Men:

Treatment of advanced, hormone-dependent prostate carcinoma.
Women:
- Preoperative reduction of myoma size to reduce the symptoms of bleeding and pain in women with symptomatic uterine myomas.
- In assisted reproduction techniques to prevent premature LH surges.
- Symptomatic uterine myomas; when suppression of the ovarian hormonogenesis is indicated as a preoperative measure to reduce the size of individual myomas prior to scheduled myoma nucleation or hysterectomy.
- Symptomatic endometriosis confirmed by laparoscopy; when suppression of the ovarian hormonogenesis is indicated to the extent that surgical therapy is not primarily indicated.
- Children: Treatment of confirmed central precocious puberty (girls under 9 years, boys under 10 years).

The product should only be used under the supervision of an appropriate specialist having requisite facilities for regular monitoring of response.
The treatment of children with triptorelin should be under the overall supervision of the pediatric endocrinologist or of a pediatrician or endocrinologist with expertise in the treatment of central precocious puberty. It is important that the injection of the sustained release form be performed strictly in accordance with the instructions given below.

Following reconstitution, the suspension has to be injected immediately.
The dosage of one syringe, equivalent to 3.75 mg triptorelin, is injected every 28 days either subcutaneously (e.g. into the skin of the abdomen, the buttock or thigh) or deep intramuscularly. The injection site should be changed each time. Before the start of the therapy, preparations containing estrogen (e.g. oral contraceptives) should be discontinued. In the case of uterine myoma and endometriosis, non-hormonal contraceptives should be used during the first treatment month.

Men: Once every four weeks an injection with one syringe, equivalent to 3.75 mg triptorelin. In order to continually suppress testosterone levels, it is important to comply with a 4-weekly administration.
Women:
- Uterine myomas and endometriosis: Once every four weeks an injection with one syringe, equivalent to 3.75 mg triptorelin. The treatment must be initiated in the first 5 days of the cycle.
- Assisted reproduction techniques: single administration on cycle days 2 or 3 (follicular phase) or cycle day 22 (luteal phase).

Children:

Dosing at the beginning of treatment should be based on body weight; one injection of triptorelin should be injected on days 0, 14, and 28. Thereafter one injection every 4 weeks. Should the effect be insufficient, the injections may be given every 3 weeks.
Dosing should be based on body weight. Children weighing less than 20 kg are injected with 1.875 mg (half dose), children between 20 and 30 kg receive 2.5 mg (2/3 dose), and children with more than 30 kg body weight are injected with 3.75 mg Triptorelin (full dose).
Note for specific patient groups:
- There is no need to adjust the dose for the elderly.
- According to current data, dose reduction or prolongation of the dosage interval in patients with impaired renal function is not necessary.
Duration of Administration
Men:
Prostate carcinoma: Treatment with DECAPEPTYL®CR is usually a long-term therapy.
Women:
Uterine myomas and endometriosis: The duration of treatment depends on the initial degree of severity of endometriosis and on the evolution of its clinical manifestations (functional and anatomical) and on the evolution of the volume of the uterine myomas, determined by ultrasonography during treatment. Normally, the maximum attainable result is achieved after 3 to 4 injections.
In view of the possible effect on bone density, DECAPEPTYL®CR therapy should not exceed duration of 6 months.
Children:
Central precocious puberty (CPP): Treatment should be stopped if a bone maturation of older than 12 years in girls and older than 13 years in boys has been achieved.
The treatment with DECAPEPTYL® CR is usually a long-term therapy, which must not be discontinued without instruction of the physician.

General: - Known hypersensitivity to gonadotrophin-releasing hormone (GnRH) or any other GnRH analogue,triptorelin, poly-(glycolic acid-co-lactic acid), dextran, or to any of the excipients. - Hypersensitivity to gonadotrophin-releasing hormone (GnRH) or any other GnRH analogue. In women: - Pregnancy. - Lactation

General:
The use of GnRH agonists may cause 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. Particular caution is necessary in patients with additional risk factors for osteoporosis (e.g. chronic alcohol abuse, smokers, long-term therapy with drugs that reduce bone mineral density; e.g. anticonvulsants or corticoids, family history of osteoporosis, malnutrition).
Rarely, treatment with GnRH agonist may reveal the presence of a previously unknown gonadotrophin cell pituitary adenoma. These patients may present with a pituitary apoplexy characterized 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.Mood changes, including depression have been reported. Patients with known depression should be monitored closely during therapy.

Children:
The chronological age at the beginning of therapy should be under 9 years in girls and under 10 years in boys.
In girls, initial ovarian stimulation at treatment initiation, followed by the treatment-induced oestrogen withdrawal, may lead, in the first month, to vaginal bleeding of mild or moderate intensity. After finalizing the therapy, development of puberty characteristics will occur. Information with regards to future fertility is still limited. In most girls, menses will start on average one year after ending the therapy, which in most cases is regular.
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 treatment. The suggested theory is that the low concentrations of estrogen during treatment with GnRH agonists weakens 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.
The treatment of children with progressive brain tumours should follow a careful individual appraisal of the risks and benefits. Pseudo-precocious puberty (gonadal or adrenal tumour or hyperplasia) and gonadotrophin-independent precocious puberty (testicular toxicosis, familial Leydig cell hyperplasia) should be precluded. Allergic and anaphylactic reactions have been reported in adults and children.
These include both local site reactions and systemic symptoms. The pathogenesis could not be elucidated. A higher reporting rate was seen in children.
Women:
DECAPEPTYL®CR should only be prescribed after careful diagnosis (e.g. laparoscopy). It should be confirmed that the patient is not pregnant before prescription of triptorelin. Since menses should stop during DECAPEPTYL®CR treatment, the patient should be instructed to notify her physician if regular menstruation persists.
Loss of bone mineral density
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. After withdrawal of treatment, the bone loss is generally reversible within 6 - 9 months. In the majority of women, currently available data suggest that recovery of bone loss occurs after cessation of therapy. No specific data is available for patients with established osteoporosis or with risk factors for osteoporosis (e.g. chronic alcohol abuses, smokers, long-term therapy with drugs that reduce bone mineral density, e.g. anticonvulsants or corticoids, family history of osteoporosis, malnutrition, e.g. anorexia nervosa). Since reduction in bone mineral density is likely to be more detrimental in these patients, treatment with triptorelin 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.
Assisted reproduction techniques
Assisted reproduction techniques are associated with an increased risk of multiple pregnancies, pregnancy loss, ectopic pregnancies and congenital malformations. These risks are also valid with usage of DECAPEPTYL®CR as adjunct therapy in controlled ovarian hyperstimulation. The use of DECAPEPTYL® in controlled ovarian hyperstimulation may increase the risk of ovarian hyperstimulation syndrome (OHSS) and ovarian cysts.
Follicular recruitment, induced by the use of GnRH analogues and gonadotrophins, may be markedly increased in a minority of predisposed patients, particularly in case of Polycystic Ovarian Syndrome. As with other GnRH analogues, there have been reports of OHSS associated with the use of triptorelin in combination with gonadotrophins.

Ovarian Hyperstimulation Syndrome (OHSS)

OHSS is a medical event distinct from uncomplicated ovarian enlargement. OHSS is a syndrome that can manifest itself with increasing degrees of severity. It comprises marked ovarian enlargement, high serum sex steroids, and an increase in vascular permeability which can result in an accumulation of fluid in the peritoneal, pleural and, rarely, in the pericardial cavities. The following symptoms may be observed in severe cases of OHSS: abdominal pain, abdominal distension, severe ovarian enlargement, weight gain, dyspnoea, oliguria and gastrointestinal symptoms including nausea, vomiting and diarrhoea. Clinical evaluation may reveal hypovolaemia, haemoconcentration, electrolyte imbalances, ascites, haemoperitoneum, pleural effusions, hydrothorax, acute pulmonary distress, and thromboembolic events. Excessive ovarian response to gonadotrophin treatment seldom gives rise to OHSS unless hCG is administered to trigger ovulation. Therefore in cases of OHSS, it is prudent to withhold hCG and advise the patient to refrain from coitus or to use barrier methods for at least 4 days. OHSS may progress rapidly (within 24 hours to several days) to become a serious medical event, therefore patients should be followed for at least two weeks after the hCG administration.OHSS may be more severe and more protracted if pregnancy occurs. Most often, OHSS occurs after hormonal treatment has been discontinued and reaches its maximum severity at about seven to ten days following treatment. Usually, OHSS resolves spontaneously with the onset of menses.If severe OHSS occurs, gonadotrophin treatment should be stopped if still ongoing, the patient hospitalized and specific therapy for OHSS, e.g. resting, intravenous administration of electrolytes or colloids and heparin, started. This syndrome occurs with higher incidence in patients with polycystic ovarian disease. The risk of OHSS might be higher with use of GnRH agonists in combination with gonadotrophins than with use of gonadotrophins alone.
Ovarian cysts
Ovarian cysts may occur during the initial phase of treatment with GnRH agonist. They are usually asymptomatic and non-functional.
Uterine myomas and endometriosis
Prolongation of menstrual bleeding during treatment is abnormal (apart from the first month), and should lead to verification of plasma estrogen level. Should this level be less than 50 pg/ml, possible associated organic lesions should be sought. After withdrawal of treatment, ovarian function resumes, e.g. menstrual bleeding will resume after approximately 7-12 weeks after the final injection. Non-hormonal contraception should be used during the initial month of treatment as ovulation may be triggered by the initial secretion of gonadotrophins. It should also be used from 4 weeks after the last injection until resumption of menstruation or until another contraceptive method has been established. During treatment of uterine myomas, uterus and myoma size should be measured regularly by means of, e.g. ultrasonography. Disproportionally rapid reduction of uterine volume in comparison with that of the myoma has, in a few cases, caused bleeding and sepsis. There have been several reports of bleeding in patients with sub-mucous fibroids after treatment with GnRH analogue, the bleeding usually started 6 - 10 weeks after initiation of therapy.
Men:
Initially, triptorelin, 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 orchiectomy (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, triptorelin does not induce any further decrease in serum testosterone levels. Long-term androgen deprivation either by bilateral orchiectomy or administration of GnRH analogues 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, physician should assess the benefit / risk ratio including the potential for Torsade de pointes prior to initiating DECAPEPTYL®CR. 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 analogues and an increase in cardiovascular mortality. Patients at high risk for metabolic or cardiovascular diseases should be carefully assessed before commencing treatment and adequately monitored during androgen deprivation therapy.Administration of triptorelin in therapeutic doses results 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 analogues may therefore be misleading.

DECAPEPTYL®CR contains sodium but less than 1 mmol (23mg) sodium per dose.

When triptorelin is co-administered with drugs affecting pituitary secretion of gonadotrophins caution should be given and it is recommended that the patient’s hormonal status should be supervised. Since androgen deprivation treatment may prolong the QT interval, the concomitant use of DECAPEPTYL®CR 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.
No studies on interactions with other medicinal products have been performed. The possibility of interactions with other medicinal products including histamine-releasing substances cannot be excluded.
Interference of calcium antagonists with the mechanism of action underlying GnRH and GnRH analogues is theoretically conceivable. Initial test results on the long-term suppressability of serum testosterone with the depot form of triptorelin during simultaneous therapy with calcium antagonists have, however, provided no evidence of such an interaction.

In women of childbearing potential, pregnancy should be excluded prior to initiation of therapy.
Non-hormonal methods of contraception should be employed during therapy until menses resumes in women of childbearing potential. Triptorelin should not be used during pregnancy since concurrent use of GnRH agonists is associated with a theoretical risk of abortion or foetal abnormality. Very limited data on the use of triptorelin during pregnancy do not indicate an increased risk of congenital malformations. However, long-term follow-up studies on development are far too limited.
Animal data do not indicate direct or indirect harmful effects with respect to pregnancies or postnatal developments, but there are indications for foetotoxicity and delayed parturition. Based on the pharmacological effects, disadvantageous influence on the pregnancy and the offspring cannot be excluded and DECAPEPTYL®CR should not be used during pregnancy. When triptorelin is used for infertility treatment, there is no clinical evidence to suggest a causal connection between triptorelin and any subsequent abnormalities of oocyte development or pregnancy or outcome.
It is not known whether triptorelin is excreted in human milk. Because of the potential for adverse reactions from triptorelin in nursing infants, breastfeeding should be discontinued prior to and throughout administration.

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.

Adverse experiences reported among patients treated with triptorelin during clinical trials and from post-marketing surveillance are shown below.
In men, since testosterone levels normally increase during first week of treatment, worsening of symptoms and complaints may occur (e.g. urinary obstruction, skeletal pain due to metastases, compression of the spinal cord, muscular fatigue and lymphatic oedema of the legs). In some cases urinary tract obstruction decreases the kidney function. Neurological compression with asthenia and paraesthesia in the legs has been observed.

Children:
Common (≥ 1/100 to < 1/10): mood changes, depression.
Uncommon (≥ 1/1000 to < 1/100): anaphylactic reaction, vomiting, nausea, vaginal haemorrhage, vaginal discharge.
Not known: hypersensitivity reaction, affect liability, nervousness, headache, vision blurred, visual impairment, hot flushes, epistaxis, abdominal discomfort, abdominal pain, rash, angioneurotic oedema, uriticaria, alopecia, erythema, epiphysiolysis, myalgia, genital haemorrhage, injection site erythema, injection site inflammation, malaise, pain, injection site pain, blood pressure increased, weight increased.
A few cases of slipped capital femoral epiphysis have been reported during use with triptorelin.
Cases of pre-existing pituitary adenomas enlargement were reported during treatment with LH-RH agonists, however, it has not yet been observed with triptorelin therapy.

Women:
Very Common (≥ 1/10): libido decreased, mood changes, sleep disorder, headache, hot flushes, abdominal pain, hyperhidrosis, bone pain, vaginal haemorrhage, vulvovaginal dryness, dyspareunia, dysmenorrhoea, ovarian hyperstimulation syndrome, ovarian hypertrophy, pelvic pain, asthenia.
Common (≥ 1/100 to < 1/10): hypersensitivity, depressed mood, depression, nausea, myalgia, arthralgia, fatigue, injection site reaction, injection site pain, irritability.
Uncommon (≥ 1/1000 to < 1/100): anaphylactic reactions, paraesthesia, visual impairment, back pain, blood lactate dehydrogenase increased, gamma glutamyl transferase increased, aspartate aminotransferase increased, alanine aminotransferase increased, blood cholesterol increased.
Not known: confusional state, anxiety, dizziness, vision blurred, vertigo, dyspnoea, abdominal discomfort, diarrhoea, vomiting, pruritus, rash, angioedema, uriticaria, bone disorders, muscle spasm, muscular weakness, breast pain, menorrhagia, metrorrhagia, amenorrhoea, injection site inflammation, pyrexia, malaise, blood pressure increased, weight increased, weight decreased.
Slight trabecular bone loss may occur. This is generally reversible within 6-9 months after treatment discontinuation.
Due to the subsequent administration of gonadotrophins which compensate the adverse events, the symptoms do not last more than a couple of days. In assisted reproduction, fertility therapy with GnRH-analogues may lead to ovarian hyperstimulation. Therefore, follicle growth and luteal phase should be carefully monitored by ultrasonography. Additionally, multiple pregnancies have been reported.
During treatment of uterine myoma, uterus and myoma size should be measured regularly by means of e.g. ultrasonography. Un-proportionally rapid reduction of uterine volume in comparison with that of the myoma has, in few cases, caused bleeding and sepsis.
At the beginning of treatment, the symptoms of endometriosis including pelvis pain, dysmenorrhoea may be exacerbated very commonly (≥ 10%) during the initial transient increase in plasma oestradiol levels. These symptoms are transient and usually disappear in one or two weeks. Genital haemorrhage including menorrhagia, metrorrhagia may occur in the month following the first injection. Ovarian hypertrophy, pelvic and abdominal pain may be observed.

Men:
Very Common (≥ 1/10): libido decreased, hot flushes, bone pain, dysuria, erectile dysfunction.
Common (≥ 1/100 to < 1/10): hypersensitivity, mood changes, depressed mood, depression, sleep disorders, headache, nausea, hyperhidrosis, myalgia, arthralgia, gynecomastia, fatigue, injection site reaction, injection site pain, irritability.
Uncommon (≥ 1/1000 to < 1/100): anaphylactic reaction, decreased appetite, embolism, hypertension, asthma aggravated, upper abdominal pain, dry mouth, hypotrichosis, alopecia, testicular atrophy, blood lactate dehydrogenase increased, gamma-glutamyl transferase increased, aspartate aminotransferase increased, alanine aminotransferase increased, weight increased, weight decreased.
Not known: nasopharyngitis, increased appetite, gout, diabetes mellitus, insomnia, confusional state, decreased activity, euphoric mood, anxiety, loss of libido, dizziness, paraesthesia, memory impairment, dysgeusia, somnolence, dysstasia, abnormal sensation in eye, visual impairment, vision blurred, tinnitus,vertigo, hypotension, dyspnoea, orthopnoea, epistaxis, abdominal pain, constipation, diarrhoea, vomiting, abdominal distension, flatulence, gastralgia, acne, pruritus, rash, blister, angioedema, urticaria, purpura, back pain, musculoskeletal pain, pain in extremity, muscle spasms, muscular weakness, joint stiffness, joint swelling, musculoskeletal stiffness, osteoarthritis, breast pain, testicular pain, ejaculation failure, asthenia, injection site erythema, injection site inflammation, oedema, pain, chills, chest pain, influenza like illness, pyrexia, malaise, blood creatinine increased, blood pressure increased, blood urea increased, blood alkaline phosphatase increased, body temperature increased, QT prolongation.

There is insufficient experience of overdosing with triptorelin to draw conclusions on possible adverse effects. Considering the package form and the pharmaceutical form, overdosing is not expected. If overdose occurs, symptomatic management is indicated.

Pharmacotherapeutic group: Gonadorelin analogues.

ATC code: L02AE04.
Triptorelin is a synthetic decapeptide analogue of the natural gonadotrophin releasing hormone (GnRH). GnRH is a decapeptide, which is synthesized in the hypothalamus and regulates the biosynthesis and release of the gonadotrophins LH (luteinizing hormone) and FSH (follicle stimulating hormone) by the pituitary. Triptorelin stimulates the pituitary more strongly to secretion of LH and FSH than a comparable dose of gonadorelin, whereas the duration of action is longer. The increase of LH and FSH levels will initially lead to an increase of serum testosterone concentrations in men or serum oestrogen concentrations in women. Chronic administration of a GnRH agonist results in an inhibition of pituitary LH- and FSH-secretion. This inhibition leads to a reduction in steroidogenesis, by which the serum estradiol concentration in women and the serum testosterone concentration in men fall to within the postmenopausal or castrate range, respectively, i.e. a hypogonadotrophic hypogonadal state.
In children with precocious puberty, the concentration of estradiol or testosterone will decrease to within the prepubertal range. Plasma DHEAS (dihydroepiandrostenedion sulphate) levels are not influenced.
Therapeutically, this leads to a decrease in growth of testosterone-sensitive prostate tumours in men, and to reduction of endometriosis foci and oestrogen-dependent uterus myomas in women. Regarding uterine myoma, maximal benefit of treatment is observed in women with anaemia (haemoglobin ≤ 8 g/dl). In children suffering from CPP, triptorelin treatment leads to a suppression of the secretion of gonadotrophins, estradiol, and testosterone to prepubertal levels. This results in arrest or even regression of pubertal signs and an increase in adult height prediction in CPP patients.
In assisted reproduction techniques, triptorelin inhibits the preterm LH secretion and following luteinisation of immature follicles.
The suppression profile for the serum estradiol level was the same in women who received the injection in the follicular phase, and in those who received the injection in the luteal phase. The menstruation of the women in the luteal phase started 9 days after single administration and afterwards after about 85 days. The menstruation of the women in the follicular phase started 81 days after injection.

After intramuscular administration of DECAPEPTYL®CR, the plasma concentrations of triptorelin are determined by the (slow) degradation of the poly-(glycolic acid, lactic acid) polymer. The mechanism inherent to this administration form enables this controlled release of triptorelin from the polymer.
After i.m. or s.c. application of a triptorelin depot-formulation (controlled-release microcapsules), a rapid increase in the concentration of triptorelin in plasma is recorded, with a maximum in the first hours. Then the triptorelin concentration declines notably within 24 hours. On day 4 the value reaches a second maximum, falling below the detection limit in a biexponential course after 44 days. After s.c. injections the triptorelin increase is more gradual and in a somewhat lower concentration than after I.M. injections. After s.c. injection, the decline in the triptorelin concentration takes longer, with values falling below the detection limit after 65 days.
During treatment over a period of 6 months and an administration every 28 days, there was no evidence of triptorelin accumulation in both modes of administration. Plasma triptorelin values decreased to approx. 100 pg/ml before the next application after i.m. or s.c. application (median values). It is to be assumed that the non-systemically available proportion of triptorelin is metabolized at the injection site, e.g. by macrophages.
In the pituitary, the systemically available triptorelin is inactivated by N-terminal cleavage via pyroglutamyl-peptidase and a neutral endopeptidase. In the liver and the kidneys, triptorelin is degraded to biologically inactive peptides and amino acids. 40 minutes after the end of an infusion of 100 μg triptorelin (over 1 hour) 3-14% of the administered dose has already been eliminated by the kidney.
For patients with an impaired renal function, adaptation and individualization of therapy with the triptorelin depot-formulation seems to be unnecessary, on account of the subordinate significance of the renal elimination route and the broad therapeutic range of triptorelin as an active component.
Bioavailability:
Men: The systemic bioavailability of the active component triptorelin from the intramuscular depot is 38.3% in the first 13 days. Further release is linear at 0.92% of the dose per day on average. Bioavailability after s.c. application is 69% of i.m. availability.
Women: After 27 test days, 35.7% of the applied dose can be detected on average, with 25.5% being released in the first 13 days and further release being linear at 0.73% of the dose per day on average.
General: Calculation of the model-depending kinetic parameters (t½, Kel, etc.) is inapplicable in presentations with a strongly protracted release of the active component.

N/A

One pre-filled syringe with powder contains:
Poly (glycolic acid-co-lactic acid) (1:1), Propyleneglycol dicaprylocaprate.
One pre-filled syringe with one ml suspension agent contains:
Dextran 70, Polysorbate 80, Sodium chloride, Sodium dihydrogen phosphate dihydrate, Sodium hydroxide, Water for injection.

In the absence of compatibility studies this medicinal product should not be mixed with other medicinal products.

See outer carton. Reconstituted suspension. 3 minutes. It must be applied immediately after preparation as per instructions..

Store at 2˚C- 8˚C (in a refrigerator). Keep the container in the outer carton.

Powder: Pre-filled syringe
Solvent: Pre-filled syringe

Pre-filled syringes (borosilicate glass type I, clear) with a connector (polypropylene), black chlorobutyl rubber stopper (plunger stopper, type I) and injection needle.
Pack sizes:
1 pre-filled syringe (powder) plus 1 pre-filled syringe (solvent)
3 pre-filled syringes (powder) plus 3 pre-filled syringes (solvent)
Not all pack sizes may be marketed in your country

The following information is intended for healthcare professionals only:
INSTRUCTIONS FOR USE
Important Information:
1. Store DECAPEPTYL CR in the packaging in the refrigerator.
2. Make sure to inject DECAPEPTYL CR within 3 minutes of the reconstitution.

Overview of the DECAPEPTYL CR components:

1. Preparation
To ensure correct preparation of the suspension, the following instructions must be strictly followed:

2. Reconstitution
To mix the suspension:
• Inject all the liquid into the syringe with the powder.
• Slowly push the suspension back and forth into the two syringes until it is homogenously milky white to faintly yellow. Take care to hold the syringes straight; do not bend.

 

3. Injection
• Screw the syringe with the suspension ready for injection off the connector.
• Screw the injection needle onto the syringe.
• Inject the suspension within 3 minutes.

 

DECAPEPTYL CR is for single use only and any unused suspension should be discarded