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Nutropin AQ (somatropin) injection, for subcutaneous use

Summary about Nutropin AQ

Growth hormone (GH) or somatotropin is a peptide produced by the somatotroph cells in the anterior pituitary gland. It binds to a transmembrane receptor and leads to the production of insulin-like growth factor I (IGF-I), IGF binding protein 3 (IGFBP-3), and the acid-labile subunit (ALS). This 3-peptide compound is brought to target cells, binds to IGF-I receptor, and stimulates metabolic functions. In infancy, childhood and adolescence GH is essential for normal linear growth.

Figure 1: Nutropin AQ NuSpin pen (Source: )

Nutropin AQ treats adults and children who don’t make enough GH on their own (a condition called growth hormone deficiency), and children who have growth failure.

Nutropin AQ therapy is approved for the following conditions where growth hormone treatment may be necessary, including:

Pediatric Growth Hormone Deficiency

Pediatric Growth Hormone Deficiency (PGHD) may happen when the body is unable to produce enough growth hormone (GH) or use it effectively. GH produced in the body plays a critical role in helping young bodies grow and develop, including improving muscle metabolism, growing bones, and breaking down fats. When levels of GH are too low, there may be an impact on growth and many functions of the body.

PGHD may be present at birth or develop at any time during childhood or adolescence. There are many possible causes of PGHD. Damage to, or an abnormality in, the pituitary gland or the hypothalamus (the part of your brain that controls the pituitary gland) are among them.

Idiopathic Short Stature

When a child or a teenager is growing poorly, but his or her body appears to be making normal amounts of growth hormone (GH), he or she is said to have Idiopathic Short Stature (ISS). “Idiopathic” means the cause is unknown; “short stature” means the child or teenager is markedly shorter than others of his or her age and gender.

Turner Syndrome

Turner syndrome (TS) is a genetic condition that affects about 1 in every 2,500 female live births. TS occurs when one of a girl’s two X chromosomes is absent or incomplete. The most common feature of TS is short stature, which affects nearly 100% of girls with TS. That’s because the missing or incomplete X chromosome contains a gene that helps girls grow to a normal height.

From birth through their teen years, girls with TS grow more slowly than unaffected children. In fact, the average adult height of women with TS is about 4’8”, while unaffected women average about 5’4”.



Chronic Kidney Disease

Chronic Kidney Disease (CKD) is a loss of kidney function over a period of months or years. Most young people with CKD produce as much growth hormone (GH) as anyone their age. The problem is that their kidneys aren’t filtering waste from their blood as well as they should. Because so much waste is trapped in their blood, their bodies aren’t able to use GH effectively. Because of CKD, GH and insulin-like growth factor (IGF) can’t connect properly. GH signals IGF to travel to muscles, organs, and bones and tells the bones to grow. It also helps improve muscle metabolism. When GH and IGF aren’t working together, it means:

  • Growth may be slowed or stopped
  • Muscles, organs, and bones may not get the GH they need to develop properly

Adult-onset Adult Growth Hormone Deficiency

Adult-onset Adult Growth Hormone Deficiency (AGHD) may occur when an adult’s pituitary gland does not work effectively. Adult-onset AGHD may have been caused by damage to the pituitary gland or hypothalamus, which may impact its ability to make enough GH.

This damage is most commonly caused by a tumor in and around the pituitary. Such a tumor may compress the gland, or the damage may occur when the tumor is removed through neurosurgery. The pituitary gland may also be damaged by infection, blood vessel disease, severe head injury, or radiation treatment. Damage to the pituitary gland may affect the production of one or more pituitary hormones, including GH.

Childhood-onset Adult Growth Hormone Deficiency

Childhood-onset Adult Growth Hormone Deficiency (AGHD) is the continuation of a disorder that began in infancy or childhood. Childhood-onset AGHD may have been caused by:

  • An abnormality in the pituitary gland or the hypothalamus (a part of the brain that controls the pituitary)
  • Genetic problems with the production of growth hormone
  • Damage to the pituitary gland or the surrounding area due to tumors, infection, radiation treatment, or severe head injury.

Nutropin AQ is available in the following pen cartridge and NuSpin forms:

  • Pen Cartridge: 10 mg/2 mL (yellow color band), and 20 mg/2 mL (purple color band)
  • NuSpin: 5 mg/2 mL (clear device), 10 mg/2 mL (green device), and 20 mg/2 mL (blue device)

Nutropin AQ is contrainidicated in following cases:

  • Acute critical illness
  • Children with Prader-Willi Syndrome who are severely obese or have severe respiratory impairment – reports of sudden death
  • Active malignancy
  • Hypersensitivity to somatropin or its excipients
  • Active proliferative or severe non-proliferative diabetic retinopathy
  • Children with closed epiphyses
  • Known hypersensitivity to somatropin or excipients
  • Diabetic retinopathy.


Nutropin (somatropin)

Active Ingredient


Administration Route


Alcohol Warning

No data about interaction

Available Strength

Nutropin AQ is available in the following pen cartridge and NuSpin forms:
  • Pen Cartridge: 10 mg/2 mL (yellow color band), and 20 mg/2 mL (purple color band)
  • NuSpin: 5 mg/2 mL (clear device), 10 mg/2 mL (green device), and 20 mg/2 mL (blue device)

Breastfeeding Warning

Caution is recommended. Excretion into human milk is unknown.

Following subcutaneous administration of radiolabelled medication in animal studies, radioactivity was transferred to milk reaching four  times the concentration found in maternal plasma. However, absorption of the intact protein in the gastrointestinal tract of the infant is considered extremely unlikely.

Clinical Pharmacology


Tissue Growth:
The primary and most intensively studied action of somatropin is the stimulation of linear growth. This effect is demonstrated in children with GHD.

Skeletal Growth:
The measurable increase in bone length after administration of somatropin results from its effect on the cartilaginous growth areas of long bones. Studies in vitro have shown that the incorporation of sulfate into proteoglycans is not due to a direct effect of somatropin, but rather is mediated by the somatomedins or insulin-like growth factors (IGFs). The somatomedins, among them IGF-I, are polypeptide hormones which are synthesized in the liver, kidney, and various other tissues. IGF-I levels are low in the serum of hypopituitary dwarfs and hypophysectomized humans or animals, and increase after treatment with somatropin.

Cell Growth:
It has been shown that the total number of skeletal muscle cells is markedly decreased in children with short stature lacking endogenous GH compared with normal children, and that treatment with somatropin results in an increase in both the number and size of muscle cells.

Organ Growth:
Somatropin influences the size of internal organs, and it also increases red cell mass.

Protein Metabolism:
Linear growth is facilitated in part by increased cellular protein synthesis. This synthesis and growth are reflected by nitrogen retention which can be quantitated by observing the decline in urinary nitrogen excretion and blood urea nitrogen following the initiation of somatropin therapy.

Carbohydrate Metabolism:
Hypopituitary children sometimes experience fasting hypoglycemia that may be improved by treatment with somatropin. In healthy subjects, large doses of somatropin may impair glucose tolerance. Although the precise mechanism of the diabetogenic effect of somatropin is not known, it is attributed to blocking the action of insulin rather than blocking insulin secretion. Insulin levels in serum actually increase as somatropin levels increase. Administration of human growth hormone to normal adults and patients with growth hormone deficiency results in increases in mean serum fasting and postprandial insulin levels, although mean values remain in the normal range. In addition, mean fasting and postprandial glucose and hemoglobin A1c levels remain in the normal range.

Lipid Metabolism:
Somatropin stimulates intracellular lipolysis, and administration of somatropin leads to an increase in plasma free fatty acids and triglycerides. Untreated GHD is associated with increased body fat stores, including increased abdominal visceral and subcutaneous adipose tissue. Treatment of growth hormone deficient patients with somatropin results in a general reduction of fat stores, and decreased serum levels of low density lipoprotein (LDL) cholesterol.

Mineral Metabolism:
Administration of somatropin results in an increase in total body potassium and phosphorus and to a lesser extent sodium. This retention is thought to be the result of cell growth. Serum levels of phosphate increase in children with GHD after somatropin therapy due to metabolic activity associated with bone growth. Serum calcium levels are not altered. Although calcium excretion in the urine is increased, there is a simultaneous increase in calcium absorption from the intestine. Negative calcium balance, however, may occasionally occur during somatropin treatment.

Connective Tissue Metabolism:
Somatropin stimulates the synthesis of chondroitin sulfate and collagen, and increases the urinary excretion of hydroxyproline.



The absolute bioavailability of somatropin after subcutaneous administration in healthy adult males has been determined to be 81 ± 20%. The mean terminal t1/2 after subcutaneous administration is significantly longer than that seen after intravenous administration (2.1 ± 0.43 hours vs. 19.5 ± 3.1 minutes) indicating that the subcutaneous absorption of the compound is slow and rate-limiting.


Animal studies with somatropin showed that GH localizes to highly perfused organs, particularly the liver and kidney. The volume of distribution at steady state for somatropin in healthy adult males is about 50 mL/kg body weight, approximating the serum volume.


Both the liver and kidney have been shown to be important metabolizing organs for GH. Animal studies suggest that the kidney is the dominant organ of clearance. GH is filtered at the glomerulus and reabsorbed in the proximal tubules. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation.


The mean terminal t1/2 after intravenous administration of somatropin in healthy adult males is estimated to be 19.5 ± 3.1 minutes. Clearance of rhGH after intravenous administration in healthy adults and children is reported to be in the range of 116–174 mL/hr/kg.

Bioequivalence of Formulations

Nutropin AQ has been determined to be bioequivalent to Nutropin based on the statistical evaluation of area under the curve (AUC) and maximum concentration (Cmax).

Special Populations

Pediatric: Available literature data suggests that somatropin clearances are similar in adults and children.

Geriatrics: Limited published data suggest that the plasma clearance and average steady-state plasma concentration of somatropin may not be different between young and elderly patients.

Race: Reported values for half-lives for endogenous GH in normal adult black males are not different from observed values for normal adult white males. No data for other races are available.

Growth Hormone Deficiency: Reported values for clearance of somatropin in adults and children with GHD range 138–245 mL/hr/kg and are similar to those observed in healthy adults and children. Mean terminal t1/2 values following intravenous and subcutaneous administration in adult and pediatric GHD patients are also similar to those observed in healthy adult males.

Chronic Kidney Disease: Children and adults with CKD and end-stage renal disease (ESRD) tend to have decreased clearance compared to normals. In a study with six pediatric patients 7 to 11 years of age, the clearance of Nutropin was reduced by 21.5% and 22.6% after the intravenous infusion and subcutaneous injection, respectively, of 0.05 mg/kg of Nutropin compared to normal healthy adults. Endogenous GH production may also increase in some individuals with ESRD. However, no somatropin accumulation has been reported in children with CKD or ESRD dosed with current regimens.

Turner Syndrome: No pharmacokinetic data are available for exogenously administered somatropin. However, reported half-lives, absorption, and elimination rates for endogenous GH in this population are similar to the ranges observed for normal subjects and GHD populations.

Hepatic Insufficiency: A reduction in somatropin clearance has been noted in patients with severe liver dysfunction. The clinical significance of this decrease is unknown.

Gender: No gender-specific pharmacokinetic studies have been done with Nutropin AQ. The available literature indicates that the pharmacokinetics of somatropin are similar in men and women.


Approximate Retail Price


solution for injection:

  • 10 mg (4 NuSpin pen, 10 mg): $6,035.28

solution for injection:

  • 20 mg (1 NuSpin pen, 20 mg): $3,025.90

solution for injection:

  • 5 mg (1 NuSpin pen, 5 mg): $692.11

Dosage Form

Injection for subcutaneous use

Dose Schedule

Pediatric GHD: Up to 0.3 mg/kg/week

Pubertal Patients: Up to 0.7 mg/kg/week

Idiopathic Short Stature: Up to 0.3 mg/kg/week

Chronic Kidney Disease: Up to 0.35 mg/kg/week

Turner Syndrome: Up to 0.375 mg/kg/week

Adult GHD: Either a non-weight based or weight-based dosing regimen may be followed, with doses adjusted based on treatment response and IGF-I concentrations.

Non-weight-based: A starting dose of approximately 0.2 mg/day (range 0.15−0.3 mg/day) increased gradually every 1−2 months by increments of approximately 0.1−0.2 mg/day.

Weight-based: Initiate from not more than 0.006 mg/kg/day; the dose may be increased up to a maximum of 0.025 mg/kg/day in patients ≤ 35 years old or 0.0125 mg/kg/day in patients >35 years old.

Drug Class

H01AC – Somatropin and somatropin agonists

Drug Unit


Food Warning

No known interactions

Included In
Health Insurance Plan

Nutropin AQ sometimes is covered by health insurance if considered medically necessary, but some patients have had coverage denied. The Magic Foundation offers help making the case for coverage or appealing a denial, and outlines patients’ experiences getting approval.

Interacting Drug

Inhibitors of 11ß-Hydroxysteroid Dehydrogenase Type 1:
May require the initiation of glucocorticoid replacement therapy. Patients treated with glucocorticoid replacement for previously diagnosed hypoadrenalism may require an increase in their maintenance dosesGlucocorticoid Replacement Therapy:
Should be carefully adjustedCytochrome P450-Metabolized Drugs:
Monitor carefully if used with somatropinOral Estrogen:
Larger doses of somatropin may be required in womenInsulin and/or Oral/Injectable Hypoglycemic Agents:
May require adjustment

Is Available Generically

No. There is currently no therapeutically equivalent version of Nutropin AQ available.

Is Proprietary


Label Details

Legal Status


Is not subject to the Controlled Substances Act.


Genentech, Inc.

Maximum Intake

The Nutropin AQ NuSpin 5 allows for administration of a minimum dose of 0.05 mg to a maximum dose of 1.75 mg, in increments of 0.05 mg.

The Nutropin AQ NuSpin 10 allows for administration of a minimum dose of 0.1 mg to a maximum dose of 3.5 mg, in increments of 0.1 mg.

The Nutropin AQ NuSpin 20 allows for administration of a minimum dose of 0.2 mg to a maximum dose of 7.0 mg, in increments of 0.2 mg.

Mechanism of Action

Somatropin binds to the human growth hormone receptor (GHR). Upon binding, soatropin causes dimerization of GHR, activation of the GHR-associated JAK2 tyrosine kinase, and tyrosyl phosphorylation of both JAK2 and GHR. These events recruit and/or activate a variety of signaling molecules, including MAP kinases, insulin receptor substrates, phosphatidylinositol 3′ phosphate kinase, diacylglycerol, protein kinase C, intracellular calcium, and Stat transcription factors. These signaling molecules contribute to the GH-induced changes in enzymatic activity, transport function, and gene expression that ultimately culminate in changes in growth and metabolism.

Non Proprietary Name



Short-term overdosage could lead initially to hypoglycemia and subsequently to hyperglycemia. Furthermore, overdose with somatropin is likely to cause fluid retention.

Long-term overdosage could result in signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess growth hormone

Pregnancy Category


AU TGA pregnancy category B2: Drugs which have been taken by only a limited number of pregnant women and women of childbearing age, without an increase in the frequency of malformation or other direct or indirect harmful effects on the human fetus having been observed. Studies in animals are inadequate or may be lacking, but available data show no evidence of an increased occurrence of fetal damage.

US FDA pregnancy category C: Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks.

Pregnancy Warning

Use is not recommended unless clearly needed.

Animal studies did not show any teratogenicity or adverse effects on gestation, morphogenesis, parturition, lactation, postnatal development, or reproductive capacity of the offspring; a slight increase in fetal death and increased body weight of pups, and reduced pregnancy rate, increased litter size, irregular estrus cycles, and decreased sperm motility in the parents were seen. There are no controlled data in human pregnancy.

Prescribing Info

Prescription Status

Prescription drug

Proprietary Name

Nutropin AQ

Related Drugs

Tesamorelin, Mecasermin rinfabate, Sermorelin, Mecasermin, Somatrem





Acute Critical Illness: Potential benefit of treatment continuation should be weighed against the potential risk.

Prader-Willi Syndrome in Children: Evaluate for signs of upper airway obstruction and sleep apnea before initiation of treatment for GHD. Discontinue treatment if these signs occur.

Neoplasm: Monitor patients with preexisting tumors for progression or recurrence. Increased risk of a second neoplasm in childhood cancer survivors treated with somatropin – in particular meningiomas in patients treated with radiation to the head for their first neoplasm.

Impaired Glucose Tolerance and Diabetes Mellitus: May be unmasked. Periodically monitor glucose levels in all patients. Doses of concurrent antihyperglycemic drugs in diabetics may require adjustment.

Intracranial Hypertension: Exclude preexisting papilledema. May develop and is usually reversible after discontinuation or dose reduction.

Hypersensitivity: Serious hypersensitivity reactions may occur. In the event of an allergic reaction, seek prompt medical attention.

Fluid Retention (i.e., edema, arthralgia, carpal tunnel syndrome – especially in adults): May occur frequently. Reduce dose as necessary.

Hypoadrenalism: Monitor patients for reduced serum cortisol levels and/or need for glucocorticoid dose increases in those with known hypoadrenalism.

Hypothyroidism: May first become evident or worsen.

Slipped Capital Femoral Epiphysis: May develop. Evaluate children with the

onset of a limp or hip/knee pain.

Progression of Preexisting Scoliosis: May develop.

Pancreatitis: Consider pancreatitis in patients with persistent severe abdominal pain.