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DECAPEPTYL SR 11.25MG POWDER FOR SUSPENSION FOR INJECTION

Active substance: TRIPTORELIN ACETATE

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SUMMARY OF PRODUCT CHARACTERISTICS

1

NAME OF THE MEDICINAL PRODUCT
Decapeptyl SR 11.25mg, powder for suspension for injection.

2

QUALITATIVE AND QUANTITATIVE COMPOSITION
Triptorelin (I.N.N.) 15mg, as triptorelin acetate.
The vial contains an overage to ensure that a dose of 11.25mg is administered
to the patient.
For a full list of excipients, see section 6.1.

3

PHARMACEUTICAL FORM
Powder for suspension for injection, sustained release formulation.

4

CLINICAL PARTICULARS

4.1

Therapeutic indications
Treatment of patients with locally advanced, non-metastatic prostate cancer, as an
alternative to surgical castration (see section 5.1).
Treatment of metastatic prostate cancer.
As adjuvant treatment to radiotherapy in patients with high-risk localised or locally
advanced prostate cancer.
As neoadjuvant treatment prior to radiotherapy in patients with high-risk localised or
locally advanced prostate cancer.
As adjuvant treatment to radical prostatectomy in patients with locally advanced
prostate cancer at high risk of disease progression.
Treatment of endometriosis.
Treatment of precocious puberty (onset before 8 years in girls and 10 years in boys).

4.2

Posology and method of administration

Prostate cancer
One intramuscular injection should be administered every 3 months.
No dosage adjustment is necessary in the elderly.
Decapeptyl is also available as a 1-month treatment (Decapeptyl SR 3 mg) and as a 6month treatment (Decapeptyl SR 22.5 mg) for prostate cancer.

In patients treated with GnRH analogues for metastatic prostate cancer, treatment
is usually continued upon development of castrate-resistant prostate cancer.
Reference should be made to relevant guidelines.
Endometriosis
One intramuscular injection should be administered every 3 months. The treatment
must be initiated in the first five days of the menstrual cycle. Treatment duration
depends on the initial severity of the endometriosis and the changes observed in the
clinical features (functional and anatomical) during treatment. The maximum duration
of treatment should be 6 months (two injections).
A further course of treatment with Decapeptyl SR 11.25 mg, or with other GnRH
agonists, beyond 6 months should not be undertaken due to concerns about bone
density losses.
Decapeptyl is also available as a 1-month treatment (Decapeptyl SR 3 mg) for
endometriosis.
Precocious puberty (before 8 years in girls and 10 years in boys)
One intramuscular injection should be administered every 3 months.
The treatment of children with Decapeptyl SR 11.25 mg should be under the overall
supervision of a paediatric endocrinologist or of a paediatrician or endocrinologist
with expertise in the treatment of central precocious puberty.
Treatment should be stopped around the physiological age of puberty in boys and
girls and should not be continued in girls with a bone maturation of more than 12
years. There are limited data available in boys relating to the optimum time to stop
treatment based on bone age, however it is advised that treatment is stopped in boys
with a bone maturation age of 13-14 years.

4.3

Contraindications

Hypersensitivity to GnRH, its analogues or any other component of the
medicinal product (see section 4.8).
Pregnancy and lactation
4.4

Special warnings and precautions for use
The use of GnRH agonists may cause a reduction in bone mineral density. In men,
preliminary data suggest that the use of a bisphosphonate in combination with a
GnRH agonist may reduce bone mineral loss. No specific data is available for patients
with established osteoporosis or with risk factors for osteoporosis (e.g. chronic
alcohol abuse, smokers, long-term therapy with drugs that reduce bone mineral
density, e.g. anticonvulsants or corticosteroids, family history of osteoporosis,
malnutrition, e.g. anorexia nervosa). Particular caution is therefore necessary since
reduction in bone mineral density is likely to be more detrimental in these patients.
Treatment with Decapeptyl SR 11.25mg should be considered on an individual basis
and only be initiated if the benefits of treatment outweigh the risk following a very
careful appraisal. Consideration should be given to additional measures in order to
counteract loss of bone mineral density.
It should be confirmed that the patient is not pregnant before prescription of
triptorelin.
Rarely, treatment with GnRH agonists may reveal the presence of a previously
unknown gonadotroph cell pituitary adenoma. These patients may present with a
pituitary apoplexy characterised by sudden headache, vomiting, visual impairment
and ophthalmoplegia.
There is an increased risk of incident depression (which may be severe) in patients
undergoing treatment with GnRH agonists, such as triptorelin. Patients should be
informed accordingly and treated as appropriate if symptoms occur. Patients with
known depression should be monitored closely during therapy.
Prostate cancer
Initially, Decapeptyl SR 11.25mg, like other GnRH agonists, causes a transient
increase in serum testosterone levels. As a consequence, isolated cases of transient
worsening of signs and symptoms of prostate cancer may occasionally develop during
the first weeks of treatment. During the initial phase of treatment, consideration
should be given to the additional administration of a suitable anti-androgen to
counteract the initial rise in serum testosterone levels and the worsening of clinical
symptoms.
A small number of patients may experience a temporary worsening of signs and
symptoms of their prostate cancer (tumour flare) and temporary increase in cancer
related pain (metastatic pain), which can be managed symptomatically.

As with other GnRH agonists, isolated cases of spinal cord compression or urethral
obstruction have been observed. If spinal cord compression or renal impairment
develops, standard treatment of these complications should be instituted, and in
extreme cases an immediate orchidectomy (surgical castration) should be considered.
Careful monitoring is indicated during the first weeks of treatment, particularly in
patients suffering from vertebral metastasis, at the risk of spinal cord compression,
and in patients with urinary tract obstruction.
After surgical castration, Decapeptyl SR 11.25mg does not induce any further
decrease in serum testosterone levels.
Long-term androgen deprivation either by bilateral orchidectomy or administration of
GnRH agonists is associated with increased risk of bone loss and may lead to
osteoporosis and increased risk of bone fracture.
Long-term androgen deprivation therapy may prolong the QT interval. Physicians
should consider whether the benefits of androgen deprivation therapy outweigh the
potential risks in patients with congenital long QT syndrome, electrolyte
abnormalities, or congestive heart failure or in patients receiving class IA or class III
antiarrhythmic medications.
In addition, from epidemiological data, it has been observed that patients may
experience metabolic changes (e.g. glucose intolerance), or an increased risk of
cardiovascular disease during androgen deprivation therapy. However, prospective
data did not confirm the link between treatment with GnRH agonists and an increase
in cardiovascular mortality. Patients at high risk for metabolic or cardiovascular
diseases should be carefully assessed before commencing treatment and their glucose,
cholesterol and blood pressure adequately monitored during androgen deprivation
therapy.
Metabolic changes may be more severe in these high risk patients. Patients at high
risk of metabolic or cardiovascular disease and receiving androgen deprivation
therapy should be monitored at appropriate intervals not exceeding 3 months.
Administration of triptorelin in therapeutic doses result in suppression of the pituitary
gonadal system. Normal function is usually restored after treatment is discontinued.
Diagnostic tests of pituitary gonadal function conducted during treatment and after
discontinuation of therapy with GnRH agonists may therefore be misleading.
Endometriosis
The use of GnRH agonists is likely to cause reduction in bone mineral density
averaging 1% per month during a six month treatment period. Every 10% reduction in
bone mineral density is linked with about a two to three times increased fracture risk.
In the majority of women, currently available data suggest that recovery of bone loss
occurs after cessation of therapy.

Used at the recommended dose, Decapeptyl SR 11.25mg causes constant
hypogonadotropic amenorrhoea. If vaginal haemorrhage occurs after the first month,
plasma oestradiol levels should be measured and if levels are below 50 pg/mL,
possible organic lesions should be investigated.
After withdrawal of treatment, ovarian function resumes and ovulation occurs
approximately 5 months after the last injection. A non-hormonal method of
contraception should be used throughout treatment including for 3 months after the
duration of the last injection.
Since menses should stop during Decapeptyl SR 11.25mg treatment, the patient
should be instructed to notify her physician if regular menstruation persists.
Precocious puberty
Treatment of children with progressive brain tumours should follow a careful
individual appraisal of the risks and benefits.
In girls, initial ovarian stimulation at treatment initiation, followed by the treatmentinduced oestrogen withdrawal, may lead, in the first month, to vaginal bleeding of
mild or moderate intensity.
After discontinuation of treatment the development of puberty characteristics will
occur.
Information with regards to future fertility is still limited. In most girls, regular
menses will start on average one year after ending the therapy.
Pseudo-precocious puberty (gonadal or adrenal tumour or hyperplasia) and
gonadotropin-independent precocious puberty (testicular toxicosis, familial Leydig
cell hyperplasia) should be precluded.
Bone mineral density may decrease during GnRH agonist therapy for central
precocious puberty. However, after cessation of treatment subsequent bone mass
accrual is preserved, and peak bone mass in late adolescence does not seem to be
affected by treatment.
Slipped capital femoral epiphysis can be seen after withdrawal of GnRH agonist
treatment. The suggested theory is that the low concentrations of oestrogen during
treatment with GnRH agonists weaken the epiphysial plate. The increase in growth
velocity after stopping the treatment subsequently results in a reduction of the
shearing force needed for displacement of the epiphysi

4.5

Interaction with other medicinal products and other forms of interaction

Drugs which raise prolactin levels should not be prescribed concomitantly as they
reduce the level of GnRH receptors in the pituitary.
When Decapeptyl SR 22.5mg is co-administered with drugs affecting pituitary
secretion of gonadotropins, caution should be exercised and it is recommended that
the patient’s hormonal status be supervised.
Since androgen deprivation treatment may prolong the QT interval, the concomitant
use of triptorelin with medicinal products known to prolong the QT interval or
medicinal products able to induce torsade de pointes such as class IA (e.g. quinidine,
procainamide) or class III (e.g. amiodarone, sotalol) antiarrhythmic medicinal
products should be carefully evaluated (see Section 4.4).

4.6

Pregnancy and lactation
Triptorelin should not be used during pregnancy since concurrent use of
GnRH agonists is associated with a theoretical risk of abortion or foetal
abnormality. Prior to treatment, potentially fertile women should be examined
to exclude pregnancy. Non-hormonal methods of contraception should be
employed during therapy until menses resume.
Animal studies have not revealed any teratogenic effects. During post-marketing
surveillance and in a limited number of pregnant women who were exposed
inadvertently to triptorelin, there were no reports of malformation or foetotoxicity
attributable to the product. However, as the number of patients is too small to draw
conclusions regarding the risk of foetal malformations or foetotoxicity, if a patient
becomes pregnant while receiving triptorelin, therapy should be discontinued.

Triptorelin is not recommended for use during lactation.
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, the ability to drive and use machines may be impaired
should the patient experience dizziness, somnolence and visual disturbances
(being possible undesirable effects of treatment), or resulting from the
underlying disease.

4.8

Undesirable effects
Clinical trials experience
General tolerance in men
As seen with other GnRH agonist therapies or after surgical castration, the most
commonly observed adverse events related to triptorelin treatment were due to its
expected pharmacological effects: Initial increase in testosterone levels, followed by
almost complete suppression of testosterone. These effects included hot flushes
(50%), erectile dysfunction (4%) and decreased libido (3%).

The following adverse reactions, considered as at least possibly related to triptorelin
treatment, were reported. Most of these are known to be related to biochemical or
surgical castration. The frequency of the adverse reactions is classified as follows:
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).



Uncommon AEs
0.1% -<1%

Rare AEs
0.01%-<0.1%
Purpura



Common AEs
1% -<10%





Tinnitus

Additional postmarketing AEs







Blood and
lymphatic system
disorders
Ear and labyrinth
disorders

Very Common
AEs
10%



System Organ
Class

Vertigo

Endocrine
disorders
Eye disorders

Diabetes mellitus

Gynaecomastia

Abnormal sensation
in eye
Visual disturbance

Vision blurred

Nausea

Abdominal pain
Constipation
Diarrhoea
Vomiting

Abdominal distension
Dry mouth
Dysgeusia
Flatulence

Fatigue
Injection site
erythema
Injection site
inflammation
Injection site pain
Injection site
reaction
Oedema

Lethargy
Pain
Rigors
Somnolence

Chest pain
Dysstasia
Influenza like illness
Pyrexia

Malaise

Immune system
disorders

Anaphylactic reaction
Hypersensitivity

Hypersensitivity
reaction

Infections and
infestations

Nasopharyngitis

Gastrointestinal
disorders

General disorders
and
administration site
conditions

Asthenia
Hyperhidrosis

Investigations

Alanine
aminotransferase
increased
Aspartate
aminotransferase
increased
Blood creatinine
increased
Blood urea
increased
Weight increased

Metabolism and
nutrition disorders

Blood alkaline
phosphatase
increased
Body temperature
increased
Weight decreased

Blood pressure
increased

Joint stiffness
Joint swelling

Bone pain

Anorexia
Gout
Increased appetite

Musculoskeletal
and connective

Back pain

Musculoskeletal
pain

Arthralgia
Muscle cramp

System Organ
Class

Very Common
AEs
10%

Common AEs
1% -<10%
Pain in extremity

Uncommon AEs
0.1% -<1%
Muscular weakness
Myalgia

Rare AEs
0.01%-<0.1%
Musculoskeletal
stiffness
Osteoarthritis

Paraesthesia

Memory impairment

Psychiatric
disorders

Depression
Mood changes

Insomnia
Irritability

Confusional state
Decreased activity
Euphoric mood

Reproductive
system and breast
disorders

Erectile
dysfunction
Loss of libido

Gynaecomastia
Breast pain
Testicular atrophy
Testicular pain

Ejaculation failure

Dyspnoea

Orthopnoea

Acne
Alopecia
Pruritus
Rash
Hypertension

Blister

Additional postmarketing AEs





Paraesthesia in
lower limbs

Dizziness
Headache

Respiratory,
thoracic and
mediastinal
disorders
Skin and
subcutaneous
tissue disorders

Hyperhidrosis

Vascular
disorders

Hot flush



Nervous system
disorders



tissue disorders

Anxiety and
Confusional state

Angioneurotic
oedema
Urticaria

Epistaxis
Hypotension

Triptorelin causes a transient increase in circulating testosterone levels within
the first week after the initial injection of the sustained release formulation.
With this initial increase in circulating testosterone levels, a small percentage
of patients (≤ 5%) may experience a temporary worsening of signs and
symptoms of their prostate cancer (tumour flare), usually manifested by an
increase in urinary symptoms (< 2%) and metastatic pain (5%), which can be
managed symptomatically. These symptoms are transient and usually
disappear in one to two weeks.
Isolated cases of exacerbation of disease symptoms, either urethral obstruction
or spinal cord compression by metastasis have occurred. Therefore, patients
with metastatic vertebral lesions and/or with upper or lower urinary tract
obstruction should be closely observed during the first few weeks of therapy
(see special warnings and special precautions for use).
The use of GnRH agonists to treat prostate cancer may be associated with
increased bone loss and may lead to osteoporosis and increases in the risk of
bone fracture.
General tolerance in women (see section 4.4)
As a consequence of decreased oestrogen levels, the most commonly reported
adverse events (expected in 10% of women or more) were headache,
decreased libido, sleep disorder, mood changes, dyspareunia, dysmenorrhoea,
genital haemorrhage, ovarian hyperstimulation syndrome, ovarian hypertrophy

pelvic pain, abdominal pain, vulvovaginal dryness, hyperhidrosis, hot flushes
and asthenia.
The following adverse reactions, considered as at least possibly related to
triptorelin treatment, were reported. Most of these are known to be related to
biochemical or surgical castration.
The frequency of the adverse reactions is classified as follows: very common
(≥1/10); common (≥1/100 to <1/10); uncommon (≥1/1,000 to <1/100)



General disorders
and administration
site conditions

Investigations
Musculoskeletal
and connective
tissue disorders
Nervous system
disorders

Common AEs
1% - <10%
Nausea
Abdominal pain
Abdominal
discomfort
Injection site
erythema
Injection site
inflammation
Injection site pain
Weight increased



Gastrointestinal
disorders

Very Common AEs
10%

Uncommon AEs
0.1% -<1%



System Organ
Class

Blood pressure
increased
Myalgia
Muscular weakness
Dizziness

Headache
Libido decreased
Sleep disorder
Mood changes
Dyspareunia
Dysmenorrhoea
Genital
haemorrhage
(including
menorrhagia,
metrorrhagia)
Libido decreased
Ovarian
hyperstimulation
syndrome
Ovarian
hypertrophy
Pelvic pain
Vulvovaginal
dryness

Skin and
subcutaneous tissue
disorders

Hyperhidrosis

Vascular disorders

Diarrhoea
Vomiting

Pyrexia
Malaise

Arthralgia
Muscle spasms

Psychiatric
disorders
Reproductive
system and breast
disorders

Additional postmarketing AEs

Hot flush

Respiratory,
thoracic and
mediastinal
disorders

Depression*
Breast pain

Depression**

Anxiety
andConfusional state
Amenorrhoea

Angioneurotic oedema
Pruritus
Rash
Urticaria

Dyspnoea



Eye disorders

Common AEs
1% - <10%



Very Common AEs
10%

Uncommon AEs
0.1% -<1%



System Organ
Class

Additional postmarketing AEs
Vision blurred
Visual disturbance
Vertigo

Ear and labyrinth
disorders
Immune system
disorders

Hypersensitivity
reaction

*Long term use
** Short term use

At the beginning of treatment, the symptoms of endometriosis including pelvic pain
and dysmenorrhoea are commonly exacerbated during the initial transient increase in
plasma oestradiol levels. These symptoms are transient and usually disappear in one
to two weeks.
Genital haemorrhage including menorrhagia and metrorrhagia may occur in the
month following the first injection.
General tolerance in children (see section 4.4)
The frequency of the adverse reactions is classified as follows: very common ( 1/10);
common ( 1/100 to <1/10);





System Organ Class

General disorders and
administration site
conditions



Gastrointestinal disorders

Common AEs
1% - <10%



Very Common AEs
10%

Pain
Erythema
Injection site erythema
Injection site
inflammation
Injection site pain

Investigations

Additional post-marketing
AEs
Vomiting
Abdominal pain
Abdominal discomfort
Malaise

Blood pressure increased
Weight increased
Myalgia

Musculoskeletal and
connective tissue
disorders
Nervous system
disorders
Psychiatric disorders

Headache

Reproductive system and
breast disorders

Genital haemorrhage
Vaginal bleeding

Vascular disorders

Hot flush

Affect lability
Nervousness

Respiratory, thoracic and
mediastinal disorders

Epistaxis

Eye disorders

Vision blurred
Visual disturbance

System Organ Class
Common AEs
1% - <10%


Skin and subcutaneous
tissue disorders
Immune system
disorders

Additional post-marketing
AEs



Very Common AEs
10%

Hypersensitivity
reaction

Angioneurotic oedema
Rash
Urticaria
Hypersensitivity reaction

Reporting of suspected adverse reactions
Reporting of suspected adverse reactions after authorization of the medicinal product
is important. It allows continued monitoring of the benefit/risk balance of the
medicinal product. Healthcare professionals are asked to report any suspected adverse
reactions via the national reporting system
Yellow Card Scheme
Website: www.mhra.gov.uk/yellowcard

4.9

Overdose
No case of overdose has been reported. Animal data do not predict any effects
other than those on sex hormone concentration and consequent effect on the
reproductive tract. If overdose occurs, symptomatic management is indicated.

5

PHARMACOLOGICAL PROPERTIES

5.1

Pharmacodynamic properties
Pharmacotherapeutic group:
Gonadotropin-Releasing Hormone analogue
L 02 A E 04: Antineoplastic and immunomodulator
Triptorelin is a synthetic decapeptide analogue of natural GnRH.
Prostate cancer
The first administration of Decapeptyl SR 11.25mg stimulates the release of
pituitary gonadotropins with a transient increase in testosterone levels (“flareup”) in men. Prolonged administration leads to a suppression of gonadotropins
and a fall in plasma testosterone or oestradiol to castrate levels after
approximately 20 days, which is maintained for as long as the product is
administered.

The efficacy and safety of triptorelin has been determined in clinical studies
involving 645 patients with locally advanced or metastatic prostate cancer.
Of these, three long term controlled studies compared the efficacy and safety
of triptorelin to bilateral orchidectomy as an initial therapy in patients with
locally advanced or metastatic prostate cancer (stage C or D). In one of these
three long term studies, 7 patients in the triptorelin group and 7 patients in the
orchidectomy group had also undergone prostatectomy. Triptorelin induced
biochemical castration at least as rapidly as surgical pulpectomy and was as
effective as surgical castration in the long term palliative treatment of locally
advanced or metastatic prostate cancer. Both the triptorelin and orchidectomy
groups showed improvements in dysuria and pain, and reduction in volume of
prostate. Analysis after six and eight years in two of the studies showed that
there was no significant difference in the median survival rates in the
triptorelin group versus the orchidectomy group.
A study assessing the pharmacodynamic equivalence between triptorelin 3month and 28-day prolonged release formulations in patients with locally
advanced or metastatic prostate cancer, found that equivalent testosterone
suppression was achieved, whether 3 doses of Decapeptyl SR 3mg (n=68) or a
single dose of Decapeptyl SR 11.25mg (n=63) was given. The percentage of
patients who achieved a testosterone castrate level ≤ 0.5 ng/mL at D84 was
similar in the two treatment groups (98% and 96% in the 3-month and 28-day
formulation groups, respectively). The time to achieve chemical castration
was not significantly different between the two groups.
In a phase III randomized clinical trial including 970 patients with locally
advanced prostate cancer (mainly T2c-T4 with some T1c to T2b patients with
pathological regional nodal disease) of whom 483 were assigned to short-term
androgen suppression (6 months) in combination with radiation therapy and
487 to long-term therapy (3 years), a non-inferiority analysis compared the
short-term to long-term concomitant and adjuvant hormonal treatment with
triptorelin (62.2%) or goserelin (30.1%). The 5-year overall mortality was
19.0% and 15.2%, in the short-term and long-term groups, respectively. The
observed Hazard Ratio of 1.42 with an upper one-sided 95.71% CI of 1.79 or
two-sided 95.71% CI of 1.09; 1.85 (p = 0.65 for non inferiority), demonstrate
that the combination of radiotherapy plus 6 months of androgen deprivation
therapy provides inferior survival as compared with radiotherapy plus 3 years
of androgen deprivation therapy. Overall survival at 5 years of long-term
treatment and short-term treatment shows 84.8% survival and 81.0%,
respectively.
Overall quality of life using QLQ-C30 did not differ significantly between the
two groups (P= 0.37).
Neoadjuvant triptorelin prior to radiotherapy has been shown to significantly
reduce prostate volume.
The use of a GnRH agonist may be considered after radical prostatectomy in
selected patients considered at high risk of disease progression. There are no
disease-free survival data or survival data with triptorelin in this setting.

Endometriosis
The first administration of Decapeptyl SR 11.25mg stimulates the release of
pituitary gonadotropins with a transient increase in oestradiol levels in women.
Prolonged administration leads to a suppression of gonadotropins and a fall in
plasma testosterone or oestradiol to castrate levels after approximately 20
days, which is maintained for as long as the product is administered.
Continued administration of Decapeptyl SR 11.25mg induces suppression of
oestrogen secretion and thus enables resting of ectopic endometrial tissue.
Precocious puberty
Inhibition of the increased hypophyseal gonadotropic activity in children with
precocious puberty leads to suppression of oestradiol and testosterone
secretion in girls and boys, respectively, and to lowering of the LH peak due to
the GnRH stimulation test. The consequence is a regression or stabilisation of
secondary sex characteristics and an improvement in median predicted adult
height of 2.3cm after one year’s treatment.

5.2

Pharmacokinetic properties
Following intramuscular injection of Decapeptyl SR 11.25mg in patients (men
and women), a peak of plasma triptorelin is observed in the first 3 hours after
injection. After a phase of decrease, the circulating triptorelin levels remain
stable at around 0.04-0.05ng/mL in endometriosis patients and around
0.1ng/mL in prostate cancer patients until day 90.

5.3

Preclinical safety data
The compound did not demonstrate any specific toxicity in animal
toxicological studies. The effects observed are related to the pharmacological
properties of triptorelin on the endocrine system.

6

PHARMACEUTICAL PARTICULARS

6.1

List of excipients
D, L lactide-glycolide copolymer
Mannitol
Carmellose sodium
Polysorbate 80.

6.2

Incompatibilities
This medicinal product must not be mixed with other medicinal products
except the one mentioned in 6.6.

6.3

Shelf life
2 years.
The product should be used immediately after reconstitution.

6.4

Special precautions for storage
Do not store above 25°C. Keep container in the outer carton.

6.5

Nature and contents of container
A type I, 4mL capacity glass vial with an elastomer stopper and an aluminium
cap containing the powder.
A type I, 3mL capacity glass ampoule containing 2mL of the suspension
vehicle.
Box containing 1 vial and 1 ampoule with 1 syringe and 2 needles.

6.6

Special precautions for disposal
The suspension for injection must be reconstituted using an aseptic technique
and only using the ampoule of mannitol solution 0.8% for injection that is
provided as the suspension vehicle for Decapeptyl SR 11.25mg.
The suspension vehicle should be drawn into the syringe provided using one of
the injection needles and transferred to the vial containing the powder for
injection. The vial should be shaken from side to side until a homogenous
suspension is formed, and the mixture then drawn back into the syringe
without inverting the vial. The injection needle should then be changed and
the second needle used to administer the injection. As the product is a
suspension, the injection should be administered immediately after
reconstitution to prevent sedimentation. The suspension should be discarded if
it is not administered immediately after reconstitution.

To ensure patients receive the correct dose, each vial of Decapeptyl contains a
small overage to allow for predictable losses on reconstitution and injection.
The vial is intended for single use only and any remaining product should be
discarded. Used injection needles should be disposed of in a designated sharps
container.

7

MARKETING AUTHORISATION HOLDER
Ipsen Limited
190 Bath Road
Slough
Berkshire
SL1 3XE
United Kingdom

8

MARKETING AUTHORISATION NUMBER(S)
PL 34926/0003

9

DATE OF FIRST AUTHORISATION/RENEWAL OF THE
AUTHORISATION
Date of first authorisation: 16 October 2002
Date of last renewal: 16 March 2009

10

DATE OF REVISION OF THE TEXT
13/05/2014

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Source: Medicines and Healthcare Products Regulatory Agency

Disclaimer: Every effort has been made to ensure that the information provided here is accurate, up-to-date and complete, but no guarantee is made to that effect. Drug information contained herein may be time sensitive. This information has been compiled for use by healthcare practitioners and consumers in the United States. The absence of a warning for a given drug or combination thereof in no way should be construed to indicate that the drug or combination is safe, effective or appropriate for any given patient. If you have questions about the substances you are taking, check with your doctor, nurse or pharmacist.

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