Detailed description page of ThPDB2

This page displays user query in tabular form.

Th1376 details

Primary information
ID	13007
Therapeutic ID	Th1376
Protein Name	Somatrem
Sequence	NA
Molecular Weight	22255.9518
Chemical Formula	C995H1537N263O301S8
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	The mean terminal half-life after subcutaneous administration is 2.1 +/- 0.43 hours while the mean terminal half-life after intravenous administration is determined to be 19.5 +/- 3.1 minutes [L1896, FDA Label].
Description	Despite the ability of almost all contemporary recombinant growth hormones to cause definite and demonstrable increases in growth rate in patients who are administered the drug, the use of these agents continues to be mired in persistent bioethical debate [A32292]. Such discussion revolves around whether patients' natural disposition of short stature should be considered a medical condition justifying medical treatment with such hormone therapy - especially when these hormone agents have been proven effective at increasing the height of children with or without growth hormone deficiency [A32292].
Indication/Disease	Somatrem is a recombinant human growth hormone indicated for: (a) treatment of paediatric patients with growth failure due to growth hormone deficiency (GHD), (b) treatment of paediatric patients with growth failure due to idiopathic short stature (ISS), (c) treatment of paediatric patients with growth failure due to Turner syndrome (TS), (d) treatment of paediatric patients with growth failure due to chronic kidney disease (CKD) up to the time of renal transplantation, (e) treatment of adults with childhood-onset GHD, or (f) treatment of adults with adult-onset GHD [FDA Label].
Pharmacodynamics	In vitro and in vivo preclinical and clinical testing have demonstrated that somatrem is therapeutically equivalent to pituitary derived human growth hormone (hGH) [L1896, FDA Label]. Paediatric patients who lack adequate endogenous growth hormone secretion, patients with chronic kidney disease, and patients with Turner syndrome that were treated with somatrem resulted in an increase in growth rate and an increase in insulin-like growth factor (IGF-1) levels similar to that seen with patients who possess endogenous pituitary derived hGH [L1896, FDA Label]. With normalized levels of growth hormone and related mediator agents like IGF-1, patients demonstrate normalized skeletal, cell, organ, and overall tissue growth [L1896, FDA Label].
Mechanism of Action	Somatrem - as well as endogenous growth hormone - binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects [L1896, FDA Label]. Some of these pharmacodynamic effects are primarily mediated by insulin like growth factor (IGF-1) produced in the liver and also locally (ie. skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (ie. lipolysis) [L1896, FDA Label]. Skeletal growth is accomplished at the epiphyseal plates at the ends of growing bone [FDA Label]. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and its mediator IGF-I [FDA Label]. Serum levels of IGF-I are low in children and adolescents who are growth hormone deficient, but increase during somatrem treatment [FDA Label]. New bone is consequently formed at the epiphyses for paediatric patients in response to GH and IGF-I from somatrem treatment [FDA Label]. This results in linear growth until these growth plates fuse at the end of puberty [FDA Label]. Somatrem treatment also causes an increase in both the number and the size of skeletal muscle cells [FDA Label]. Additionally, such therapy also influences the size of internal organs, including kidneys, and increases red cell mass [FDA Label]. Linear skeletal bone growth is facilitated in part by GH-stimulated protein synthesis [FDA Label]. This is demonstrated by nitrogen retention as reflected by a decline in urinary nitrogen excretion and blood urea nitrogen (BUN) during somatrem therapy [FDA Label]. GH also acts as a modulator of carbohydrate metabolism which may improve a fasting hypoglycaemia feeling that some patients with inadequate GH secretion sometimes experience [FDA Label]. Additionally, somatrem administration may decrease insulin sensitivity, resulting in increased serum fasting and postprandial insulin levels - usually more commonly in overweight or obese individuals, adults or children [FDA Label]. Moreover, mean fasting and postprandial glucose and hemoglobin A1C levels remained in the normal range [FDA Label]. Furthermore, in growth hormone deficient patients, the use of somatrem resulted in lipid mobilization, reduction in body fat stores, increased plasma fatty acids, and decreased plasma cholesterol levels [FDA Label]. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, chronic kidney disease, or Turner syndrome during somatrem therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney [FDA Label]. Serum calcium is not significantly altered in somatrem patients [FDA Label]. Sodium retention and increases in serum alkaline phosphatase can occur to patients taking somatrem [FDA Label]. As well, GH can stimulate the synthesis of chondroitin sulphate and collagen as well as the urinary excretion of hydroxyproline [FDA Label].
Toxicity	Short-term overdosage with somatrem may initially result in hypoglycaemia and then subsequently to hyperglycemia [L1896, FDA Label]. Moreover, this kind of short-term overdosage with somatrem is also likely to cause fluid retention [L1896, FDA Label]. Long-term overdose with somatrem could leads to signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess growth hormone [L1896, FDA Label]. Some animal based oral LD50 values have been reported as: mouse = 300mg/kg, rabbit = 3200 mg/kg, rat = 980 mg/kg.
Metabolism	Both the liver and kidney have been shown to be important metabolizing organs for growth hormone [L1896, FDA Label]. Animal studies suggest that the kidney is the dominant organ of clearance. Growth hormone is filtered at the glomerulus and reabsorbed in the proximal tubules [L1896, FDA Label]. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation [L1896, FDA Label].
Absorption	The absolute bioavailability of somatrem after subcutaneous administration in healthy adult males has been determined to be 81 +/- 20%. Additionally, as the subcutaneous terminal half-life is significantly longer than the intravenous terminal half-life, it appears as if the subcutaneous absorption of somatrem is slow and rate-limiting [L1896, FDA Label].
	Animal studies with somatrem showed that growth hormone localizes to highly perfused organs, particularly the liver and kidney [L1896, FDA Label]. The volume of distribution at steady state for somatrem in health adult males is approximately 50 mL/kg body weight, approximating the serum volume [L1896, FDA Label].
Clearance	The clearance of somatrem after intravenous administration in healthy adults and children is reported to be in the range of 116-174 mL/hr/kg [L1896, FDA Label].
Categories	Amino Acids, Peptides, and Proteins
Patents Number	NA
Date of Issue	NA
Date of Expiry	NA
Drug Interaction	NA
Target	Growth hormone receptor,Insulin-like growth factor 1 receptor
Brand Name	Protropin - Kit Im Sc 10mg/vial
Company	Hoffmann La Roche
Brand Description	Hoffmann La Roche
Prescribed For	Intramuscular; Subcutaneous
Chemical Name	NA
Formulation	NA
Physical Appearance	NA
Route of Administration	NA
Recommended Dosage	NA
Contraindication	NA
Side Effects	NA
Useful Link 1	Link
Useful Link 2	NA
Remarks	NA

Primary information
ID	13008
Therapeutic ID	Th1376
Protein Name	Somatrem
Sequence	NA
Molecular Weight	22255.9518
Chemical Formula	C995H1537N263O301S8
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	The mean terminal half-life after subcutaneous administration is 2.1 +/- 0.43 hours while the mean terminal half-life after intravenous administration is determined to be 19.5 +/- 3.1 minutes [L1896, FDA Label].
Description	Despite the ability of almost all contemporary recombinant growth hormones to cause definite and demonstrable increases in growth rate in patients who are administered the drug, the use of these agents continues to be mired in persistent bioethical debate [A32292]. Such discussion revolves around whether patients' natural disposition of short stature should be considered a medical condition justifying medical treatment with such hormone therapy - especially when these hormone agents have been proven effective at increasing the height of children with or without growth hormone deficiency [A32292].
Indication/Disease	Somatrem is a recombinant human growth hormone indicated for: (a) treatment of paediatric patients with growth failure due to growth hormone deficiency (GHD), (b) treatment of paediatric patients with growth failure due to idiopathic short stature (ISS), (c) treatment of paediatric patients with growth failure due to Turner syndrome (TS), (d) treatment of paediatric patients with growth failure due to chronic kidney disease (CKD) up to the time of renal transplantation, (e) treatment of adults with childhood-onset GHD, or (f) treatment of adults with adult-onset GHD [FDA Label].
Pharmacodynamics	In vitro and in vivo preclinical and clinical testing have demonstrated that somatrem is therapeutically equivalent to pituitary derived human growth hormone (hGH) [L1896, FDA Label]. Paediatric patients who lack adequate endogenous growth hormone secretion, patients with chronic kidney disease, and patients with Turner syndrome that were treated with somatrem resulted in an increase in growth rate and an increase in insulin-like growth factor (IGF-1) levels similar to that seen with patients who possess endogenous pituitary derived hGH [L1896, FDA Label]. With normalized levels of growth hormone and related mediator agents like IGF-1, patients demonstrate normalized skeletal, cell, organ, and overall tissue growth [L1896, FDA Label].
Mechanism of Action	Somatrem - as well as endogenous growth hormone - binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects [L1896, FDA Label]. Some of these pharmacodynamic effects are primarily mediated by insulin like growth factor (IGF-1) produced in the liver and also locally (ie. skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (ie. lipolysis) [L1896, FDA Label]. Skeletal growth is accomplished at the epiphyseal plates at the ends of growing bone [FDA Label]. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and its mediator IGF-I [FDA Label]. Serum levels of IGF-I are low in children and adolescents who are growth hormone deficient, but increase during somatrem treatment [FDA Label]. New bone is consequently formed at the epiphyses for paediatric patients in response to GH and IGF-I from somatrem treatment [FDA Label]. This results in linear growth until these growth plates fuse at the end of puberty [FDA Label]. Somatrem treatment also causes an increase in both the number and the size of skeletal muscle cells [FDA Label]. Additionally, such therapy also influences the size of internal organs, including kidneys, and increases red cell mass [FDA Label]. Linear skeletal bone growth is facilitated in part by GH-stimulated protein synthesis [FDA Label]. This is demonstrated by nitrogen retention as reflected by a decline in urinary nitrogen excretion and blood urea nitrogen (BUN) during somatrem therapy [FDA Label]. GH also acts as a modulator of carbohydrate metabolism which may improve a fasting hypoglycaemia feeling that some patients with inadequate GH secretion sometimes experience [FDA Label]. Additionally, somatrem administration may decrease insulin sensitivity, resulting in increased serum fasting and postprandial insulin levels - usually more commonly in overweight or obese individuals, adults or children [FDA Label]. Moreover, mean fasting and postprandial glucose and hemoglobin A1C levels remained in the normal range [FDA Label]. Furthermore, in growth hormone deficient patients, the use of somatrem resulted in lipid mobilization, reduction in body fat stores, increased plasma fatty acids, and decreased plasma cholesterol levels [FDA Label]. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, chronic kidney disease, or Turner syndrome during somatrem therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney [FDA Label]. Serum calcium is not significantly altered in somatrem patients [FDA Label]. Sodium retention and increases in serum alkaline phosphatase can occur to patients taking somatrem [FDA Label]. As well, GH can stimulate the synthesis of chondroitin sulphate and collagen as well as the urinary excretion of hydroxyproline [FDA Label].
Toxicity	Short-term overdosage with somatrem may initially result in hypoglycaemia and then subsequently to hyperglycemia [L1896, FDA Label]. Moreover, this kind of short-term overdosage with somatrem is also likely to cause fluid retention [L1896, FDA Label]. Long-term overdose with somatrem could leads to signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess growth hormone [L1896, FDA Label]. Some animal based oral LD50 values have been reported as: mouse = 300mg/kg, rabbit = 3200 mg/kg, rat = 980 mg/kg.
Metabolism	Both the liver and kidney have been shown to be important metabolizing organs for growth hormone [L1896, FDA Label]. Animal studies suggest that the kidney is the dominant organ of clearance. Growth hormone is filtered at the glomerulus and reabsorbed in the proximal tubules [L1896, FDA Label]. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation [L1896, FDA Label].
Absorption	The absolute bioavailability of somatrem after subcutaneous administration in healthy adult males has been determined to be 81 +/- 20%. Additionally, as the subcutaneous terminal half-life is significantly longer than the intravenous terminal half-life, it appears as if the subcutaneous absorption of somatrem is slow and rate-limiting [L1896, FDA Label].
	Animal studies with somatrem showed that growth hormone localizes to highly perfused organs, particularly the liver and kidney [L1896, FDA Label]. The volume of distribution at steady state for somatrem in health adult males is approximately 50 mL/kg body weight, approximating the serum volume [L1896, FDA Label].
Clearance	The clearance of somatrem after intravenous administration in healthy adults and children is reported to be in the range of 116-174 mL/hr/kg [L1896, FDA Label].
Categories	Anterior Pituitary Lobe Hormones and Analogues
Patents Number	NA
Date of Issue	NA
Date of Expiry	NA
Drug Interaction	NA
Target	Growth hormone receptor,Insulin-like growth factor 1 receptor
Brand Name	Protropin - Kit Im Sc 5mg/vial
Company	Hoffmann La Roche
Brand Description	Hoffmann La Roche
Prescribed For	Intramuscular; Subcutaneous
Chemical Name	NA
Formulation	NA
Physical Appearance	NA
Route of Administration	NA
Recommended Dosage	NA
Contraindication	NA
Side Effects	NA
Useful Link 1	Link
Useful Link 2	NA
Remarks	NA

Primary information
ID	13009
Therapeutic ID	Th1376
Protein Name	Somatrem
Sequence	NA
Molecular Weight	22255.9518
Chemical Formula	C995H1537N263O301S8
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	The mean terminal half-life after subcutaneous administration is 2.1 +/- 0.43 hours while the mean terminal half-life after intravenous administration is determined to be 19.5 +/- 3.1 minutes [L1896, FDA Label].
Description	Despite the ability of almost all contemporary recombinant growth hormones to cause definite and demonstrable increases in growth rate in patients who are administered the drug, the use of these agents continues to be mired in persistent bioethical debate [A32292]. Such discussion revolves around whether patients' natural disposition of short stature should be considered a medical condition justifying medical treatment with such hormone therapy - especially when these hormone agents have been proven effective at increasing the height of children with or without growth hormone deficiency [A32292].
Indication/Disease	Somatrem is a recombinant human growth hormone indicated for: (a) treatment of paediatric patients with growth failure due to growth hormone deficiency (GHD), (b) treatment of paediatric patients with growth failure due to idiopathic short stature (ISS), (c) treatment of paediatric patients with growth failure due to Turner syndrome (TS), (d) treatment of paediatric patients with growth failure due to chronic kidney disease (CKD) up to the time of renal transplantation, (e) treatment of adults with childhood-onset GHD, or (f) treatment of adults with adult-onset GHD [FDA Label].
Pharmacodynamics	In vitro and in vivo preclinical and clinical testing have demonstrated that somatrem is therapeutically equivalent to pituitary derived human growth hormone (hGH) [L1896, FDA Label]. Paediatric patients who lack adequate endogenous growth hormone secretion, patients with chronic kidney disease, and patients with Turner syndrome that were treated with somatrem resulted in an increase in growth rate and an increase in insulin-like growth factor (IGF-1) levels similar to that seen with patients who possess endogenous pituitary derived hGH [L1896, FDA Label]. With normalized levels of growth hormone and related mediator agents like IGF-1, patients demonstrate normalized skeletal, cell, organ, and overall tissue growth [L1896, FDA Label].
Mechanism of Action	Somatrem - as well as endogenous growth hormone - binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects [L1896, FDA Label]. Some of these pharmacodynamic effects are primarily mediated by insulin like growth factor (IGF-1) produced in the liver and also locally (ie. skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (ie. lipolysis) [L1896, FDA Label]. Skeletal growth is accomplished at the epiphyseal plates at the ends of growing bone [FDA Label]. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and its mediator IGF-I [FDA Label]. Serum levels of IGF-I are low in children and adolescents who are growth hormone deficient, but increase during somatrem treatment [FDA Label]. New bone is consequently formed at the epiphyses for paediatric patients in response to GH and IGF-I from somatrem treatment [FDA Label]. This results in linear growth until these growth plates fuse at the end of puberty [FDA Label]. Somatrem treatment also causes an increase in both the number and the size of skeletal muscle cells [FDA Label]. Additionally, such therapy also influences the size of internal organs, including kidneys, and increases red cell mass [FDA Label]. Linear skeletal bone growth is facilitated in part by GH-stimulated protein synthesis [FDA Label]. This is demonstrated by nitrogen retention as reflected by a decline in urinary nitrogen excretion and blood urea nitrogen (BUN) during somatrem therapy [FDA Label]. GH also acts as a modulator of carbohydrate metabolism which may improve a fasting hypoglycaemia feeling that some patients with inadequate GH secretion sometimes experience [FDA Label]. Additionally, somatrem administration may decrease insulin sensitivity, resulting in increased serum fasting and postprandial insulin levels - usually more commonly in overweight or obese individuals, adults or children [FDA Label]. Moreover, mean fasting and postprandial glucose and hemoglobin A1C levels remained in the normal range [FDA Label]. Furthermore, in growth hormone deficient patients, the use of somatrem resulted in lipid mobilization, reduction in body fat stores, increased plasma fatty acids, and decreased plasma cholesterol levels [FDA Label]. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, chronic kidney disease, or Turner syndrome during somatrem therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney [FDA Label]. Serum calcium is not significantly altered in somatrem patients [FDA Label]. Sodium retention and increases in serum alkaline phosphatase can occur to patients taking somatrem [FDA Label]. As well, GH can stimulate the synthesis of chondroitin sulphate and collagen as well as the urinary excretion of hydroxyproline [FDA Label].
Toxicity	Short-term overdosage with somatrem may initially result in hypoglycaemia and then subsequently to hyperglycemia [L1896, FDA Label]. Moreover, this kind of short-term overdosage with somatrem is also likely to cause fluid retention [L1896, FDA Label]. Long-term overdose with somatrem could leads to signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess growth hormone [L1896, FDA Label]. Some animal based oral LD50 values have been reported as: mouse = 300mg/kg, rabbit = 3200 mg/kg, rat = 980 mg/kg.
Metabolism	Both the liver and kidney have been shown to be important metabolizing organs for growth hormone [L1896, FDA Label]. Animal studies suggest that the kidney is the dominant organ of clearance. Growth hormone is filtered at the glomerulus and reabsorbed in the proximal tubules [L1896, FDA Label]. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation [L1896, FDA Label].
Absorption	The absolute bioavailability of somatrem after subcutaneous administration in healthy adult males has been determined to be 81 +/- 20%. Additionally, as the subcutaneous terminal half-life is significantly longer than the intravenous terminal half-life, it appears as if the subcutaneous absorption of somatrem is slow and rate-limiting [L1896, FDA Label].
	Animal studies with somatrem showed that growth hormone localizes to highly perfused organs, particularly the liver and kidney [L1896, FDA Label]. The volume of distribution at steady state for somatrem in health adult males is approximately 50 mL/kg body weight, approximating the serum volume [L1896, FDA Label].
Clearance	The clearance of somatrem after intravenous administration in healthy adults and children is reported to be in the range of 116-174 mL/hr/kg [L1896, FDA Label].
Categories	Growth Hormone
Patents Number	NA
Date of Issue	NA
Date of Expiry	NA
Drug Interaction	NA
Target	Growth hormone receptor,Insulin-like growth factor 1 receptor
Brand Name	Protropin Inj Pws 10mg/vial
Company	Genentech, Inc.
Brand Description	Genentech, Inc.
Prescribed For	Intramuscular
Chemical Name	NA
Formulation	NA
Physical Appearance	NA
Route of Administration	NA
Recommended Dosage	NA
Contraindication	NA
Side Effects	NA
Useful Link 1	Link
Useful Link 2	NA
Remarks	NA

Primary information
ID	13010
Therapeutic ID	Th1376
Protein Name	Somatrem
Sequence	NA
Molecular Weight	22255.9518
Chemical Formula	C995H1537N263O301S8
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	The mean terminal half-life after subcutaneous administration is 2.1 +/- 0.43 hours while the mean terminal half-life after intravenous administration is determined to be 19.5 +/- 3.1 minutes [L1896, FDA Label].
Description	Despite the ability of almost all contemporary recombinant growth hormones to cause definite and demonstrable increases in growth rate in patients who are administered the drug, the use of these agents continues to be mired in persistent bioethical debate [A32292]. Such discussion revolves around whether patients' natural disposition of short stature should be considered a medical condition justifying medical treatment with such hormone therapy - especially when these hormone agents have been proven effective at increasing the height of children with or without growth hormone deficiency [A32292].
Indication/Disease	Somatrem is a recombinant human growth hormone indicated for: (a) treatment of paediatric patients with growth failure due to growth hormone deficiency (GHD), (b) treatment of paediatric patients with growth failure due to idiopathic short stature (ISS), (c) treatment of paediatric patients with growth failure due to Turner syndrome (TS), (d) treatment of paediatric patients with growth failure due to chronic kidney disease (CKD) up to the time of renal transplantation, (e) treatment of adults with childhood-onset GHD, or (f) treatment of adults with adult-onset GHD [FDA Label].
Pharmacodynamics	In vitro and in vivo preclinical and clinical testing have demonstrated that somatrem is therapeutically equivalent to pituitary derived human growth hormone (hGH) [L1896, FDA Label]. Paediatric patients who lack adequate endogenous growth hormone secretion, patients with chronic kidney disease, and patients with Turner syndrome that were treated with somatrem resulted in an increase in growth rate and an increase in insulin-like growth factor (IGF-1) levels similar to that seen with patients who possess endogenous pituitary derived hGH [L1896, FDA Label]. With normalized levels of growth hormone and related mediator agents like IGF-1, patients demonstrate normalized skeletal, cell, organ, and overall tissue growth [L1896, FDA Label].
Mechanism of Action	Somatrem - as well as endogenous growth hormone - binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects [L1896, FDA Label]. Some of these pharmacodynamic effects are primarily mediated by insulin like growth factor (IGF-1) produced in the liver and also locally (ie. skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (ie. lipolysis) [L1896, FDA Label]. Skeletal growth is accomplished at the epiphyseal plates at the ends of growing bone [FDA Label]. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and its mediator IGF-I [FDA Label]. Serum levels of IGF-I are low in children and adolescents who are growth hormone deficient, but increase during somatrem treatment [FDA Label]. New bone is consequently formed at the epiphyses for paediatric patients in response to GH and IGF-I from somatrem treatment [FDA Label]. This results in linear growth until these growth plates fuse at the end of puberty [FDA Label]. Somatrem treatment also causes an increase in both the number and the size of skeletal muscle cells [FDA Label]. Additionally, such therapy also influences the size of internal organs, including kidneys, and increases red cell mass [FDA Label]. Linear skeletal bone growth is facilitated in part by GH-stimulated protein synthesis [FDA Label]. This is demonstrated by nitrogen retention as reflected by a decline in urinary nitrogen excretion and blood urea nitrogen (BUN) during somatrem therapy [FDA Label]. GH also acts as a modulator of carbohydrate metabolism which may improve a fasting hypoglycaemia feeling that some patients with inadequate GH secretion sometimes experience [FDA Label]. Additionally, somatrem administration may decrease insulin sensitivity, resulting in increased serum fasting and postprandial insulin levels - usually more commonly in overweight or obese individuals, adults or children [FDA Label]. Moreover, mean fasting and postprandial glucose and hemoglobin A1C levels remained in the normal range [FDA Label]. Furthermore, in growth hormone deficient patients, the use of somatrem resulted in lipid mobilization, reduction in body fat stores, increased plasma fatty acids, and decreased plasma cholesterol levels [FDA Label]. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, chronic kidney disease, or Turner syndrome during somatrem therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney [FDA Label]. Serum calcium is not significantly altered in somatrem patients [FDA Label]. Sodium retention and increases in serum alkaline phosphatase can occur to patients taking somatrem [FDA Label]. As well, GH can stimulate the synthesis of chondroitin sulphate and collagen as well as the urinary excretion of hydroxyproline [FDA Label].
Toxicity	Short-term overdosage with somatrem may initially result in hypoglycaemia and then subsequently to hyperglycemia [L1896, FDA Label]. Moreover, this kind of short-term overdosage with somatrem is also likely to cause fluid retention [L1896, FDA Label]. Long-term overdose with somatrem could leads to signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess growth hormone [L1896, FDA Label]. Some animal based oral LD50 values have been reported as: mouse = 300mg/kg, rabbit = 3200 mg/kg, rat = 980 mg/kg.
Metabolism	Both the liver and kidney have been shown to be important metabolizing organs for growth hormone [L1896, FDA Label]. Animal studies suggest that the kidney is the dominant organ of clearance. Growth hormone is filtered at the glomerulus and reabsorbed in the proximal tubules [L1896, FDA Label]. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation [L1896, FDA Label].
Absorption	The absolute bioavailability of somatrem after subcutaneous administration in healthy adult males has been determined to be 81 +/- 20%. Additionally, as the subcutaneous terminal half-life is significantly longer than the intravenous terminal half-life, it appears as if the subcutaneous absorption of somatrem is slow and rate-limiting [L1896, FDA Label].
	Animal studies with somatrem showed that growth hormone localizes to highly perfused organs, particularly the liver and kidney [L1896, FDA Label]. The volume of distribution at steady state for somatrem in health adult males is approximately 50 mL/kg body weight, approximating the serum volume [L1896, FDA Label].
Clearance	The clearance of somatrem after intravenous administration in healthy adults and children is reported to be in the range of 116-174 mL/hr/kg [L1896, FDA Label].
Categories	Hormones
Patents Number	NA
Date of Issue	NA
Date of Expiry	NA
Drug Interaction	NA
Target	Growth hormone receptor,Insulin-like growth factor 1 receptor
Brand Name	NA
Company	NA
Brand Description	NA
Prescribed For	NA
Chemical Name	NA
Formulation	NA
Physical Appearance	NA
Route of Administration	NA
Recommended Dosage	NA
Contraindication	NA
Side Effects	NA
Useful Link 1	Link
Useful Link 2	NA
Remarks	NA

Primary information
ID	13011
Therapeutic ID	Th1376
Protein Name	Somatrem
Sequence	NA
Molecular Weight	22255.9518
Chemical Formula	C995H1537N263O301S8
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	The mean terminal half-life after subcutaneous administration is 2.1 +/- 0.43 hours while the mean terminal half-life after intravenous administration is determined to be 19.5 +/- 3.1 minutes [L1896, FDA Label].
Description	Despite the ability of almost all contemporary recombinant growth hormones to cause definite and demonstrable increases in growth rate in patients who are administered the drug, the use of these agents continues to be mired in persistent bioethical debate [A32292]. Such discussion revolves around whether patients' natural disposition of short stature should be considered a medical condition justifying medical treatment with such hormone therapy - especially when these hormone agents have been proven effective at increasing the height of children with or without growth hormone deficiency [A32292].
Indication/Disease	Somatrem is a recombinant human growth hormone indicated for: (a) treatment of paediatric patients with growth failure due to growth hormone deficiency (GHD), (b) treatment of paediatric patients with growth failure due to idiopathic short stature (ISS), (c) treatment of paediatric patients with growth failure due to Turner syndrome (TS), (d) treatment of paediatric patients with growth failure due to chronic kidney disease (CKD) up to the time of renal transplantation, (e) treatment of adults with childhood-onset GHD, or (f) treatment of adults with adult-onset GHD [FDA Label].
Pharmacodynamics	In vitro and in vivo preclinical and clinical testing have demonstrated that somatrem is therapeutically equivalent to pituitary derived human growth hormone (hGH) [L1896, FDA Label]. Paediatric patients who lack adequate endogenous growth hormone secretion, patients with chronic kidney disease, and patients with Turner syndrome that were treated with somatrem resulted in an increase in growth rate and an increase in insulin-like growth factor (IGF-1) levels similar to that seen with patients who possess endogenous pituitary derived hGH [L1896, FDA Label]. With normalized levels of growth hormone and related mediator agents like IGF-1, patients demonstrate normalized skeletal, cell, organ, and overall tissue growth [L1896, FDA Label].
Mechanism of Action	Somatrem - as well as endogenous growth hormone - binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects [L1896, FDA Label]. Some of these pharmacodynamic effects are primarily mediated by insulin like growth factor (IGF-1) produced in the liver and also locally (ie. skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (ie. lipolysis) [L1896, FDA Label]. Skeletal growth is accomplished at the epiphyseal plates at the ends of growing bone [FDA Label]. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and its mediator IGF-I [FDA Label]. Serum levels of IGF-I are low in children and adolescents who are growth hormone deficient, but increase during somatrem treatment [FDA Label]. New bone is consequently formed at the epiphyses for paediatric patients in response to GH and IGF-I from somatrem treatment [FDA Label]. This results in linear growth until these growth plates fuse at the end of puberty [FDA Label]. Somatrem treatment also causes an increase in both the number and the size of skeletal muscle cells [FDA Label]. Additionally, such therapy also influences the size of internal organs, including kidneys, and increases red cell mass [FDA Label]. Linear skeletal bone growth is facilitated in part by GH-stimulated protein synthesis [FDA Label]. This is demonstrated by nitrogen retention as reflected by a decline in urinary nitrogen excretion and blood urea nitrogen (BUN) during somatrem therapy [FDA Label]. GH also acts as a modulator of carbohydrate metabolism which may improve a fasting hypoglycaemia feeling that some patients with inadequate GH secretion sometimes experience [FDA Label]. Additionally, somatrem administration may decrease insulin sensitivity, resulting in increased serum fasting and postprandial insulin levels - usually more commonly in overweight or obese individuals, adults or children [FDA Label]. Moreover, mean fasting and postprandial glucose and hemoglobin A1C levels remained in the normal range [FDA Label]. Furthermore, in growth hormone deficient patients, the use of somatrem resulted in lipid mobilization, reduction in body fat stores, increased plasma fatty acids, and decreased plasma cholesterol levels [FDA Label]. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, chronic kidney disease, or Turner syndrome during somatrem therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney [FDA Label]. Serum calcium is not significantly altered in somatrem patients [FDA Label]. Sodium retention and increases in serum alkaline phosphatase can occur to patients taking somatrem [FDA Label]. As well, GH can stimulate the synthesis of chondroitin sulphate and collagen as well as the urinary excretion of hydroxyproline [FDA Label].
Toxicity	Short-term overdosage with somatrem may initially result in hypoglycaemia and then subsequently to hyperglycemia [L1896, FDA Label]. Moreover, this kind of short-term overdosage with somatrem is also likely to cause fluid retention [L1896, FDA Label]. Long-term overdose with somatrem could leads to signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess growth hormone [L1896, FDA Label]. Some animal based oral LD50 values have been reported as: mouse = 300mg/kg, rabbit = 3200 mg/kg, rat = 980 mg/kg.
Metabolism	Both the liver and kidney have been shown to be important metabolizing organs for growth hormone [L1896, FDA Label]. Animal studies suggest that the kidney is the dominant organ of clearance. Growth hormone is filtered at the glomerulus and reabsorbed in the proximal tubules [L1896, FDA Label]. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation [L1896, FDA Label].
Absorption	The absolute bioavailability of somatrem after subcutaneous administration in healthy adult males has been determined to be 81 +/- 20%. Additionally, as the subcutaneous terminal half-life is significantly longer than the intravenous terminal half-life, it appears as if the subcutaneous absorption of somatrem is slow and rate-limiting [L1896, FDA Label].
	Animal studies with somatrem showed that growth hormone localizes to highly perfused organs, particularly the liver and kidney [L1896, FDA Label]. The volume of distribution at steady state for somatrem in health adult males is approximately 50 mL/kg body weight, approximating the serum volume [L1896, FDA Label].
Clearance	The clearance of somatrem after intravenous administration in healthy adults and children is reported to be in the range of 116-174 mL/hr/kg [L1896, FDA Label].
Categories	Hormones, Hormone Substitutes, and Hormone Antagonists
Patents Number	NA
Date of Issue	NA
Date of Expiry	NA
Drug Interaction	NA
Target	Growth hormone receptor,Insulin-like growth factor 1 receptor
Brand Name	NA
Company	NA
Brand Description	NA
Prescribed For	NA
Chemical Name	NA
Formulation	NA
Physical Appearance	NA
Route of Administration	NA
Recommended Dosage	NA
Contraindication	NA
Side Effects	NA
Useful Link 1	Link
Useful Link 2	NA
Remarks	NA

Primary information
ID	13012
Therapeutic ID	Th1376
Protein Name	Somatrem
Sequence	NA
Molecular Weight	22255.9518
Chemical Formula	C995H1537N263O301S8
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	The mean terminal half-life after subcutaneous administration is 2.1 +/- 0.43 hours while the mean terminal half-life after intravenous administration is determined to be 19.5 +/- 3.1 minutes [L1896, FDA Label].
Description	Despite the ability of almost all contemporary recombinant growth hormones to cause definite and demonstrable increases in growth rate in patients who are administered the drug, the use of these agents continues to be mired in persistent bioethical debate [A32292]. Such discussion revolves around whether patients' natural disposition of short stature should be considered a medical condition justifying medical treatment with such hormone therapy - especially when these hormone agents have been proven effective at increasing the height of children with or without growth hormone deficiency [A32292].
Indication/Disease	Somatrem is a recombinant human growth hormone indicated for: (a) treatment of paediatric patients with growth failure due to growth hormone deficiency (GHD), (b) treatment of paediatric patients with growth failure due to idiopathic short stature (ISS), (c) treatment of paediatric patients with growth failure due to Turner syndrome (TS), (d) treatment of paediatric patients with growth failure due to chronic kidney disease (CKD) up to the time of renal transplantation, (e) treatment of adults with childhood-onset GHD, or (f) treatment of adults with adult-onset GHD [FDA Label].
Pharmacodynamics	In vitro and in vivo preclinical and clinical testing have demonstrated that somatrem is therapeutically equivalent to pituitary derived human growth hormone (hGH) [L1896, FDA Label]. Paediatric patients who lack adequate endogenous growth hormone secretion, patients with chronic kidney disease, and patients with Turner syndrome that were treated with somatrem resulted in an increase in growth rate and an increase in insulin-like growth factor (IGF-1) levels similar to that seen with patients who possess endogenous pituitary derived hGH [L1896, FDA Label]. With normalized levels of growth hormone and related mediator agents like IGF-1, patients demonstrate normalized skeletal, cell, organ, and overall tissue growth [L1896, FDA Label].
Mechanism of Action	Somatrem - as well as endogenous growth hormone - binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects [L1896, FDA Label]. Some of these pharmacodynamic effects are primarily mediated by insulin like growth factor (IGF-1) produced in the liver and also locally (ie. skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (ie. lipolysis) [L1896, FDA Label]. Skeletal growth is accomplished at the epiphyseal plates at the ends of growing bone [FDA Label]. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and its mediator IGF-I [FDA Label]. Serum levels of IGF-I are low in children and adolescents who are growth hormone deficient, but increase during somatrem treatment [FDA Label]. New bone is consequently formed at the epiphyses for paediatric patients in response to GH and IGF-I from somatrem treatment [FDA Label]. This results in linear growth until these growth plates fuse at the end of puberty [FDA Label]. Somatrem treatment also causes an increase in both the number and the size of skeletal muscle cells [FDA Label]. Additionally, such therapy also influences the size of internal organs, including kidneys, and increases red cell mass [FDA Label]. Linear skeletal bone growth is facilitated in part by GH-stimulated protein synthesis [FDA Label]. This is demonstrated by nitrogen retention as reflected by a decline in urinary nitrogen excretion and blood urea nitrogen (BUN) during somatrem therapy [FDA Label]. GH also acts as a modulator of carbohydrate metabolism which may improve a fasting hypoglycaemia feeling that some patients with inadequate GH secretion sometimes experience [FDA Label]. Additionally, somatrem administration may decrease insulin sensitivity, resulting in increased serum fasting and postprandial insulin levels - usually more commonly in overweight or obese individuals, adults or children [FDA Label]. Moreover, mean fasting and postprandial glucose and hemoglobin A1C levels remained in the normal range [FDA Label]. Furthermore, in growth hormone deficient patients, the use of somatrem resulted in lipid mobilization, reduction in body fat stores, increased plasma fatty acids, and decreased plasma cholesterol levels [FDA Label]. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, chronic kidney disease, or Turner syndrome during somatrem therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney [FDA Label]. Serum calcium is not significantly altered in somatrem patients [FDA Label]. Sodium retention and increases in serum alkaline phosphatase can occur to patients taking somatrem [FDA Label]. As well, GH can stimulate the synthesis of chondroitin sulphate and collagen as well as the urinary excretion of hydroxyproline [FDA Label].
Toxicity	Short-term overdosage with somatrem may initially result in hypoglycaemia and then subsequently to hyperglycemia [L1896, FDA Label]. Moreover, this kind of short-term overdosage with somatrem is also likely to cause fluid retention [L1896, FDA Label]. Long-term overdose with somatrem could leads to signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess growth hormone [L1896, FDA Label]. Some animal based oral LD50 values have been reported as: mouse = 300mg/kg, rabbit = 3200 mg/kg, rat = 980 mg/kg.
Metabolism	Both the liver and kidney have been shown to be important metabolizing organs for growth hormone [L1896, FDA Label]. Animal studies suggest that the kidney is the dominant organ of clearance. Growth hormone is filtered at the glomerulus and reabsorbed in the proximal tubules [L1896, FDA Label]. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation [L1896, FDA Label].
Absorption	The absolute bioavailability of somatrem after subcutaneous administration in healthy adult males has been determined to be 81 +/- 20%. Additionally, as the subcutaneous terminal half-life is significantly longer than the intravenous terminal half-life, it appears as if the subcutaneous absorption of somatrem is slow and rate-limiting [L1896, FDA Label].
	Animal studies with somatrem showed that growth hormone localizes to highly perfused organs, particularly the liver and kidney [L1896, FDA Label]. The volume of distribution at steady state for somatrem in health adult males is approximately 50 mL/kg body weight, approximating the serum volume [L1896, FDA Label].
Clearance	The clearance of somatrem after intravenous administration in healthy adults and children is reported to be in the range of 116-174 mL/hr/kg [L1896, FDA Label].
Categories	Peptide Hormones
Patents Number	NA
Date of Issue	NA
Date of Expiry	NA
Drug Interaction	NA
Target	Growth hormone receptor,Insulin-like growth factor 1 receptor
Brand Name	NA
Company	NA
Brand Description	NA
Prescribed For	NA
Chemical Name	NA
Formulation	NA
Physical Appearance	NA
Route of Administration	NA
Recommended Dosage	NA
Contraindication	NA
Side Effects	NA
Useful Link 1	Link
Useful Link 2	NA
Remarks	NA

Primary information
ID	13013
Therapeutic ID	Th1376
Protein Name	Somatrem
Sequence	NA
Molecular Weight	22255.9518
Chemical Formula	C995H1537N263O301S8
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	The mean terminal half-life after subcutaneous administration is 2.1 +/- 0.43 hours while the mean terminal half-life after intravenous administration is determined to be 19.5 +/- 3.1 minutes [L1896, FDA Label].
Description	Despite the ability of almost all contemporary recombinant growth hormones to cause definite and demonstrable increases in growth rate in patients who are administered the drug, the use of these agents continues to be mired in persistent bioethical debate [A32292]. Such discussion revolves around whether patients' natural disposition of short stature should be considered a medical condition justifying medical treatment with such hormone therapy - especially when these hormone agents have been proven effective at increasing the height of children with or without growth hormone deficiency [A32292].
Indication/Disease	Somatrem is a recombinant human growth hormone indicated for: (a) treatment of paediatric patients with growth failure due to growth hormone deficiency (GHD), (b) treatment of paediatric patients with growth failure due to idiopathic short stature (ISS), (c) treatment of paediatric patients with growth failure due to Turner syndrome (TS), (d) treatment of paediatric patients with growth failure due to chronic kidney disease (CKD) up to the time of renal transplantation, (e) treatment of adults with childhood-onset GHD, or (f) treatment of adults with adult-onset GHD [FDA Label].
Pharmacodynamics	In vitro and in vivo preclinical and clinical testing have demonstrated that somatrem is therapeutically equivalent to pituitary derived human growth hormone (hGH) [L1896, FDA Label]. Paediatric patients who lack adequate endogenous growth hormone secretion, patients with chronic kidney disease, and patients with Turner syndrome that were treated with somatrem resulted in an increase in growth rate and an increase in insulin-like growth factor (IGF-1) levels similar to that seen with patients who possess endogenous pituitary derived hGH [L1896, FDA Label]. With normalized levels of growth hormone and related mediator agents like IGF-1, patients demonstrate normalized skeletal, cell, organ, and overall tissue growth [L1896, FDA Label].
Mechanism of Action	Somatrem - as well as endogenous growth hormone - binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects [L1896, FDA Label]. Some of these pharmacodynamic effects are primarily mediated by insulin like growth factor (IGF-1) produced in the liver and also locally (ie. skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (ie. lipolysis) [L1896, FDA Label]. Skeletal growth is accomplished at the epiphyseal plates at the ends of growing bone [FDA Label]. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and its mediator IGF-I [FDA Label]. Serum levels of IGF-I are low in children and adolescents who are growth hormone deficient, but increase during somatrem treatment [FDA Label]. New bone is consequently formed at the epiphyses for paediatric patients in response to GH and IGF-I from somatrem treatment [FDA Label]. This results in linear growth until these growth plates fuse at the end of puberty [FDA Label]. Somatrem treatment also causes an increase in both the number and the size of skeletal muscle cells [FDA Label]. Additionally, such therapy also influences the size of internal organs, including kidneys, and increases red cell mass [FDA Label]. Linear skeletal bone growth is facilitated in part by GH-stimulated protein synthesis [FDA Label]. This is demonstrated by nitrogen retention as reflected by a decline in urinary nitrogen excretion and blood urea nitrogen (BUN) during somatrem therapy [FDA Label]. GH also acts as a modulator of carbohydrate metabolism which may improve a fasting hypoglycaemia feeling that some patients with inadequate GH secretion sometimes experience [FDA Label]. Additionally, somatrem administration may decrease insulin sensitivity, resulting in increased serum fasting and postprandial insulin levels - usually more commonly in overweight or obese individuals, adults or children [FDA Label]. Moreover, mean fasting and postprandial glucose and hemoglobin A1C levels remained in the normal range [FDA Label]. Furthermore, in growth hormone deficient patients, the use of somatrem resulted in lipid mobilization, reduction in body fat stores, increased plasma fatty acids, and decreased plasma cholesterol levels [FDA Label]. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, chronic kidney disease, or Turner syndrome during somatrem therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney [FDA Label]. Serum calcium is not significantly altered in somatrem patients [FDA Label]. Sodium retention and increases in serum alkaline phosphatase can occur to patients taking somatrem [FDA Label]. As well, GH can stimulate the synthesis of chondroitin sulphate and collagen as well as the urinary excretion of hydroxyproline [FDA Label].
Toxicity	Short-term overdosage with somatrem may initially result in hypoglycaemia and then subsequently to hyperglycemia [L1896, FDA Label]. Moreover, this kind of short-term overdosage with somatrem is also likely to cause fluid retention [L1896, FDA Label]. Long-term overdose with somatrem could leads to signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess growth hormone [L1896, FDA Label]. Some animal based oral LD50 values have been reported as: mouse = 300mg/kg, rabbit = 3200 mg/kg, rat = 980 mg/kg.
Metabolism	Both the liver and kidney have been shown to be important metabolizing organs for growth hormone [L1896, FDA Label]. Animal studies suggest that the kidney is the dominant organ of clearance. Growth hormone is filtered at the glomerulus and reabsorbed in the proximal tubules [L1896, FDA Label]. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation [L1896, FDA Label].
Absorption	The absolute bioavailability of somatrem after subcutaneous administration in healthy adult males has been determined to be 81 +/- 20%. Additionally, as the subcutaneous terminal half-life is significantly longer than the intravenous terminal half-life, it appears as if the subcutaneous absorption of somatrem is slow and rate-limiting [L1896, FDA Label].
	Animal studies with somatrem showed that growth hormone localizes to highly perfused organs, particularly the liver and kidney [L1896, FDA Label]. The volume of distribution at steady state for somatrem in health adult males is approximately 50 mL/kg body weight, approximating the serum volume [L1896, FDA Label].
Clearance	The clearance of somatrem after intravenous administration in healthy adults and children is reported to be in the range of 116-174 mL/hr/kg [L1896, FDA Label].
Categories	Peptides
Patents Number	NA
Date of Issue	NA
Date of Expiry	NA
Drug Interaction	NA
Target	Growth hormone receptor,Insulin-like growth factor 1 receptor
Brand Name	NA
Company	NA
Brand Description	NA
Prescribed For	NA
Chemical Name	NA
Formulation	NA
Physical Appearance	NA
Route of Administration	NA
Recommended Dosage	NA
Contraindication	NA
Side Effects	NA
Useful Link 1	Link
Useful Link 2	NA
Remarks	NA

Primary information
ID	13014
Therapeutic ID	Th1376
Protein Name	Somatrem
Sequence	NA
Molecular Weight	22255.9518
Chemical Formula	C995H1537N263O301S8
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	The mean terminal half-life after subcutaneous administration is 2.1 +/- 0.43 hours while the mean terminal half-life after intravenous administration is determined to be 19.5 +/- 3.1 minutes [L1896, FDA Label].
Description	Despite the ability of almost all contemporary recombinant growth hormones to cause definite and demonstrable increases in growth rate in patients who are administered the drug, the use of these agents continues to be mired in persistent bioethical debate [A32292]. Such discussion revolves around whether patients' natural disposition of short stature should be considered a medical condition justifying medical treatment with such hormone therapy - especially when these hormone agents have been proven effective at increasing the height of children with or without growth hormone deficiency [A32292].
Indication/Disease	Somatrem is a recombinant human growth hormone indicated for: (a) treatment of paediatric patients with growth failure due to growth hormone deficiency (GHD), (b) treatment of paediatric patients with growth failure due to idiopathic short stature (ISS), (c) treatment of paediatric patients with growth failure due to Turner syndrome (TS), (d) treatment of paediatric patients with growth failure due to chronic kidney disease (CKD) up to the time of renal transplantation, (e) treatment of adults with childhood-onset GHD, or (f) treatment of adults with adult-onset GHD [FDA Label].
Pharmacodynamics	In vitro and in vivo preclinical and clinical testing have demonstrated that somatrem is therapeutically equivalent to pituitary derived human growth hormone (hGH) [L1896, FDA Label]. Paediatric patients who lack adequate endogenous growth hormone secretion, patients with chronic kidney disease, and patients with Turner syndrome that were treated with somatrem resulted in an increase in growth rate and an increase in insulin-like growth factor (IGF-1) levels similar to that seen with patients who possess endogenous pituitary derived hGH [L1896, FDA Label]. With normalized levels of growth hormone and related mediator agents like IGF-1, patients demonstrate normalized skeletal, cell, organ, and overall tissue growth [L1896, FDA Label].
Mechanism of Action	Somatrem - as well as endogenous growth hormone - binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects [L1896, FDA Label]. Some of these pharmacodynamic effects are primarily mediated by insulin like growth factor (IGF-1) produced in the liver and also locally (ie. skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (ie. lipolysis) [L1896, FDA Label]. Skeletal growth is accomplished at the epiphyseal plates at the ends of growing bone [FDA Label]. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and its mediator IGF-I [FDA Label]. Serum levels of IGF-I are low in children and adolescents who are growth hormone deficient, but increase during somatrem treatment [FDA Label]. New bone is consequently formed at the epiphyses for paediatric patients in response to GH and IGF-I from somatrem treatment [FDA Label]. This results in linear growth until these growth plates fuse at the end of puberty [FDA Label]. Somatrem treatment also causes an increase in both the number and the size of skeletal muscle cells [FDA Label]. Additionally, such therapy also influences the size of internal organs, including kidneys, and increases red cell mass [FDA Label]. Linear skeletal bone growth is facilitated in part by GH-stimulated protein synthesis [FDA Label]. This is demonstrated by nitrogen retention as reflected by a decline in urinary nitrogen excretion and blood urea nitrogen (BUN) during somatrem therapy [FDA Label]. GH also acts as a modulator of carbohydrate metabolism which may improve a fasting hypoglycaemia feeling that some patients with inadequate GH secretion sometimes experience [FDA Label]. Additionally, somatrem administration may decrease insulin sensitivity, resulting in increased serum fasting and postprandial insulin levels - usually more commonly in overweight or obese individuals, adults or children [FDA Label]. Moreover, mean fasting and postprandial glucose and hemoglobin A1C levels remained in the normal range [FDA Label]. Furthermore, in growth hormone deficient patients, the use of somatrem resulted in lipid mobilization, reduction in body fat stores, increased plasma fatty acids, and decreased plasma cholesterol levels [FDA Label]. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, chronic kidney disease, or Turner syndrome during somatrem therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney [FDA Label]. Serum calcium is not significantly altered in somatrem patients [FDA Label]. Sodium retention and increases in serum alkaline phosphatase can occur to patients taking somatrem [FDA Label]. As well, GH can stimulate the synthesis of chondroitin sulphate and collagen as well as the urinary excretion of hydroxyproline [FDA Label].
Toxicity	Short-term overdosage with somatrem may initially result in hypoglycaemia and then subsequently to hyperglycemia [L1896, FDA Label]. Moreover, this kind of short-term overdosage with somatrem is also likely to cause fluid retention [L1896, FDA Label]. Long-term overdose with somatrem could leads to signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess growth hormone [L1896, FDA Label]. Some animal based oral LD50 values have been reported as: mouse = 300mg/kg, rabbit = 3200 mg/kg, rat = 980 mg/kg.
Metabolism	Both the liver and kidney have been shown to be important metabolizing organs for growth hormone [L1896, FDA Label]. Animal studies suggest that the kidney is the dominant organ of clearance. Growth hormone is filtered at the glomerulus and reabsorbed in the proximal tubules [L1896, FDA Label]. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation [L1896, FDA Label].
Absorption	The absolute bioavailability of somatrem after subcutaneous administration in healthy adult males has been determined to be 81 +/- 20%. Additionally, as the subcutaneous terminal half-life is significantly longer than the intravenous terminal half-life, it appears as if the subcutaneous absorption of somatrem is slow and rate-limiting [L1896, FDA Label].
	Animal studies with somatrem showed that growth hormone localizes to highly perfused organs, particularly the liver and kidney [L1896, FDA Label]. The volume of distribution at steady state for somatrem in health adult males is approximately 50 mL/kg body weight, approximating the serum volume [L1896, FDA Label].
Clearance	The clearance of somatrem after intravenous administration in healthy adults and children is reported to be in the range of 116-174 mL/hr/kg [L1896, FDA Label].
Categories	Pituitary and Hypothalamic Hormones and Analogues
Patents Number	NA
Date of Issue	NA
Date of Expiry	NA
Drug Interaction	NA
Target	Growth hormone receptor,Insulin-like growth factor 1 receptor
Brand Name	NA
Company	NA
Brand Description	NA
Prescribed For	NA
Chemical Name	NA
Formulation	NA
Physical Appearance	NA
Route of Administration	NA
Recommended Dosage	NA
Contraindication	NA
Side Effects	NA
Useful Link 1	Link
Useful Link 2	NA
Remarks	NA

Primary information
ID	13015
Therapeutic ID	Th1376
Protein Name	Somatrem
Sequence	NA
Molecular Weight	22255.9518
Chemical Formula	C995H1537N263O301S8
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	The mean terminal half-life after subcutaneous administration is 2.1 +/- 0.43 hours while the mean terminal half-life after intravenous administration is determined to be 19.5 +/- 3.1 minutes [L1896, FDA Label].
Description	Despite the ability of almost all contemporary recombinant growth hormones to cause definite and demonstrable increases in growth rate in patients who are administered the drug, the use of these agents continues to be mired in persistent bioethical debate [A32292]. Such discussion revolves around whether patients' natural disposition of short stature should be considered a medical condition justifying medical treatment with such hormone therapy - especially when these hormone agents have been proven effective at increasing the height of children with or without growth hormone deficiency [A32292].
Indication/Disease	Somatrem is a recombinant human growth hormone indicated for: (a) treatment of paediatric patients with growth failure due to growth hormone deficiency (GHD), (b) treatment of paediatric patients with growth failure due to idiopathic short stature (ISS), (c) treatment of paediatric patients with growth failure due to Turner syndrome (TS), (d) treatment of paediatric patients with growth failure due to chronic kidney disease (CKD) up to the time of renal transplantation, (e) treatment of adults with childhood-onset GHD, or (f) treatment of adults with adult-onset GHD [FDA Label].
Pharmacodynamics	In vitro and in vivo preclinical and clinical testing have demonstrated that somatrem is therapeutically equivalent to pituitary derived human growth hormone (hGH) [L1896, FDA Label]. Paediatric patients who lack adequate endogenous growth hormone secretion, patients with chronic kidney disease, and patients with Turner syndrome that were treated with somatrem resulted in an increase in growth rate and an increase in insulin-like growth factor (IGF-1) levels similar to that seen with patients who possess endogenous pituitary derived hGH [L1896, FDA Label]. With normalized levels of growth hormone and related mediator agents like IGF-1, patients demonstrate normalized skeletal, cell, organ, and overall tissue growth [L1896, FDA Label].
Mechanism of Action	Somatrem - as well as endogenous growth hormone - binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects [L1896, FDA Label]. Some of these pharmacodynamic effects are primarily mediated by insulin like growth factor (IGF-1) produced in the liver and also locally (ie. skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (ie. lipolysis) [L1896, FDA Label]. Skeletal growth is accomplished at the epiphyseal plates at the ends of growing bone [FDA Label]. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and its mediator IGF-I [FDA Label]. Serum levels of IGF-I are low in children and adolescents who are growth hormone deficient, but increase during somatrem treatment [FDA Label]. New bone is consequently formed at the epiphyses for paediatric patients in response to GH and IGF-I from somatrem treatment [FDA Label]. This results in linear growth until these growth plates fuse at the end of puberty [FDA Label]. Somatrem treatment also causes an increase in both the number and the size of skeletal muscle cells [FDA Label]. Additionally, such therapy also influences the size of internal organs, including kidneys, and increases red cell mass [FDA Label]. Linear skeletal bone growth is facilitated in part by GH-stimulated protein synthesis [FDA Label]. This is demonstrated by nitrogen retention as reflected by a decline in urinary nitrogen excretion and blood urea nitrogen (BUN) during somatrem therapy [FDA Label]. GH also acts as a modulator of carbohydrate metabolism which may improve a fasting hypoglycaemia feeling that some patients with inadequate GH secretion sometimes experience [FDA Label]. Additionally, somatrem administration may decrease insulin sensitivity, resulting in increased serum fasting and postprandial insulin levels - usually more commonly in overweight or obese individuals, adults or children [FDA Label]. Moreover, mean fasting and postprandial glucose and hemoglobin A1C levels remained in the normal range [FDA Label]. Furthermore, in growth hormone deficient patients, the use of somatrem resulted in lipid mobilization, reduction in body fat stores, increased plasma fatty acids, and decreased plasma cholesterol levels [FDA Label]. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, chronic kidney disease, or Turner syndrome during somatrem therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney [FDA Label]. Serum calcium is not significantly altered in somatrem patients [FDA Label]. Sodium retention and increases in serum alkaline phosphatase can occur to patients taking somatrem [FDA Label]. As well, GH can stimulate the synthesis of chondroitin sulphate and collagen as well as the urinary excretion of hydroxyproline [FDA Label].
Toxicity	Short-term overdosage with somatrem may initially result in hypoglycaemia and then subsequently to hyperglycemia [L1896, FDA Label]. Moreover, this kind of short-term overdosage with somatrem is also likely to cause fluid retention [L1896, FDA Label]. Long-term overdose with somatrem could leads to signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess growth hormone [L1896, FDA Label]. Some animal based oral LD50 values have been reported as: mouse = 300mg/kg, rabbit = 3200 mg/kg, rat = 980 mg/kg.
Metabolism	Both the liver and kidney have been shown to be important metabolizing organs for growth hormone [L1896, FDA Label]. Animal studies suggest that the kidney is the dominant organ of clearance. Growth hormone is filtered at the glomerulus and reabsorbed in the proximal tubules [L1896, FDA Label]. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation [L1896, FDA Label].
Absorption	The absolute bioavailability of somatrem after subcutaneous administration in healthy adult males has been determined to be 81 +/- 20%. Additionally, as the subcutaneous terminal half-life is significantly longer than the intravenous terminal half-life, it appears as if the subcutaneous absorption of somatrem is slow and rate-limiting [L1896, FDA Label].
	Animal studies with somatrem showed that growth hormone localizes to highly perfused organs, particularly the liver and kidney [L1896, FDA Label]. The volume of distribution at steady state for somatrem in health adult males is approximately 50 mL/kg body weight, approximating the serum volume [L1896, FDA Label].
Clearance	The clearance of somatrem after intravenous administration in healthy adults and children is reported to be in the range of 116-174 mL/hr/kg [L1896, FDA Label].
Categories	Pituitary Hormones
Patents Number	NA
Date of Issue	NA
Date of Expiry	NA
Drug Interaction	NA
Target	Growth hormone receptor,Insulin-like growth factor 1 receptor
Brand Name	NA
Company	NA
Brand Description	NA
Prescribed For	NA
Chemical Name	NA
Formulation	NA
Physical Appearance	NA
Route of Administration	NA
Recommended Dosage	NA
Contraindication	NA
Side Effects	NA
Useful Link 1	Link
Useful Link 2	NA
Remarks	NA

Primary information
ID	13016
Therapeutic ID	Th1376
Protein Name	Somatrem
Sequence	NA
Molecular Weight	22255.9518
Chemical Formula	C995H1537N263O301S8
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	The mean terminal half-life after subcutaneous administration is 2.1 +/- 0.43 hours while the mean terminal half-life after intravenous administration is determined to be 19.5 +/- 3.1 minutes [L1896, FDA Label].
Description	Despite the ability of almost all contemporary recombinant growth hormones to cause definite and demonstrable increases in growth rate in patients who are administered the drug, the use of these agents continues to be mired in persistent bioethical debate [A32292]. Such discussion revolves around whether patients' natural disposition of short stature should be considered a medical condition justifying medical treatment with such hormone therapy - especially when these hormone agents have been proven effective at increasing the height of children with or without growth hormone deficiency [A32292].
Indication/Disease	Somatrem is a recombinant human growth hormone indicated for: (a) treatment of paediatric patients with growth failure due to growth hormone deficiency (GHD), (b) treatment of paediatric patients with growth failure due to idiopathic short stature (ISS), (c) treatment of paediatric patients with growth failure due to Turner syndrome (TS), (d) treatment of paediatric patients with growth failure due to chronic kidney disease (CKD) up to the time of renal transplantation, (e) treatment of adults with childhood-onset GHD, or (f) treatment of adults with adult-onset GHD [FDA Label].
Pharmacodynamics	In vitro and in vivo preclinical and clinical testing have demonstrated that somatrem is therapeutically equivalent to pituitary derived human growth hormone (hGH) [L1896, FDA Label]. Paediatric patients who lack adequate endogenous growth hormone secretion, patients with chronic kidney disease, and patients with Turner syndrome that were treated with somatrem resulted in an increase in growth rate and an increase in insulin-like growth factor (IGF-1) levels similar to that seen with patients who possess endogenous pituitary derived hGH [L1896, FDA Label]. With normalized levels of growth hormone and related mediator agents like IGF-1, patients demonstrate normalized skeletal, cell, organ, and overall tissue growth [L1896, FDA Label].
Mechanism of Action	Somatrem - as well as endogenous growth hormone - binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects [L1896, FDA Label]. Some of these pharmacodynamic effects are primarily mediated by insulin like growth factor (IGF-1) produced in the liver and also locally (ie. skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (ie. lipolysis) [L1896, FDA Label]. Skeletal growth is accomplished at the epiphyseal plates at the ends of growing bone [FDA Label]. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and its mediator IGF-I [FDA Label]. Serum levels of IGF-I are low in children and adolescents who are growth hormone deficient, but increase during somatrem treatment [FDA Label]. New bone is consequently formed at the epiphyses for paediatric patients in response to GH and IGF-I from somatrem treatment [FDA Label]. This results in linear growth until these growth plates fuse at the end of puberty [FDA Label]. Somatrem treatment also causes an increase in both the number and the size of skeletal muscle cells [FDA Label]. Additionally, such therapy also influences the size of internal organs, including kidneys, and increases red cell mass [FDA Label]. Linear skeletal bone growth is facilitated in part by GH-stimulated protein synthesis [FDA Label]. This is demonstrated by nitrogen retention as reflected by a decline in urinary nitrogen excretion and blood urea nitrogen (BUN) during somatrem therapy [FDA Label]. GH also acts as a modulator of carbohydrate metabolism which may improve a fasting hypoglycaemia feeling that some patients with inadequate GH secretion sometimes experience [FDA Label]. Additionally, somatrem administration may decrease insulin sensitivity, resulting in increased serum fasting and postprandial insulin levels - usually more commonly in overweight or obese individuals, adults or children [FDA Label]. Moreover, mean fasting and postprandial glucose and hemoglobin A1C levels remained in the normal range [FDA Label]. Furthermore, in growth hormone deficient patients, the use of somatrem resulted in lipid mobilization, reduction in body fat stores, increased plasma fatty acids, and decreased plasma cholesterol levels [FDA Label]. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, chronic kidney disease, or Turner syndrome during somatrem therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney [FDA Label]. Serum calcium is not significantly altered in somatrem patients [FDA Label]. Sodium retention and increases in serum alkaline phosphatase can occur to patients taking somatrem [FDA Label]. As well, GH can stimulate the synthesis of chondroitin sulphate and collagen as well as the urinary excretion of hydroxyproline [FDA Label].
Toxicity	Short-term overdosage with somatrem may initially result in hypoglycaemia and then subsequently to hyperglycemia [L1896, FDA Label]. Moreover, this kind of short-term overdosage with somatrem is also likely to cause fluid retention [L1896, FDA Label]. Long-term overdose with somatrem could leads to signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess growth hormone [L1896, FDA Label]. Some animal based oral LD50 values have been reported as: mouse = 300mg/kg, rabbit = 3200 mg/kg, rat = 980 mg/kg.
Metabolism	Both the liver and kidney have been shown to be important metabolizing organs for growth hormone [L1896, FDA Label]. Animal studies suggest that the kidney is the dominant organ of clearance. Growth hormone is filtered at the glomerulus and reabsorbed in the proximal tubules [L1896, FDA Label]. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation [L1896, FDA Label].
Absorption	The absolute bioavailability of somatrem after subcutaneous administration in healthy adult males has been determined to be 81 +/- 20%. Additionally, as the subcutaneous terminal half-life is significantly longer than the intravenous terminal half-life, it appears as if the subcutaneous absorption of somatrem is slow and rate-limiting [L1896, FDA Label].
	Animal studies with somatrem showed that growth hormone localizes to highly perfused organs, particularly the liver and kidney [L1896, FDA Label]. The volume of distribution at steady state for somatrem in health adult males is approximately 50 mL/kg body weight, approximating the serum volume [L1896, FDA Label].
Clearance	The clearance of somatrem after intravenous administration in healthy adults and children is reported to be in the range of 116-174 mL/hr/kg [L1896, FDA Label].
Categories	Pituitary Hormones, Anterior
Patents Number	NA
Date of Issue	NA
Date of Expiry	NA
Drug Interaction	NA
Target	Growth hormone receptor,Insulin-like growth factor 1 receptor
Brand Name	NA
Company	NA
Brand Description	NA
Prescribed For	NA
Chemical Name	NA
Formulation	NA
Physical Appearance	NA
Route of Administration	NA
Recommended Dosage	NA
Contraindication	NA
Side Effects	NA
Useful Link 1	Link
Useful Link 2	NA
Remarks	NA

Primary information
ID	13017
Therapeutic ID	Th1376
Protein Name	Somatrem
Sequence	NA
Molecular Weight	22255.9518
Chemical Formula	C995H1537N263O301S8
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	The mean terminal half-life after subcutaneous administration is 2.1 +/- 0.43 hours while the mean terminal half-life after intravenous administration is determined to be 19.5 +/- 3.1 minutes [L1896, FDA Label].
Description	Despite the ability of almost all contemporary recombinant growth hormones to cause definite and demonstrable increases in growth rate in patients who are administered the drug, the use of these agents continues to be mired in persistent bioethical debate [A32292]. Such discussion revolves around whether patients' natural disposition of short stature should be considered a medical condition justifying medical treatment with such hormone therapy - especially when these hormone agents have been proven effective at increasing the height of children with or without growth hormone deficiency [A32292].
Indication/Disease	Somatrem is a recombinant human growth hormone indicated for: (a) treatment of paediatric patients with growth failure due to growth hormone deficiency (GHD), (b) treatment of paediatric patients with growth failure due to idiopathic short stature (ISS), (c) treatment of paediatric patients with growth failure due to Turner syndrome (TS), (d) treatment of paediatric patients with growth failure due to chronic kidney disease (CKD) up to the time of renal transplantation, (e) treatment of adults with childhood-onset GHD, or (f) treatment of adults with adult-onset GHD [FDA Label].
Pharmacodynamics	In vitro and in vivo preclinical and clinical testing have demonstrated that somatrem is therapeutically equivalent to pituitary derived human growth hormone (hGH) [L1896, FDA Label]. Paediatric patients who lack adequate endogenous growth hormone secretion, patients with chronic kidney disease, and patients with Turner syndrome that were treated with somatrem resulted in an increase in growth rate and an increase in insulin-like growth factor (IGF-1) levels similar to that seen with patients who possess endogenous pituitary derived hGH [L1896, FDA Label]. With normalized levels of growth hormone and related mediator agents like IGF-1, patients demonstrate normalized skeletal, cell, organ, and overall tissue growth [L1896, FDA Label].
Mechanism of Action	Somatrem - as well as endogenous growth hormone - binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects [L1896, FDA Label]. Some of these pharmacodynamic effects are primarily mediated by insulin like growth factor (IGF-1) produced in the liver and also locally (ie. skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (ie. lipolysis) [L1896, FDA Label]. Skeletal growth is accomplished at the epiphyseal plates at the ends of growing bone [FDA Label]. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and its mediator IGF-I [FDA Label]. Serum levels of IGF-I are low in children and adolescents who are growth hormone deficient, but increase during somatrem treatment [FDA Label]. New bone is consequently formed at the epiphyses for paediatric patients in response to GH and IGF-I from somatrem treatment [FDA Label]. This results in linear growth until these growth plates fuse at the end of puberty [FDA Label]. Somatrem treatment also causes an increase in both the number and the size of skeletal muscle cells [FDA Label]. Additionally, such therapy also influences the size of internal organs, including kidneys, and increases red cell mass [FDA Label]. Linear skeletal bone growth is facilitated in part by GH-stimulated protein synthesis [FDA Label]. This is demonstrated by nitrogen retention as reflected by a decline in urinary nitrogen excretion and blood urea nitrogen (BUN) during somatrem therapy [FDA Label]. GH also acts as a modulator of carbohydrate metabolism which may improve a fasting hypoglycaemia feeling that some patients with inadequate GH secretion sometimes experience [FDA Label]. Additionally, somatrem administration may decrease insulin sensitivity, resulting in increased serum fasting and postprandial insulin levels - usually more commonly in overweight or obese individuals, adults or children [FDA Label]. Moreover, mean fasting and postprandial glucose and hemoglobin A1C levels remained in the normal range [FDA Label]. Furthermore, in growth hormone deficient patients, the use of somatrem resulted in lipid mobilization, reduction in body fat stores, increased plasma fatty acids, and decreased plasma cholesterol levels [FDA Label]. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, chronic kidney disease, or Turner syndrome during somatrem therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney [FDA Label]. Serum calcium is not significantly altered in somatrem patients [FDA Label]. Sodium retention and increases in serum alkaline phosphatase can occur to patients taking somatrem [FDA Label]. As well, GH can stimulate the synthesis of chondroitin sulphate and collagen as well as the urinary excretion of hydroxyproline [FDA Label].
Toxicity	Short-term overdosage with somatrem may initially result in hypoglycaemia and then subsequently to hyperglycemia [L1896, FDA Label]. Moreover, this kind of short-term overdosage with somatrem is also likely to cause fluid retention [L1896, FDA Label]. Long-term overdose with somatrem could leads to signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess growth hormone [L1896, FDA Label]. Some animal based oral LD50 values have been reported as: mouse = 300mg/kg, rabbit = 3200 mg/kg, rat = 980 mg/kg.
Metabolism	Both the liver and kidney have been shown to be important metabolizing organs for growth hormone [L1896, FDA Label]. Animal studies suggest that the kidney is the dominant organ of clearance. Growth hormone is filtered at the glomerulus and reabsorbed in the proximal tubules [L1896, FDA Label]. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation [L1896, FDA Label].
Absorption	The absolute bioavailability of somatrem after subcutaneous administration in healthy adult males has been determined to be 81 +/- 20%. Additionally, as the subcutaneous terminal half-life is significantly longer than the intravenous terminal half-life, it appears as if the subcutaneous absorption of somatrem is slow and rate-limiting [L1896, FDA Label].
	Animal studies with somatrem showed that growth hormone localizes to highly perfused organs, particularly the liver and kidney [L1896, FDA Label]. The volume of distribution at steady state for somatrem in health adult males is approximately 50 mL/kg body weight, approximating the serum volume [L1896, FDA Label].
Clearance	The clearance of somatrem after intravenous administration in healthy adults and children is reported to be in the range of 116-174 mL/hr/kg [L1896, FDA Label].
Categories	Somatropin and Somatropin Agonists
Patents Number	NA
Date of Issue	NA
Date of Expiry	NA
Drug Interaction	NA
Target	Growth hormone receptor,Insulin-like growth factor 1 receptor
Brand Name	NA
Company	NA
Brand Description	NA
Prescribed For	NA
Chemical Name	NA
Formulation	NA
Physical Appearance	NA
Route of Administration	NA
Recommended Dosage	NA
Contraindication	NA
Side Effects	NA
Useful Link 1	Link
Useful Link 2	NA
Remarks	NA

Primary information
ID	13018
Therapeutic ID	Th1376
Protein Name	Somatrem
Sequence	NA
Molecular Weight	22255.9518
Chemical Formula	C995H1537N263O301S8
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	The mean terminal half-life after subcutaneous administration is 2.1 +/- 0.43 hours while the mean terminal half-life after intravenous administration is determined to be 19.5 +/- 3.1 minutes [L1896, FDA Label].
Description	Despite the ability of almost all contemporary recombinant growth hormones to cause definite and demonstrable increases in growth rate in patients who are administered the drug, the use of these agents continues to be mired in persistent bioethical debate [A32292]. Such discussion revolves around whether patients' natural disposition of short stature should be considered a medical condition justifying medical treatment with such hormone therapy - especially when these hormone agents have been proven effective at increasing the height of children with or without growth hormone deficiency [A32292].
Indication/Disease	Somatrem is a recombinant human growth hormone indicated for: (a) treatment of paediatric patients with growth failure due to growth hormone deficiency (GHD), (b) treatment of paediatric patients with growth failure due to idiopathic short stature (ISS), (c) treatment of paediatric patients with growth failure due to Turner syndrome (TS), (d) treatment of paediatric patients with growth failure due to chronic kidney disease (CKD) up to the time of renal transplantation, (e) treatment of adults with childhood-onset GHD, or (f) treatment of adults with adult-onset GHD [FDA Label].
Pharmacodynamics	In vitro and in vivo preclinical and clinical testing have demonstrated that somatrem is therapeutically equivalent to pituitary derived human growth hormone (hGH) [L1896, FDA Label]. Paediatric patients who lack adequate endogenous growth hormone secretion, patients with chronic kidney disease, and patients with Turner syndrome that were treated with somatrem resulted in an increase in growth rate and an increase in insulin-like growth factor (IGF-1) levels similar to that seen with patients who possess endogenous pituitary derived hGH [L1896, FDA Label]. With normalized levels of growth hormone and related mediator agents like IGF-1, patients demonstrate normalized skeletal, cell, organ, and overall tissue growth [L1896, FDA Label].
Mechanism of Action	Somatrem - as well as endogenous growth hormone - binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects [L1896, FDA Label]. Some of these pharmacodynamic effects are primarily mediated by insulin like growth factor (IGF-1) produced in the liver and also locally (ie. skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (ie. lipolysis) [L1896, FDA Label]. Skeletal growth is accomplished at the epiphyseal plates at the ends of growing bone [FDA Label]. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and its mediator IGF-I [FDA Label]. Serum levels of IGF-I are low in children and adolescents who are growth hormone deficient, but increase during somatrem treatment [FDA Label]. New bone is consequently formed at the epiphyses for paediatric patients in response to GH and IGF-I from somatrem treatment [FDA Label]. This results in linear growth until these growth plates fuse at the end of puberty [FDA Label]. Somatrem treatment also causes an increase in both the number and the size of skeletal muscle cells [FDA Label]. Additionally, such therapy also influences the size of internal organs, including kidneys, and increases red cell mass [FDA Label]. Linear skeletal bone growth is facilitated in part by GH-stimulated protein synthesis [FDA Label]. This is demonstrated by nitrogen retention as reflected by a decline in urinary nitrogen excretion and blood urea nitrogen (BUN) during somatrem therapy [FDA Label]. GH also acts as a modulator of carbohydrate metabolism which may improve a fasting hypoglycaemia feeling that some patients with inadequate GH secretion sometimes experience [FDA Label]. Additionally, somatrem administration may decrease insulin sensitivity, resulting in increased serum fasting and postprandial insulin levels - usually more commonly in overweight or obese individuals, adults or children [FDA Label]. Moreover, mean fasting and postprandial glucose and hemoglobin A1C levels remained in the normal range [FDA Label]. Furthermore, in growth hormone deficient patients, the use of somatrem resulted in lipid mobilization, reduction in body fat stores, increased plasma fatty acids, and decreased plasma cholesterol levels [FDA Label]. Serum levels of inorganic phosphorus may increase slightly in patients with inadequate secretion of endogenous GH, chronic kidney disease, or Turner syndrome during somatrem therapy due to metabolic activity associated with bone growth as well as increased tubular reabsorption of phosphate by the kidney [FDA Label]. Serum calcium is not significantly altered in somatrem patients [FDA Label]. Sodium retention and increases in serum alkaline phosphatase can occur to patients taking somatrem [FDA Label]. As well, GH can stimulate the synthesis of chondroitin sulphate and collagen as well as the urinary excretion of hydroxyproline [FDA Label].
Toxicity	Short-term overdosage with somatrem may initially result in hypoglycaemia and then subsequently to hyperglycemia [L1896, FDA Label]. Moreover, this kind of short-term overdosage with somatrem is also likely to cause fluid retention [L1896, FDA Label]. Long-term overdose with somatrem could leads to signs and symptoms of gigantism and/or acromegaly consistent with the known effects of excess growth hormone [L1896, FDA Label]. Some animal based oral LD50 values have been reported as: mouse = 300mg/kg, rabbit = 3200 mg/kg, rat = 980 mg/kg.
Metabolism	Both the liver and kidney have been shown to be important metabolizing organs for growth hormone [L1896, FDA Label]. Animal studies suggest that the kidney is the dominant organ of clearance. Growth hormone is filtered at the glomerulus and reabsorbed in the proximal tubules [L1896, FDA Label]. It is then cleaved within renal cells into its constituent amino acids, which return to the systemic circulation [L1896, FDA Label].
Absorption	The absolute bioavailability of somatrem after subcutaneous administration in healthy adult males has been determined to be 81 +/- 20%. Additionally, as the subcutaneous terminal half-life is significantly longer than the intravenous terminal half-life, it appears as if the subcutaneous absorption of somatrem is slow and rate-limiting [L1896, FDA Label].
	Animal studies with somatrem showed that growth hormone localizes to highly perfused organs, particularly the liver and kidney [L1896, FDA Label]. The volume of distribution at steady state for somatrem in health adult males is approximately 50 mL/kg body weight, approximating the serum volume [L1896, FDA Label].
Clearance	The clearance of somatrem after intravenous administration in healthy adults and children is reported to be in the range of 116-174 mL/hr/kg [L1896, FDA Label].
Categories	Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins
Patents Number	NA
Date of Issue	NA
Date of Expiry	NA
Drug Interaction	NA
Target	Growth hormone receptor,Insulin-like growth factor 1 receptor
Brand Name	NA
Company	NA
Brand Description	NA
Prescribed For	NA
Chemical Name	NA
Formulation	NA
Physical Appearance	NA
Route of Administration	NA
Recommended Dosage	NA
Contraindication	NA
Side Effects	NA
Useful Link 1	Link
Useful Link 2	NA
Remarks	NA