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Clinical Pharmacology


Somatropin has a pronounced effect on the metabolism of fats, proteins and carbohydrates. In children with growth hormone deficiency (GH), somatropin stimulates the growth of skeletal bones in length by acting on the epiphysis plates of the tubular bones. In both adults and children, somatropin contributes to the normalization of body structure by increasing muscle mass and reducing body fat. Visceral adipose tissue is especially sensitive to the action of somatropin. In addition to enhancing lipolysis, somatropin reduces the flow of triglycerides into body fat. Under the action of somatropin, the concentration of insulin-like growth factor I (IGF-I) and its binding protein (IGF-CB3, insulin-like growth factor binding protein) increases.

In addition, the following effects were demonstrated.

Fat exchange. Somatropin activates LDL receptors in the liver and changes the profile of lipids and lipoproteins in the blood. In general, the use of somatropin in patients with GH deficiency leads to a decrease in LDL and apolipoprotein B in the blood. A decrease in cholesterol concentration is also observed.

Carbohydrate exchange. Somatropin increases insulin release, but the glucose concentration of glucose does not usually change. Children with hypopituitarism may develop fasting hypoglycemia. This condition is reversible with the introduction of somatropin.

Water and mineral metabolism. GH deficiency is associated with a decrease in plasma and extracellular fluid volume. The administration of somatropin leads to a rapid increase in both parameters. Somatropin contributes to the retention of sodium, potassium and phosphorus.

Bone metabolism. Somatropin stimulates bone metabolism. Long-term treatment with somatropin in children with GH deficiency and osteoporosis leads to the normalization of the mineral composition and bone density.

Physical activity. Long-term replacement therapy with somatropin leads to an increase in muscle strength and physical endurance. Cardiac output is also increasing, although the mechanism of this action is not fully understood. Reduced peripheral vascular resistance may partly explain this effect of somatropin.



After s / c administration, the bioavailability of somatropin is approximately 80% in both healthy individuals and in patients with GH deficiency. When s / c administration of the drug Omnitrop® at a dose of 5 mg healthy volunteers Cmax somatropin in plasma and its Tmax accounted for (72 ± 28) mcg / l and (4 ± 2) h, respectively.


Average t1/2 somatropin after i / v administration in adult patients with GH deficiency is about 0.4 hours. However, after s / c administration, T1/2 drug reaches 3 hours

Selected patient groups

The absolute bioavailability of somatropin after s / c injection does not differ in men and women.

There are no data on the effect on the pharmacokinetic parameters of growth hormone age, race, abnormal liver function, kidney or heart.


In children with growth retardation as a result of the following diseases and conditions:

  • insufficient secretion of growth hormone;
  • Shereshevsky-Turner syndrome;
  • Prader-Willi syndrome (SPV);
  • chronic renal failure (CRF) with a decrease in kidney function by more than 50%;
  • babies born with low growth rates for this gestational age.

In adults, as a replacement therapy:

  • confirmed pronounced congenital or acquired growth hormone deficiency.


1 ml of solution contains:
active substance: somatropin 6.7 mg,
auxiliary substancesVA: sodium hydrogen phosphate heptahydrate, sodium dihydrogen phosphate dihydrate, poloxamer, benzyl alcohol (preservative), mannitol, phosphoric acid - q.s. to pH 6.2 ± 0.2, sodium hydroxide - q.s. to pH 6.2 ± 0.2, water d / u.

Somatropin is marketed under different brands and generic names, and comes in different dosage forms:

Brand nameManufacturerCountryDosage form
Omnitrop Sandoz Switzerland solution
Jintropin Jensiens China vials
Rastan Pharmstandard Ufavita Russia cartridge

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Dosage and Administration

Somatropin is administered subcutaneously, slowly, 1 time per day, usually at night. Injection sites should be changed to prevent the development of lipoatrophy.

Doses are selected individually, taking into account the severity of GH deficiency, body mass or surface area, and efficacy in the treatment process.

In children with insufficient secretion of GH

a dose of 0.025-0.035 mg / kg / day or 0.7-1 mg / m² / day is recommended. Treatment begins as soon as possible at an earlier age and continues until puberty and / or until the bone growth zones are closed. It is possible to stop treatment when the desired result is achieved.

With Shereshevsky-Turner syndrome

a dose of 0.045-0.050 mg / kg / day or 1.4 mg / m² / day is recommended.

With SPV (Prader-Willi syndrome)

To increase growth and improve body composition in children, the recommended dose is 0.035 mg / kg / day or 1.0 mg / m² / day. The daily dose of the drug should not exceed 2.7 mg. Treatment should not be administered to children with an increase in growth of less than 1 cm per year and almost closed epiphyseal zones of bone growth.

With CRF in children,

accompanied by growth retardation, the recommended dose of 0.045-0.050 mg / kg / day. In case of insufficient growth dynamics, higher doses of the drug may be required. Revision of the optimal dose is possible after 6 months of treatment.

With growth disorders in children,

born with low growth rates for a given gestational age, a dose of 0.035 mg / kg / day or 1.0 mg / m² / day is recommended until the desired growth is achieved. Treatment should be stopped if the increase in growth does not exceed 1 cm after the first year of drug treatment. Also, therapy should be stopped if the increase in growth does not exceed 2 cm per year, if it is found that the bone age is 14 years old (for girls) or > 16 years (for boys), there are closed growth zones.

In adults with severe GH deficiency, substitution therapy is recommended to start with a low dose, 0.15-0.3 mg / day, followed by a gradual increase depending on the serum IHF-I concentration. In patients with a normal initial concentration of IGF-I, the dose of the drug should be adjusted so that the IGF-I values ​​are at the upper limit of normal, without going beyond the 2 standard deviations from the mean. Maintenance dose is selected individually, but, as a rule, does not exceed 1 mg / day (3 IU / day). Women may need higher doses than men, since men over time have increased sensitivity to IGF-I. In this regard, in women, especially those receiving oral estrogen replacement therapy, there is a risk of receiving somatropin treatment in an insufficient dose, while men may receive an overdose treatment with somatropin. Therefore, the optimal dose of somatropin should be monitored every 6 months. Patients older than 60 years of age should begin therapy with a starting dose of 0.1-0.2 mg / day, and then slowly increase to the individually necessary. A minimum effective dose (rarely more than 0.5 mg) should be used.

Adverse reactions

According to the World Health Organization (WHO), undesirable effects are classified according to the frequency of their development as follows: very often (≥1 / 10), often (from ≥1 / 100 to A special feature of patients with GH deficiency is an extracellular fluid deficiency. somatropin, this deficiency is quickly resolved.In adult patients, adverse reactions associated with fluid retention, such as peripheral edema, stiffness of the limbs, arthralgia, myalgia and paresthesia, are often observed. These reactions vary from moderate to moderate, they develop in the first months of treatment and pass spontaneously or with a decrease in dose.The likelihood of these reactions depends on the dose of the drug, the patient’s age and is probably irreversibly associated with age when GH is deficient. side effects are unknown.

Benign, malignant and unspecified neoplasms

very rare: leukemia. In children, in very rare cases there have been cases of leukemia with GH deficiency in the treatment with somatotropin, however, it was found that this frequency is similar to that in children with a normal concentration of GH.

Immune system disorders

often: the formation of antibodies to somatropin. When administering somatropin, approximately 1% of patients produce antibodies to it. The binding capacity of these antibodies is small and there are no clinical manifestations of such antibody production.

Endocrine Disorders

rarely: type 2 diabetes.

Nervous system disorders

often: in adults - paresthesia.

infrequently: in adults - carpal tunnel syndrome, in children - paresthesia;

rarely: benign intracranial hypertension.

Disorders of the gastrointestinal tract

infrequently: in children - pancreatitis

Disorders of the musculoskeletal and connective tissue

often: in adults - stiff limbs, arthralgia, myalgia.

infrequently: in children - stiffness of the limbs, arthralgia, myalgia.

General disorders and disorders at the site of administration

often: in adults, peripheral edema. In children, transient skin reactions at the injection site;

infrequently: in children - peripheral edema.



Diabetes mellitus, cranial hypertension, concomitant therapy with glucocorticosteroids, hypothyroidism (including during replacement therapy with thyroid hormones).

Drug interactions

The results of the study of drug interactions in adult patients with GH deficiency suggest that the administration of somatropin increases the clearance of drugs metabolized by the microsomal isoenzymes of cytochrome P450 in the liver, especially those that are metabolized by the 3A4 isoenzyme - sex hormones, glucocorticosteroids, anticonvulsant drugs and cyclosporine, the curbant, glucose-corticosteroids, anticonvulsant drugs and cyclosporin, the curbant, glucose-corticosteroids, anticonvulsant drugs and cyclosporine, the fungal hormone, glucocorticosteroids, anticonvulsant drugs and cyclosporin; to reduce their plasma concentrations. The clinical significance of this impact has not yet been determined.

Glucocorticosteroids inhibit the stimulating effect of somatropin on growth processes. Concomitant therapy with other hormones, such as gonadotropin, anabolic steroids, estrogens and thyroid hormones, may also affect the efficacy of the drug (in relation to final growth).

Special instructions

Insulin resistance:

Somatropin can cause a state of insulin resistance, and in some patients hyperglycemia, so you should first identify the presence of impaired glucose tolerance. In rare cases, the administration of somatropin can develop type 2 diabetes, but in the vast majority of these cases, patients had risk factors such as obesity (including obesity with PWV), a family history, taking glucocorticosteroids, or a previously existing impaired glucose tolerance. In patients with diabetes mellitus when prescribing somatropin, dose adjustment of hypoglycemic drugs may be necessary.

In children with an increased risk of developing diabetes mellitus (family history of diabetes mellitus, obesity, severe insulin resistance, acantcoratodermia), a glucose tolerance test should be performed. When detecting diabetes, the use of somatropin is not allowed.


In the treatment with somatropin, an enhanced conversion of thyroxin (T4) to triiodothyronine (TK) was detected, which may cause corresponding changes in the blood plasma.

Despite the fact that in healthy volunteers, as a rule, the concentration of thyroid hormones in the blood remained within the normal range, theoretically, clinical manifestation of subclinical hypothyroidism is possible. On the other hand, patients receiving levothyroxine sodium as a hormone replacement therapy may develop hyperthyroidism. On this basis, it is strongly recommended to monitor thyroid function after the initiation of therapy with somatropin, as well as with each change in its dose.

Adrenal function:

It was noted that somatropin decreases plasma cortisol concentration, possibly by affecting carrier proteins or increasing hepatic clearance. The clinical significance of these observations may be limited, however, replacement glucocorticosteroid therapy before prescribing Omnitrop® should be optimized.

Malignant neoplasms:

In case of insufficiency of GH arising after antitumor therapy, attention should be paid to possible signs of a recurrence of a malignant neoplasm.

In patients with endocrine disorders, including GH deficiency, a shift in the femoral epiphyses may occur more often than in the general population. Detection of lameness during therapy with somatropin requires clinical examination and careful observation.

Benign intracranial hypertension:

If severe or recurrent headaches, visual impairment, nausea and / or vomiting occur, fundoscopy is recommended to diagnose possible edema of the optic nerve head. However, it should be remembered that at first the rise in intracranial pressure may not be accompanied by swelling of the optic nerve head. Thus, the absence of edema of the optic nerve does not exclude intracranial hypertension. When confirming the diagnosis, should, if necessary, cancel the drug.

At present, there are no clear guidelines on the use of somatropin in patients with corrected intracranial hypertension. However, experience with clinical use suggests that the resumption of treatment with somatropin in many cases does not lead to a recurrence of intracranial hypertension. If the use of somatropin was resumed, careful monitoring of the possible appearance of symptoms of intracranial hypertension is necessary.

Elderly patients:

experience in people older than 80 years is limited.


in patients with PWV, treatment must necessarily be coupled with a calorie-restricted diet.

There have been reports of deaths associated with the use of somatropin in children with SST who have at least one of the following risk factors: severe obesity, a history of respiratory failure, sleep apnea, or an unidentified respiratory infection. Patients with SPV in the presence of one or more of these factors may have a greater risk. Patients with PWV should be examined to identify upper airway obstruction (VDP), sleep apnea and respiratory infections before starting somatropin.

At detection of obstruction of VDP, consultation of the ENT specialist for treatment of obstruction before the beginning of use of somatropin is necessary.

Diagnosis of sleep apnea is carried out before starting to use the drug with the help of approved methods such as polysomnography or nighttime oximetry, and, if a suspicion of this syndrome appears, you should carefully monitor the patient's condition. If during the treatment with somatropin there are signs of obstruction of the VDP (including the appearance or increase in snoring), treatment should be interrupted and an unscheduled otolaryngological examination should be carried out.

All patients with SPV should be monitored for sleep apnea and, if suspected, their condition should be monitored. In addition, all patients with PWV should monitor the occurrence of respiratory infections, diagnose them as early as possible and carry out massive antimicrobial therapy. All patients with PWV should actively monitor their body weight both before the use of somatropin, and during it. Scoliosis is a frequent occurrence with SPV, it can progress in any child with the rapid growth of the organism. Therefore, during treatment with somatropin, it is necessary to monitor the possible signs of scoliosis. Despite this, the use of somatropin does not increase the likelihood of the development or severity of scoliosis.The experience of long-term use in adults and patients with PWV is limited. In children and adolescents with growth deficiency and low weight for gestational age at birth (MWH), before starting therapy with somatropin, other causes of growth deficiency and the possibility of using other treatment methods should be evaluated. In children and adolescents with MWH, it is recommended to measure the fasting insulin concentration and blood glucose before starting therapy and, further, annually.

In children and adolescents with MWF, it is recommended to measure the concentration of IGF-I before treatment and twice a year after its onset. If repeated measurements of the concentration of IGF-I exceed +2 standard deviations relative to typical values ​​for a given age and degree of sexual development, then for the correction of the dose of somatropin, the ratio of IGF-I concentrations to IGFB-3 (IGF binding protein) should be taken into account.

The experience of therapy in patients with MVGV during puberty is limited, therefore, it is not recommended to begin treatment during this period. Experience of use in patients with Silver-Russell syndrome is also limited. When treating children and adolescents with MWH, it should be borne in mind that when discontinuing therapy until the maximum possible growth is reached, some of the increase in growth may be lost.

Growth disorder in chronic renal failure:

With CRF, the functional activity of the kidneys before the start of therapy should be less than 50% of normal. To confirm growth impairment, it is necessary to track growth over the course of the year preceding therapy. During this period, conservative treatment is prescribed (including the control of acidosis, hyperparathyroidism, and nutritional status), which continues with the start of the main therapy. When kidney transplantation treatment should be discontinued.

Currently, there is no data on the amount of growth increase in the appointment of Omnitrop® to patients with chronic renal failure.

Critical conditions:

Reparative effects of somatropin in adult patients in critical condition as a result of complications after open-heart and abdominal operations, multiple injuries from accidents, and acute respiratory failure were evaluated in two placebo-controlled studies.

Mortality in patients who were prescribed 5.3 mg or 8 mg of somatropin per day was higher than in the placebo group (42% and 19%, respectively). According to these results, the listed patient groups should not be given somatropin. It is necessary to change the place of subcutaneous injections in connection with the possibility of the development of lipoatrophies. This preparation contains less than 1 mmol of sodium (23 mg) in 1 ml, which is a negligible amount. Since benzyl alcohol is present in the composition of Omnitrop®, it should not be given to premature infants or newborns, since this component can cause toxic and anaphylactic reactions in children under 3 years of age.

Antibodies: in a small number of patients, antibodies to somatropin may be formed, which, due to their low affinity, do not affect the growth process. However, the determination of the presence of antibodies to somatropin should be performed in all patients with an inexplicable decrease / absence of effect.

Growth disorder in children born with low growth rates for a given gestational age:

Before starting treatment, all other causes of lack of growth should be excluded. Also in these children it is recommended to control the level of glucose in the blood.

Pancreatitis in children:

children receiving somatropin have an increased risk of developing pancreatitis. In spite of the fact that this complication is rare, it is necessary to exclude pancreatitis in all children with abdominal pain.


In a small number of GD-deficient patients treated with somatropin, cases of leukemia have been described.However, at the moment there is no evidence that the risk of developing leukemia is increased in the absence of other risk factors.


Cases of overdose are unknown.

Acute overdose can lead to hypoglycemia first, and then to hyperglycemia. With prolonged overdose, there may be signs and symptoms characteristic of an excess of human GH (the development of acromegaly and / or gigantism, as well as the development of hypothyroidism, a decrease in serum cortisol concentration).

Treatment: drug withdrawal, symptomatic therapy.

  • Active ingredient: Somatropin (recombinant human growth hormone)

Studies and clinical trials of Somatropin (Click to expand)
  1. Stability study of somatropin by capillary zone electrophoresis
  2. The Second International Standard for Somatropin (Recombinant DNA-derived Human Growth Hormone): Preparation and Calibration in an International Collaborative Study
  3. Somatonorm® (somatrem) and Genotropin® (somatropin): Two case studies
  4. Experience of reviewing the follow-on biologics including Somatropin and erythropoietin in Japan
  5. Cost-effectiveness of somatropin for the treatment of short children born small for gestational age
  6. Intranasal delivery of recombinant human growth hormone (somatropin) in sheep using chitosan-based powder formulations
  8. Direct ovarian stimulation by ovarian injection of rFSH and somatropin for the poor responders in IVF-ET program
  9. Injection Force Dynamics of Improved NordiFlex [somatropin (rDNA origin)] Versus the Current Version of Norditropin NordiFlex
  10. P-40 Economic evaluation of somatropin (Norditropin®) for the treatment of short children born SGA in Sweden
  11. Exercise capacity and hormonal response in adults with childhood onset growth hormone deficiency during long-term somatropin treatment
  18. Somatropin Zorbtive™
  19. Somatropin (Zorbtive™)
  20. Somatropin (Zorbtive™)
  21. Mammalian Cell-Derived Somatropin
  22. Somatropin Therapy for Children with Prader- Willi Syndrome
  23. Relative Bioavailability of Two Drug Products of Somatropin Obtained from Either the Milk of Transgenic Cows or Bacterial Culture
  24. Additional regulatory approval for devices delivering somatropin.

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