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Active substance: SOMATROPIN (RBE)

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GENOTROPIN MINIQUICK 0.2 mg powder and solvent for solution for injection.


GENOTROPIN MINIQUICK 0.2 mg powder and solvent for solution for injection.
One cartridge contains 0.2 mg per 0.25 ml of somatropin* after reconstitution
corresponding to a concentration of 0.8 mg/ml.

* produced in Escherichia coli cells by recombinant DNA technology.
For a full list of excipients, see section 6.1.


Powder and solvent for solution for injection. A two chamber cartridge with a white
powder in the front compartment and a clear solution in the rear compartment.




Therapeutic indications
Growth disturbance due to insufficient secretion of growth hormone (growth hormone
deficiency, GHD) and growth disturbance associated with Turner syndrome or
chronic renal insufficiency.

Growth disturbance [current height standard deviation score (SDS) < - 2.5 and
parental adjusted height SDS < - 1] in short children born small for gestational age
(SGA), with a birth weight and/or length below - 2 SD, who failed to show catch-up
growth [height velocity (HV) SDS < 0 during the last year] by 4 years of age or later.
Prader-Willi syndrome (PWS), for improvement of growth and body composition.
The diagnosis of PWS should be confirmed by appropriate genetic testing.
Replacement therapy in adults with pronounced growth hormone deficiency.
Adult Onset: Patients who have severe growth hormone deficiency associated with
multiple hormone deficiencies as a result of known hypothalamic or pituitary
pathology, and who have at least one known deficiency of a pituitary hormone not
being prolactin. These patients should undergo an appropriate dynamic test in order to
diagnose or exclude a growth hormone deficiency.
Childhood Onset: Patients who were growth hormone deficient during childhood as a
result of congenital, genetic, acquired, or idiopathic causes. Patients with childhood
onset GHD should be re-evaluated for growth hormone secretory capacity after
completion of longitudinal growth. In patients with a high likelihood for persistent
GHD, i.e. a congenital cause or GHD secondary to a pituitary/hypothalamic disease
or insult, an Insulin-like Growth Factor-I (IGF-I) SDS < - 2 off growth hormone
treatment for at least 4 weeks should be considered sufficient evidence of profound
All other patients will require IGF-I assay and one growth hormone stimulation test.


Posology and method of administration
The dosage and administration schedule should be individualised.
The injection should be given subcutaneously and the site varied to prevent
Growth disturbance due to insufficient secretion of growth hormone in children:
Generally a dose of 0.025 - 0.035 mg/kg body weight per day or 0.7 - 1.0 mg/m² body
surface area per day is recommended. Even higher doses have been used.
Where childhood onset GHD persists into adolescence, treatment should be continued
to achieve full somatic development (e.g. body composition, bone mass). For
monitoring, the attainment of a normal peak bone mass defined as a T score > - 1 (i.e.

standardised to average adult peak bone mass measured by dual energy X-ray
absorptiometry taking into account sex and ethnicity) is one of the therapeutic
objectives during the transition period. For guidance on dosing see adult section
Prader-Willi syndrome, for improvement of growth and body composition in
children: Generally a dose of 0.035 mg/kg body weight per day or 1.0 mg/m2 body
surface area per day is recommended. Daily doses of 2.7 mg should not be exceeded.
Treatment should not be used in children with a growth velocity of less than 1 cm per
year and near closure of epiphyses.
Growth disturbance due to Turner syndrome: A dose of 0.045 - 0.050 mg/kg body
weight per day or 1.4 mg/m² body surface area per day is recommended.
Growth disturbance in chronic renal insufficiency: A dose of 0.045 - 0.050 mg/kg
body weight per day (1.4 mg/m² body surface area per day) is recommended. Higher
doses can be needed if growth velocity is too low. A dose correction can be needed
after six months of treatment.
Growth disturbance in short children born small for gestational age: A dose of 0.035
mg/kg body weight per day (1 mg/m² body surface area per day) is usually
recommended until final height is reached (see section 5.1). Treatment should be
discontinued after the first year of treatment if the height velocity SDS is below + 1.
Treatment should be discontinued if height velocity is < 2 cm/year and, if
confirmation is required, bone age is > 14 years (girls) or > 16 years (boys),
corresponding to closure of the epiphyseal growth plates.

Dosage recommendations in Paediatric Patients
mg/kg body weight
mg/m² body surface area
dose per day
dose per day
Growth hormone deficiency
0.025 - 0.035
0.7 - 1.0
in children
Prader-Willi syndrome in
Turner syndrome
0.045 - 0.050
Chronic renal insufficiency
0.045 - 0.050
Children born small for
gestational age
Growth hormone deficient adult patients: In patients who continue growth hormone
therapy after childhood GHD, the recommended dose to restart is 0.2 – 0.5 mg per
day. The dose should be gradually increased or decreased according to individual
patient requirements as determined by the IGF-I concentration.
In patients with adult-onset GHD, therapy should start with a low dose, 0.15 – 0.3 mg
per day. The dose should be gradually increased according to individual patient
requirements as determined by the IGF-I concentration.

In both cases treatment goal should be IGF-I concentrations within 2 SDS from the
age corrected mean. Patients with normal IGF-I concentrations at the start of the
treatment should be administered growth hormone up to an IGF-I level into upper
range of normal, not exceeding the 2 SDS. Clinical response and side effects may also
be used as guidance for dose titration. It is recognised that there are patients with
GHD who do not normalise IGF-I levels despite a good clinical response, and thus do
not require dose escalation. The maintenance dose seldom exceeds 1.0 mg per day.
Women may require higher doses than men, with men showing an increasing IGF-I
sensitivity over time. This means that there is a risk that women, especially those on
oral oestrogen replacement are under-treated while men are over-treated. The
accuracy of the growth hormone dose should therefore be controlled every 6 months.
As normal physiological growth hormone production decreases with age, dose
requirements are reduced. In patients above 60 years, therapy should start with a dose
of 0.1 - 0.2 mg per day and should be slowly increased according to individual patient
requirements. The minimum effective dose should be used. The maintenance dose in
these patients seldom exceeds 0.5 mg per day.


Hypersensitivity to the active substance or to any of the excipients.
Somatropin must not be used when there is any evidence of activity of a tumour.
Intracranial tumours must be inactive and antitumour therapy must be completed
prior to starting growth hormone therapy. Treatment should be discontinued if there is
evidence of tumour growth.
GENOTROPIN should not be used for growth promotion in children with closed
Patients with acute critical illness suffering complications following open heart
surgery, abdominal surgery, multiple accidental trauma, acute respiratory failure or
similar conditions should not be treated with GENOTROPIN (regarding patients
undergoing substitution therapy, see section 4.4).


Special warnings and precautions for use

Diagnosis and therapy with GENOTROPIN should be initiated and monitored by
physicians who are appropriately qualified and experienced in the diagnosis and
management of patients with the therapeutic indication of use.
The maximum recommended daily dose should not be exceeded (see section 4.2).
Insulin sensitivity
Somatropin may reduce insulin sensitivity. For patients with diabetes mellitus, the
insulin dose may require adjustment after somatropin therapy is instituted. Patients

with diabetes, glucose intolerance, or additional risk factors for diabetes should be
monitored closely during somatropin therapy.
Thyroid function
Growth hormone increases the extrathyroidal conversion of T4 to T3 which may
result in a reduction in serum T4 and an increase in serum T3 concentrations. Whereas
the peripheral thyroid hormone levels have remained within the reference ranges in
the majority of healthy subjects, hypothyroidism theoretically may develop in subjects
with subclinical hypothyroidism. Consequently, monitoring of thyroid function should
therefore be conducted in all patients. In patients with hypopituitarism on standard
replacement therapy, the potential effect of growth hormone treatment on thyroid
function must be closely monitored.
In growth hormone deficiency secondary to treatment of malignant disease, it is
recommended to pay attention to signs of relapse of the malignancy. In childhood
cancer survivors, an increased risk of a second neoplasm has been reported in patients
treated with somatropin after their first neoplasm. Intracranial tumours, in particular
meningiomas, in patients treated with radiation to the head for their first neoplasm,
were the most common of these second neoplasms
In patients with endocrine disorders, including growth hormone deficiency, slipped
epiphyses of the hip may occur more frequently than in the general population.
Children limping during treatment with somatropin, should be examined clinically.
Benign intracranial hypertension
In case of severe or recurrent headache, visual problems, nausea and/or vomiting, a
funduscopy for papilloedema is recommended. If papilloedema is confirmed, a
diagnosis of benign intracranial hypertension should be considered and, if appropriate,
the growth hormone treatment should be discontinued. At present there is insufficient
evidence to give specific advice on the continuation of growth hormone treatment in
patients with resolved intracranial hypertension. If growth hormone treatment is
restarted, careful monitoring for symptoms of intracranial hypertension is necessary.
Leukaemia has been reported in a small number of growth hormone deficiency
patients, some of whom have been treated with somatropin. However, there is no
evidence that leukaemia incidence is increased in growth hormone recipients without
predisposition factors.
As with all somatropin containing products, a small percentage of patients may
develop antibodies to GENOTROPIN. GENOTROPIN has given rise to the formation
of antibodies in approximately 1% of patients. The binding capacity of these
antibodies is low and there is no effect on growth rate. Testing for antibodies to
somatropin should be carried out in any patient with otherwise unexplained lack of
Elderly patients

Experience in patients above 80 years is limited. Elderly patients may be more
sensitive to the action of GENOTROPIN, and therefore may be more prone to
develop adverse reactions.
Acute critical illness
The effects of GENOTROPIN on recovery were studied in two placebo controlled
trials involving 522 critically ill adult patients suffering complications following open
heart surgery, abdominal surgery, multiple accidental trauma or acute respiratory
failure. Mortality was higher in patients treated with 5.3 or 8 mg GENOTROPIN daily
compared to patients receiving placebo, 42% vs. 19%. Based on this information,
these types of patients should not be treated with GENOTROPIN. As there is no
information available on the safety of growth hormone substitution therapy in acutely
critically ill patients, the benefits of continued treatment in this situation should be
weighed against the potential risks involved.
In all patients developing other or similar acute critical illness, the possible benefit of
treatment with Genotropin must be weighed against the potential risk involved.
Although rare, pancreatitis should be considered in somatropin-treated patients,
especially children who develop abdominal pain.
Prader-Willi syndrome
In patients with Prader-Willi syndrome, treatment should always be in combination
with a calorie-restricted diet.
There have been reports of fatalities associated with the use of growth hormone in
pediatric patients with Prader-Willi syndromewho had one or more of the following
risk factors: severe obesity (those patients exceeding a weight/height of 200 %),
history of respiratory impairment or sleep apnoea, or unidentified respiratory
infection. Patients with one or more of these factors may be at increased risk.
Before initiation of treatment with somatropin in patients with Prader-Willi syndrome,
signs for upper airway obstruction, sleep apnoea, or respiratory infections should be
If during the evaluation of upper airway obstruction, pathological findings are
observed, the child should be referred to an ear, nose and throat (ENT) specialist for
treatment and resolution of the respiratory disorder prior to initiating growth hormone
Sleep apnoea should be assessed before onset of growth hormone treatment by
recognised methods such as polysomnography or overnight oxymetry, and monitored
if sleep apnoea is suspected.
If during treatment with somatropin patients show signs of upper airway obstruction
(including onset of or increased snoring), treatment should be interrupted, and a new
ENT assessment performed.

All patients with Prader-Willi syndromeshould be monitored if sleep apnoea is
Patients should be monitored for signs of respiratory infections, which should be
diagnosed as early as possible and treated aggressively.
All patients with Prader-Willi syndromeshould also have effective weight control
before and during growth hormone treatment.
Scoliosis is common in patients with Prader-Willi syndrome. Scoliosis may progress
in any child during rapid growth. Signs of scoliosis should be monitored during
Experience with prolonged treatment in adults and in patients with Prader-Willi
syndrome is limited.
Small for gestational age
In short children born SGA other medical reasons or treatments that could explain
growth disturbance should be ruled out before starting treatment.
In SGA children it is recommended to measure fasting insulin and blood glucose
before start of treatment and annually thereafter. In patients with increased risk for
diabetes mellitus (e.g. familial history of diabetes, obesity, severe insulin resistance,
acanthosis nigricans) oral glucose tolerance testing (OGTT) should be performed. If
overt diabetes occurs, growth hormone should not be administered.
In SGA children it is recommended to measure the IGF-I level before start of
treatment and twice a year thereafter. If on repeated measurements IGF-I levels
exceed +2 SD compared to references for age and pubertal status, the IGF-I / IGFBP3 ratio could be taken into account to consider dose adjustment.
Experience in initiating treatment in SGA patients near onset of puberty is limited. It
is therefore not recommended to initiate treatment near onset of puberty. Experience
in patients with Silver-Russell syndrome is limited.
Some of the height gain obtained with treating short children born SGA with growth
hormone may be lost if treatment is stopped before final height is reached.
Chronic renal insufficiency
In chronic renal insufficiency, renal function should be below 50 percent of normal
before institution of therapy. To verify growth disturbance, growth should be followed
for a year preceding institution of therapy. During this period, conservative treatment
for renal insufficiency (which includes control of acidosis, hyperparathyroidism and
nutritional status) should have been established and should be maintained during
treatment. The treatment should be discontinued at renal transplantation.
To date, no data on final height in patients with chronic renal insufficiency treated
with Genotropin are available.

Interaction with other medicinal products and other forms of interaction

Concomitant treatment with glucocorticoids may inhibit the growth-promoting effects
of somatropin containing products. Therefore, patients treated with glucocorticoids
should have their growth monitored carefully to assess the potential impact of
glucocorticoid treatment on growth.
Data from an interaction study performed in growth hormone deficient adults,
suggests that somatropin administration may increase the clearance of compounds
known to be metabolised by cytochrome P450 isoenzymes. The clearance of
compounds metabolised by cytochrome P 450 3A4 (e.g. sex steroids, corticosteroids,
anticonvulsants and ciclosporin) may be especially increased resulting in lower
plasma levels of these compounds. The clinical significance of this is unknown.
Also see section 4.4 for statements regarding diabetes mellitus and thyroid disorder
and section 4.2 for statement on oral oestrogen replacement therapy.


Pregnancy and lactation

Animal studies are insufficient with regard to effects on pregnancy, embryofoetal
development, parturition or postnatal development (See section 5.3). No clinical
studies on exposed pregnancies are available. Therefore, somatropin containing
products are not recommended during pregnancy and in women of childbearing
potential not using contraception.
There have been no clinical studies conducted with somatropin containing products in
breast-feeding women. It is not known whether somatropin is excreted in human milk,
but absorption of intact protein from the gastrointestinal tract of the infant is
extremely unlikely. Therefore caution should be exercised when somatropin
containing products are administered to breast-feeding women.


Effects on ability to drive and use machines
GENOTROPIN has no influence on the ability to drive and use machines.


Undesirable effects
Patients with growth hormone deficiency are characterized by extracellular volume
deficit. When treatment with somatropin is started this deficit is rapidly corrected. In
adult patients adverse effects related to fluid retention, such as oedema peripheral,
musculoskeletal stiffness, arthralgia, myalgia and paraesthesia are common. In
general these adverse effects are mild to moderate, arise within the first months of
treatment and subside spontaneously or with dose-reduction.

The incidence of these adverse effects is related to the administered dose, the age of
patients, and possibly inversely related to the age of patients at the onset of growth
hormone deficiency. In children such adverse effects are uncommon.
Genotropin has given rise to the formation of antibodies in approximately 1 % of the
patients. The binding capacity of these antibodies has been low and no clinical
changes have been associated with their formation, see section 4.4.
The following undesirable effects have been observed and reported during treatment
with Genotropin with the following frequencies: Very common ( 1/10); common
( 1/100 to <1/10); uncommon ( 1/1,000 to <1/100); rare ( 1/10,000 to <1/1,000);
very rare (<1/10,000).

Neoplasms benign, malignant and unspecified (including cysts and polyps):
Very rare:
Immune system disorders:
Formation of antibodies
Endocrine disorders:
Diabetes mellitus type II
Nervous system disorders:
In adults: paraesthesia

In adults: carpal tunnel syndrome. In children: paraesthesia


Benign intracranial hypertension

Skin and subcutaneous tissue disorders:
In children: transient injection site reactions
Musculoskeletal and connective tissue disorders:
In adults: musculoskeletal stiffness, arthralgia, myalgia

In children: musculoskeletal stiffness, arthralgia, myalgia

General disorders and administration site conditions:
In adults: oedema peripheral

In children: oedema peripheral

Somatropin has been reported to reduce serum cortisol levels, possibly by affecting
carrier proteins or by increased hepatic clearance. The clinical relevance of these
findings may be limited. Nevertheless, corticosteroid replacement therapy should be
optimised before initiation of GENOTROPIN therapy.
In the post-marketing experience rare cases of sudden death have been reported in
patients affected by Prader-Willi syndrome treated with somatropin, although no
causal relationship has been demonstrated.

Very rare cases of leukaemia have been reported in growth hormone deficient
children treated with Genotropin, but the incidence appears to be similar to that in
children without growth hormone deficiency, see section 4.4.



Acute overdosage could lead initially to hypoglycaemia and subsequently to
Long-term overdosage could result in signs and symptoms consistent with the known
effects of human growth hormone excess.




Pharmacodynamic properties
Pharmacotherapeutic group: Anterior pituitary lobe hormones and analogues, ATC
code: H01A C01
Somatropin is a potent metabolic hormone of importance for the metabolism of lipids,
carbohydrates and proteins. In children with inadequate endogenous growth hormone,
somatropin stimulates linear growth and increases growth rate. In adults, as well as in
children, somatropin maintains a normal body composition by increasing nitrogen
retention and stimulation of skeletal muscle growth, and by mobilisation of body fat.
Visceral adipose tissue is particularly responsive to somatropin. In addition to
enhanced lipolysis, somatropin decreases the uptake of triglycerides into body fat
stores. Serum concentrations of IGF-I and IGFBP3 (Insulin-like Growth Factor
Binding Protein 3) are increased by somatropin. In addition, the following actions
have been demonstrated:

Lipid metabolism: Somatropin induces hepatic LDL cholesterol receptors,
and affects the profile of serum lipids and lipoproteins. In general,
administration of somatropin to growth hormone deficient patients results in
reductions in serum LDL and apolipoprotein B. A reduction in serum total
cholesterol may also be observed.


Carbohydrate metabolism: Somatropin increases insulin but fasting blood
glucose is commonly unchanged. Children with hypopituitarism may
experience fasting hypoglycemia. This condition is reversed by somatropin.


Water and mineral metabolism: Growth hormone deficiency is associated
with decreased plasma and extracellular volumes. Both are rapidly increased
after treatment with somatropin. Somatropin induces the retention of sodium,
potassium and phosphorus.


Bone metabolism: Somatropin stimulates the turnover of skeletal bone. Longterm administration of somatropin to growth hormone deficient patients with
osteopenia results in an increase in bone mineral content and density at
weight-bearing sites.


Physical capacity: Muscle strength and physical exercise capacity are
improved after long-term treatment with somatropin. Somatropin also
increases cardiac output, but the mechanism has yet to be clarified. A
decrease in peripheral vascular resistance may contribute to this effect.

In clinical trials in short children born SGA doses of 0.033 and 0.067 mg/kg body
weight per day have been used for treatment until final height. In 56 patients who
were continuously treated and have reached (near) final height, the mean change from
height at start of treatment was +1.90 SDS (0.033 mg/kg body weight per day) and
+2.19 SDS (0.067 mg/kg body weight per day). Literature data from untreated SGA
children without early spontaneous catch-up suggest a late growth of 0.5 SDS. Longterm safety data are still limited.


Pharmacokinetic properties
The bioavailability of subcutaneously administered somatropin is approximately 80
% in both healthy subjects and growth hormone deficient patients. A subcutaneous
dose of 0.035 mg/kg of somatropin results in plasma Cmax and tmax values in the range
of 13-35 ng/ml and 3-6 hours respectively.
The mean terminal half-life of somatropin after intravenous administration in growth
hormone deficient adults is about 0.4 hours. However, after subcutaneous
administration, half-lives of 2-3 hours are achieved. The observed difference is likely
due to slow absorption from the injection site following subcutaneous administration.
The absolute bioavailability of somatropin seems to be similar in males and females
following s.c. administration.
Information about the pharmacokinetics of somatropin in geriatric and paediatric
populations, in different races and in patients with renal, hepatic or cardiac
insufficiency is either lacking or incomplete.


Preclinical safety data
In studies regarding general toxicity, local tolerance and reproduction toxicity no
clinically relevant effects have been observed.

In vitro and in vivo genotoxicity studies on gene mutations and induction of
chromosome aberrations have been negative.
An increased chromosome fragility has been observed in one in-vitro study on
lymphocytes taken from patients after long term treatment with somatropin and
following the addition of the radiomimetic drug bleomycin. The clinical significance
of this finding is unclear.
In another study, no increase in chromosomal abnormalities was found in the
lymphocytes of patients who had received long term somatropin therapy.




List of excipients

Powder (front compartment):

Solvent (rear compartment):

Glycine (E640)
Sodium dihydrogen phosphate anhydrous
Disodium phosphate anhydrous (E339)
Mannitol (E421)

Water for injections
Mannitol (E421)


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


Shelf life
3 years.
After reconstitution: Chemical and physical in-use stability has been demonstrated for
24 hours at 2°C - 8°C.
From a microbiological point of view, the product should be used immediately. If not
used immediately, in-use storage times and conditions prior to use are the
responsibility of the user and would normally not be longer than 24 hours at 2ºC -

8ºC, unless reconstitution has taken place in controlled and validated aseptic


Special precautions for storage
Before reconstitution:
Store in a refrigerator (2ºC – 8ºC). Do not freeze. Keep the syringe in the outer carton
in order to protect from light.
Before opening, the product may be taken out of the refrigerator, without being
replaced, for a maximum period of 6 months at a temperature not above 25°C. The
date when the medicinal product is taken out and the new expiry date should be
recorded. This new expiry date should never exceed the one initially mentioned on
the outer carton. If the medicinal product has not been used before the new expiry
date, it should be disposed of.
After reconstitution:
Do not freeze. Keep the syringe in the outer carton in order to protect from light. For
storage conditions of the reconstituted medicinal product, see section 6.3.


Nature and contents of container
Powder and 0.25 ml solvent in a two chamber glass cartridge (type I glass) separated
by a rubber plunger (bromobutyl), supplied as a single dose syringe. The cartridge is
sealed at both ends with rubber stoppers (bromobutyl) and is enclosed in a plastic
sleeve with a plunger rod and a finger grip.
Package sizes
7 x 0.2 mg, 28 (4 x 7 x 0.2 mg)
7 x 0.4 mg, 28 (4 x 7 x 0.4 mg)
7 x 0.6 mg, 28 (4 x 7 x 0.6 mg)
7 x 0.8 mg, 28 (4 x 7 x 0.8 mg)
7 x 1.0 mg, 28 (4 x 7 x 1.0 mg)

4 x 1.2 mg, 7 x 1.2 mg, 28 (4 x 7 x 1.2 mg)
4 x 1.4 mg, 7 x 1.4 mg, 28 (4 x 7 x 1.4 mg)
4 x 1.6 mg, 7 x 1.6 mg, 28 (4 x 7 x 1.6 mg)
4 x 1.8 mg, 7 x 1.8 mg, 28 (4 x 7 x 1.8 mg)
4 x 2.0 mg, 7 x 2.0 mg, 28 (4 x 7 x 2.0 mg)

Not all pack sizes may be marketed.


Special precautions for disposal
Only reconstitute the powder with the solvent supplied.
The solution is prepared by screwing the plunger rod inwards so that the solvent will
be mixed with the powder in the two chamber cartridge. Do not shake vigorously; this
might cause denaturation of the active ingredient. The injection needle should be
screwed on before reconstitution. The reconstituted solution is colourless or slightly
opalescent. The reconstituted solution for injection is to be inspected prior to use and
only clear solutions without particles should be used.

Comprehensive instructions for the preparation and administration of the
reconstituted Genotropin product are given in the package leaflet, section 3,
”Injecting genotropin” and in the relevant Instructions for Use.
GENOTROPIN MINIQUICK is for single use only. Any unused product or waste
material should be disposed of in accordance with local requirements.


Pfizer Limited
Ramsgate Road,
Kent CT13 9NJ, UK


PL 00057/0989


14 September 1998 / 20 April 2010



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Source: Medicines and Healthcare Products Regulatory Agency

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