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OCTREOTIDE 100 MICROGRAMS/1 ML SOLUTION FOR INJECTION

Active substance(s): OCTREOTIDE ACETATE

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1. NAME OF THE MEDICINAL PRODUCT
Octreotide 100 micrograms/1 ml Solution for Injection

2

QUALITATIVE AND QUANTITATIVE COMPOSITION
The active substance is octreotide acetate.
Each 1 ml of solution for injection contains 100 micrograms of Octreotide as octreotide
acetate.
Octreotide solutions for injection contain less than 1 mmol (23 mg) of sodium per 1 ml of
solution (i.e. essentially "sodium-free").
For the full list of excipients, see section 6.1.

3

PHARMACEUTICAL FORM
Solution for injection.
Clear, colourless.

4.1 Therapeutic indications
Symptomatic control and reduction of growth hormone (GH) and IGF-1 plasma levels in patients
with acromegaly who are inadequately controlled by surgery or radiotherapy. Octreotide is also
indicated for acromegalic patients unfit or unwilling to undergo surgery, or in the interim period
until radiotherapy becomes fully effective.
Relief of symptoms associated with functional gastro-entero-pancreatic (GEP) endocrine
tumours, e.g. carcinoid tumours with features of the carcinoid syndrome (see section 5.1).
Octreotide is not an anti-tumour therapy and is not curative in these patients.
Prevention of complications following pancreatic surgery.
Emergency management to stop bleeding and to protect from re-bleeding owing to gastrooesophageal varices in patients with cirrhosis. Octerotide is to be used in association with
specific treatment such as endoscopic sclerotherapy.

Treatment of TSH-secreting pituitary adenomas:
• When secretion has not normalised after surgery and/or radiotherapy;
• In patients in whom surgery is inappropriate;
• In irradiated patients, until radiotherapy is effective.
4.2 Posology and method of administration

Posology
Acromegaly
Initially 0.05 to 0.1 mg by subcutaneous (s.c.) injection every 8 to 12 hours. Dosage adjustment should
be based on monthly assessment of GH and IGF-1 levels (target: GH <2.5 ng/mL); IGF-1 within
normal range) and clinical symptoms, and on tolerability. In most patients, the optimal daily dose will
be 0.3 mg. A maximum dose of 1.5 mg per day should not be exceeded. For patients on a stable dose
of Octreotide assessment of GH should be made every 6 months.
If no relevant reduction in GH levels and no improvement in clinical symptoms have been achieved
within 3 months of starting treatment with Octreotide therapy should be discontinued.
Gastro-entero-pancreatic endocrine tumours
Initially 0.05 mg once or twice daily by s.c. injection. Depending on clinical response, effect on levels
of tumour-produced hormones (in case of carcinoid tumours, on the urinary excretion of 5hydroxyindole acetic acid), and on tolerability, dosage can be gradually increased to 0.1 to 0.2 mg 3
times daily. Under exceptional circumstances, higher doses may be required. Maintenance doses have
to adjust individually.
In carcinoid tumours, if there is no beneficial response within 1 week of treatment with Octreotide at
the maximum tolerate dose, therapy should not be continued.
Complications following pancreatic surgery
0.1 mg 3 times daily by s.c. injection for 7 consecutive days, starting on the day of surgery at least 1
hour before laparotomy.
Bleeding gastro-oesophageal varices
25 micrograms/hour for 5 days by continuous intravenous (i.v.) infusion, Octroetide can be used in
dilution with physiological saline.
In cirrhotic patients with bleeding gastro-oesophageal varices. Octreotide has been well tolerated at
continuous i.v. doses of up to 50 micrograms/hour for 5 days.
Treatment of TSH-secreting pituitary adenomas
The dosage most generally effective is 100 micrograms three times a day by s.c. injection. The dose
can be adjusted according to the responses of TSH and thyroid hormones. At least 5 days of treatment
will be needed to judge the efficacy.

Use in the elderly
There is no evidence of reduced tolerability or altered dosage requirements in elderly patients treated
with Octreotide.
Use in children
Experience with Octreotide in children is limited.
Use in children
Experience with Octreotide in children is limited.
Use in patients with impaired liver function
In patients with lever cirrhosis, the half-life of the drug may be increased, necessitating adjustment of
the maintenance dosage.
Use in patients with impaired renal function
Impaired renal function did not affect the total exposure (AUC) to octreotide administered as s.c.
injection, therefore no dose adjustment of Octreotide is necessary.
4.3 Contraindications
Known hypersensitivity to the active substance or to any of the excipients listed in section 6.1.
4.4 Special warnings and precautions for use
General
As GH-secreting pituitary tumours may sometimes expand, causing serious complications (e.g.
visual field defects), it is essential that all patients be carefully monitored. If evidence of
tumour expansion appears, alternative procedures may be advisable.
The therapeutic benefits of a reduction in growth hormone (GH) levels and normalisation of
insulin-like growth factor 1 (IGF-1) concentration in female acromegalic patients could
potentially restore fertility. Female patients of childbearing potential should be advised to use
adequate contraception if necessary during treatment with octreotide (see section 4.6).
Thyroid function should be monitored in patients receiving prolonged treatment with
octreotide.
Hepatic function should be monitored during octreotide therapy.
Cardiovascular related events
Common cases of bradycardia have been reported. Dose adjustment of medicinal products such
as beta blockers, calcium channel blockers or agents to control fluid and electrolyte balance
may be necessary (see section 4.5).

Gallbladder and related events
Octreotide inhibits secretion of cholecystokinin, resulting in reduced contractility of the
gallbladder and an increased risk of sludge and stone formation. The incidence of gallstone
formation with Octreotide treatment is estimated to be between 15 to 30%. The incidence in the
general population is 5 to 20%. Ultrasonic examination of the gallbladder before, and at about
6- to 12-month intervals during Octreotide therapy is therefore recommended. The presence of
gallstones in Octreotide treated patients is largely asymptomatic; symptomatic stone should be
treated either by dissolution therapy with bile acids or by surgery.
GEP endocrine tumours
During the treatment of GEP endocrine tumours, there may be rare instances of sudden escape
from symptomatic control by Octreotide with rapid recurrence of severe symptoms. If the
treatment is stopped, symptoms may worsen or recur.
Glucose metabolism
Because of its inhibitory action on growth hormone, glucagon, and insulin. Octreotide may
affect glucose regulation. Post-prandial glucose tolerance may be impaired and, in some
instances, the state of persistent hyperglycaemia may be induced as a result of chronic
administration. Hypoglycaemia has also been reported.
In patients with insulinomas, octreotide because of its greater relative potency in inhibiting the
secretion of GH and glucagon than that of insulin, and because of the shorter duration of its
inhibitory action on insulin, may increase the depth and prolong the duration of
hypoglycaemia. These patients should be closely monitored during initiation of Octreotide
therapy and at each change of dosage. Marked fluctuation in blood glucose concentration may
possibly be reduced by smaller, more frequently administered doses.
Insulin requirements of patients with Type I diabetes mellitus therapy may be reduced by
administration of Octreotide. In non-diabetics and type II diabetics with partially intact insulin
reserves, Octreotide administration can result in post-prandial increase in glycaemia. It is
therefore recommended to monitor glucose tolerance and antidiabetic treatment.
Oesophageal varices
Since, following bleeding episodes from oesophageal varices, there is an increased risk for the
development of insulin-dependent diabetes or for changes in insulin requirement in patients
with pre-existing diabetes, an appropriate monitoring of blood glucose levels is mandatory.
Local site reactions
In a 52-week toxicity study in rats, predominantly in males, sarcomas were noted at the s.c.
injection site only at the highest dose (about 8 times the maximum human dose based on body
surface area). No hyperplastic or neoplastic lesions occurred at the s.c. injection site in a 52-

week dog toxicity study. There have been no reports of tumour formation at the injection sites
in patients treated with Octreotide for up to 15 years. All the information available at present
indicates that the findings in rats are species specific and have no significance for the use of the
drug in humans (see section 5.3).
Nutrition
Octreotide may alter absorption of dietary fats in some patients.
Depressed vitamin B12 levels and abnormal Schilling’s test have been observed in some
patients receiving octreotide therapy. Monitoring of vitamin B12 levels is recommended during
therapy with Octreotide in patients who have a history of vitamin B12 deprivation.
4.5 Interaction with other medicinal products and other forms of interaction
Dose adjustment of medicinal products such as beta blocker, calcium channel blockers, or agents
to control fluid and electrolyte balance may be necessary when Octreotide is administered
concomitantly (see section 4.4).
Dose adjustments of insulin and antidiabetic medicinal products may be required when
Octreotide s administered concomitantly (see section 4.4).
Octreotide has been found to reduce the intestinal absorption of ciclosporin and to delay that of
cimetidine.
Concomitant administration of octreotide and bromocriptine increase the bioavailability of
bromocriptine.
Limited published data indicate that somatostatin analogues might decrease the metabolic
clearance of compounds known to be metabolised by cytochrome P450 enzymes, which may be
due to the suppression of growth hormone. Since it cannot be excluded that octreotide may have
this effect, other drugs mainly metabolised by CYP3A4 and which have a low therapeutic index
should therefore be used with caution (e.g. quinidine, terfenadine).
4.6 Fertility, pregnancy and lactation
Pregnancy
There is a limited amount of data (less than 300 pregnancy outcomes) from the use of octreotide in
pregnant women, and in approximately one third of the cases the pregnancy outcome are unknown.
The majority of reports were received after post-marketing use of octreotide and more than 50% of
exposed pregnancies were reported in patients with acromegaly. Most women were exposed to
octreotide during the first trimester of pregnancy at doses ranging from 100-1200 micrograms/day of
Octreotide s.c. or 10-40 mg/month of octreotide powder and solvent for suspension for injection
(intramuscular use). Congenital anomalies were reported in about 4% of pregnancy cases for which
the outcome is known. No causal relationship to octreotide is suspected for these cases.

Animal studies do not indicate direct or indirect harmful effects with respected to reproductive toxicity
(see section 5.3).
As a precautionary measure, it is preferable to avoid the use of Octreotide during pregnancy (see
section 4.4).
Breastfeeding
It is unknown whether octreotide is excreted in human breast milk. Animal studies have shown
excretion of octreotide in breast milk. Patients should not breast-feed during Octreotide treatment.
Fertility
It is not known whether octreotide has an effect on human fertility. Late descent of the testes was
found for male offsprings of dam treated during pregnancy and lactation. Octreotide, however, did not
impair fertility in male and female rats at doses of up to 1 mg/kg body weight per day (see section
5.3).
4.7 Effects on ability to drive and use machines
Octreotide has no or negligible influence on the ability to driver and/or use machines. Patients should
be advised to be cautious when driving or using machines if they experience dizziness,
asthenia/fatigue, or headache during treatment with Octreotide.
4.8 Undesirable effects
Summary of the safety profile
The most frequent adverse reactions reported during octreotide therapy include gastrointestinal
disorders, nervous system disorders, hepatobiliary disorders, and metabolism and nutritional disorders.
The most commonly reported adverse reactions in clinical trial with octreotide administration were
diarrhoea, abdominal pain, nausea, flatulence, headache, cholelithiasis, hyperglycaemia and
constipation. Other commonly reported adverse reactions were dizziness, localised pain, biliary
sludge, thyroid dysfunction (e.g. decreased thyroid stimulating hormone [TSH], decreased total T4,
and decreased free T4), loose stools, impaired glucose tolerance, vomiting, asthenia and
hypoglycaemia.
Tabulated list of adverse reactions
The following adverse drug reactions, listed in Table 1, have been accumulated from clinical studies
with octreotide:
Adverse drug reactions (Table 1) are ranked under heading of frequency, the most frequent first, using
the following convention: very common (≥1/10); common (≥1/100, <1/10); uncommon (≥1/1,000,
<1/100); rare (≥1/10,000, <1/1,000) very rare (<1/10,000), including isolated reports. Within each

frequency grouping, adverse reactions are ranked in order of decreasing seriousness.
Table 1 Adverse drug reactions reported in clinical studies
Gastrointestinal disorders
Very common:
Diarrhoea, abdominal pain, nausea, constipation, flatulence
Common:
Dyspepsia, vomiting, abdominal bloating, steatorrhoea, loose
stools, discolouration of faeces.
Nervous system disorders
Very common:
Headache
Common:
Dizziness
Endocrine disorders
Common:
Hypothyroidism, thyroid dysfunction (e.g. decreased TSH,
decreased total T4, and decreased free T4)
Hepatobiliary disorders
Very common:
Cholelithiasis
Common:
Cholecystitis, biliary sludge, hyperbilirubinaemia
Metabolism and nutrition disorders
Very common:
Hyperglycaemia
Common:
Hypoglycaemia, impaired glucose tolerance, anorexia
Uncommon:
Dehydration
General disorders and administration site conditions
Very common:
Injection site reactions
Common:
Asthenia
Investigations
Common:
Elevated transaminase levels
Skin and subcutaneous tissue disorders
Common:
Pruritus, rash, alopecia
Respiratory disorders
Common:
Dyspnoea
Cardiac disorders
Common:
Bradycardia
Uncommon:
Tachycardia
Post-marketing
Spontaneously reported adverse reactions, presented in Table 2, are reported voluntarily and it is not
always possible to reliably establish frequency or a causal relationship to drug exposure.
Table 2 Adverse drug reactions derived from spontaneous reports
Immune system disorders
Anaphylaxis, allergy/hypersensitivity reactions
Hepatobiliary disorders
Acute pancreatitis, acute hepatitis without cholestasis, cholestatic hepatitis,
cholestasis, jaundice, cholestatic jaundice

Cardiac disorders
Arrhythmias
Investigations
Increased alkaline phosphatase levels, increased gamma glutamyl transferase levels
Description of selected adverse reactions
Gastrointestinal disorders
In rare instances, gastrointestinal side effects may resemble acute intestinal obstruction, with
progressive abdominal distension, severe epigastric pain, abdominal tenderness and guarding.
The frequency of gastrointestinal adverse events is known to decrease over time with continued
treatment.
Occurrence of gastrointestinal side effects may be reduced by avoiding meals around the time of
Octreotide s.c. administration, that is, by injecting between meals or on retiring to bed.
Injection site reactions
Pain or a sensation of stinging, tingling or burning at the site of s.c. injection, with redness and
swelling, rarely lasting more than 15 minutes. Local discomfort may be reduced by allowing the
solution to reach room temperature before injection, or by injecting a smaller volume using a more
concentrated solution.
Metabolism and nutrition disorders
Although measured faecal fat excretion may increase, there is no evidence to date that long-term
treatment with octreotide has led to nutritional deficiency due to malabsorption.
Pancreatic enzymes
In very rare instances, acute pancreatitis has been reported within the first hours or days of Octreotide
s.c. treatment and resolved on withdrawal of the drug. In addition, cholelithiasis induced pancreatitis
has been reported for patients on long-term Octreotide s.c. treatment.
Cardiac disorders
In both acromegalic and carcinoid syndrome patients, ECG changes were observed such as QT
prolongation, axis shifts, early repolarisation, low voltage, R/S transition, early R wave progression,
and non-specific ST-T wave changes. The relationship of these events to octreotide acetate is not
established because many of these patients have underlying cardiac diseases (see section 4.4).
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,
Website: www.mhra.gov.uk/yellowcard
4.9 Overdose

A limited number of accidental overdoses of octreotide in adults and children have been
reported. In adults, the doses ranged from 2,400-6,000 micrograms/day administered by
continuous infusion (100-250 micrograms/hour) or subcutaneously (1,500 micrograms three
times a day). The adverse events reported were arrhythmia, hypotension, cardiac arrest, brain
hypoxia, pancreatitis, hepatitis steatosis, diarrhoea, weakness, lethargy, weight loss,
hepatomegaly, and lactic acidosis.
In children, the doses ranged from 50-3,000 micrograms/day administered by continuous
infusion (2.1-500 micrograms/hour) or subcutaneously (50-100 micrograms). The only adverse
event reported was mild hyperglycaemia.
No unexpected adverse events have been reported in cancer patients receiving octreotide at doses of 330 mg/day in divided doses subcutaneously.
The management of overdosage should be symptomatic.

5

PHARMACOLOGICAL PROPERTIES

5.1

Pharmacodynamic properties
Pharmacotherapeutic group: Somatostatin and analogues.
ATC code: H01CB02
Octreotide is a synthetic octapeptide derivative of naturally occurring somatostatin with similar
pharmacological effects, but with a considerably prolonged duration of action. It inhibits
pathologically increased secretion of growth hormone (GH) and of peptides and serotonin
produced within the GEP endocrine system.
In animals, Octreotide is a more potent inhibitor of GH, glucagon and insulin release than
somatostatin is, with greater selectivity for GH and glucagon suppression.
In healthy subjects, octreotide has been shown to inhibit:
• Release of GH stimulated by arginine, exercise- and insulin-induced hypoglycaemia
• Postprandial release of insulin, glucagon, gastrin, other peptides of the GEP endocrine
system, and arginine-stimulated release of insulin and glucagon.
• Thyrotropin-releasing hormone (TRH)-stimulated release of thyroid-stimulating
hormone (TSH).
Unlike somatostatin, octreotide inhibits GH secretion preferentially over insulin and its
administration is not followed by rebound hypersecretion of hormones (i.e. GH in patients with
acromegaly).
In acromegalic patients octreotide lowers plasma levels of GH and IGF-1. A GH reduction by
50% or more occurs in up to 90% patients, and a reduction of serum GH to <5 ng/mL can be
achieved in about half of the cases. In most patients, octreotide markedly reduces the clinical

symptoms of the disease, such as headache, skin and soft tissue swelling, hyperhidrosis,
arthralgia, paraesthesia. In patients with a large pituitary adenoma, octreotide treatment may
result in some shrinkage of the tumour mass.
In patients with functional tumours of the GEP endocrine system, octreotide, because of its
diverse endocrine effects, modifies a number of clinical features. Clinical improvement and
symptomatic benefit occur in patients who still have symptoms related to their tumours,
despite previous therapies, which may include surgery, hepatic artery embolization, and
various chemotherapies, e.g. streptozocin and 5-fluorouracil.
Octreotide’s effects in the different tumour types are as follows:
Carcinoid tumours
Administration of octreotide may result in improvement of symptoms, particularly of flush and
diarrhoea. In many cases, this is accompanied by a fall in plasma serotonin and reduced
urinary excretion of 5-hydroxyindole acetic acid.
VIPomas
The biochemical characteristic of these tumours is overproduction of vasoactive intestinal
peptide (VIP). In most cases, administration of octreotide results in alleviation of the severe
secretory diarrhoea typical of the condition, with consequent improvement in quality of life.
This is accompanied by an improvement in associated electrolyte abnormalities, e.g.
hypokalaemia, enabling enteral and parenteral fluid and electrolyte supplementation to be
withdrawn. In some patients, computed tomography scanning suggests a slowing or arrest of
progression of the tumour, or even tumour shrinkage, particularly of hepatic metastases.
Clinical improvement is usually accompanied by a reduction in plasma VIP levels, which may
fall into the normal reference range.
Glucagonomas
Administration of octreotide results in most cases in substantial improvement of the necrolytic
migratory rash which is characteristic of the condition. The effect of octreotide on the state of
mild diabetes mellitus which frequently occurs is not marked and, in general, does not result in
a reduction of requirements for insulin or oral hypoglycaemic agents. Octreotide produces
improvement of diarrhoea, and hence weight gain, in those patients affected. Although
administration of octreotide often leads to an immediate reduction in plasma glucagon levels,
this decrease is generally not maintained over a prolonged period of administration, despite
continued symptomatic improvement.
Gastrinomas/Zollinger-Ellison syndrome
Therapy with proton pump inhibitors or H2 receptor blocking agents generally controls gastric
acid hypersecretion. However, diarrhoea, which is also a prominent symptom, may not be
adequately alleviated by proton pump inhibitors or H2 receptor blocking agents. Octreotide

can help to further reduce gastric acid hypersecretion and improve symptoms, including
diarrhoea, as it provides suppression of elevated gastrin levels, in some patients.
Insulinomas
Administration of octreotide produces a fall in circulating immunoreactive insulin, which may,
however, be of short duration (about 2 hours). In patients with operable tumours, octreotide
may help to restore and maintain normoglycaemia pre-operatively. In patients with inoperable
benign or malignant tumours, glycaemic control may be improved without concomitant
sustained reduction in circulating insulin levels.
Complications following pancreatic surgery
For patients undergoing pancreatic surgery, the peri- and post-operative administration of
Octreotide reduces the incidence of typical post-operative complications (e.g. pancreatic
fistula, abscess and subsequent sepsis, post-operative acute pancreatitis).
Bleeding gastro-oesophageal varices
In patients presenting with bleeding gastro-oesophageal varices due to underlying cirrhosis,
octreotide administration in combination with specific treatment (e.g. sclerotherapy) is
associated with better control of bleeding and early re-bleeding, reduced transfusion
requirements, and improved 5-day survival. While the precise mode of action of octreotide is
not fully elucidated, it is postulated that octreotide reduces splanchnic blood flow through
inhibition of vaso-active hormones (e.g. VIP, glucagon).
Treatment of TSH-secreting pituitary adenomas
The treatment effects of octreotide were prospectively observed in 21 patients and pooled with
series of 37 published cases. Among 42 patients with evaluable biochemical data, there were
81% of patients (n-=34) with satisfactory results (at least 50% reduction of TSH and
substantial reduction of thyroid hormones), whereas 67% (n=28) had normalisations of TSH
and thyroid hormones. In these patients, the response was maintained throughout the duration
of treatment (up to 61 months, mean, 15.7 months).
Regarding clinical symptoms, a clear improvement was reported in 19 out of 32 patients with
clinical hyperthyroidism. Tumour volume reduction greater than 20% was observed in 11
cases (41%) with a decrease greater than 50% in 4 cases (15%). The earliest reduction was
reported after 14 days of treatment.
5.2 Pharmacokinetic properties

Absorption
After s.c. injection, Octreotide is rapidly and completely absorbed. Peak plasma concentrations are
reached after 30 minutes.

Distribution
The volume of distribution is around 0.27 l/kg and the total body clearance is 160 mL/min. Plasma
protein binding amount to 65%. The amount of Octreotide bound to blood cells is negligible.
Elimination
The elimination half-life after s.c. administration is 100 minutes.
After i.v. injection, the elimination is biphasic with half-lives of 10 and 90 minutes. Most of the
peptide is eliminated via the faeces, while approximately 32% is excreted unchanged into the urine.
Special patient population
Impaired renal function did not affect the total exposure (AUC) to octreotide administered as s.c.
injection.
The elimination capacity may be reduced in patients with liver cirrhosis, but not in patients with fatty
liver disease.
5.3 Preclinical safety data
Acute and repeated dose toxicology, genotoxicity, carcinogenicity and reproductive toxicology studies
in animals reveals no specific safety concerns for humans.
Reproduction studies in animals revealed no evidence of teratogenic, embryo/foetal or other
reproduction effects due to octreotide at parental doses of up to 1 mg/kg/day. Some retardation of
physiological growth was noted in the offspring of rats which was transient and attributable to GH
inhibition brought about by excessive pharmacodynamics activity (see section 4.6).
No specific studies were conducted in juvenile rats. In the pre- and post-natal developmental studies,
reduced growth and naturation was observed in the F1 offspring of dams given octreotide during the
entire pregnancy and lactation period. Delayed descent of the testes were observed for male F1
offsprings, but fertility of the affected F1 male pups remained normal. Thus, the abovementioned
observations were transient and considered to be the consequence of GH inhibition.
Carcinogenicity/Chronic toxicity
In rats receiving octreotide acetate at daily doses up to 1.25 mg/kg body weight, fibrosarcomas
were observed, predominantly in a number of male animals, at the s.c. injection site after 52, 104
and 113/116 weeks. Local tumours also occurred in the control rats, however development of
these tumours were attributed to disordered fibroplasia produced by sustained irritant effects at
the injection sites, enhanced by the acidic lactic acid/mannitol vehicle. This non-specific tissue
reaction appeared to be particular to rats. Neoplastic lesions were not observed either in mice
receiving daily s.c. injections of octreotide at doses up to 2 mg/kg for 98 weeks, r in dogs treated
with daily s.c. doses of the drug for 52 weeks.

6

PHARMACEUTICAL PARTICULARS

6.1

List of excipients

Glacial acetic acid (pH adjustment),
Sodium acetate trihydrate (pH adjustment),
Sodium chloride,
Water for injections.
6.2 Incompatibilities
The octreotide acetate is not stable in Total Parenteral Nutrition (TPN) solutions.
This medicinal product must not be mixed with other medicinal products, except those mentioned in
section 6.6.

6.3

Shelf life
Medicinal product as packaged for sale: 3 years
Shelf-life after first opening: The product must be used immediately and any unused drugproduct must be discarded.

6.4 Special precautions for storage
Medicinal product as packaged for sale: store in a refrigerator (2°C - 8ºC).
Do not freeze. Keep the vial in the outer carton in order to protect from light.
For storage conditions after dilution of the medicinal product, see section 6.6.
6.5 Nature and contents of container
2 ml Type I amber glass vials for injection, with a teflon-faced rubber stopper, aluminium seal and
flip-off plastic cap, containing 1 ml of Octreotide solution for injection.
Packs of 5 and 30 vials containing 1 ml of solution for injection.
Not all pack sizes may be marketed.
6.6

Special precautions for disposal
Each vial contains a clear colourless solution, free from foreign matter. Single dose vials (50
micrograms/ml, 100 micrograms/ml and 500 micrograms/ml injection) are for single use only.
Subcutaneous injections

Patients who will be injecting themselves must receive precise instructions from the doctor or
nurse.
To reduce local discomfort, let the solution reach room temperature before injection.
Avoid multiple injections at short intervals at the same site.
To prevent contamination, it is recommended that the cap of the multidose vial (200
micrograms/ml) should be punctured no more than 10 times.
Intravenous infusion
Prior to administration the solution should be inspected visually for changes of colour or solid
particles. The diluted solutions of Octreotide (octreotide acetate) in 0.9% sodium chloride
solution for injection and stored in PVC bags or in polypropylene syringes are physically and
chemically stable for seven days when stored at below 25°C. From a microbiological point of
view, the diluted solution should preferably be used immediately. If the solution is not used
immediately, storage prior to use is the responsibility of the user and normally should not be
longer than 24 hours at 2 to 8°C unless dilution has taken place in controlled and validated
aseptic conditions. Before administration the solution has to be brought to room temperature
again.
When Octreotide is to be administered as intravenous infusion, the contents of one 500
micrograms vial should normally be dissolved in 60 mL physiological saline, and the resulting
solution should be infused by means of an infusion pump. This should be repeated as often as
necessary until the prescribed duration of treatment is reached. Octreotide has also been
infused in lower concentrations.
Any unused solution or waste material should be disposed of in accordance with local
requirements.
7. MARKETING AUTHORISATION HOLDER
Hospira UK Limited
Horizon
Honey Lane
Hurley, Maidenhead
SL6 6RJ
UK

8

MARKETING AUTHORISATION NUMBER(S)
PL 04515/0218

9

DATE OF FIRST AUTHORISATION/RENEWAL OF THE
AUTHORISATION

16/02/2012

10

DATE OF REVISION OF THE TEXT
27/05/2016

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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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