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Somapacitan-beco is a human growth hormone (hGH) analog with a single substitution in the amino acid backbone (L101C) to which an albumin-binding moiety has been attached. The albumin-binding moiety (side-chain) consists of an albumin binder and a hydrophilic spacer attached to position 101 of the protein. The protein part consists of 191 amino acids. Somapacitan-beco is produced in Escherichia coli by recombinant DNA technology. The molecular formula (including the albumin-binding moiety) is C1038H1609N273O319S9 and the molecular weight is 23305.10 g/mol, of which the albumin-binding moiety is 1191.39 g/mol.
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SOGROYA (somapacitan-beco) injection is supplied as a sterile, clear to slightly opalescent and colorless to slightly yellow solution for subcutaneous use in a single-patient-use prefilled pen with a deliverable volume of 1.5 mL.
Each mL of SOGROYA prefilled pen contains 6.7 mg of somapacitan-beco, histidine (0.68 mg), mannitol (44 mg), phenol (4 mg), poloxamer 188 (1 mg), and Water for Injection, USP. The pH is approximately 6.8. Hydrochloric acid and sodium hydroxide may be added to adjust the pH.
The following clinically significant adverse drug reactions are described elsewhere in the labeling:
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
Pediatric Patients with GHD
SOGROYA was studied in a 52-week randomized, open-label, active-controlled, parallel-group clinical study in 200 treatment-naïve, prepubertal pediatric patients with growth hormone deficiency [see Clinical Studies (14.1)]. Table 2 shows common adverse reactions that occurred in ≥5% of patients treated with either SOGROYA or somatropin in this trial.
Table 2. Adverse Reactions occurring ≥5% in SOGROYA or Somatropin-Treated Pediatric Patients (52 Weeks of Treatment)
| Somatropin (N=68) | SOGROYA (N=132) | ||
| Adverse Reactions | % | % | |
| Nasopharyngitis a | 16.2 | 16.7 | |
| Headache | 8.8 | 12.1 | |
| Pyrexiab | 11.8 | 9.1 | |
| Pain in extremityc | 2.9 | 9.8 | |
| Injection site reactiond | 5.9 | 6.1 | |
| Diarrheae | 5.9 | 4.5 | |
| Nausea/vomitingf | 5.9 | 4.5 | |
| Bronchitis | 7.4 | 3 | |
|
a Nasopharyngitis in the SOGROYA treatment group included nasopharyngitis (11.4%), rhinitis (3.8%), pharyngitis streptococcal (0.8%), acute sinusitis (0.8%), nasal congestion (0.8%), pharyngitis (0.8%), and sinusitis (0.8%). b Pyrexia in the SOGROYA treatment group included pyrexia (8.3%) and hyperthermia (0.8%). c Pain in extremity in the SOGROYA treatment group included pain in extremity (9.1%) and growing pains (0.8%). d Injection site reaction in the SOGROYA treatment group included injection site bruising (1.5%), injection site pain (1.5%), injection site hematoma (1.5%), injection site reaction (0.8%), and injection site swelling (0.8%) e Diarrhea in the SOGROYA treatment group included diarrhea (2.3%), gastroenteritis viral (1.5%), and gastrointestinal viral infection (0.8%) f Nausea/vomiting in the SOGROYA treatment group included vomiting (4.5%) and nausea (1.5%) |
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Adult Patients with GHD
SOGROYA was studied in adult patients with GHD in a 35-week, placebo-controlled, double-blind trial with an active- control arm [see Clinical Studies (14.2)]. Adverse reactions occurring >2% with SOGROYA are presented in Table 3.
Table 3. Adverse Reactions occurring >2% in Adults with GHD Treated with SOGROYA and More Frequently# than in Placebo-Treated Patients for 34 Weeks
| Placebo (N=61) | SOGROYA (N=120) | |
| Adverse Reactions | % | % |
| Back pain | 3.3 | 10 |
| Arthralgia | 1.6 | 6.7 |
| Dyspepsia | 3.3 | 5 |
| Sleep disorder | 1.6 | 4.2 |
| Dizziness | 1.6 | 4.2 |
| Tonsillitis | 1.6 | 3.3 |
| Peripheral edema | 1.6 | 3.3 |
| Vomiting | 1.6 | 3.3 |
| Adrenal insufficiency | 1.6 | 3.3 |
| Hypertension | 1.6 | 3.3 |
| Blood creatine phosphokinase increase | 0 | 3.3 |
| Weight increased | 0 | 3.3 |
| Anemia | 0 | 2.5 |
| # Included adverse reactions reported with at least 1% greater incidence in SOGROYA group compared to the placebo group | ||
More SOGROYA treated patients shifted from normal baseline levels to elevated phosphate and creatine phosphokinase levels at the end of the trial compared to the placebo group (17.5% vs 4.9% and 9.2% vs. 6.6%, respectively); these laboratory changes occurred intermittently, and were non-progressive.
The following adverse reactions have been identified during post-approval use of somatropins. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
Musculoskeletal and connective tissue disorders – osteonecrosis in pediatric patients.
Table 4 includes a list of drugs with clinically important drug interactions when administered concomitantly with SOGROYA and instructions for preventing or managing them.
Table 4. Clinically Important Drug Interactions with SOGROYA
| Replacement Glucocorticoid Treatment | |
| Clinical Impact: | Microsomal enzyme 11β-hydroxysteroid dehydrogenase type 1 (11βHSD-1) is required for conversion of cortisone to its active metabolite, cortisol, in hepatic and adipose tissue. GH inhibits 11βHSD-1. Consequently, individuals with untreated GH deficiency have relative increases in 11βHSD-1 and serum cortisol. Initiation of SOGROYA may result in inhibition of 11βHSD-1 and reduced serum cortisol concentrations. |
| Intervention: | Patients treated with glucocorticoid replacement for hypoadrenalism may require an increase in their maintenance or stress doses following initiation of SOGROYA [see Warnings and Precautions (5.7)]. |
| Examples: | Cortisone acetate and prednisone may be affected more than others because conversion of these drugs to their biologically active metabolites is dependent on the activity of 11βHSD-1. |
| Cytochrome P450-Metabolized Drugs | |
| Clinical Impact: | Limited published data indicate that GH treatment increases cytochrome P450 (CP450)-mediated antipyrine clearance. SOGROYA may alter the clearance of compounds known to be metabolized by CP450 liver enzymes. |
| Intervention: | Careful monitoring is advisable when SOGROYA is administered in combination with drugs metabolized by CP450 liver enzymes. |
| Oral Estrogen | |
| Clinical Impact: | Oral estrogens may reduce the serum IGF-1 response to SOGROYA. |
| Intervention: | Patients receiving oral estrogen replacement may require higher SOGROYA dosages [see Dosage and Administration (2.5)]. |
| Insulin and/or Other Hypoglycemic Agents | |
| Clinical Impact: | Treatment with SOGROYA may decrease insulin sensitivity, particularly at higher doses. |
| Intervention: | Patients with diabetes mellitus may require adjustment of their doses of insulin and/or other hypoglycemic agents [see Warnings and Precautions (5.4)]. |
SOGROYA contains somapacitan-beco, which is not a controlled substance.
Inappropriate use of SOGROYA may result in significant negative health consequences.
SOGROYA is not associated with drug related withdrawal adverse reactions.
Included as part of the PRECAUTIONS section.
Increased mortality has been reported after treatment with somatropin in patients with acute critical illness due to complications following open-heart surgery, abdominal surgery and multiple accidental trauma, as well as patients with acute respiratory failure [see Contraindications (4)]. The safety of continuing SOGROYA treatment in patients receiving replacement doses for approved indications who concurrently develop these illnesses has not been established. SOGROYA is not indicated for the treatment of non-GH deficient adults.
Serious systemic hypersensitivity reactions including anaphylactic reactions and angioedema have been reported with postmarketing use of somatropin. Inform patients and/or caregivers that such reactions are possible, and that prompt medical attention should be sought if an allergic reaction occurs. SOGROYA is contraindicated in patients with known hypersensitivity to somatropin or any excipients in SOGROYA [see Contraindications (4)].
Active Malignancy
There is an increased risk of malignancy progression with somatropin treatment in patients with active malignancy [see Contraindications (4)]. Any preexisting malignancy should be inactive, and its treatment complete prior to instituting therapy with SOGROYA. Discontinue SOGROYA if there is evidence of recurrent activity.
Risk of Second Neoplasm in Pediatric Patients
In childhood cancer survivors who were treated with radiation to the brain/head for their first neoplasm and who developed subsequent growth hormone deficiency (GHD) and were treated with somatropin, an increased risk of second neoplasm has
been reported. Intracranial tumors, in particular meningiomas, were the most common of these second neoplasms. Monitor all patients with a history of GHD secondary to an intracranial neoplasm while on somatropin therapy for progression or recurrence of the tumor.
New Malignancy During Treatment
Because children with certain rare genetic causes of short stature have an increased risk of developing malignancies, thoroughly consider the risks and benefits of starting SOGROYA in these patients. If treatment with SOGROYA is initiated, carefully monitor these patients for development of neoplasms.
There is risk of malignant changes of preexisting nevi with somatropin treatment in patients. Monitor patients on SOGROYA therapy carefully for increased growth or potential malignant changes of preexisting nevi. Advise patients/caregivers to report marked changes in behavior, onset of headaches, vision disturbances, and/or changes in the appearance of preexisting nevi.
Treatment with somatropin may decrease insulin sensitivity, particularly at higher doses. New onset type 2 diabetes mellitus has been reported in patients taking somatropin. Patients with undiagnosed pre-diabetes and diabetes mellitus may experience worsened glycemic control and become symptomatic. Monitor glucose levels periodically in all patients receiving SOGROYA, especially in those with risk factors for diabetes mellitus, such as obesity, Turner syndrome, or a family history of diabetes mellitus. Patients with preexisting type 1 or type 2 diabetes mellitus or pre-diabetes should be monitored closely. The doses of antidiabetic agents may require adjustment when SOGROYA is initiated.
Intracranial hypertension with papilledema, visual changes, headache, nausea, and/or vomiting has been reported in patients treated with somatropin. Symptoms usually occurred within the first eight (8) weeks after the initiation of somatropin therapy. In all reported cases, intracranial hypertension-associated signs and symptoms rapidly resolved after cessation of therapy or a reduction of the somatropin dose.
Perform fundoscopic examination before initiating treatment with SOGROYA to exclude preexisting papilledema and periodically thereafter. If papilledema is identified prior to initiation, evaluate the etiology and treat the underlying cause before initiating SOGROYA. If papilledema is observed by fundoscopy during SOGROYA treatment, treatment should be stopped. If intracranial hypertension is confirmed, treatment with SOGROYA can be restarted at a lower dose after intracranial hypertension-associated signs and symptoms have resolved.
Fluid retention during SOGROYA replacement therapy may occur. Clinical manifestations of fluid retention (e.g. edema and nerve compression syndromes including carpal tunnel syndrome/paresthesia) are usually transient and dose dependent.
Patients receiving somatropin therapy who have or are at risk for corticotropin deficiency may be at risk for reduced serum cortisol levels and/or unmasking of central (secondary) hypoadrenalism. In addition, patients treated with glucocorticoid replacement for previously diagnosed hypoadrenalism may require an increase in their maintenance or stress doses following initiation of SOGROYA treatment. Monitor patients with known hypoadrenalism for reduced serum cortisol levels and/or need for glucocorticoid dose increases [see Drug Interactions (7)].
Undiagnosed/untreated hypothyroidism may prevent an optimal response to SOGROYA. In patients with GH deficiency, central (secondary) hypothyroidism may first become evident or worsen during treatment with somatropin therapy.
Therefore, patients should have periodic thyroid function tests and thyroid hormone replacement therapy should be initiated or appropriately adjusted when indicated.
Slipped capital femoral epiphysis may occur more frequently in patients undergoing rapid growth. Slipped capital femoral epiphysis may lead to osteonecrosis. Cases of slipped capital femoral epiphysis with or without osteonecrosis have been reported in pediatric patients with short stature receiving somatropin. Evaluate pediatric patients receiving SOGROYA with the onset of a limp or complaints of persistent hip or knee pain for slipped capital femoral epiphysis and osteonecrosis and manage accordingly.
Somatropin increases growth rate, and progression of preexisting scoliosis can occur in patients who experience rapid growth. Somatropin has not been shown to increase the occurrence of scoliosis. Monitor patients with a history of scoliosis for disease progression.
Cases of pancreatitis have been reported in patients receiving somatropin. The risk may be greater in pediatric patients compared with adults. Consider pancreatitis in patients who develop persistent severe abdominal pain.
When SOGROYA is administered subcutaneously at the same site over a long period of time, tissue lipohypertrophy or lipoatrophy may result. Rotate injection sites when administering SOGROYA to reduce this risk [see Dosage and Administration (2.1)].
There have been reports of fatalities after initiating therapy with somatropin in pediatric patients with Prader-Willi syndrome who had one or more of the following risk factors: severe obesity, history of upper airway obstruction or sleep apnea, or unidentified respiratory infection. Male patients with one or more of these factors may be at greater risk than females.
SOGROYA is not indicated for the treatment of pediatric patients who have growth failure due to genetically confirmed Prader-Willi syndrome.
Serum levels of inorganic phosphorus and alkaline phosphatase may increase after SOGROYA therapy. Serum levels of parathyroid hormone may increase with somatropin treatment.
Long term studies in animals with somapacitan-beco to evaluate carcinogenic potential have not been conducted.
Somapacitan-beco was not mutagenic or clastogenic in a standard battery of genotoxicity tests (bacterial mutagenicity (Ames), human lymphocyte chromosome aberration, rat bone marrow micronucleus).
In rat studies evaluating male and female fertility, somapacitan-beco was administered by subcutaneous injection at doses of 1, 2, and 4 mg/kg twice weekly. Males were dosed from four weeks before pairing until termination and females were dosed beginning two weeks prior to mating through gestation day 7. No adverse effects were observed on male or female fertility in rats at doses up to 4 mg/kg (29 times the MRHD, based on AUC).
Acute overdosage could lead initially to hypoglycemia and subsequently to hyperglycemia. Overdose with SOGROYA 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 endogenous growth hormone.
SOGROYA is contraindicated in patients with:
Somapacitan-beco binds to a dimeric GH receptor in the cell membrane of target 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-1 (IGF-1) produced in the liver, while others are primarily a consequence of the direct effects of somapacitan-beco.
IGF-1 was measured to assess the pharmacodynamic (PD) properties of somapacitan-beco. Somapacitan-beco normalizes the mean IGF-1 standard deviation score (SDS) level from a baseline value below -2 to a value within the reference range (-2 to +2) in treatment-naïve adult patients with GHD [see Clinical Studies (14)].
In adult patients with GHD (n=26), somapacitan-beco induces a less than dose proportional IGF-1 response at steady state. Maximum IGF-1 concentrations were observed within 2 to 4 days after dosing. Similar to the somapacitan-beco exposure time course, a steady state IGF-1 response was reached after 1 to 2 weekly doses with limited cumulative IGF-1 response.
In pediatric patients with GHD aged 2.5 to 11 years, somapacitan-beco produces a dose linear IGF-1 response, with a change of 0.02 mg/kg on average resulting in a change in IGF-1 standard deviation score (SDS) of 0.32. Approximately 97% of pediatric patients achieved an average IGF-1 SDS level within normal range after 52 weeks of treatment with once weekly Sogroya in Study NCT03811535. IGF-1 SDS levels were -2.03 at baseline and the IGF-1 SDS level change from baseline was 2.36.
Somapacitan-beco has pharmacokinetic properties compatible with once weekly administration. The reversible binding to endogenous albumin delays elimination of somapacitan and thereby prolongs the in vivo half-life and duration of action.
The pharmacokinetics (PK) of somapacitan-beco following subcutaneous administration have been investigated at clinically relevant doses (e.g., 0.01 to 0.32 mg/kg in healthy adults, 0.02 to 0.12 mg/kg in adults with GHD, and 0.02 to 0.16 mg/kg in pediatric patient with GHD).
Overall, somapacitan-beco displays non-linear pharmacokinetics, however in the clinically relevant dose range of somapacitan-beco in adults with GHD, somapacitan-beco pharmacokinetics are approximately linear. After subcutaneous administration of 0.02 – 0.16 mg/kg/week somapacitan-beco in pediatric patients with GHD, a non-linear dose-exposure relationship with a greater than dose proportional increase in exposure was observed.
In adults with GHD, a maximum concentration of somapacitan-beco is reached 4 to 24 hours post dose.
Steady state exposure is achieved following 1 to 2 weeks of once weekly administration of subcutaneous somapacitan-beco.
In pediatric patients with GHD, maximum somapacitan-beco concentrations occurred 8 to 25 hours after dosing at doses from
0.02 mg/kg/week to 0.16 mg/kg/week and increased with increasing dose level. Steady state was achieved following 1 to 2 weekly administration.
Somapacitan-beco is extensively bound (>99%) to plasma proteins.
Based on population PK analyses, the estimated volume of distribution (V/F) of somapacitan-beco in adult GHD patients is approximately 14.6 L and 1.7 L in pediatric patients with GHD.
The plasma elimination half-life of somapacitan-beco is approximately 2 to 3 days in adult patients with GHD. Following a dose of 0.16 mg/kg/week, the terminal half-life of somapacitan-beco was about 34 hours in pediatric patients with GHD. Somapacitan-beco was cleared within one week after treatment discontinuation.
Metabolism: Somapacitan-beco is metabolized via proteolytic cleavage of the linker sequence between the peptide backbone and albumin binder sidechain.
Excretion: The primary excretion routes of somapacitan-beco-related material are via the urine and feces. Approximately 81% of the dose is excreted in the urine and approximately 13% is excreted in the feces. No intact somapacitan-beco is excreted indicating full breakdown of somapacitan-beco prior to excretion.
Body weight: Adults with GHD -The exposure of somapacitan-beco decreases with increasing body weight. However, the somapacitan-beco dose range of 0.1 to 8 mg/week provides adequate systemic exposure to reach target IGF-1 levels over the weight range of 34.5-150.5 kg evaluated in the clinical trials.
Pediatric patients with GHD: Based on pharmacokinetic analysis, gender and race do not have a clinically meaningful effect on the pharmacokinetics. The exposure of somapacitan-beco decreases with increasing body weight. However, the somapacitan-beco dose of 0.16 mg/kg/week provides adequate systemic exposure for pediatrics to reach target IGF-1 levels over the weight range of 9.9 to 61.8 kg evaluated in the clinical trials.
Geriatric patients: Adult patients greater than 65 years of age and geriatric patients have a higher exposure than younger subjects at the same somapacitan-beco dose [see Dosage and Administration (2.5) and Use in Specific Populations (8.5)].
Female patients receiving estrogen: Female patients and in particular female patients on oral estrogen, have lower exposure than males at the same somapacitan-beco dose [see Dosage and Administration (2.5) and Drug Interactions (7)].
Hepatic impairment: A somapacitan-beco dose of 0.08 mg/kg at steady state resulted in comparable somapacitan-beco exposure between patients with normal hepatic function and mild hepatic impairment (Child-Pugh A). However, higher exposure was observed in patients with moderate hepatic impairment (Child-Pugh B) (ratios to normal hepatic function were 4.69 and 3.52-fold increase for AUC0-168h and Cmax, respectively). Lower somapacitan-beco stimulated IGF-1 levels were observed in patients with mild and moderate hepatic impairment (ratios to normal hepatic function were 0.85 and 0.75, respectively) [see Dosage and Administration (2.5) and Use in Specific Populations (8.6)].
Renal impairment: In general, somapacitan-beco exposure tended to increase with decreasing estimated glomerular filtration rate. A somapacitan-beco dose of 0.08 mg/kg at steady state resulted in higher exposures in patients with renal impairment, that was most pronounced for patients with severe renal impairment and patients requiring hemodialysis (AUC0-168h ratios to normal renal function were 1.75 and 1.63, respectively). Higher IGF-1 AUC0-168h levels were also observed in patients with moderate and severe renal impairment and in patients requiring hemodialysis (ratios to normal renal function were 1.35, 1.40 and 1.24, respectively).
The observed incidence of anti-drug antibodies is highly dependent on the sensitivity and specificity of the assay. Differences in assay methods preclude meaningful comparisons of the incidence of anti-drug antibodies in the studies described below with the incidence of anti-drug antibodies in other studies, include those of SOGROYA or other growth hormone analogs.
No anti-somapacitan-beco antibodies were detected in the clinical trials in adult patients with GHD.
Anti-somapacitan-beco binding antibodies were evaluated in samples collected at baseline, week 13, and week 52 of treatment in the 52-week main period of the phase 3 trial in pediatric patients with GHD receiving somapacitan-beco. Of the 132 subjects exposed to somapacitan-beco, 16 (12.1%) showed detectable binding antibodies to somapacitan-beco at any time during the main period of the trial following exposure to SOGROYA. 14 out of 16 subjects showed detectable binding antibodies to somapacitan-beco only at one timepoint. Of the 68 patients exposed to daily somatropin, detectable binding antibodies were detected in 7 (10.3%) children. Of these, 6 children had positive antibody samples only at one timepoint.
There was no identified clinically significant effect of anti-drug antibodies on pharmacokinetics, pharmacodynamics, safety, or effectiveness of SOGROYA over the treatment duration. No neutralizing antibodies to somapacitan-beco were detected.
Advise patients and/or caregivers to read the FDA-approved patient labeling (Patient Information and Instructions for Use).
