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Mechanism of Action
Somatropin (as well as endogenous growth hormone) binds to dimeric growth hormone receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects. Some of these pharmacodynamic effects are primarily mediated by insulin-like growth factor (IGF-1) produced in the liver and also locally (e.g., skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (e.g., lipolysis).
In vitro and in vivo preclinical and clinical testing have demonstrated that Nutropin AQ is therapeutically equivalent to pituitary-derived hGH. Pediatric patients who lack adequate endogenous growth hormone (GH) secretion, patients with chronic kidney disease (CKD), and patients with Turner syndrome (TS) that were treated with Nutropin AQ or Nutropin resulted in an increase in growth rate and an increase in IGF-1 levels similar to that seen with pituitary-derived hGH.
- Skeletal Growth: Nutropin AQ stimulates skeletal growth in pediatric patients with growth failure due to a lack of adequate secretion of endogenous GH or secondary to CKD and in patients with TS. Skeletal growth is accomplished at the epiphyseal plates at the ends of a growing bone. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and one of its mediators, IGF-I. Serum levels of IGF-I are low in children and adolescents who are GHD, but increase during treatment with somatropin. In pediatric patients, new bone is formed at the epiphyses in response to GH and IGF-I. This results in linear growth until these growth plates fuse at the end of puberty.
- Cell Growth: Treatment with somatropin results in an increase in both the number and the size of skeletal muscle cells.
- Organ Growth: GH influences the size of internal organs, including kidneys, and increases red cell mass. Treatment of hypophysectomized or genetic dwarf rats with somatropin results in organ growth that is proportional to the overall body growth. In normal rats subjected to nephrectomy-induced uremia, somatropin promoted skeletal and body growth.
Linear growth is facilitated in part by GH-stimulated protein synthesis. This is reflected by nitrogen retention as demonstrated by a decline in urinary nitrogen excretion and blood urea nitrogen (BUN) during somatropin therapy.
GH is a modulator of carbohydrate metabolism. For example, patients with inadequate secretion of GH sometimes experience fasting hypoglycemia that is improved by treatment with Nutropin AQ. Somatropin therapy may decrease insulin sensitivity. Untreated patients with CKD and TS have an increased incidence of glucose intolerance. Administration of somatropin to adults or children resulted in increases in serum fasting and postprandial insulin levels, more commonly in overweight or obese individuals. In addition, mean fasting and postprandial glucose and hemoglobin A1C levels remained in the normal range.
The retention of total body potassium in response to somatropin administration apparently results from cellular growth. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, CKD, or TS during Nutropin AQ therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney. Serum calcium is not significantly altered in these patients. Sodium retention also occurs. Adults with childhood-onset GHD show low bone mineral density (BMD). Nutropin AQ therapy results in increases in serum alkaline phosphatase [see WARNINGS AND PRECAUTIONS].
Connective Tissue Metabolism
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).
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.
Table 2: Summary of Nutropin AQ Pharmacokinetic Parameters
in Healthy Adult Males 0.1 mg fatroroximatelv 0.3 IUa)/kg SC
|a Based on current International Standard of 3
IU = 1 mg.
Abbreviations: AUC0-∞ =area under the curve, Cmax=maximum concentration, CL/Fsc systemic clearance, CV%=coefficient of variation in %; SC=subcutaneous, Fsc=subcutaneous bioavailability (not determined), t1/2=half-life.
Figure 1: Single Dose Mean Growth Hormone Concentrations
in Healthy Adult Males
Pubertal Patients with Growth Hormone Deficiency (GHD)
One open label, multicenter, randomized clinical trial of two dosages of Nutropin was performed in pubertal patients with GHD. Ninety-seven patients (mean age 13.9 years, 83 male, 14 female) currently being treated with approximately 0.3 mg/kg/wk of GH were randomized to 0.3 mg/kg/wk or 0.7 mg/kg/wk Nutropin doses. All patients were already in puberty (Tanner stage ≥ 2) and had bone ages ≤ 14 years in males or ≤ 12 years in females. Mean baseline height standard deviation score (SDS) was -1.3.
The mean last measured height in all 97 patients after a mean duration of 2.7 ± 1.2 years, by analysis of covariance (ANCOVA) adjusting for baseline height, is shown below.
Table 3: Last Measured Height* by Sex and Nutropin Dose for Pubertal Patients with GHD
|Last Measured Height* (cm)||Height Difference Between Groups (cm)|
|Age (yr)||0.3 mg/kg/wk||0.7 mg/kg/wk||Mean ± SE|
|Mean ± SD (range)||Mean ± SD||Mean ± SD|
|Male|| 17.2 ± 1.3
(13.6 to 19.4)
| 170.9 ± 7.9
| 174.5 ± 7.9
|3.6 ± 1.7|
|Female|| 15.8 ± 1.8
(11.9 to 19.3)
| 154.7 ± 6.3
| 157.6 ± 6.3
|2.9 ± 3.4|
|*Adjusted for baseline height|
The mean height SDS at last measured height (n=97) was -0.7 ± 1.0 in the 0.3 mg/kg/wk group and -0.1 ± 1.2 in the 0.7 mg/kg/wk group. For patients completing 3.5 or more years (mean 4.1 years) of Nutropin treatment (15/49 patients in the 0.3 mg/kg/wk group and 16/48 patients in the 0.7 mg/kg/wk group), the mean last measured height was 166.1 ± 8.0 cm in the 0.3 mg/kg/wk group and 171.8 ± 7.1 cm in the 0.7 mg/kg/wk group, adjusting for baseline height and sex.
The mean change in bone age was approximately one year for each year in the study in both dose groups. Patients with baseline height SDS above -1.0 were able to attain normal adult heights with the 0.3 mg/kg/wk dose of Nutropin (mean height SDS at near-adult height =-0.1, n= 15).
Thirty-one patients had bone mineral density (BMD) determined by dual energy x-ray absorptiometry (DEXA) scans at study conclusion. The two dose groups did not differ significantly in mean SDS for total body BMD (-0.9 ± 1.9 in the 0.3 mg/kg/wk group vs. -0.8 ± 1.2 in the 0.7 mg/kg/wk group, n=20) or lumbar spine BMD (—1.0 ± 1.0 in the 0.3 mg/kg/wk group vs. -0.2 ± 1.7 in the 0.7 mg/kg/wk group, n=21).
Over a mean duration of 2.7 years, patients in the 0.7 mg/kg/wk group were more likely to have IGF-I values above the normal range than patients in the 0.3 mg/kg/wk group (27.7% vs. 9.0% of IGF-I measurements for individual patients). The clinical significance of elevated IGF-I values is unknown.
Pediatric Patients with Growth Failure Secondary to Chronic Kidney Disease (CKD)
Two multicenter, randomized, controlled clinical trials were conducted to determine whether treatment with Nutropin prior to renal transplantation in patients with CKD could improve their growth rates and height deficits. One study was a double-blind, placebo-controlled trial and the other was an open-label, randomized trial. The dose of Nutropin in both controlled studies was 0.05 mg/kg/day (0.35 mg/kg/week) administered daily by subcutaneous injection. Combining the data from those patients completing two years in the two controlled studies results in 62 patients treated with Nutropin and 28 patients in the control groups (either placebo-treated or untreated). The mean first year growth rate was 10.8 cm/yr for Nutropin-treated patients, compared with a mean growth rate of 6.5 cm/yr for placebo/untreated controls (p < 0.00005). The mean second year growth rate was 7.8 cm/yr for the Nutropin-treated group, compared with 5.5 cm/yr for controls (p < 0.00005). There was a significant increase in mean height SDS in the Nutropin group (-2.9 at baseline to -1.5 at Month 24, n=62) but no significant change in the controls (-2.8 at baseline to -2.9 at Month 24, n=28). The mean third year growth rate of 7.6 cm/yr in the Nutropin-treated patients (n=27) suggests that Nutropin stimulates growth beyond two years. However, there are no control data for the third year because control patients crossed over to Nutropin treatment after two years of participation. The gains in height were accompanied by appropriate advancement of skeletal age. These data demonstrate that Nutropin therapy improves growth rate and corrects the acquired height deficit associated with CKD.
The North American Pediatric Renal Transplant Cooperative Study (NAPRTCS) has reported data for growth post-transplant in children who did not receive GH prior to transplantation as well as children who did receive Nutropin during the clinical trials prior to transplantation. The average change in height SDS during the initial two years post-transplant was 0.15 for the 2,391 patients who did not receive GH pre-transplant and 0.28 for the 57 patients who did1. For patients who were followed for 5 years post-transplant, the corresponding changes in height SDS were also similar between groups.
Pediatric Patients with Turner Syndrome (TS)
Three US studies, two long-term, open-label, multicenter, historically controlled studies (Studies 1 and 2), and one long-term, randomized, dose-response study (Study 3) and one Canadian, long-term, randomized, open-label, multicenter, concurrently controlled study, were conducted to evaluate the efficacy of somatropin treatment of short stature due to TS.
In the US Studies 1 and 2, the effect of long-term GH treatment (0.375 mg/kg/week given either 3 times per week or daily) on adult height was determined by comparing adult heights in the treated patients with those of age-matched historical controls with TS who received no growth-promoting therapy. In Study 1, estrogen treatment was delayed until patients were at least age 14. GH therapy resulted in a mean adult height gain of 7.4 cm (mean duration of GH therapy of 7.6 years) vs. matched historical controls by ANCOVA.
In Study 2, patients treated with early Nutropin therapy (before 11 years of age) were randomized to receive estrogen-replacement therapy (conjugated estrogens, 0.3 mg escalating to 0.625 mg daily) at either age 12 or 15 years. Compared with matched historical controls, early Nutropin therapy (mean duration of 5.6 years) combined with estrogen replacement at age 12 years resulted in an adult height gain of 5.9 cm (n=26), whereas girls who initiated estrogen at age 15 years (mean duration of Nutropin therapy 6.1 years) had a mean adult height gain of 8.3 cm (n=29). Patients who initiated Nutropin after age 11 (mean age 12.7 years; mean duration of Nutropin therapy 3.8 years) had a mean adult height gain of 5.0 cm (n=51).
Thus, in Studies 1 and 2, the greatest improvement in adult height was observed in patients who received early GH treatment and estrogen after age 14 years.
In Study 3, a randomized, blinded dose-response study, patients were treated from a mean age of 11.1 years for a mean duration of 5.3 years with a weekly GH dose of either 0.27 mg/kg or 0.36 mg/kg administered in divided doses 3 or 6 times weekly. The mean near-final height of GH-treated patients was 148.7 ± 6.5 cm (n=31). When compared to historical control data, the mean gain in adult height was approximately 5 cm.
The Canadian randomized study compared near-adult height outcomes for GH-treated patients to those of a concurrent control group who received no injections. The somatropin-treated patients received a dosage of 0.3 mg/kg/week given in divided doses 6 times per week from a mean age of 11.7 years for a mean duration of 4.7 years. Puberty was induced with a standardized estrogen regimen initiated at 13 years of age for both treatment groups. The somatropin-treated group (n=27) attained a mean (+ SD) near final height of 146.0 ± 6.2 cm; the untreated control group (n= 19) attained a near final height of 142.1 ± 4.8 cm. By ANCOVA (with adjustments for baseline height and mid-parental height), the effect of GH-treatment was a mean height increase of 5.4 cm (p=0.001).
In summary, patients with TS (total n= 181 from the 4 studies above) treated to adult height achieved statistically significant average height gains ranging from 5.0-8.3 cm.
Table 4: Summary of Efficacy Results in Turner Syndromea
| GH Duration
| Adult Height
|US 3||RDT||31||11.1||8-13.5||5.3|| ~5
|a Data shown are mean values.
b RCT: randomized controlled trial; MHT: matched historical controlled trial; RDT: randomized dose-response trial.
c Analysis of covariance vs. controls.
d Compared with historical data.
*A=GH age < 11 yr, estrogen age 15 yr.
B=GH age < 11 yr, estrogen age 12 yr.
C=GH age > 11 yr, estrogen at Month 12.
Pediatric Patient with Idiopathic Short Stature (ISS)
A long-term, open-label, multicenter study was conducted to examine the safety and efficacy of Nutropin in pediatric patients with ISS, also called non-growth hormone deficient short stature. For the first year, 122 pre-pubertal subjects over the age of 5 years with stimulated serum GH ≥ 10 ng/mL were randomized into two treatment groups of approximately equal size; one group was treated with Nutropin 0.3 mg/kg weekly divided into three doses per week and the other group served as untreated controls. For the second and subsequent years of the study, all subjects were re-randomized to receive the same total weekly dose of Nutropin (0.3 mg/kg weekly) administered either daily or three times weekly. Treatment with Nutropin was continued until a subject's bone age was > 15.0 years (boys) or > 14.0 years (girls) and the growth rate was < 2 cm/yr, after which subjects were followed until adult height was achieved. The mean baseline values were: height SDS-2.8, IGF-I SDS -0.9, age 9.4 years, bone age 7.8 years, growth rate 4.4 cm/yr, mid-parental target height SDS -0.7, and Bayley-Pinneau predicted adult height SDS -2.3. Nearly all subjects had predicted adult height that was less than mid-parental target height.
During the one-year controlled phase of the study, the mean height velocity increased by 0.5 ± 1.8 cm (mean ± SD) in the no-treatment control group and by 3.1 ± 1.7 cm in the Nutropin group (p < 0.0001). For the same period of treatment the mean height SDS increased by 0.4 ± 0.2 and remained unchanged (0.0 ± 0.2) in the control group (p < 0.001).
Of the 118 subjects who were treated with Nutropin (70%) reached near-adult height (hereafter called adult height) after 2-10 years of Nutropin therapy. Their last measured height, including post-treatment follow-up, was obtained at a mean age of 18.3 years in males and 17.3 years in females. The mean duration of therapy was 6.2 and 5.5 years, respectively. Adult height was greater than pretreatment predicted adult height in 49 of 60 males (82%) and 19 of 23 females (83%). The mean difference between adult height and pretreatment predicted adult height was 5.2 cm (2.0 inches) in males and 6.0 cm (2.4 inches) in females (p < 0.0001 for both). The table (below) summarizes the efficacy data.
Table 5: Long-Term Efficacy in ISS (Mean ± SD)
|Adult height (cm)||166.3 ± 5.8||153.1 ± 4.8|
|Pretreatment predicted adult height (cm)||161.1 ± 5.5||147.1 ± 5.1|
|Adult height minus pretreatment predicted adult height (cm)||+5.2 ± 5.0a||+6.0 ± 5.0a|
|Adult height SDS||-1.5 ± 0.8||-1.6 ± 0.7|
|Pretreatment predicted adult height SDS||-2.2 ± 0.8||-2.5 ± 0.8|
|Adult height minus pretreatment predicted adult height SDS||+0.7 ± 0.7a||+0.9 ± 0.8a|
|ap < 0.0001 versus zero.|
Nutropin therapy resulted in an increase in mean IGF-I SDS from -0.9 ± 1.0 to -0.2 ± 0.9 in Treatment Year 1. During continued treatment, mean IGF-I levels remained close to the normal mean. IGF-I SDS above +2 occurred sporadically in 14 subjects.
Adult Growth Hormone Deficiency
Two multicenter, double-blind, placebo-controlled clinical trials were conducted in growth hormone-deficient adults. Study 1 was conducted in subjects with adult-onset GHD (n= 166), mean age 48.3 years, at doses of 0.0125 or 0.00625 mg/kg/day; doses of 0.025 mg/kg/day were not tolerated in these subjects. Study 2 was conducted in previously treated subjects with childhood-onset GHD (n=64), mean age 23.8 years, at randomly assigned doses of 0.025 or 0.0125 mg/kg/day. The studies were designed to assess the effects of replacement therapy with Nutropin on body composition.
Significant changes from baseline to Month 12 of treatment in body composition (i.e., total body % fat mass, trunk % fat mass, and total body % lean mass by DEXA scan) were seen in all Nutropin groups in both studies (p < 0.0001 for change from baseline and vs. placebo), whereas no statistically significant changes were seen in either of the placebo groups. In the adult-onset study, the Nutropin group improved mean total body fat from 35.0% to 31.5%, mean trunk fat from 33.9% to 29.5%, and mean lean body mass from 62.2% to 65.7%, whereas the placebo group had mean changes of 0.2% or less (p=not significant). Due to the possible effect of GH-induced fluid retention on DEXA measurements of lean body mass, DEXA scans were repeated approximately 3 weeks after completion of therapy; mean % lean body mass in the Nutropin group was 65.0%, a change of 2.8% from baseline, compared with a change of 0.4% in the placebo group (p < 0.0001 between groups).
In the childhood-onset study, the high-dose Nutropin group improved mean total body fat from 38.4% to 32.1%, mean trunk fat from 36.7% to 29.0%, and mean lean body mass from 59.1% to 65.5%; the low-dose Nutropin group improved mean total body fat from 37.1% to 31.3%, mean trunk fat from 37.9% to 30.6%, and mean lean body mass from 60.0% to 66.0%; the placebo group had mean changes of 0.6% or less (p=not significant).
Table 6: Mean Changes from Baseline to Month 12 in Proportion
of Fat and Lean by DEXA for Adult- and Childhood- Onset GHD Studies
| Adult Onset
0.025 mg/ kg/day
| Placebo vs. Pooled
|Total body percent fat|
|Baseline to Month 12 change||-0.1||-3.6||< 0.0001||+ 0.2||-5.8||-6.3||< 0.0001|
|Baseline to post-washout change||-0.4||-2.8||< 0.0001||NA||NA||NA||—|
|Trunk percent fat|
|Baseline to Month 12 change||0.0||-4.3||< 0.0001||+0.6||-7.3||-7.6||< 0.0001|
|Baseline to post-washout change||-0.3||-3.4||—||NA||NA||NA||—|
|Total body percent lean|
|Baseline to Month 12 change||+0.2||+3.6||< 0.0001||-0.2||+6.0||+6.4||< 0.0001|
|Baseline to post-washout change||+0.4||+2.8||< 0.0001||NA||NA||NA||—|
In the adult-onset study, significant decreases from baseline to Month 12 in low-density lipoprotein (LDL) cholesterol and LDL:high-density lipoprotein (HDL) ratio were seen in the Nutropin group compared to the placebo group, p < 0.02; there were no statistically significant between-group differences in change from baseline to Month 12 in total cholesterol, HDL cholesterol, or triglycerides. In the childhood-onset study significant decreases from baseline to Month 12 in total cholesterol, LDL cholesterol, and LDL:HDL ratio were seen in the high-dose Nutropin group only, compared to the placebo group, p < 0.05. There were no statistically significant between-group differences in HDL cholesterol or triglycerides from baseline to Month 12.
In the childhood-onset study, 55% of the patients had decreased spine BMD (z-score < -l) at baseline. The administration of Nutropin (n= 16) (0.025 mg/kg/day) for two years resulted in increased spine BMD from baseline when compared to placebo (n= 13) (4.6% vs. 1.0%, respectively, p < 0.03); a transient decrease in spine BMD was seen at six months in the Nutropin-treated patients. Thirty-five percent of subjects treated with this dose had supraphysiological levels of IGF-I at some point during the study, which may carry unknown risks. No significant improvement in total body BMD was found when compared to placebo. A lower GH dose (0.0125 mg/kg/day) did not show significant increments in either of these bone parameters when compared to placebo. No statistically significant effects on BMD were seen in the adult-onset study where patients received GH (0.0125 mg/kg/day) for one year.
Muscle strength, physical endurance, and quality of life measurements were not markedly abnormal at baseline, and no statistically significant effects of Nutropin therapy were observed in the two studies.
A subsequent 32-week, multicenter, open-label, controlled clinical trial was conducted using Nutropin AQ, Nutropin Depot, or no treatment in adults with both adult-onset and childhood-onset GHD. Subjects were randomized into the three groups to evaluate effects on body composition, including change in visceral adipose tissue (VAT) as determined by computed tomography (CT) scan.
For subjects evaluable for change in VAT in the Nutropin AQ (n=44) and untreated (n= 19) groups, the mean age was 46.2 years and 78% had adult-onset GHD. Subjects in the Nutropin AQ group were treated at doses up to 0.012 mg/kg per day in women (all of whom received estrogen replacement therapy) and men under age 35 years, and up to 0.006 mg/kg per day in men over age 35 years.
The mean absolute change in VAT from baseline to Week 32 was -10.7 cm2 in the Nutropin AQ group and + 8.4 cm2 in the untreated group (p=0.013 between groups). There was a 6.7% VAT loss in the Nutropin AQ group (mean percent change from baseline to Week 32) compared with a 7.5% increase in the untreated group (p=0.012 between groups). The effect of reducing VAT in adult GHD patients with Nutropin AQ on long-term cardiovascular morbidity and mortality has not been determined.
Table 7: Visceral Adipose Tissue by Computed Tomography Scan:
Percent Change and Absolute Change from Baseline to Week 32 in Study 3
(n = 44)
| Treatment Difference
|Baseline VAT (cm2) (mean)||126.2||123.3|
|Change in VAT (cm2) (adjusted mean)||-10.7||+8.4||-19.1||0.013a|
|Percent change in VAT (adjusted mean)||-6.7||+7.5||-14.2||0.012a|
| a ANCOVA using baseline VAT as a covariate
VAT=visceral adipose tissue.
Last reviewed on RxList: 5/25/2012
This monograph has been modified to include the generic and brand name in many instances.
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