change indicates improvement.

2 Mean data shown for convenience, categorical analysis performed using van Elteren test

ITT: Intent-To-Treat; RDO: Retrieved Drop Outs; LOCF: Last Observation Carried Forward

3.54 1

<0.001 1

Although a treatment effect was demonstrated in the overall study population, the data suggested that a

larger treatment effect relative to placebo was seen in the subgroup of patients with moderate dementia

associated with Parkinson’s disease. Similarly a larger treatment effect was observed in those patients

with visual hallucinations (see Table 6).

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Adjusted treatment

difference

p-value versus placebo

Table 6

Dementia associated with

Parkinson’s Disease

ADAS-Cog

Rivastigmine

ADAS-Cog

Placebo

ADAS-Cog

Rivastigmine

ADAS-Cog

Placebo

Patients with visual

hallucinations

Patients without visual

hallucinations

ITT + RDO population

Mean baseline ± SD

Mean change at

24 weeks ± SD

(n=107)

25.4 ± 9.9

1.0 ± 9.2

(n=60)

27.4 ± 10.4

-2.1 ± 8.3

(n=220)

23.1 ± 10.4

2.6 ± 7.6

(n=101)

22.5 ± 10.1

0.1 ± 6.9

Adjusted treatment

difference

p-value versus placebo

4.27 1

0.002 1

2.09 1

0.015 1

Patients with moderate

dementia (MMSE 10-17)

Patients with mild dementia

(MMSE 18-24)

ITT + RDO population

Mean baseline ± SD

Mean change at

24 weeks ± SD

(n=87)

32.6 ± 10.4

2.6 ± 9.4

(n=44)

33.7 ± 10.3

-1.8 ± 7.2

(n=237)

20.6 ± 7.9

1.9 ± 7.7

(n=115)

20.7 ± 7.9

-0.2 ± 7.5

2.14 1

0.010 1

1 Based on ANCOVA with treatment and country as factors and baseline ADAS-Cog as a covariate. A

positive change indicates improvement.

ITT: Intent-To-Treat; RDO: Retrieved Drop Outs

4.73 1

0.002 1

5.2 Pharmacokinetic properties

Absorption

Rivastigmine is rapidly and completely absorbed. Peak plasma concentrations are reached in

approximately 1 hour. As a consequence of rivastigmine’s interaction with its target enzyme, the

increase in bioavailability is about 1.5-fold greater than that expected from the increase in dose.

Absolute bioavailability after a 3 mg dose is about 36%±13%. Administration of rivastigmine with

food delays absorption (t max ) by 90 min and lowers C max and increases AUC by approximately 30%.

Distribution

Protein binding of rivastigmine is approximately 40%. It readily crosses the blood brain barrier and

has an apparent volume of distribution in the range of 1.8–2.7 l/kg.

Metabolism

Rivastigmine is rapidly and extensively metabolised (half-life in plasma approximately 1 hour),

primarily via cholinesterase-mediated hydrolysis to the decarbamylated metabolite. In vitro , this

metabolite shows minimal inhibition of acetylcholinesterase (<10%). Based on evidence from in vitro

and animal studies the major cytochrome P450 isoenzymes are minimally involved in rivastigmine

metabolism. Total plasma clearance of rivastigmine was approximately 130 l/h after a 0.2 mg

intravenous dose and decreased to 70 l/h after a 2.7 mg intravenous dose.

Excretion

Unchanged rivastigmine is not found in the urine; renal excretion of the metabolites is the major route

of elimination. Following administration of 14 C-rivastigmine, renal elimination was rapid and

essentially complete (>90%) within 24 hours. Less than 1% of the administered dose is excreted in the

faeces. There is no accumulation of rivastigmine or the decarbamylated metabolite in patients with

Alzheimer’s disease.

Elderly subjects

10

Adjusted treatment

difference

p-value versus placebo

While bioavailability of rivastigmine is greater in elderly than in young healthy volunteers, studies in

Alzheimer patients aged between 50 and 92 years showed no change in bioavailability with age.

Subjects with hepatic impairment

The C max of rivastigmine was approximately 60% higher and the AUC of rivastigmine was more than

twice as high in subjects with mild to moderate hepatic impairment than in healthy subjects.

Subjects with renal impairment

C max and AUC of rivastigmine were more than twice as high in subjects with moderate renal

impairment compared with healthy subjects; however there were no changes in C max and AUC of

rivastigmine in subjects with severe renal impairment.

5.3 Preclinical safety data

Repeated-dose toxicity studies in rats, mice and dogs revealed only effects associated with an

exaggerated pharmacological action. No target organ toxicity was observed. No safety margins to

human exposure were achieved in the animal studies due to the sensitivity of the animal models used.

Rivastigmine was not mutagenic in a standard battery of in vitro and in vivo tests, except in a

chromosomal aberration test in human peripheral lymphocytes at a dose 10 4 times the maximum

clinical exposure. The in vivo micronucleus test was negative.

No evidence of carcinogenicity was found in studies in mice and rats at the maximum tolerated dose,

although the exposure to rivastigmine and its metabolites was lower than the human exposure. When

normalised to body surface area, the exposure to rivastigmine and its metabolites was approximately

equivalent to the maximum recommended human dose of 12 mg/day; however, when compared to the

maximum human dose, a multiple of approximately 6-fold was achieved in animals.

In animals, rivastigmine crosses the placenta and is excreted into milk. Oral studies in pregnant rats

and rabbits gave no indication of teratogenic potential on the part of rivastigmine.

6. PHARMACEUTICAL PARTICULARS

6.1 List of excipients

Gelatin

Magnesium stearate

Hypromellose

Microcrystalline cellulose

Silica, colloidal anhydrous

Yellow iron oxide (E172)

Red iron oxide (E172)

Titanium dioxide (E171)

6.2 Incompatibilities

Not applicable.

6.3 Shelf life

5 years

6.4 Special precautions for storage

Do not store above 30°C.

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6.5 Nature and contents of container

-

Blister of clear PVC tray with blue lidding foil with 14 capsules. Each box contains 2, 4 or 8

blisters.

-

HDPE bottles with plastic closure with induction innerseal. Each bottle contains 250 capsules.

Not all pack sizes may be marketed.

6.6 Special precautions for disposal

No special requirements.

7. MARKETING AUTHORISATION HOLDER

HEXAL AG

Industriestraße 25

83607 Holzkirchen

Germany

8. MARKETING AUTHORISATION NUMBER(S)

EU/1/09/589/001

EU/1/09/589/002

EU/1/09/589/003

EU/1/09/589/004

9

DATE OF FIRST AUTHORISATION/RENEWAL OF THE AUTHORISATION

11/12/2009

10. DATE OF REVISION OF THE TEXT

….

Detailed information is available on the European Medicines Agency (EMA) website:

http://www.ema.europa.eu

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1. NAME OF THE MEDICINAL PRODUCT

Rivastigmine HEXAL 3 mg hard capsules

2. QUALITATIVE AND QUANTITATIVE COMPOSITION

Each capsule contains rivastigmine hydrogen tartrate corresponding to rivastigmine 3 mg.

For a full list of excipients, see section 6.1.

3. PHARMACEUTICAL FORM

Hard capsule

Off-white to slightly yellow powder in a capsule with orange cap and orange body, with red imprint

“RIV 3 mg” on the body.