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DECAPEPTYL SR 11.25 MG POWDER AND SOLVENT FOR SUSPENSION FOR INJECTION

Active substance(s): TRIPTORELIN PAMOATE / TRIPTORELIN PAMOATE

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SUMMARY OF PRODUCT CHARACTERISTICS
1

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

2

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

3

PHARMACEUTICAL FORM
Powder and solvent 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 6-month 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 (gonadotropin releasing hormone), its analogues or to any
of the excipients listed in section 6.1.
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 11.25 mg 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 11.25 mg, 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 11.25 mg 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.

Androgen deprivation therapy may prolong the QT interval.

In patients with a history of or risk factors for QT prolongation and in patients
receiving concomitant medicinal products that might prolong the QT interval
(see section 4.5) physicians should assess the benefit risk ratio including the
potential for Torsade de pointes prior to initiating Decapeptyl SR 11.25 mg.
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 11.25 mg 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 11.25 mg 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 epiphysis.

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 11.25 mg 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 Decapeptyl SR 11.25 mg 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, disopyramide) or class III (e.g.
amiodarone, sotalol, dofetilide, ibutilide) antiarrhythmic medicinal products,
methadone, moxifloxacin, antipsychotics, etc. should be carefully evaluated
(see section 4.4).

4.6

Fertility, 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 postmarketing 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
Since patients suffering from locally advanced or metastatic, hormone-dependent
prostate cancer are generally old and have other diseases frequently encountered in
this aged population, more than 90% of the patients included in clinical trials reported
adverse events, and often the causality is difficult to assess. 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. These effects included hot flushes and decreased libido.
With the exception of immuno-allergic (rare) and injection site (< 5%) reactions, all
adverse events are known to be related to testosterone changes.
The following adverse reactions considered as at least possibly related to triptorelin
treatment were reported. Most of these events 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, < 1/10); uncommon (≥1/1000, < 1/100); rare (≥1/10000, < 1/1000).

Additional
postmarketing
AEs

System Organ
Class

Very Common

Common

Uncommon

Infections and
infestations

Rare
Nasopharyngitis

Frequency
not known

Thrombocytosis

Blood and
lymphatic
system
disorders
Hypersensitivity

Immune system
disorders

Anaphylactic
reaction

Anaphylactic
shock

Anxiety

Anorexia
Diabetes
mellitus
Gout
Hyperlipidaemi
a
Increased
appetite

Metabolism and
nutrition
disorders

Psychiatric
disorders

Libido
decreased

Depression*
Loss of libido
Mood change*

Insomnia
Irritability

Confusional state
Decreased
activity
Euphoric mood

Nervous system
disorders

Paraesthesia in
lower limbs

Dizziness
Headache

Paraesthesia

Memory
impairment

Eye disorders

Visual
impairment

Abnormal
sensation in eye
Visual
disturbance

Ear and
labyrinth
disorders

Tinnitus
Vertigo

Cardiac
Disorders

Palpitations

QT
prolongation
(see sections
4.4 and 4.5)

Vascular
disorders

Hot flush

Hypertension

Respiratory,
thoracic and
mediastinal
disorders
Dry mouth
Nausea

Gastrointestinal
disorders

Skin and
subcutaneous
tissue disorders

Hyperhidrosis

Musculoskeletal
and connective
tissue disorders

Back pain

Musculoskeletal
pain
Pain in
extremity

General
disorders and
administration
site conditions

Dyspnoea
Epistaxis

Orthopnoea

Abdominal pain
Constipation
Diarrhoea
Vomiting

Abdominal
distension
Dysgeusia
Flatulence

Acne
Alopecia
Erythema
Pruritus
Rash
Urticaria

Blister
Purpura

Arthralgia
Bone pain
Muscle cramp
Muscular
weakness
Myalgia

Joint stiffness
Joint swelling
Musculoskeletal
stiffness
Osteoarthritis

Erectile
dysfunction
(including
ejaculation
failure,
ejaculation
disorder)
Asthenia

Pelvic pain

Breast pain
Gynaecomastia
Testicular
atrophy
Testicular pain

Injection site
reaction
(including
erythema,
inflammation
and pain)
Oedema

Lethargy
Oedema
peripheral
Pain
Rigors
Somnolence

Angioneurotic
oedema

Urinary
incontinence

Nocturia
Urinary
retention

Renal and
urinary
disorders

Reproductive
system and
breast disorders

Hypotension

Chest pain
Dysstasia
Influenza like
illness
Pyrexia

Malaise

Investigations

Weight
increased

Alanine
aminotransferas
e increased
Aspartate
aminotransferas
e increased
Blood creatinine
increased
Blood pressure
increased
Blood urea
increased
Gammaglutamyl
transferase
increased
Weight
decreased

Blood alkaline
phosphatase
increased

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 Section 4.4).

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, libido decreased, 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, < 1/10); uncommon (≥1/1000, < 1/100); rare (≥1/10000, < 1/1000).
System Organ
Class

Additional postmarketing AEs

Very Common
Immune system
disorders

Common
Hypersensitivity

Nervous system
disorders

Eye disorders

Frequency not
known
Anaphylactic
shock

Decreased
appetite
Fluid retention

Metabolism and
nutrition
disorders

Psychiatric
disorders

Uncommon

Libido decreased
Mood disorder
Sleep disorder
(including
insomnia)
Headache

Depression*
Nervousness

Affect lability
Anxiety
Depression**
Disorientation

Dizziness

Dysgeusia
Hypoasthesia
Syncope
Memory
impairment
Disturbance in
attention
Paraesthesia
Tremor
Dry eye
Visual
Impairment

Ear and
labyrinth
disorders

Vertigo

Cardiac
Disorders

Palpitations

Confusional state

Visual
disturbance

Vascular
disorders

Hot flush

Hypertension

Dyspnoea
Epistaxis

Respiratory,
thoracic and
mediastinal
disorders
Abdominal pain

Gastrointestinal
disorders

Skin and
subcutaneous
tissue disorders

Abdominal
discomfort
Nausea
Acne
Hyperhidrosis
Seborrhoea

Musculoskeletal
and connective
tissue disorders
Reproductive
system and
breast disorders

General
disorders and
administration
site conditions

Breast disorder
Dyspareunia
Genital bleeding
(including vaginal
bleeding
withdrawal bleed)
Ovarian
hyperstimulation
syndrome
Ovarian
hypertrophy
Pelvic pain
Vulvovaginal
dryness
Asthenia

Arthralgia
Muscle spasms
Pain in
extremities
Breast pain

Abdominal
distension
Dry mouth
Flatulence
Mouth ulceration
Vomiting
Alopecia
Dry skin
Hirsutism
Onychoclasis
Pruritus
Rash
Back pain
Myalgia

Diarrhoea

Coital bleeding
Cystocele
Menstrual
disorder
(including
dysmenorrhoea,
metrorrhagia and
menorrhagia)
Ovarian cyst
Vaginal discharge

Amenorrhoea

Angioneurotic
oedema
Urticaria

Muscular
weakness

Malaise
Pyrexia

Injection site
reaction
(including pain,
swelling,
erythema and
inflammation)
Oedema
peripheral
Weight decreased

Investigations
Weight increased

Blood alkaline
phosphatase
increased
Blood pressure
increased

Long term use: This frequency is based on class-effect frequencies common for all GnRH agonists

** Short term use: This frequency is based on class-effect frequencies common for all
GnRH agonists

At the beginning of treatment, the symptoms of endometriosis including pelvic pain
and dysmenorrhoea may be very commonly exacerbated (≥ 10%) 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); uncommon (≥1/1000, < 1/100).
System Organ
Class
Very Common
Immune system
disorders

Common
Hypersensitivity

Uncommon

Metabolism and
Nutrition
Disorders

Obesity

Psychiatric
disorders

Mood altered

Additional postmarketing AEs
Frequency not
known
Anaphylactic
shock (seen in
adult men and
women)

Affect lability
Depression
Nervousness

Nervous system
disorders

Headache

Visual
impairment

Eye disorders

Vascular
disorders

Hot flush

Visual
disturbance

Hypertension

Epistaxis

Respiratory,
thoracic and
mediastinal
disorders
Abdominal pain

Gastrointestinal
disorders

Vomiting
Constipation
Nausea

Skin and
subcutaneous
tissue disorders
Musculoskeletal
and connective
tissue disorders
Reproductive
system and
breast disorders

Acne

Angioneurotic
oedema
Myalgia

Breast pain

Vaginal bleeding
(including vaginal
haemorrhage
withdrawal bleed,
uterine
haemorrhage,
vaginal discharge,
vaginal bleeding
including
spotting)

General
disorders and
administration
site conditions

Pruritus
Rash
Urticaria
Neck pain

Injection site
reaction
(including
injection site pain,
injection site
erythema and
injection site
inflammation)

Investigations
Weight increased

Malaise

Blood prolactin
increased
Blood pressure
increased

General
Increased lymphocytes count has been reported with patients undergoing GnRH
agonist treatment. This secondary lymphocytosis is apparently related to GnRH
induced castration and seems to indicate that gonadal hormones are involved in
thymic involution.

Reporting of suspected adverse reactions
Reporting suspected adverse reactions after authorisation 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
Yellow Card Scheme at: 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 11.25 mg 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 more than 1000 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 another
triptorelin 3-month formulation 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
triptorelin 28 day (n=68) or a single dose of triptorelin-3 month (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. The same pharmacodynamics equivalence has been demonstrated with
Decapeptyl SR 11.25 mg and Decapeptyl SR 3 mg.

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 11.25 mg 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 11.25 mg 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 11.25 mg in patients
(men and women), a peak of plasma triptorelin is observed in the first 3 hours
after injection. After a declining concentration phase, which continues during
the first month, circulating triptorelin levels remain constant until the end of
the third month following the injection.

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
3 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 solvent for injection.
The instructions for reconstitution hereafter and in the leaflet must be strictly
followed.
The solvent should be drawn into the syringe provided using the reconstituion
needle (20 G, without safety device) and transferred to the vial containing the
powder. The suspension should be reconstituted by swirling the vial gently
from side to side for long enough until a homogeneous, milky suspension is
formed. Do not invert the vial.
It is important to check there is no unsuspended powder in the vial. The
suspension obtained should then be drawn back into the syringe, without
inverting the vial. The reconstitution needle should then be changed and the
injection needle (20 G, with safety device) used to administer the product.
As the product is a suspension, the injection should be administered
immediately after reconstitution to prevent precipitation.
For single use only.

Used needles, any unused suspension or other waste materials should be
disposed of in accordance with local requirements.

7

MARKETING AUTHORISATION HOLDER
Ipsen Limited,
190 Bath Road,
Slough,
SL1 3XE,

United Kingdom.

8

MARKETING AUTHORISATION NUMBER(S)
PL 34926/003

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
05/07/2017

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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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