Browse result page of ThPDB2
This is the result page of the browse module of ThPDB2. This page gives the information about the query submitted by the user as per the browse category. Further details of the entries can be seen by clicking on the ID or THPP_ID. Further the user can sort the entries on the basis of various fields by clicking on the respective headers. The user can also download the results in various formats.
Tabular representation:
| ID | THPP_ID | Therapeutic Name | Sequence | Molecular Weight | Chemical Formula | Isoelectric Point | Hydrophobicity | Melting Point | Half Life | Description | Disease/Indication | Pharmacodynamics | Mechanism of Action | Toxicity | Metabolism | Absorption | Volume of Distribution | Clearance | Categories | Patent Number | Date of Issue | Date of Expiry | Drug Interaction | Target | Brand Name | Company | Brand Description | Prescribed for | Chemical Name | Formulation | Physical Appearance | Route of Administation | Recommended Dosage | Contraindication | Side Effects | Useful Links 1 | Useful Links 2 | Remarks |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 10038 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty. | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | Gonadotropin-releasing hormone receptor | Eligard | Atrix Labs/QLT In | Atrix Labs/QLT In | Eligard is used to treat the symptoms of prostate cancer in men. | 5-oxo-L-prolyl-L-histidyl-L-tryptophyl-L-seryl-L-tyrosyl-D-leucyl-L-arginyl-N-ethyl-L-prolinamide acetate | ELIGARD is prefilled and supplied in two separate, sterile syringes whose contents are mixed immediately prior to administration. The two syringes are joined and the single dose product is mixed until it is homogenous. One syringe contains the ATRIGEL De | Suspension | Subcutaneous Injection | 7.5mg-1 injection/month, 22.5mg-1 injection per 3 month, 30mg-1 injection per 4 month, 45 mg- 1 injection every 6 month. | Hypersensitivity and pregnancy | Rare pain or unusual sensations in your back; numbness, weakness, or tingly feeling in your legs or feet; muscle weakness or loss of use; loss of bowel or bladder control; or liver problems - nausea, upper stomach pain, itching, tired feeling, loss of apetite. | Link | NA | NA |
| 10039 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Enantone | Takeda | Takeda | NA | NA | NA | Solution | Injection | One3.75 mg DPS mnthly or one 11.25 mg DPS every 3 month as a single SC/IM injection. | Hypersensitivity, undiagnosed abnormal vag bleeding, pregnancy, lactation | Weightloss, Parosmia (distortion of the sense of smell, as in smelling odours that are not present), Nausea (feeling of having an urge to vomit), Musculoskeletal Stiffness (stiffness of the body's muscles, joints, tendons, ligaments and nerves), Mood Swinng. | Link | NA | NA |
| 10040 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Leuplin | Cardinal Health | Cardinal Health | NA | NA | NA | NA | Injection | NA | NA | NA | Link | NA | NA |
| 10041 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | LeuProMaxx | Baxter/Teva | Baxter/Teva | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10042 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Leupromer | Oso Biopharmaceuticals Manufacturing LLC | Oso Biopharmaceuticals Manufacturing LLC | NA | NA | NA | NA | Injection | NA | NA | NA | Link | NA | NA |
| 10043 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Lupron | Abbott/TAP Pharmaceuticals | Abbott/TAP Pharmaceuticals | NA | NA | NA | NA | Injection | 7.5 mg for 1-month, 22.5 mg for 3-month, 30 mg for 4-month, and 45 mg for 6-month administration are prescribed for the palliative treatment of advanced prostate cancer, 3.75 mg for 1-month and 11.25 mg for 3-month administration are used for the manageme. | Allergic, pregnancy, lactation | NA | Link | NA | NA |
| 10044 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Lutrate | Hospira Inc. | Hospira Inc. | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10045 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Memryte | Curaxis | Curaxis | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10046 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Prostap 3 | Sanofi-Aventis Inc. , Sun Pharmaceutical Industries Ltd. , Takeda Pharmaceutical Co. Ltd. , Teva Pharmaceutical Industries Ltd. , Tolmar Inc. | Sanofi-Aventis Inc. , Sun Pharmaceutical Industries Ltd. , Takeda Pharmaceutical Co. Ltd. , Teva Pharmaceutical Industries Ltd. , Tolmar Inc. | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10047 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Prostap SR, Camcevi, Fensolvi, Lupaneta Pack 1-month, Lupron, Lupron Depot-ped, Zeulide Depot | Takeda UK Limited, Eon Labs, Physicians Total Care Inc. | Takeda UK Limited, Eon Labs, Physicians Total Care Inc. | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10048 | Th1007 | Leuprolide | >Th1007_Leuprolide PHWSYLLR | 1209.398 | C59H84N16O12 | NA | 0.1 | NA | Approximately 3 hours | Leuprolide is a synthetic 9 residue peptide analog of gonadotropin releasing hormone belonging to the class of drugs called hormones or hormone antagonists. It is used to treat advanced prostate cancer, uterine fibroids and endometriosis (under investigation for possible use in the treatment of mild to moderate Alzheimer's disease). | To treat prostate cancer, endometriosis, uterine fibroids and premature puberty | Leuprolide is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis thus used in the palliative treatment of advanced prostate cancer. | Leuprolide binds to the gonadotropin releasing hormone receptor and acts as an efficient inhibitor of gonadotropin secretion. | Subcutaneous administration of 250 to 500 times the recommended human dose in rats, expressed on a per body weight basis, resulted in dyspnea, decreased activity, and local irritation at the injection site. There is no evidence at present that there is a | Primarily degraded by peptidase (instead of cytochrome P450 enzymes). | Bioavailability by subcutaneous administration is comparable to that by intravenous administration. | 27 L [intravenous bolus administration to healthy male volunteers] | Excretion in urine, 8.34 L/hour [healthy male receiving a 1-mg IV bolus] | Adrenal Cortex Hormones, Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Antineoplastic Agents, Antineoplastic Agents, Hormonal, Antineoplastic and Immunomodulating Agents, Drugs causing inadvertant photosensitivity, Drugs that are Mainly Renally Excreted, Endocrine Therapy, Fertility Agents, Fertility Agents, Female, Gonadotropin Releasing Hormone Receptor Agonist, Gonadotropin Releasing Hormone Receptor Agonists, Gonadotropin-releasing hormone agonist, Gonadotropins, Hormones and Related Agents, Hyperglycemia-Associated Agents, Hypothalamic Hormones, Moderate Risk QTc-Prolonging Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptides, Photosensitizing Agents, Pituitary Hormone-Releasing Hormones, Proteins, QTc Prolonging Agents, Reproductive Control Agents | NA | NA | NA | NA | NA | Viadur | Bayer AG | Bayer AG | NA | 5-Oxo-L-prolyl-L-histidyl-L-tryptophyl-L-seryl-L-tyrosyl-D-leucyl-Lleucyl-L-arginyl-N-ethyl-L-prolinamide acetate | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10098 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | US6440392 | 27-Aug-2002 | 2-Feb-2021 | Eskalith (lithium) | Calcitonin receptor | Calcimar | Sanofi Aventis | Sanofi Aventis | To treat Paget's disease of bone | NA | Each mL of sterile solution contains calcitonin salmon 200 IU. Nonmedicinal ingredients include acetic acid, phenol, sodium acetate, sodium chloride, sodium hydroxide and water for injection. | Solution | Subcutaneous or intramuSubcutaneousular Injection | Based on body weight and injected every 12 hours | Allergy | Feeling light-headed, fainting; or muscle stiffness. | Link | NA | NA |
| 10099 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | US5733569 | 31-Mar-1998 | 31-Mar-2015 | Eskalith-CR (lithium) | NA | NA | NA | NA | For treatment of postmenopausal osteoporosis | NA | NA | NA | NA | NA | NA | Swelling in your feet | Link | NA | NA |
| 10100 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | Foscavir (foscarnet) | NA | NA | NA | NA | To reduce high levels of calcium in the blood (hypercalcemia) | NA | NA | NA | NA | NA | NA | Swelling or irritation of the skin where an injection was given. | Link | NA | NA |
| 10101 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | Lithium Carbonate ER (lithium) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Warmth, redness, itching, or tingly feeling under your skin; nausea, loss of appetite, stomach pain | NA | NA | NA |
| 10102 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | Lithobid (lithium) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Vomiting; skin rash or itching; increased urination, especially at night; eye pain | NA | NA | NA |
| 10103 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | Lithonate (lithium) | NA | Fortical | Upsher-Smith Laboratories, Inc., Physicians Total Care, Inc. | Upsher-Smith Laboratories, Inc., Physicians Total Care, Inc. | Used to treat osteoporosis in women who have been in menopause for at least 5 years. To be used along with adequate calcium and vitamin D intake. | NA | Calcitonin-salmon 2200 International Units/mL, corresponding to 200 International Units per actuation (0.09 mL) and Sodium Chloride, Citric Acid, Phenylethyl Alcohol, Benzyl Alcohol, Polysorbate 80, Hydrochloric Acid or Sodium Hydroxide (added as necess | Nasal spray | Intranasal use | Each spray delivers 200 International Units calcitonin-salmon in a volume of 0.09 mL. | Allergy | Tremors or shaking, feeling like you might pass out, severe nasal irritation. | Link | NA | NA |
| 10104 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | Lithotabs (lithium) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Bleeding from your nose, runny or stuffy nose, dryness, itching, tenderness, or general discomfort of your nose, crusting, scabs, or sores inside your nose, redness in or around your nose. | Link | NA | NA |
| 10105 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Warmth, redness, or tingly feeling under your skin, headache, back pain, nausea. | Link | NA | NA |
| 10106 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | NA | NA | Miacalcin | Novartis, Mylan Institutional LLC, Physicians Total Care, Inc., Sebela Pharmaceuticals Inc. | Novartis, Mylan Institutional LLC, Physicians Total Care, Inc., Sebela Pharmaceuticals Inc. | Miacalcin Nasal Spray is used to treat osteoporosis in women who have been in menopause for at least 5 years. To be supplemented with adequate calcium and vitamin D intake. | NA | Each milliliter contains calcitonin-salmon 200 I.U., acetic acid, USP, 2.25 mg; phenol, USP, 5.0 mg; sodium acetate trihydrate, USP, 2.0 mg; sodium chloride, USP, 7.5 mg; water for injection, USP, qs to 1.0 mL | Solution | Subcutaneous or intramuSubcutaneousular Injection | For treatment of symptomatic Paget's disease of bone, 100 International Units (0.5 mL) per day administered subcutaneously or intramuscularly and for early treatment of hypercalcemia, 4 International Units/kg body weight every 12 hours by subcutaneous or | Allergic, nasal or sinus problem such as nasal deformities, a chronic infection, or nasal pain. | Tremors or shaking, feeling like you might pass out, severe nasal irritation. | Link | NA | NA |
| 10107 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Bleeding from your nose, runny or stuffy nose, dryness, itching, tenderness, or general discomfort of your nose. | Link | NA | NA |
| 10108 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Crusting, scabs, or sores inside your nose, redness in or around your nose. | Link | NA | NA |
| 10109 | Th1014 | Salmon Calcitonin | >Th1014_Salmon_Calcitonin CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP | 3431.853 | C145H240N44O48S2 | 8.86 | -0.537 | NA | 0.83-1.33 hours | Synthetic peptide of 32 residues, formulated as a nasal spray. | Used for the treatment of post-menopausal osteoporosis. | Calcitonin inhibits bone removal by osteoclasts and promotes bone formation by osteoblasts, leading to a net increase in bone mass. Calcitonin also reduces plasma calcium levels and enhances secretion of ions in the kidney. | Calcitonin binds to the calcitonin receptor, found mainly in osteoclasts which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway. | It is devoid of embryotoxic, teratogenic and mutagenic potential. | Primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. | Rapidly absorbed and eliminated. Bioavailability is high following subcutaneous and intramuscular injection in humans and similar for the two routes of administration (71% and 66%, respectively). | 0.15 to 0.3 L/kg | Studies with injectable calcitonin show increase in the excretion of filtered calcium, phosphate, and sodium by decreasing their tubular reabsorption in the kidney. | Amino Acids, Peptides, and Proteins, Bone Density Conservation Agents, Bone Density, drug effects, Calcitonin Preparations, Calcium Homeostasis, Calcium-Regulating Hormones and Agents, Drugs that are Mainly Renally Excreted, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Parathyroid and Antiparathyroid Agents, Parathyroid Hormones and Analogues, Peptide Hormones, Peptides, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Warmth, redness, or tingly feeling under your skin, headache, back pain, nausea. | Link | NA | NA |
| 10129 | Th1018 | Secretin | >Th1018_Secretin HSDGTFTSELSRLREGARLQRLLQGLV | 3039.44 | C130H220N44O39 | 9.45 | -0.463 | NA | 0.75 hours | This drug is the synthetic form of natural secretin. It is prepared using solid phase peptide synthesis. Secretin is a peptide hormone produced in the S cells of the duodenum. Its main effect is to regulate the pH of the small intestine contents through the control of gastric acid secretion and buffering with bicarbonate. It was the first hormone to be discovered. | For diagnosis of pancreatic exocrine dysfunction and gastrinoma | Secretin is a hormone produced in the S cells of the duodenum in response to low local pH. It stimulates the secretion of bicarbonate from bicarbonate producing organs(liver, pancreas, Brunner's glands) when the pH drops below a set value. This helps neutralize the gastric acid entering the duodenum from the stomach. It also inhibits acid secretion from the stomach by reducing gastrin release from the G cells of the stomach. | Secretin binds to the secretin receptor found on the lining of S cells in the duodenum and G cells in the stomach. Binding leads to the secrection of bicarbonate or the reduction of the secretion of gastrin. Properly functioning organs (duodenum, pancreas and stomach) should be responsive to this hormone. | n acute toxicity studies with mice and rabbits, a dose of 20 μg/kg of synthetic human secretin was not lethal with no clinical symptoms of toxicity. | NA | Following intravenous bolus administration of 0.4 mcg/kg, synthetic human secretin concentration rapidly declines to baseline secretin levels within 90 to 120 minutes | 2.7 L | 580.9 ± 51.3 mL/min | Amino Acids, Peptides, and Proteins, Diagnostic Agents, Gastrointestinal Agents, Gastrointestinal Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Peptide Hormones, Peptides, Proteins, Secretin, Secretin-class Hormone, Tests for Pancreatic Function | NA | NA | NA | Clidinium. Anticholinergic agents such as secretin may diminish the stimulatory effect of secretin. Avoid using drugs with substantial anticholinergic effects in patients receiving secretin whenever possible. If such agents must be used in combina | Secretin receptor | SecreFlo | Repligen Corp | Repligen Corp | Testing for stimulation of pancreatic secretions, including bicarbonate, to aid in the diagnosis of pancreatic exocrine dysfunction. | H-His-Ser-Asp-Gly-Thr-Phe-Thr-Ser-Glu-Leu-Ser-Arg-Leu-Arg-Asp-Ser- Ala-Arg-Leu-Gln-Arg-Leu-Leu-Gln-Gly-Leu-Val-NH2 | NA | Lyophilized white powder | Intravenous infusion | NA | Allergy | Abdominal discomfort, Nausea, Mild bradycardia (reduced heart rate), Decreased blood pressure and Diaphoresis (profuse perspiration) | Link | NA | NA |
| 10130 | Th1018 | Secretin | >Th1018_Secretin HSDGTFTSELSRLREGARLQRLLQGLV | 3039.44 | C130H220N44O40 | 9.45 | -0.463 | NA | 0.75 hours | This drug is the synthetic form of natural secretin. It is prepared using solid phase peptide synthesis. Secretin is a peptide hormone produced in the S cells of the duodenum. Its main effect is to regulate the pH of the small intestine contents through the control of gastric acid secretion and buffering with bicarbonate. It was the first hormone to be discovered. | For diagnosis of pancreatic exocrine dysfunction and gastrinoma | Secretin is a hormone produced in the S cells of the duodenum in response to low local pH. It stimulates the secretion of bicarbonate from bicarbonate producing organs(liver, pancreas, Brunner's glands) when the pH drops below a set value. This helps neutralize the gastric acid entering the duodenum from the stomach. It also inhibits acid secretion from the stomach by reducing gastrin release from the G cells of the stomach. | Secretin binds to the secretin receptor found on the lining of S cells in the duodenum and G cells in the stomach. Binding leads to the secrection of bicarbonate or the reduction of the secretion of gastrin. Properly functioning organs (duodenum, pancreas and stomach) should be responsive to this hormone. | n acute toxicity studies with mice and rabbits, a dose of 20 μg/kg of synthetic human secretin was not lethal with no clinical symptoms of toxicity. | NA | Following intravenous bolus administration of 0.4 mcg/kg, synthetic human secretin concentration rapidly declines to baseline secretin levels within 90 to 120 minutes | 2.7 L | 580.9 ± 51.3 mL/min | Amino Acids, Peptides, and Proteins, Diagnostic Agents, Gastrointestinal Agents, Gastrointestinal Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Peptide Hormones, Peptides, Proteins, Secretin, Secretin-class Hormone, Tests for Pancreatic Function | NA | NA | NA | Tiotropium.The stimulatory effect of Secretin may be reduced by anticholinergics such as Tiotropium. Concomitant use of Secretin and drugs with substantial anticholinergic effects should be avoided. | NA | ChiRhoStim | ChiRhoClin, Inc | ChiRhoClin, Inc | Testing for stimulation of gastrin secretion to aid in the diagnosis of gastrinoma. | NA | As a 10 mL single-dose vial which contains 16 mcg of purified synthetic human secretin, 1.5 mg of Lcysteine hydrochloride, 20 mg of mannitol, and 9 mg of sodium chloride. When reconstituted in 8 mL of Sodium Chloride Injection USP, each mL of solution contains 2 mcg synthetic human secretin for intravenous use. The pH of the reconstituted solution has a range of 3 to 6.5. | white lyophilized sterile powder | Intravenous infusion | 0.2 mcg/kg by intravenous injection over 1 minute | NA | Nausea Vomiting Flushing Upset stomach | Link | NA | NA |
| 10131 | Th1018 | Secretin | >Th1018_Secretin HSDGTFTSELSRLREGARLQRLLQGLV | 3039.44 | C130H220N44O41 | 9.45 | -0.463 | NA | 0.75 hours | This drug is the synthetic form of natural secretin. It is prepared using solid phase peptide synthesis. Secretin is a peptide hormone produced in the S cells of the duodenum. Its main effect is to regulate the pH of the small intestine contents through the control of gastric acid secretion and buffering with bicarbonate. It was the first hormone to be discovered. | For diagnosis of pancreatic exocrine dysfunction and gastrinoma | Secretin is a hormone produced in the S cells of the duodenum in response to low local pH. It stimulates the secretion of bicarbonate from bicarbonate producing organs(liver, pancreas, Brunner's glands) when the pH drops below a set value. This helps neutralize the gastric acid entering the duodenum from the stomach. It also inhibits acid secretion from the stomach by reducing gastrin release from the G cells of the stomach. | Secretin binds to the secretin receptor found on the lining of S cells in the duodenum and G cells in the stomach. Binding leads to the secrection of bicarbonate or the reduction of the secretion of gastrin. Properly functioning organs (duodenum, pancreas and stomach) should be responsive to this hormone. | n acute toxicity studies with mice and rabbits, a dose of 20 μg/kg of synthetic human secretin was not lethal with no clinical symptoms of toxicity. | NA | Following intravenous bolus administration of 0.4 mcg/kg, synthetic human secretin concentration rapidly declines to baseline secretin levels within 90 to 120 minutes | 2.7 L | 580.9 ± 51.3 mL/min | Amino Acids, Peptides, and Proteins, Diagnostic Agents, Gastrointestinal Agents, Gastrointestinal Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Peptide Hormones, Peptides, Proteins, Secretin, Secretin-class Hormone, Tests for Pancreatic Function | NA | NA | NA | Tolterodine.The stimulatory effect of Secretin may be reduced by anticholinergics such as Tolterodine. Concomitant use of Secretin and drugs with substantial anticholinergic effects should be avoided. If combination therapy must be used, Secretin | NA | Secretin Inj 75unit/vial | Ferring Pharmaceuticals | Ferring Pharmaceuticals | Testing for stimulation of pancreatic secretions to facilitate the identification of the ampulla of Vater and accessory papilla during endoscopic retrograde cholangiopancreatography(ERCP). | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10132 | Th1018 | Secretin | >Th1018_Secretin HSDGTFTSELSRLREGARLQRLLQGLV | 3039.44 | C130H220N44O42 | 9.45 | -0.463 | NA | 0.75 hours | This drug is the synthetic form of natural secretin. It is prepared using solid phase peptide synthesis. Secretin is a peptide hormone produced in the S cells of the duodenum. Its main effect is to regulate the pH of the small intestine contents through the control of gastric acid secretion and buffering with bicarbonate. It was the first hormone to be discovered. | For diagnosis of pancreatic exocrine dysfunction and gastrinoma | Secretin is a hormone produced in the S cells of the duodenum in response to low local pH. It stimulates the secretion of bicarbonate from bicarbonate producing organs(liver, pancreas, Brunner's glands) when the pH drops below a set value. This helps neutralize the gastric acid entering the duodenum from the stomach. It also inhibits acid secretion from the stomach by reducing gastrin release from the G cells of the stomach. | Secretin binds to the secretin receptor found on the lining of S cells in the duodenum and G cells in the stomach. Binding leads to the secrection of bicarbonate or the reduction of the secretion of gastrin. Properly functioning organs (duodenum, pancreas and stomach) should be responsive to this hormone. | n acute toxicity studies with mice and rabbits, a dose of 20 μg/kg of synthetic human secretin was not lethal with no clinical symptoms of toxicity. | NA | Following intravenous bolus administration of 0.4 mcg/kg, synthetic human secretin concentration rapidly declines to baseline secretin levels within 90 to 120 minutes | 2.7 L | 580.9 ± 51.3 mL/min | Amino Acids, Peptides, and Proteins, Diagnostic Agents, Gastrointestinal Agents, Gastrointestinal Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Peptide Hormones, Peptides, Proteins, Secretin, Secretin-class Hormone, Tests for Pancreatic Function | NA | NA | NA | Trihexyphenidyl.The stimulatory effect of Secretin may be reduced by anticholinergics such as Trihexyphenidyl. Concomitant use of Secretin and drugs with substantial anticholinergic effects should be avoided. If combination therapy must be used, S | NA | Secremax | Repligen Corp | Repligen Corp | Used to treat GI spasm, irritable bowel syndrome, hyperperistalsis, peptic ulcer, functional diarrhoea, morning sickness, motion sickness and Dismenorrhoea. | NA | NA | Solution | Intravenous | NA | NA | NA | Link | NA | NA |
| 10133 | Th1018 | Secretin | >Th1018_Secretin HSDGTFTSELSRLREGARLQRLLQGLV | 3039.44 | C130H220N44O43 | 9.45 | -0.463 | NA | 0.75 hours | This drug is the synthetic form of natural secretin. It is prepared using solid phase peptide synthesis. Secretin is a peptide hormone produced in the S cells of the duodenum. Its main effect is to regulate the pH of the small intestine contents through the control of gastric acid secretion and buffering with bicarbonate. It was the first hormone to be discovered. | For diagnosis of pancreatic exocrine dysfunction and gastrinoma | Secretin is a hormone produced in the S cells of the duodenum in response to low local pH. It stimulates the secretion of bicarbonate from bicarbonate producing organs(liver, pancreas, Brunner's glands) when the pH drops below a set value. This helps neutralize the gastric acid entering the duodenum from the stomach. It also inhibits acid secretion from the stomach by reducing gastrin release from the G cells of the stomach. | Secretin binds to the secretin receptor found on the lining of S cells in the duodenum and G cells in the stomach. Binding leads to the secrection of bicarbonate or the reduction of the secretion of gastrin. Properly functioning organs (duodenum, pancreas and stomach) should be responsive to this hormone. | n acute toxicity studies with mice and rabbits, a dose of 20 μg/kg of synthetic human secretin was not lethal with no clinical symptoms of toxicity. | NA | Following intravenous bolus administration of 0.4 mcg/kg, synthetic human secretin concentration rapidly declines to baseline secretin levels within 90 to 120 minutes | 2.7 L | 580.9 ± 51.3 mL/min | Amino Acids, Peptides, and Proteins, Diagnostic Agents, Gastrointestinal Agents, Gastrointestinal Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Peptide Hormones, Peptides, Proteins, Secretin, Secretin-class Hormone, Tests for Pancreatic Function | NA | NA | NA | Trimethobenzamide.The stimulatory effect of Secretin may be reduced by anticholinergics such as Trimethobenzamide. Concomitant use of Secretin and drugs with substantial anticholinergic effects should be avoided. If combination therapy must be use | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10134 | Th1018 | Secretin | >Th1018_Secretin HSDGTFTSELSRLREGARLQRLLQGLV | 3039.44 | C130H220N44O44 | 9.45 | -0.463 | NA | 0.75 hours | This drug is the synthetic form of natural secretin. It is prepared using solid phase peptide synthesis. Secretin is a peptide hormone produced in the S cells of the duodenum. Its main effect is to regulate the pH of the small intestine contents through the control of gastric acid secretion and buffering with bicarbonate. It was the first hormone to be discovered. | For diagnosis of pancreatic exocrine dysfunction and gastrinoma | Secretin is a hormone produced in the S cells of the duodenum in response to low local pH. It stimulates the secretion of bicarbonate from bicarbonate producing organs(liver, pancreas, Brunner's glands) when the pH drops below a set value. This helps neutralize the gastric acid entering the duodenum from the stomach. It also inhibits acid secretion from the stomach by reducing gastrin release from the G cells of the stomach. | Secretin binds to the secretin receptor found on the lining of S cells in the duodenum and G cells in the stomach. Binding leads to the secrection of bicarbonate or the reduction of the secretion of gastrin. Properly functioning organs (duodenum, pancreas and stomach) should be responsive to this hormone. | n acute toxicity studies with mice and rabbits, a dose of 20 μg/kg of synthetic human secretin was not lethal with no clinical symptoms of toxicity. | NA | Following intravenous bolus administration of 0.4 mcg/kg, synthetic human secretin concentration rapidly declines to baseline secretin levels within 90 to 120 minutes | 2.7 L | 580.9 ± 51.3 mL/min | Amino Acids, Peptides, and Proteins, Diagnostic Agents, Gastrointestinal Agents, Gastrointestinal Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Nerve Tissue Proteins, Neuropeptides, Peptide Hormones, Peptides, Proteins, Secretin, Secretin-class Hormone, Tests for Pancreatic Function | NA | NA | NA | Trospium.The stimulatory effect of Secretin may be reduced by anticholinergics such as Trospium. Concomitant use of Secretin and drugs with substantial anticholinergic effects should be avoided. If combination therapy must be used, Secretin effica | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10145 | Th1021 | Thyrotropin Alfa | >Th1021_Thyrotropin_Alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 | 25 ± 10 hours | Thyrotropin alfa is a recombinant form of thyroid stimulating hormone used in performing certain tests in patients who have or have had thyroid cancer. It is also used along with a radioactive agent to destroy remaining thyroid tissue in certain patients. | For detection of residueal or recurrent thyroid cancer | Binding of thyrotropin alfa to TSH receptors on normal thyroid epithelial cells or on well-differentiated thyroid cancer tissue stimulates iodine uptake and organification. Thyrogen is an exogenous source of human TSH that offers an additional diagnostic tool in the follow-up of patients with a history of well-differentiated thyroid cancer. | Binding of thyrotropin Alfa to the thyrotropin receptors found on any residual thyroid cells or tissues stimulates radioactive iodine uptake for better radiodiagnostic imaging. | NA | NA | Time to peak: Median: 10 hours (range: 3-24 hours) After a single intramuscular injection of 0.9 mg of thyrotropin alfa: Cmax= 116+38mU/L, Tmax=22+8.5 hours. AUC=5088+1728 mU·hr/L. | NA | Through kidney and liver | Agents used to treat hypothyroidism, Anterior Pituitary Lobe Hormones and Analogues, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | US5840566 | 24-Nov-1998 | 24-Nov-2015 | NA | Thyrotropin receptor | Thyrogen | Genzyme Corporation , Genzyme Europe Bv | Genzyme Corporation , Genzyme Europe Bv | It is used in performing certain tests in patients who have or have had thyroid cancer. It is also used along with a radioactive agent to destroy remaining thyroid tissue in certain patients who have had their thyroid gland removed because of thyroid canc | NA | Each vial of THYROGEN contains 1.1 mg thyrotropin alfa, 36 mg Mannitol, 5.1 mg Sodium Phosphate, and 2.4 mg Sodium Chloride. | Lyophilized powder | IntramuSubcutaneousular preferably the buttocks | A 0.9 mg intramuscular injection to the buttock followed by a second 0.9 mg intramuscular injection to the buttock 24 hours later. | Allergic | Rash; hives; itching; difficulty breathing; tightness in the chest | Link | NA | NA |
| 10146 | Th1021 | Thyrotropin Alfa | >Th1021_Thyrotropin_Alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 | 25 ± 10 hours | Thyrotropin alfa is a recombinant form of thyroid stimulating hormone used in performing certain tests in patients who have or have had thyroid cancer. It is also used along with a radioactive agent to destroy remaining thyroid tissue in certain patients. | For detection of residueal or recurrent thyroid cancer | Binding of thyrotropin alfa to TSH receptors on normal thyroid epithelial cells or on well-differentiated thyroid cancer tissue stimulates iodine uptake and organification. Thyrogen is an exogenous source of human TSH that offers an additional diagnostic tool in the follow-up of patients with a history of well-differentiated thyroid cancer. | Binding of thyrotropin Alfa to the thyrotropin receptors found on any residual thyroid cells or tissues stimulates radioactive iodine uptake for better radiodiagnostic imaging. | NA | NA | Time to peak: Median: 10 hours (range: 3-24 hours) After a single intramuscular injection of 0.9 mg of thyrotropin alfa: Cmax= 116+38mU/L, Tmax=22+8.5 hours. AUC=5088+1728 mU·hr/L. | NA | Through kidney and liver | Agents used to treat hypothyroidism, Anterior Pituitary Lobe Hormones and Analogues, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Swelling of the mouth, face, lips, or tongue; confusion; one-sided weakness | Link | NA | NA |
| 10147 | Th1021 | Thyrotropin Alfa | >Th1021_Thyrotropin_Alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 | 25 ± 10 hours | Thyrotropin alfa is a recombinant form of thyroid stimulating hormone used in performing certain tests in patients who have or have had thyroid cancer. It is also used along with a radioactive agent to destroy remaining thyroid tissue in certain patients. | For detection of residueal or recurrent thyroid cancer | Binding of thyrotropin alfa to TSH receptors on normal thyroid epithelial cells or on well-differentiated thyroid cancer tissue stimulates iodine uptake and organification. Thyrogen is an exogenous source of human TSH that offers an additional diagnostic tool in the follow-up of patients with a history of well-differentiated thyroid cancer. | Binding of thyrotropin Alfa to the thyrotropin receptors found on any residual thyroid cells or tissues stimulates radioactive iodine uptake for better radiodiagnostic imaging. | NA | NA | Time to peak: Median: 10 hours (range: 3-24 hours) After a single intramuscular injection of 0.9 mg of thyrotropin alfa: Cmax= 116+38mU/L, Tmax=22+8.5 hours. AUC=5088+1728 mU·hr/L. | NA | Through kidney and liver | Agents used to treat hypothyroidism, Anterior Pituitary Lobe Hormones and Analogues, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins, Thyroid Products | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Severe or persistent dizziness or headache; shortness of breath or other breathing problems; slurred speech; vision problems. | Link | NA | NA |
| 10205 | Th1027 | Insulin Regular | >Th1027_Insulin_Regular GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | 5.39 | 0.218 | 81 | 2-3.4 hours | Insulin regular is a 51 residue peptide hormone, composed of two amino acid chains covalently linked by disulfide bonds. The structure is identical to native human insulin. Recombinant insulin is synthesized by recombinant DNA techncology. Inserting the human insulin gene into the Escherichia coli bacteria or Saccharomyces cerevisiae produces insulin for human use. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults and children with type 1 and type 2 diabetes mellitus. | Insulin regular is a short-acting insulin. When subcutaneously administered, the onset of action (as evidenced by a decrease in glucose level) occurs 30 minutes post-dose. Maximal effect occurs between 1.5 and 3.5 hours post-dose. The glucose-lowering effect occurs 8 hours post-dose. Compared to other rapid-acting insulin analogs, insulin regular has a slower onset of action and longer duration of action. | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | Hypoglycemia is caused due to insulin toxicity. | Predominantly cleared by metabolic degradation via a receptor-mediated process. | Generally well absorbed. | 0.15 L/kg | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin, metabolism, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | Liraglutide's coadministration may increase the risk of hypoglycemia. A lower dose of the antidiabetic agent may be needed. | Insulin receptor,Insulin-like growth factor 1 receptor,Retinoblastoma-associated protein,Cathepsin D,Insulin-degrading enzyme,Neuroendocrine convertase 2,Carboxypeptidase E,Neuroendocrine convertase 1,Protein NOV homolog,Low-density lipoprotein receptor-r | Humulin R | Eli Lilly and Company | Eli Lilly and Company | Treating diabetes mellitus. | NA | It contains human insulin (rDNA origin) 100 units/mL, glycerin 16 mg/mL and metacresol 2.5 mg/mL, endogenous zinc (approximately 0.015 mg/100 units) and water for injection. The pH is 7.0 to 7.8. Sodiumhydroxide and/or hydrochloric acid may be added durin | Sterile, clear, aqueous, and colorless solution | Subcutaneous Injection in the abdominal wall, the | Humulin R (insulin (human recombinant)) U-100, when used subcutaneously, is usually given three or more times daily before meals. The average range of total daily insulin requirement for maintenance therapy in insulin-treated patients without severe insulin resistance lies between 0.5 and 1 unit/kg/day. | During episodes of hypoglycemia and in patients hypersensitive to humulin R. | Rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue; wheezing; muscle pain; changes in vision; chills; confusion; dizziness; drowsiness; fainting; fast or irregular heartbeat; headache; loss of apetite. | Link | NA | NA |
| 10206 | Th1027 | Insulin Regular | >Th1027_Insulin_Regular GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | 5.39 | 0.218 | 81 | 2-3.4 hours | Insulin regular is a 51 residue peptide hormone, composed of two amino acid chains covalently linked by disulfide bonds. The structure is identical to native human insulin. Recombinant insulin is synthesized by recombinant DNA techncology. Inserting the human insulin gene into the Escherichia coli bacteria or Saccharomyces cerevisiae produces insulin for human use. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults and children with type 1 and type 2 diabetes mellitus. | Insulin regular is a short-acting insulin. When subcutaneously administered, the onset of action (as evidenced by a decrease in glucose level) occurs 30 minutes post-dose. Maximal effect occurs between 1.5 and 3.5 hours post-dose. The glucose-lowering effect occurs 8 hours post-dose. Compared to other rapid-acting insulin analogs, insulin regular has a slower onset of action and longer duration of action. | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | Hypoglycemia is caused due to insulin toxicity. | Predominantly cleared by metabolic degradation via a receptor-mediated process. | Generally well absorbed. | 0.15 L/kg | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin, metabolism, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | NA | NA | ACTRAPID INJECTION 100 IU/ml | NOVO NORDISK PHARMA (SINGAPORE) PTE LTD | NOVO NORDISK PHARMA (SINGAPORE) PTE LTD | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10207 | Th1027 | Insulin Regular | >Th1027_Insulin_Regular GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | 5.39 | 0.218 | 81 | 2-3.4 hours | Insulin regular is a 51 residue peptide hormone, composed of two amino acid chains covalently linked by disulfide bonds. The structure is identical to native human insulin. Recombinant insulin is synthesized by recombinant DNA techncology. Inserting the human insulin gene into the Escherichia coli bacteria or Saccharomyces cerevisiae produces insulin for human use. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults and children with type 1 and type 2 diabetes mellitus. | Insulin regular is a short-acting insulin. When subcutaneously administered, the onset of action (as evidenced by a decrease in glucose level) occurs 30 minutes post-dose. Maximal effect occurs between 1.5 and 3.5 hours post-dose. The glucose-lowering effect occurs 8 hours post-dose. Compared to other rapid-acting insulin analogs, insulin regular has a slower onset of action and longer duration of action. | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | Hypoglycemia is caused due to insulin toxicity. | Predominantly cleared by metabolic degradation via a receptor-mediated process. | Generally well absorbed. | 0.15 L/kg | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin, metabolism, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | NA | NA | INSULATARD INJECTION 100 iu/ml | NOVO NORDISK PHARMA (SINGAPORE) PTE LTD | NOVO NORDISK PHARMA (SINGAPORE) PTE LTD | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10208 | Th1027 | Insulin Regular | >Th1027_Insulin_Regular GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | 5.39 | 0.218 | 81 | 2-3.4 hours | Insulin regular is a 51 residue peptide hormone, composed of two amino acid chains covalently linked by disulfide bonds. The structure is identical to native human insulin. Recombinant insulin is synthesized by recombinant DNA techncology. Inserting the human insulin gene into the Escherichia coli bacteria or Saccharomyces cerevisiae produces insulin for human use. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults and children with type 1 and type 2 diabetes mellitus. | Insulin regular is a short-acting insulin. When subcutaneously administered, the onset of action (as evidenced by a decrease in glucose level) occurs 30 minutes post-dose. Maximal effect occurs between 1.5 and 3.5 hours post-dose. The glucose-lowering effect occurs 8 hours post-dose. Compared to other rapid-acting insulin analogs, insulin regular has a slower onset of action and longer duration of action. | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | Hypoglycemia is caused due to insulin toxicity. | Predominantly cleared by metabolic degradation via a receptor-mediated process. | Generally well absorbed. | 0.15 L/kg | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin, metabolism, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | NA | NA | Novolin R | Novo Nordisk | Novo Nordisk | Used for the treatment of patients with diabetes mellitus, for the control of hyperglycemia | NA | It contains human insulin (rDNA origin) 100 units/mL, glycerol 16 mg/mL, metacresol 3 mg/mL, zinc chloride approximately 7 mcg/mL and water for injection. The pH is adjusted to 7.4. Hydrochloric acid 2N or sodium hydroxide 2N may be added to adjust pH. No | Sterile, clear, aqueous, and colorless solution | Subcutaneous and Intravenous infusion | The injection of Novolin R (recombinant dna origin) should be followed by a meal within approximately 30 minutes of administration The average range of total daily insulin requirement for maintenance therapy in insulin-treated patients lies between 0.5 and 1.0 IU/kg. | During episodes of hypoglycemia and in patients with hypersensitivity to Novolin R | Hypoglycemia, or low blood sugar, is the most common side effect. Symptoms include headache, hunger, dizziness, sweating, irritability, trouble concentrating, rapid breathing, fast heartbeat, fainting, or seizure (severe hypoglycemia can be fatal). | Link | NA | NA |
| 10209 | Th1027 | Insulin Regular | >Th1027_Insulin_Regular GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | 5.39 | 0.218 | 81 | 2-3.4 hours | Insulin regular is a 51 residue peptide hormone, composed of two amino acid chains covalently linked by disulfide bonds. The structure is identical to native human insulin. Recombinant insulin is synthesized by recombinant DNA techncology. Inserting the human insulin gene into the Escherichia coli bacteria or Saccharomyces cerevisiae produces insulin for human use. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults and children with type 1 and type 2 diabetes mellitus. | Insulin regular is a short-acting insulin. When subcutaneously administered, the onset of action (as evidenced by a decrease in glucose level) occurs 30 minutes post-dose. Maximal effect occurs between 1.5 and 3.5 hours post-dose. The glucose-lowering effect occurs 8 hours post-dose. Compared to other rapid-acting insulin analogs, insulin regular has a slower onset of action and longer duration of action. | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | Hypoglycemia is caused due to insulin toxicity. | Predominantly cleared by metabolic degradation via a receptor-mediated process. | Generally well absorbed. | 0.15 L/kg | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin, metabolism, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10215 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | Antagon (ganirelix) | Follicle-stimulating hormone receptor,Lutropin-choriogonadotropic hormone receptor | Menopur | Ferring Pharmaceuticals | Ferring Pharmaceuticals | Menotropins are used to stimulate ovulation (the release of an egg) when a woman's ovaries can produce a follicle but hormonal stimulation is deficient. Menotropins are also used to stimulate the development of multiple eggs for in vitro fertilization. Li | NA | Each vial of MENOPUR contains 75 International Units of follicle-stimulating hormone (FSH) activity and 75 International Units of luteinizing hormone (LH) activity, plus 21 mg lactose monohydrate and 0.005 mg Polysorbate 20 and Sodium Phosphate Buffer (So | Sterile, lyophilized powder which is reconstitution with Sterile 0.9% Sodium Chloride Injection. | Subcutaneous Injection | The dosing scheme for patients undergoing IVF follows a stepwise approach and is individualized for each woman. The recommended initial dose of MENOPUR for women who have received a GnRH agonist for pituitary suppression is 225 International Units. MENOPU | Hypersensitivity, high level of FSH indicating primary ovarian failure, cause fetal harm when administerd to prergnant woman, ex hormone dependent tumors of the reproductive tract and accessory organs. | Less than 2% of female patients treated with menotropins develop ovarian hyperstimulation syndrome (OHSS), especially after the first cycle of therapy. Symptoms of OHSS include swelling of the hands or legs, abdominal pain and swelling, shortness of breathing. | Link | NA | NA |
| 10216 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | Follicle stimulating hormone / ganirelix | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Tumors of pituitary gland or hypothalamus and abnormal uterine bleeding of undetermined origin | Ovarian enlargement presenting as abdominal or pelvic pain, tenderness, pressure, or swelling; nausea, vomiting, or diarrhea; shortness of breath; pain, warmth, or tenderness centralized in an arm or leg; fever or chills. | Link | NA | NA |
| 10217 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | Follistim / Antagon (follicle stimulating hormone / ganirelix) | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Ovarian cyst or enlargement of undetermined origin, not due to polycystic ovary syndrome | Headache or drowsiness; weakness or aching of muscles or joints; breast enlargement or tenderness; pain, swelling, or irritation at the injection site; or rash. | Link | NA | NA |
| 10218 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | NA | NA | Repronex | Ferring Pharmaceuticals | Ferring Pharmaceuticals | Repronex is generally used as part of an assisted reproductive technology (ART) program to treat infertility in women. | NA | Each vial of Repronex (menotropins for injection) contains 75 International Units (IU) or 150 IU of follicle-stimulating hormone (FSH) activity and 75 IU or 150 IU of luteinizing hormone (LH) activity, respectively, plus 20 mg lactose monohydrate in a ste | Sterile, lyophilized form | Subcutaneous or intramuSubcutaneousular Injection. | The initial dose of Repronex (menotropins for injection) for patients who have received GnRH agonist or antagonist pituitary suppression is 150 IU daily for the first 5 days of treatment. Based on clinical monitoring (including serum estradiol levels and | A high FSH level indicating primary ovarian failure. | Rash; hives; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); breast pain or enlarged breasts; calf, leg, or arm pain, swelling, redness, or tenderness; change in balance | Link | NA | NA |
| 10219 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | An organic intracranial lesion such as a pituitary tumor. | Change in color of skin to a bluish color (eg, on the lips, nail beds, fingers, toes); changes in speech or vision; chest, jaw, or arm pain; confusion; coughing up blood; fainting; fast breathing; fast heartbeat. | Link | NA | NA |
| 10220 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Ovarian cysts or enlargement not due to polycystic ovary syndrome. | Flu-like symptoms; one-sided weakness; pale skin; shortness of breath; sudden, severe nausea or vomiting; unusual sweating; weakness; yellowing of the skin or eyes. | Link | NA | NA |
| 10221 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Uncontrolled thyroid and adrenal dysfunction. | NA | NA | NA | NA |
| 10222 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | The presence of any cause of infertility other than anovulation unless they are candidates for in vitro-fertilization. | NA | NA | NA | NA |
| 10223 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Abnormal bleeding of undetermined origin. | NA | NA | NA | NA |
| 10224 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Prior hypersensitivity to menotropins | NA | NA | NA | NA |
| 10225 | Th1029 | Menotropins | >Th1029_Menotropins APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 23390.3 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | NA | Menotropins contains follicle stimulating hormone and luteinizing hormone purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunit alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. | For the treatment of female infertility | Menotropins is used to treat female infertility, stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Menotropins is a combination drug which binds to the Follicle stimulating hormone receptor (which results in ovulation in the absence of sufficient endogenous Luteinizing hormone)and it also binds to the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH,therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure.FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Biological Products, Complex Mixtures, Fertility Agents, Fertility Agents, Female, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Reproductive Control Agents, Sex Hormones and Modulators of the Genital System | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Repronex (menotropins for injection) is not indicated in women who are pregnant. There are limited human data on the effects of menotropins when administered during pregnancy. | NA | NA | NA | NA |
| 10252 | Th1035 | Glucagon recombinant | >Th1035_Glucagon_recombinant HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | -1.197 | NA | 0.43 hours for an intramuscular dose | Glucagon is a 29 residue peptide hormone, synthesized in a special non- pathogenic laboratory strain of Escherichia coli bacteria that has been genetically altered by the addition of the gene for glucagons. | Used to treat severe hypoglycemia, also used in gastrointestinal imaging. | Used in the treatment of hypoglycemia and in gastric imaging, glucagon increases blood glucose concentration and is used in the treatment of hypoglycemia. Glucagon acts only on liver glycogen, converting it to glucose through the release of insulin. It also relaxes the smooth muscles of the gastrointestinal tract. | Glucagon binds the glucagon receptor(G protein-coupled receptor located in the plasma membrane) which then initiates a dual signaling pathway using both adenylate cyclase activation and increased intracellular calcium. Adenylate cyclase manufactures cAMP (cyclic AMP), which activates protein kinase A (cAMP-dependent protein kinase). This enzyme, in turn, activates phosphorylase kinase, which, in turn, phosphorylates glycogen phosphorylase, converting into the active form called phosphorylase A. Phosphorylase A is the enzyme responsible for the release of glucose-1-phosphate from glycogen polymers. This yields glucose molecules to be released into the blood. Glucagon receptors are found in the liver, kidney, brain and pancreatic islet cells. The glucagon mediated signals lead to an increase in insulin excretion | atients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium. Phentolamine may be given to control blood pressure. Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia. | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma. | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes. A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes | 0.25 L/kg | 13.5 mL/min/kg [Adults with IV 1 mg] | Amino Acids, Peptides, and Proteins, Antihypoglycemic Agent, Decreased GI Motility, Decreased GI Smooth Muscle Tone, Decreased Glycolysis, Gastrointestinal Agents, Gastrointestinal Hormones, Gastrointestinal Motility Inhibitor, Glucagon, antagonists & inhibitors, Glycogenolytic Agents, Glycogenolytic Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Increased Gluconeogenesis, Increased Glycogenolysis, Pancreatic Hormones, Peptide Hormones, Peptides, Proglucagon, Protein Precursors, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | GlucaGen | Novo Nordisk, Boehringer Ingelheim Pharmaceuticals, Inc. | Novo Nordisk, Boehringer Ingelheim Pharmaceuticals, Inc. | GlucaGen is used to treat severe hypoglycemic (low blood sugar) reactions which may occur in patients with diabetes mellitus treated with insulin. It is also used as a diagniostic aid. GlucaGen is indicated for use during radiologic examinations to tempor | NA | The reconstituted solution contains glucagon as hydrochloride 1 mg/mL (1 unit/mL) and lactose monohydrate (107 mg). GlucaGen is supplied at pH 2.5-3.5 and is soluble in water. | Sterile, lyophilized white powder | Subcutaneous, intramuSubcutaneousular, or Intraven | Inject 1 mL (adults and children, weighing more than 55 lbs (25 kg)) or 0.5 mL (children weighing less than 55 lbs (25 kg)) subcutaneously, intramuscularly, or intravenously. If the weight is not known: children younger than 6 years should be given a 0.5 | Hypersensitivity | Severe side effects are very rare, although nausea and vomiting may occur occasionally especially with doses above 1 mg or with rapid injection (less than 1 minute). You may also have rapid heart beat for a short while. | Link | NA | NA |
| 10253 | Th1035 | Glucagon recombinant | >Th1035_Glucagon_recombinant HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | -1.197 | NA | 0.58 hours for glucagon nasal powder | Glucagon is a 29 residue peptide hormone, synthesized in a special non- pathogenic laboratory strain of Escherichia coli bacteria that has been genetically altered by the addition of the gene for glucagons. | Used to treat severe hypoglycemia, also used in gastrointestinal imaging. | Used in the treatment of hypoglycemia and in gastric imaging, glucagon increases blood glucose concentration and is used in the treatment of hypoglycemia. Glucagon acts only on liver glycogen, converting it to glucose through the release of insulin. It also relaxes the smooth muscles of the gastrointestinal tract. | Glucagon binds the glucagon receptor(G protein-coupled receptor located in the plasma membrane) which then initiates a dual signaling pathway using both adenylate cyclase activation and increased intracellular calcium. Adenylate cyclase manufactures cAMP (cyclic AMP), which activates protein kinase A (cAMP-dependent protein kinase). This enzyme, in turn, activates phosphorylase kinase, which, in turn, phosphorylates glycogen phosphorylase, converting into the active form called phosphorylase A. Phosphorylase A is the enzyme responsible for the release of glucose-1-phosphate from glycogen polymers. This yields glucose molecules to be released into the blood. Glucagon receptors are found in the liver, kidney, brain and pancreatic islet cells. The glucagon mediated signals lead to an increase in insulin excretion | atients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium. Phentolamine may be given to control blood pressure. Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia. | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma. | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes. A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes | 0.25 L/kg | 13.5 mL/min/kg [Adults with IV 1 mg] | Amino Acids, Peptides, and Proteins, Antihypoglycemic Agent, Decreased GI Motility, Decreased GI Smooth Muscle Tone, Decreased Glycolysis, Gastrointestinal Agents, Gastrointestinal Hormones, Gastrointestinal Motility Inhibitor, Glucagon, antagonists & inhibitors, Glycogenolytic Agents, Glycogenolytic Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Increased Gluconeogenesis, Increased Glycogenolysis, Pancreatic Hormones, Peptide Hormones, Peptides, Proglucagon, Protein Precursors, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | NA | NA | Baqsimi | Eli Lilly and Company | Eli Lilly and Company | very low blood sugar (severe hypoglycemia) in people with diabetes ages 4 years and above. | C153H225N43O49S | Glucagon is a single-chain polypeptide containing 29 amino acid residues and has a molecular weight of 3483, and is identical to human glucagon. | preservative-free, white powder | intranasal administration in an intranasal device | The recommended dose of BAQSIMI is 3 mg administered as one actuation of the intranasal device into one nostril. If there has been no response after 15 minutes, an additional 3 mg dose of BAQSIMI from a new device may be administered while waiting for emergency assistance. | BAQSIMI is contraindicated in patients with: Pheochromocytoma because of the risk of substantial increase in blood pressure Insulinoma because of the risk of hypoglycemia Known hypersensitivity to glucagon or to any of the excipients in BAQSIMI. Allergic reactions have been reported with glucagon and include anaphylactic shock with breathing difficulties and hypotension | nausea vomiting headache runny nose discomfort in your nose stuffy nose redness in your eyes itchy nose, throat and eyes watery eyes | Link | NA | NA |
| 10254 | Th1035 | Glucagon recombinant | >Th1035_Glucagon_recombinant HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | -1.197 | NA | 0.53 hours for subcutaneous auto-injector or pre-filled syringe | Glucagon is a 29 residue peptide hormone, synthesized in a special non- pathogenic laboratory strain of Escherichia coli bacteria that has been genetically altered by the addition of the gene for glucagons. | Used to treat severe hypoglycemia, also used in gastrointestinal imaging. | Used in the treatment of hypoglycemia and in gastric imaging, glucagon increases blood glucose concentration and is used in the treatment of hypoglycemia. Glucagon acts only on liver glycogen, converting it to glucose through the release of insulin. It also relaxes the smooth muscles of the gastrointestinal tract. | Glucagon binds the glucagon receptor(G protein-coupled receptor located in the plasma membrane) which then initiates a dual signaling pathway using both adenylate cyclase activation and increased intracellular calcium. Adenylate cyclase manufactures cAMP (cyclic AMP), which activates protein kinase A (cAMP-dependent protein kinase). This enzyme, in turn, activates phosphorylase kinase, which, in turn, phosphorylates glycogen phosphorylase, converting into the active form called phosphorylase A. Phosphorylase A is the enzyme responsible for the release of glucose-1-phosphate from glycogen polymers. This yields glucose molecules to be released into the blood. Glucagon receptors are found in the liver, kidney, brain and pancreatic islet cells. The glucagon mediated signals lead to an increase in insulin excretion | atients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium. Phentolamine may be given to control blood pressure. Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia. | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma. | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes. A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes | 0.25 L/kg | 13.5 mL/min/kg [Adults with IV 1 mg] | Amino Acids, Peptides, and Proteins, Antihypoglycemic Agent, Decreased GI Motility, Decreased GI Smooth Muscle Tone, Decreased Glycolysis, Gastrointestinal Agents, Gastrointestinal Hormones, Gastrointestinal Motility Inhibitor, Glucagon, antagonists & inhibitors, Glycogenolytic Agents, Glycogenolytic Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Increased Gluconeogenesis, Increased Glycogenolysis, Pancreatic Hormones, Peptide Hormones, Peptides, Proglucagon, Protein Precursors, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | NA | NA | Gvoke | Xeris Pharmaceuticals, Inc. | Xeris Pharmaceuticals, Inc. | symptoms of severe Hypoglycemia. | C153H225N43O49S | Glucagon is a single chain containing 29 amino acid residues and has a molecular weight of 3483 and is identical to human glucagon. Glucagon is produced by solid phase synthesis with subsequent purification. | clear, colorless to pale yellow, sterile solution | subcutaneous injection | Adults and Pediatric Patients Aged 12 and Older: The recommended dose of GVOKE is 1 mg administered by subcutaneous injection into lower abdomen, outer thigh, or outer upper arm. If there has been no response after 15 minutes, an additional 1 mg dose of GVOKE from a new device may be administered while waiting for emergency assistance. Pediatric Patients Aged 2 To Under 12 Years Of Age: The recommended dose for pediatric patients who weigh less than 45 kg is 0.5 mg GVOKE administered by subcutaneous injection into the lower abdomen, outer thigh, or outer upper arm. The recommended dose for pediatric patients who weigh 45 kg or greater is 1 mg GVOKE administered by subcutaneous injection into the lower abdomen, outer thigh, or outer upper arm. If there has been no response after 15 minutes, an additional weight appropriate dose of GVOKE from a new device may be administered while waiting for emergency assistance. | GVOKE is contraindicated in patients with: Pheochromocytoma Insulinoma because of the risk of hypoglycemia Known hypersensitivity to glucagon or to any of the excipients in GVOKE. Allergic reactions have been reported with glucagon and include anaphylactic shock with breathing difficulties and hypotension | nausea, vomiting, and swelling where the injection was given | Link | NA | NA |
| 10255 | Th1035 | Glucagon recombinant | >Th1035_Glucagon_recombinant HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | -1.197 | NA | NA | Glucagon is a 29 residue peptide hormone, synthesized in a special non- pathogenic laboratory strain of Escherichia coli bacteria that has been genetically altered by the addition of the gene for glucagons. | Used to treat severe hypoglycemia, also used in gastrointestinal imaging. | Used in the treatment of hypoglycemia and in gastric imaging, glucagon increases blood glucose concentration and is used in the treatment of hypoglycemia. Glucagon acts only on liver glycogen, converting it to glucose through the release of insulin. It also relaxes the smooth muscles of the gastrointestinal tract. | Glucagon binds the glucagon receptor(G protein-coupled receptor located in the plasma membrane) which then initiates a dual signaling pathway using both adenylate cyclase activation and increased intracellular calcium. Adenylate cyclase manufactures cAMP (cyclic AMP), which activates protein kinase A (cAMP-dependent protein kinase). This enzyme, in turn, activates phosphorylase kinase, which, in turn, phosphorylates glycogen phosphorylase, converting into the active form called phosphorylase A. Phosphorylase A is the enzyme responsible for the release of glucose-1-phosphate from glycogen polymers. This yields glucose molecules to be released into the blood. Glucagon receptors are found in the liver, kidney, brain and pancreatic islet cells. The glucagon mediated signals lead to an increase in insulin excretion | atients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium. Phentolamine may be given to control blood pressure. Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia. | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma. | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes. A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes | 0.25 L/kg | 13.5 mL/min/kg [Adults with IV 1 mg] | Amino Acids, Peptides, and Proteins, Antihypoglycemic Agent, Decreased GI Motility, Decreased GI Smooth Muscle Tone, Decreased Glycolysis, Gastrointestinal Agents, Gastrointestinal Hormones, Gastrointestinal Motility Inhibitor, Glucagon, antagonists & inhibitors, Glycogenolytic Agents, Glycogenolytic Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Increased Gluconeogenesis, Increased Glycogenolysis, Pancreatic Hormones, Peptide Hormones, Peptides, Proglucagon, Protein Precursors, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | Walfarin- Glucagon may increase the anticoagulant effect of warfarin (Coumadin) and other anticoagulants causing an increase in the slow clotting of blood and a greater risk of developing an episode of bleeding. | NA | Glucagon | Eli Lilly, Fresenius Kabi USA, LLC,TYA Pharmaceuticals, A-S Medication Solutions, Physicians Total Care, Inc. | Eli Lilly, Fresenius Kabi USA, LLC,TYA Pharmaceuticals, A-S Medication Solutions, Physicians Total Care, Inc. | Glucagon is used to increase the blood glucose level in severe hypoglycemia (low blood glucose). Glucagon is a glucose-elevating drug | NA | Glucagon is available as an emergency kit. The kit contains freeze-dried glucagon as a powder for injection 1 ml syringe of diluent. The powder contains 1 mg (1 unit) of glucagon and 49 mg of lactose. The diluent contains 12 mg/ml of glycerine, water for | Powder | Subcutaneously or intramuSubcutaneousularly Inject | Adults and children weighing 44 pounds or more should receive 1mg (1 unit) of glucagon | Allergy | Nausea and vomiting may occur occasionally after injection of glucagon, but this may be a symptom of the hypoglycemia for which glucagon is being given. Rare allergic-type reactions may occur with glucagon including itching, respiratory distress, or low blood pressure. | Link | NA | NA |
| 10256 | Th1035 | Glucagon recombinant | >Th1035_Glucagon_recombinant HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | -1.197 | NA | NA | Glucagon is a 29 residue peptide hormone, synthesized in a special non- pathogenic laboratory strain of Escherichia coli bacteria that has been genetically altered by the addition of the gene for glucagons. | Used to treat severe hypoglycemia, also used in gastrointestinal imaging. | Used in the treatment of hypoglycemia and in gastric imaging, glucagon increases blood glucose concentration and is used in the treatment of hypoglycemia. Glucagon acts only on liver glycogen, converting it to glucose through the release of insulin. It also relaxes the smooth muscles of the gastrointestinal tract. | Glucagon binds the glucagon receptor(G protein-coupled receptor located in the plasma membrane) which then initiates a dual signaling pathway using both adenylate cyclase activation and increased intracellular calcium. Adenylate cyclase manufactures cAMP (cyclic AMP), which activates protein kinase A (cAMP-dependent protein kinase). This enzyme, in turn, activates phosphorylase kinase, which, in turn, phosphorylates glycogen phosphorylase, converting into the active form called phosphorylase A. Phosphorylase A is the enzyme responsible for the release of glucose-1-phosphate from glycogen polymers. This yields glucose molecules to be released into the blood. Glucagon receptors are found in the liver, kidney, brain and pancreatic islet cells. The glucagon mediated signals lead to an increase in insulin excretion | atients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium. Phentolamine may be given to control blood pressure. Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia. | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma. | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes. A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes | 0.25 L/kg | 13.5 mL/min/kg [Adults with IV 1 mg] | Amino Acids, Peptides, and Proteins, Antihypoglycemic Agent, Decreased GI Motility, Decreased GI Smooth Muscle Tone, Decreased Glycolysis, Gastrointestinal Agents, Gastrointestinal Hormones, Gastrointestinal Motility Inhibitor, Glucagon, antagonists & inhibitors, Glycogenolytic Agents, Glycogenolytic Hormones, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Increased Gluconeogenesis, Increased Glycogenolysis, Pancreatic Hormones, Peptide Hormones, Peptides, Proglucagon, Protein Precursors, Proteins, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | Indomethacin (Indocin, Indocin-SR) reduces the effect of glucagon. | NA | Ogluo | Tetris Pharma B.V | Tetris Pharma B.V | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10269 | Th1039 | Lutropin alfa | >Th1039_Lutropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 30000 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | approximately 18 hours | Lutropin alfa is a recombinant human luteinizing hormone produced in yeast with 2 subunits, alpha = 92 residues, beta = 121 residues. It is a heterodimeric glycoprotein. Each monomeric unit is a glycoprotein molecule. In females, an acute rise of LH(LH surge) triggers ovulation and the development of the corpus luteum. In males, it stimulates Leydig cell production of testosterone. Lutropin alfa was the first and only recombinant human form of luteinizing hormone (LH) developed for use in the stimulation of follicular development. | For treatment of female infertility | Used to facilitate female conception, lutropin alfa performs the same actions as luteinizing hormone, which is normally produced in the pituitary gland. Lutropin is usually given in combination with follitropin alfa. In females, a LH surge about halfway through the menstrual cycle triggers the onset of ovulation. LH also induces the ovulated follicle to become a corpus luteum, which then secretes progesterone. | Binds to the luteinizing hormone receptor which then activates adenylate cylcase through G protein mediation. Adenylate cyclase then activates many other pathways leading to steroid hormone production and other follicle maturation processes. | Lutropin alfa is not indicated for people under 16 and over 60, pregnant and lactating women, patients with uncontrolled thyroid and adrenal failure, patients with active, untreated tumours of the hypothalamus and pituitary gland, and in any patient with a condition that makes a normal pregnancy possible such as primary ovarian failure or fibroid tumors of the uterus. | <5% of dose excreted renally as unchanged drug. | bioavailability is 56% | 10 L | 2-3 L/h [healthy female following subcutaneous administration]. Total body clearance is approximately 2 to 3 L/h with less than 5 percent of the dose being excreted unchanged renally. | Genito Urinary System and Sex Hormones, Gonadotropins | US5767251 | 16-Jun-1998 | 16-Jun-2015 | Other drugs may interact with lutropin alfa, including prescription and over-the-counter medicines, vitamins, and herbal products | Lutropin-choriogonadotropic hormone receptor | Luveris | Serono, Merck Europe B.V. | Serono, Merck Europe B.V. | Luveris is used together with follitropin alfa to treat infertility in women with LH deficiency. | NA | One vial contains 75 IU of lutropin alfa (recombinant human Luteinising Hormone {r-hLH}) and following excipeint is present; Powder:Sucrose,Disodium phosphate dihydrate,Sodium dihydrogen phosphate monohydrate,Polysorbate 20,Phosphoric acid, concentrated ( | White lyophilised pellet withg clear colourless solvent to make solution | Subcutaneous (Subcutaneous) administration | It is recommended that 75 IU Luveris be concomitantly administered subcutaneously with 75 IU to 150 IU Gonal-f as two separate injections in the initial treatment cycle | Hypersensitivity | Nausea, stomach pain, diarrhea, constipation, gas; pelvic pain, menstrual cramps; breast pain; headache; pain or irritation where the injection was given; tired feeling; or cold symptoms such as stuffy nose, sneezing, sore throat. | Link | NA | NA |
| 10270 | Th1039 | Lutropin alfa | >Th1039_Lutropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 30000 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | approximately 18 hours | Lutropin alfa is a recombinant human luteinizing hormone produced in yeast with 2 subunits, alpha = 92 residues, beta = 121 residues. It is a heterodimeric glycoprotein. Each monomeric unit is a glycoprotein molecule. In females, an acute rise of LH(LH surge) triggers ovulation and the development of the corpus luteum. In males, it stimulates Leydig cell production of testosterone. Lutropin alfa was the first and only recombinant human form of luteinizing hormone (LH) developed for use in the stimulation of follicular development. | For treatment of female infertility | Used to facilitate female conception, lutropin alfa performs the same actions as luteinizing hormone, which is normally produced in the pituitary gland. Lutropin is usually given in combination with follitropin alfa. In females, a LH surge about halfway through the menstrual cycle triggers the onset of ovulation. LH also induces the ovulated follicle to become a corpus luteum, which then secretes progesterone. | Binds to the luteinizing hormone receptor which then activates adenylate cylcase through G protein mediation. Adenylate cyclase then activates many other pathways leading to steroid hormone production and other follicle maturation processes. | Lutropin alfa is not indicated for people under 16 and over 60, pregnant and lactating women, patients with uncontrolled thyroid and adrenal failure, patients with active, untreated tumours of the hypothalamus and pituitary gland, and in any patient with a condition that makes a normal pregnancy possible such as primary ovarian failure or fibroid tumors of the uterus. | <5% of dose excreted renally as unchanged drug. | bioavailability is 56% | 10 L | 2-3 L/h [healthy female following subcutaneous administration]. Total body clearance is approximately 2 to 3 L/h with less than 5 percent of the dose being excreted unchanged renally. | Genito Urinary System and Sex Hormones, Gonadotropins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Tumours of the hypothalamus and pituitary gland | NA | Link | NA | NA |
| 10271 | Th1039 | Lutropin alfa | >Th1039_Lutropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 30000 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | approximately 18 hours | Lutropin alfa is a recombinant human luteinizing hormone produced in yeast with 2 subunits, alpha = 92 residues, beta = 121 residues. It is a heterodimeric glycoprotein. Each monomeric unit is a glycoprotein molecule. In females, an acute rise of LH(LH surge) triggers ovulation and the development of the corpus luteum. In males, it stimulates Leydig cell production of testosterone. Lutropin alfa was the first and only recombinant human form of luteinizing hormone (LH) developed for use in the stimulation of follicular development. | For treatment of female infertility | Used to facilitate female conception, lutropin alfa performs the same actions as luteinizing hormone, which is normally produced in the pituitary gland. Lutropin is usually given in combination with follitropin alfa. In females, a LH surge about halfway through the menstrual cycle triggers the onset of ovulation. LH also induces the ovulated follicle to become a corpus luteum, which then secretes progesterone. | Binds to the luteinizing hormone receptor which then activates adenylate cylcase through G protein mediation. Adenylate cyclase then activates many other pathways leading to steroid hormone production and other follicle maturation processes. | Lutropin alfa is not indicated for people under 16 and over 60, pregnant and lactating women, patients with uncontrolled thyroid and adrenal failure, patients with active, untreated tumours of the hypothalamus and pituitary gland, and in any patient with a condition that makes a normal pregnancy possible such as primary ovarian failure or fibroid tumors of the uterus. | <5% of dose excreted renally as unchanged drug. | bioavailability is 56% | 10 L | 2-3 L/h [healthy female following subcutaneous administration]. Total body clearance is approximately 2 to 3 L/h with less than 5 percent of the dose being excreted unchanged renally. | Genito Urinary System and Sex Hormones, Gonadotropins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Ovarian enlargement or ovarian cyst unrelated to polycystic ovarian disease and of unknown origin. | NA | NA | NA | NA |
| 10272 | Th1039 | Lutropin alfa | >Th1039_Lutropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 30000 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | approximately 18 hours | Lutropin alfa is a recombinant human luteinizing hormone produced in yeast with 2 subunits, alpha = 92 residues, beta = 121 residues. It is a heterodimeric glycoprotein. Each monomeric unit is a glycoprotein molecule. In females, an acute rise of LH(LH surge) triggers ovulation and the development of the corpus luteum. In males, it stimulates Leydig cell production of testosterone. Lutropin alfa was the first and only recombinant human form of luteinizing hormone (LH) developed for use in the stimulation of follicular development. | For treatment of female infertility | Used to facilitate female conception, lutropin alfa performs the same actions as luteinizing hormone, which is normally produced in the pituitary gland. Lutropin is usually given in combination with follitropin alfa. In females, a LH surge about halfway through the menstrual cycle triggers the onset of ovulation. LH also induces the ovulated follicle to become a corpus luteum, which then secretes progesterone. | Binds to the luteinizing hormone receptor which then activates adenylate cylcase through G protein mediation. Adenylate cyclase then activates many other pathways leading to steroid hormone production and other follicle maturation processes. | Lutropin alfa is not indicated for people under 16 and over 60, pregnant and lactating women, patients with uncontrolled thyroid and adrenal failure, patients with active, untreated tumours of the hypothalamus and pituitary gland, and in any patient with a condition that makes a normal pregnancy possible such as primary ovarian failure or fibroid tumors of the uterus. | <5% of dose excreted renally as unchanged drug. | bioavailability is 56% | 10 L | 2-3 L/h [healthy female following subcutaneous administration]. Total body clearance is approximately 2 to 3 L/h with less than 5 percent of the dose being excreted unchanged renally. | Genito Urinary System and Sex Hormones, Gonadotropins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Gynaecological haemorrhages of unknown origin | NA | NA | NA | NA |
| 10273 | Th1039 | Lutropin alfa | >Th1039_Lutropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 30000 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | approximately 18 hours | Lutropin alfa is a recombinant human luteinizing hormone produced in yeast with 2 subunits, alpha = 92 residues, beta = 121 residues. It is a heterodimeric glycoprotein. Each monomeric unit is a glycoprotein molecule. In females, an acute rise of LH(LH surge) triggers ovulation and the development of the corpus luteum. In males, it stimulates Leydig cell production of testosterone. Lutropin alfa was the first and only recombinant human form of luteinizing hormone (LH) developed for use in the stimulation of follicular development. | For treatment of female infertility | Used to facilitate female conception, lutropin alfa performs the same actions as luteinizing hormone, which is normally produced in the pituitary gland. Lutropin is usually given in combination with follitropin alfa. In females, a LH surge about halfway through the menstrual cycle triggers the onset of ovulation. LH also induces the ovulated follicle to become a corpus luteum, which then secretes progesterone. | Binds to the luteinizing hormone receptor which then activates adenylate cylcase through G protein mediation. Adenylate cyclase then activates many other pathways leading to steroid hormone production and other follicle maturation processes. | Lutropin alfa is not indicated for people under 16 and over 60, pregnant and lactating women, patients with uncontrolled thyroid and adrenal failure, patients with active, untreated tumours of the hypothalamus and pituitary gland, and in any patient with a condition that makes a normal pregnancy possible such as primary ovarian failure or fibroid tumors of the uterus. | <5% of dose excreted renally as unchanged drug. | bioavailability is 56% | 10 L | 2-3 L/h [healthy female following subcutaneous administration]. Total body clearance is approximately 2 to 3 L/h with less than 5 percent of the dose being excreted unchanged renally. | Genito Urinary System and Sex Hormones, Gonadotropins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Ovarian, uterine, or mammary carcinoma | NA | NA | NA | NA |
| 10274 | Th1039 | Lutropin alfa | >Th1039_Lutropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 30000 | C1014H1609N287O294S27 | 8.44 | -0.063 | 55 | approximately 18 hours | Lutropin alfa is a recombinant human luteinizing hormone produced in yeast with 2 subunits, alpha = 92 residues, beta = 121 residues. It is a heterodimeric glycoprotein. Each monomeric unit is a glycoprotein molecule. In females, an acute rise of LH(LH surge) triggers ovulation and the development of the corpus luteum. In males, it stimulates Leydig cell production of testosterone. Lutropin alfa was the first and only recombinant human form of luteinizing hormone (LH) developed for use in the stimulation of follicular development. | For treatment of female infertility | Used to facilitate female conception, lutropin alfa performs the same actions as luteinizing hormone, which is normally produced in the pituitary gland. Lutropin is usually given in combination with follitropin alfa. In females, a LH surge about halfway through the menstrual cycle triggers the onset of ovulation. LH also induces the ovulated follicle to become a corpus luteum, which then secretes progesterone. | Binds to the luteinizing hormone receptor which then activates adenylate cylcase through G protein mediation. Adenylate cyclase then activates many other pathways leading to steroid hormone production and other follicle maturation processes. | Lutropin alfa is not indicated for people under 16 and over 60, pregnant and lactating women, patients with uncontrolled thyroid and adrenal failure, patients with active, untreated tumours of the hypothalamus and pituitary gland, and in any patient with a condition that makes a normal pregnancy possible such as primary ovarian failure or fibroid tumors of the uterus. | <5% of dose excreted renally as unchanged drug. | bioavailability is 56% | 10 L | 2-3 L/h [healthy female following subcutaneous administration]. Total body clearance is approximately 2 to 3 L/h with less than 5 percent of the dose being excreted unchanged renally. | Genito Urinary System and Sex Hormones, Gonadotropins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Luveris must not be used when a condition exists which would make a normal pregnancy impossible, such as:primary ovarian failure, malformations of sexual organs incompatible with pregnancy, fibroid tumours of the uterus incompatible with pregnancy. | NA | NA | NA | NA |
| 10275 | Th1040 | Insulin Lispro | >Th1040_Insulin_Lispro GIVEQCCTSICSLYQLENYCN | 5808 | C257H387N65O76S6 | 5.39 | 0.218 | 81 | On subcutaneous administration = 1 hour | Insulin lispro is a recombinant human insulin analogue produced in a specialized laboratory strain of Escherischia coli. Plasmid DNA transfected into the bacteria encodes for an analogue of human insulin that has a lysine at residuce B28 and proline at B29; these residues are reversed in endogenous human insulin. Reversal of these amino acid residues produces a rapid-acting insulin analogue. FDA approved on 1996. | To treat type 1 or 2 diabetes mellitus. To be used in conjunction with an intermediate or long-acting insulin except when used in a continuous insulin infusion pump. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin lispro binds to the insulin receptor(IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Reversal of the proline and lysine residues at positions B28 and B29 of native insulin eliminates hydrophobic interactions and weakens some of the hydrogen bonds that contribute to the stability of the insulin dimers that comprise insulin hexamers. Hexamers of insulin lispro are produced in the presence of zinc and -cresol. These weakly associated hexamers quickly dissociate upon subcutaneous injection and are absorbed as monomers through vascular endothelial cells. These properties give insulin lispro its fast-acting properties. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | Rapidly absorbed following subcutaneous administration. It is also absorbed more quickly than regular human insulin. Peak serum levels occur 30-90 minutes after injection in healthy subjects. Absorption also differs depending on the site of injection. Aft | When administered intravenously as bolus injections of 0.1 and 0.2 U/kg dose in two separate groups of healthy subjects, the mean volume of distribution of insulin lispro appeared to decrease with increase in dose (1.55 and 0.72 L/kg, respectively). | Clearance is dose dependent. When a dose of 0.1 unit/kg and 0.2 unit/kg were administered intravenously, the mean clearance was 21.0 mL/min/kg and 9.6 mL/min/kg respectively. | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin Analog, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | US5474978 | 12-Dec-1995 | 16-Jun-2014 | The beta-blocker, acebutolol, atenolol, bisoprolol, carvedilol, may decrease symptoms of hypoglycemia. | Insulin receptor,Insulin-like growth factor 1 receptor | Humalog | Eli Lilly | Eli Lilly | Humalog is used to treat type 1 diabetes in adults. It is usually given together with another long-acting insulin. Humalog is also used together with oral medications to treat type 2 diabetes in adults. | NA | Each milliliter of HUMALOG contains insulin lispro 100 units, 16 mg glycerin, 1.88 mg dibasic sodium phosphate, 3.15 mg Metacresol, zinc oxide content adjusted to provide 0.0197 mg zinc ion, trace amounts of phenol, and Water for Injection. Insulin lispro | Sterile, aqueous, clear, and colorless solution | Subcutaneous and Intravenous infusion | The total daily insulin requirement may vary and is usually between 0.5 to 1 unit/kg/day. Insulin requirements may be altered during stress, major illness, or with changes in exercise, meal patterns, or coadministered drugs. Usual maintenance range is 0.5-1 unit/kg/day in divided doses; nonobese may require 0.4-0.6 unit/kg/day; obese may require 0.8-1.2 units/kg/day. | During episodes of hypoglycemia in patients who are hypersensitive to HUMALOG or to any of its excipients. | Low blood sugar--headache, hunger, weakness, sweating, confusion, irritability, dizziness, fast heart rate, or feeling jittery. | Link | NA | NA |
| 10276 | Th1040 | Insulin Lispro | >Th1040_Insulin_Lispro GIVEQCCTSICSLYQLENYCN | 5808 | C257H387N65O76S6 | 5.39 | 0.218 | 81 | On subcutaneous administration = 1 hour | Insulin lispro is a recombinant human insulin analogue produced in a specialized laboratory strain of Escherischia coli. Plasmid DNA transfected into the bacteria encodes for an analogue of human insulin that has a lysine at residuce B28 and proline at B29; these residues are reversed in endogenous human insulin. Reversal of these amino acid residues produces a rapid-acting insulin analogue. FDA approved on 1996. | To treat type 1 or 2 diabetes mellitus. To be used in conjunction with an intermediate or long-acting insulin except when used in a continuous insulin infusion pump. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin lispro binds to the insulin receptor(IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Reversal of the proline and lysine residues at positions B28 and B29 of native insulin eliminates hydrophobic interactions and weakens some of the hydrogen bonds that contribute to the stability of the insulin dimers that comprise insulin hexamers. Hexamers of insulin lispro are produced in the presence of zinc and -cresol. These weakly associated hexamers quickly dissociate upon subcutaneous injection and are absorbed as monomers through vascular endothelial cells. These properties give insulin lispro its fast-acting properties. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | Rapidly absorbed following subcutaneous administration. It is also absorbed more quickly than regular human insulin. Peak serum levels occur 30-90 minutes after injection in healthy subjects. Absorption also differs depending on the site of injection. Aft | When administered intravenously as bolus injections of 0.1 and 0.2 U/kg dose in two separate groups of healthy subjects, the mean volume of distribution of insulin lispro appeared to decrease with increase in dose (1.55 and 0.72 L/kg, respectively). | Clearance is dose dependent. When a dose of 0.1 unit/kg and 0.2 unit/kg were administered intravenously, the mean clearance was 21.0 mL/min/kg and 9.6 mL/min/kg respectively. | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin Analog, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | US5514646 | 7-May-1996 | 7-May-2013 | Concomitant therapy with drugs like Dextropropoxyphene, Pentoxifylline, Pramlintide, Fluoxetine, Fenofibrate and Disopyramide that may increase the blood-glucose-lowering effect of insulin lispro | NA | Admelog | Sanofi Aventis, REMEDYREPACK INC. | Sanofi Aventis, REMEDYREPACK INC. | symptoms of Type 1 or 2 Diabetes Mellitus. | C257H383N65O77S6 | Insulin lispro is produced by recombinant DNA technology utilizing a non-pathogenic laboratory strain of Escherichia coli. Insulin lispro differs from human insulin in that the amino acid proline at position B28 is replaced by lysine and the lysine in position B29 is replaced by proline. | sterile, aqueous, clear, and colorless solution. | Subcutaneous Injection | Dilute ADMELOG to concentrations from 0.1 unit/mL to 1 unit/mL using 0.9% sodium chloride. Administer ADMELOG intravenously ONLY under medical supervision with close monitoring of blood glucose and potassium levels to avoid hypoglycemia and hypokalemia | ADMELOG is contraindicated: during episodes of hypoglycemia. in patients who are hypersensitive to insulin lispro or to any of the excipients. Clinical Pharmacology | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, redness or swelling where an injection was given, itchy skin rash over the entire body, fast heartbeats, lightheadedness, weight gain, swelling in your hands or feet, shortness of breath, headache, hunger, sweating, irritability, dizziness, anxiety, shakiness, leg cramps, constipation, irregular heartbeats, fluttering in your chest, increased thirst or urination, numbness or tingling, muscle weakness, and limp feeling | Link | NA | NA |
| 10277 | Th1040 | Insulin Lispro | >Th1040_Insulin_Lispro GIVEQCCTSICSLYQLENYCN | 5808 | C257H387N65O76S6 | 5.39 | 0.218 | 81 | On subcutaneous administration = 1 hour | Insulin lispro is a recombinant human insulin analogue produced in a specialized laboratory strain of Escherischia coli. Plasmid DNA transfected into the bacteria encodes for an analogue of human insulin that has a lysine at residuce B28 and proline at B29; these residues are reversed in endogenous human insulin. Reversal of these amino acid residues produces a rapid-acting insulin analogue. FDA approved on 1996. | To treat type 1 or 2 diabetes mellitus. To be used in conjunction with an intermediate or long-acting insulin except when used in a continuous insulin infusion pump. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin lispro binds to the insulin receptor(IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Reversal of the proline and lysine residues at positions B28 and B29 of native insulin eliminates hydrophobic interactions and weakens some of the hydrogen bonds that contribute to the stability of the insulin dimers that comprise insulin hexamers. Hexamers of insulin lispro are produced in the presence of zinc and -cresol. These weakly associated hexamers quickly dissociate upon subcutaneous injection and are absorbed as monomers through vascular endothelial cells. These properties give insulin lispro its fast-acting properties. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | Rapidly absorbed following subcutaneous administration. It is also absorbed more quickly than regular human insulin. Peak serum levels occur 30-90 minutes after injection in healthy subjects. Absorption also differs depending on the site of injection. Aft | When administered intravenously as bolus injections of 0.1 and 0.2 U/kg dose in two separate groups of healthy subjects, the mean volume of distribution of insulin lispro appeared to decrease with increase in dose (1.55 and 0.72 L/kg, respectively). | Clearance is dose dependent. When a dose of 0.1 unit/kg and 0.2 unit/kg were administered intravenously, the mean clearance was 21.0 mL/min/kg and 9.6 mL/min/kg respectively. | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin Analog, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | CA2151564 | 11-Feb-2003 | 12-Jun-2015 | Concomitant therapy with ACE inhibitors like Enalapril and Ramipril may increase the blood-glucose-lowering effect of insulin lispro and thus the chance of hypoglycemia should be monitored closely. | NA | Insulin Lispro | A-S Medication Solutions, Eli Lilly and Company, REMEDYREPACK INC., ImClone LLC | A-S Medication Solutions, Eli Lilly and Company, REMEDYREPACK INC., ImClone LLC | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10278 | Th1040 | Insulin Lispro | >Th1040_Insulin_Lispro GIVEQCCTSICSLYQLENYCN | 5808 | C257H387N65O76S6 | 5.39 | 0.218 | 81 | On subcutaneous administration = 1 hour | Insulin lispro is a recombinant human insulin analogue produced in a specialized laboratory strain of Escherischia coli. Plasmid DNA transfected into the bacteria encodes for an analogue of human insulin that has a lysine at residuce B28 and proline at B29; these residues are reversed in endogenous human insulin. Reversal of these amino acid residues produces a rapid-acting insulin analogue. FDA approved on 1996. | To treat type 1 or 2 diabetes mellitus. To be used in conjunction with an intermediate or long-acting insulin except when used in a continuous insulin infusion pump. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin lispro binds to the insulin receptor(IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Reversal of the proline and lysine residues at positions B28 and B29 of native insulin eliminates hydrophobic interactions and weakens some of the hydrogen bonds that contribute to the stability of the insulin dimers that comprise insulin hexamers. Hexamers of insulin lispro are produced in the presence of zinc and -cresol. These weakly associated hexamers quickly dissociate upon subcutaneous injection and are absorbed as monomers through vascular endothelial cells. These properties give insulin lispro its fast-acting properties. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | Rapidly absorbed following subcutaneous administration. It is also absorbed more quickly than regular human insulin. Peak serum levels occur 30-90 minutes after injection in healthy subjects. Absorption also differs depending on the site of injection. Aft | When administered intravenously as bolus injections of 0.1 and 0.2 U/kg dose in two separate groups of healthy subjects, the mean volume of distribution of insulin lispro appeared to decrease with increase in dose (1.55 and 0.72 L/kg, respectively). | Clearance is dose dependent. When a dose of 0.1 unit/kg and 0.2 unit/kg were administered intravenously, the mean clearance was 21.0 mL/min/kg and 9.6 mL/min/kg respectively. | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin Analog, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | CA2151560 | 9-May-2000 | 12-Jun-2015 | Concomitant therapy with diuretics like Hydrochlorothiazide may reduce the blood-glucose-lowering effect of insulin lispro. | NA | Humalog KwikPen | Eli Lilly | Eli Lilly | Insulin lispro is used to treat type 1 diabetes in adults. It is usually given together with another long-acting insulin. Insulin lispro is also used together with oral medication to treat type 2 diabetes in adults. | NA | NA | Solution | Subcutaneous injection | Insulin lispro can be administered intravenously under medical supervision at concentrations from 0.1 unit/mL to 1 unit/mL in infusion systems containing 0.9% sodium chloride. Blood glucose and potassium levels should be closely monitored to avoid hypoglycemia. | During episodes of hypoglycemia in patients who are hypersensitive to HUMALOG or to any of its excipients. | Low blood sugar is the most common side effect. There are many causes of low blood sugar, including taking too much Humalog. Severe life-threatening allergic reactions (whole-body reactions) can happen.Reactions at the injection site (local allergic reaction. | Link | NA | NA |
| 10279 | Th1040 | Insulin Lispro | >Th1040_Insulin_Lispro GIVEQCCTSICSLYQLENYCN | 5808 | C257H387N65O76S6 | 5.39 | 0.218 | 81 | On subcutaneous administration = 1 hour | Insulin lispro is a recombinant human insulin analogue produced in a specialized laboratory strain of Escherischia coli. Plasmid DNA transfected into the bacteria encodes for an analogue of human insulin that has a lysine at residuce B28 and proline at B29; these residues are reversed in endogenous human insulin. Reversal of these amino acid residues produces a rapid-acting insulin analogue. FDA approved on 1996. | To treat type 1 or 2 diabetes mellitus. To be used in conjunction with an intermediate or long-acting insulin except when used in a continuous insulin infusion pump. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin lispro binds to the insulin receptor(IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Reversal of the proline and lysine residues at positions B28 and B29 of native insulin eliminates hydrophobic interactions and weakens some of the hydrogen bonds that contribute to the stability of the insulin dimers that comprise insulin hexamers. Hexamers of insulin lispro are produced in the presence of zinc and -cresol. These weakly associated hexamers quickly dissociate upon subcutaneous injection and are absorbed as monomers through vascular endothelial cells. These properties give insulin lispro its fast-acting properties. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | Rapidly absorbed following subcutaneous administration. It is also absorbed more quickly than regular human insulin. Peak serum levels occur 30-90 minutes after injection in healthy subjects. Absorption also differs depending on the site of injection. Aft | When administered intravenously as bolus injections of 0.1 and 0.2 U/kg dose in two separate groups of healthy subjects, the mean volume of distribution of insulin lispro appeared to decrease with increase in dose (1.55 and 0.72 L/kg, respectively). | Clearance is dose dependent. When a dose of 0.1 unit/kg and 0.2 unit/kg were administered intravenously, the mean clearance was 21.0 mL/min/kg and 9.6 mL/min/kg respectively. | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin Analog, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | Concomitant therapy with angiotensin II receptor blockers like Losartan may increase the blood-glucose-lowering effect of insulin lispro and thus the chance of hypoglycemia should be monitored closely. | NA | Liprelog | Eli Lilly & Co. Ltd. | Eli Lilly & Co. Ltd. | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10280 | Th1040 | Insulin Lispro | >Th1040_Insulin_Lispro GIVEQCCTSICSLYQLENYCN | 5808 | C257H387N65O76S6 | 5.39 | 0.218 | 81 | On subcutaneous administration = 1 hour | Insulin lispro is a recombinant human insulin analogue produced in a specialized laboratory strain of Escherischia coli. Plasmid DNA transfected into the bacteria encodes for an analogue of human insulin that has a lysine at residuce B28 and proline at B29; these residues are reversed in endogenous human insulin. Reversal of these amino acid residues produces a rapid-acting insulin analogue. FDA approved on 1996. | To treat type 1 or 2 diabetes mellitus. To be used in conjunction with an intermediate or long-acting insulin except when used in a continuous insulin infusion pump. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin lispro binds to the insulin receptor(IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Reversal of the proline and lysine residues at positions B28 and B29 of native insulin eliminates hydrophobic interactions and weakens some of the hydrogen bonds that contribute to the stability of the insulin dimers that comprise insulin hexamers. Hexamers of insulin lispro are produced in the presence of zinc and -cresol. These weakly associated hexamers quickly dissociate upon subcutaneous injection and are absorbed as monomers through vascular endothelial cells. These properties give insulin lispro its fast-acting properties. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | Rapidly absorbed following subcutaneous administration. It is also absorbed more quickly than regular human insulin. Peak serum levels occur 30-90 minutes after injection in healthy subjects. Absorption also differs depending on the site of injection. Aft | When administered intravenously as bolus injections of 0.1 and 0.2 U/kg dose in two separate groups of healthy subjects, the mean volume of distribution of insulin lispro appeared to decrease with increase in dose (1.55 and 0.72 L/kg, respectively). | Clearance is dose dependent. When a dose of 0.1 unit/kg and 0.2 unit/kg were administered intravenously, the mean clearance was 21.0 mL/min/kg and 9.6 mL/min/kg respectively. | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin Analog, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | Concomitant therapy with somatostatin analogs like Octreotide may increase the blood-glucose-lowering effect of insulin lispro and thus the chance of hypoglycemia should be monitored closely. | NA | Humalog Pen | Eli Lilly | Eli Lilly | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10281 | Th1040 | Insulin Lispro | >Th1040_Insulin_Lispro GIVEQCCTSICSLYQLENYCN | 5808 | C257H387N65O76S6 | 5.39 | 0.218 | 81 | On subcutaneous administration = 1 hour | Insulin lispro is a recombinant human insulin analogue produced in a specialized laboratory strain of Escherischia coli. Plasmid DNA transfected into the bacteria encodes for an analogue of human insulin that has a lysine at residuce B28 and proline at B29; these residues are reversed in endogenous human insulin. Reversal of these amino acid residues produces a rapid-acting insulin analogue. FDA approved on 1996. | To treat type 1 or 2 diabetes mellitus. To be used in conjunction with an intermediate or long-acting insulin except when used in a continuous insulin infusion pump. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin lispro binds to the insulin receptor(IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Reversal of the proline and lysine residues at positions B28 and B29 of native insulin eliminates hydrophobic interactions and weakens some of the hydrogen bonds that contribute to the stability of the insulin dimers that comprise insulin hexamers. Hexamers of insulin lispro are produced in the presence of zinc and -cresol. These weakly associated hexamers quickly dissociate upon subcutaneous injection and are absorbed as monomers through vascular endothelial cells. These properties give insulin lispro its fast-acting properties. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | Rapidly absorbed following subcutaneous administration. It is also absorbed more quickly than regular human insulin. Peak serum levels occur 30-90 minutes after injection in healthy subjects. Absorption also differs depending on the site of injection. Aft | When administered intravenously as bolus injections of 0.1 and 0.2 U/kg dose in two separate groups of healthy subjects, the mean volume of distribution of insulin lispro appeared to decrease with increase in dose (1.55 and 0.72 L/kg, respectively). | Clearance is dose dependent. When a dose of 0.1 unit/kg and 0.2 unit/kg were administered intravenously, the mean clearance was 21.0 mL/min/kg and 9.6 mL/min/kg respectively. | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin Analog, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | The beta-blocker, esmolol, may decrease symptoms of hypoglycemia. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10282 | Th1040 | Insulin Lispro | >Th1040_Insulin_Lispro GIVEQCCTSICSLYQLENYCN | 5808 | C257H387N65O76S6 | 5.39 | 0.218 | 81 | On subcutaneous administration = 1 hour | Insulin lispro is a recombinant human insulin analogue produced in a specialized laboratory strain of Escherischia coli. Plasmid DNA transfected into the bacteria encodes for an analogue of human insulin that has a lysine at residuce B28 and proline at B29; these residues are reversed in endogenous human insulin. Reversal of these amino acid residues produces a rapid-acting insulin analogue. FDA approved on 1996. | To treat type 1 or 2 diabetes mellitus. To be used in conjunction with an intermediate or long-acting insulin except when used in a continuous insulin infusion pump. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin lispro binds to the insulin receptor(IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Reversal of the proline and lysine residues at positions B28 and B29 of native insulin eliminates hydrophobic interactions and weakens some of the hydrogen bonds that contribute to the stability of the insulin dimers that comprise insulin hexamers. Hexamers of insulin lispro are produced in the presence of zinc and -cresol. These weakly associated hexamers quickly dissociate upon subcutaneous injection and are absorbed as monomers through vascular endothelial cells. These properties give insulin lispro its fast-acting properties. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | Rapidly absorbed following subcutaneous administration. It is also absorbed more quickly than regular human insulin. Peak serum levels occur 30-90 minutes after injection in healthy subjects. Absorption also differs depending on the site of injection. Aft | When administered intravenously as bolus injections of 0.1 and 0.2 U/kg dose in two separate groups of healthy subjects, the mean volume of distribution of insulin lispro appeared to decrease with increase in dose (1.55 and 0.72 L/kg, respectively). | Clearance is dose dependent. When a dose of 0.1 unit/kg and 0.2 unit/kg were administered intravenously, the mean clearance was 21.0 mL/min/kg and 9.6 mL/min/kg respectively. | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Insulin, Insulin Analog, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | Concomitant therapy with sympathomimetic agents like Epinephrine may reduce the blood-glucose-lowering effect of insulin lispro. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10283 | Th1041 | Insulin Glargine | >Th1041_Insulin_Glargine GIVEQCCTSICSLYQLENYCG | 6063 | C267H404N72O78S6 | 6.88 | 0.098 | 81 | Not reported in humans; 30 hours in mammalian reticulocytes. | Insulin glargine is produced by recombinant DNA technology using a non-pathogenic laboratory strain of Escherichia coli (K12). It is an analogue of human insulin made by replacing the asparagine residue at position A21 of the A-chain with glycine and adding two arginines to the C-terminus (positions B31 and 32) of the B-chain. The resulting protein is soluble at pH 4 and forms microprecipitates at physiological pH 7.4. Small amounts of insulin glargine are slowly released from microprecipitates giving the drug a long duration of action (up to 24 hours) and no pronounced peak concentration. | To treat Type 1 or 2 diabetes mellitus in patients over 17 years old who require a long-acting (basal) insulin for the control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for glycemic control. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin glargine binds to the insulin receptor, a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism. Insulin glargine is completely soluble at pH 4, the pH of administered solution, and has low solubility at physiological pH 7.4. Upon subcuteous injection, the solution is neutralized resulting in the formation of microprecipitates. Small amounts of insulin glargine are released from microprecipitates giving the drug a relatively constant concentration over time profile over 24 hours with no pronounced peak. This release mechanism allows the drug to mimic basal insulin levels within the body. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Partly metabolized to two active metabolites with similar in vitro activity to insulin: A21-Gly-insulin and A21-Gly-des-B30-Thr-insulin. | Due to the modifications in the A and B chain, the isoelectric point shifts towards a neutral pH and insulin glargine is more stable in acidic conditions than regular insulin. As insulin glargine is less soluble at neutral pH, once injected, forms micro-p | NA | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Antimetabolites, Biological Products, Blood Glucose Lowering Agents, Complex Mixtures, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Hypolipidemic Agents, Insulin, Insulin Analog, Insulin, Long-Acting, Lipid Regulating Agents, Pancreatic Hormones, Peptide Hormones, Peptides | US7476652 | 13-Jan-2009 | 23-Jul-2023 | Somatropin may antagonize the hypoglycemic effect of insulin glargine. Monitor for changes in fasting and postprandial blood sugars. | Insulin receptor,Insulin-like growth factor 1 receptor | Lantus | Sanofi-Aventis | Sanofi-Aventis | Its used to improve glycemic control in adults and children with type 1 diabetes mellitus and in adults with type 2 diabetes mellitus. | 21A-Gly-30Ba-L-Arg-30Bb-L-Arg-human insulin | LANTUS consists of insulin glargine dissolved in a clear aqueous fluid. Each milliliter of LANTUS contains 100 Units (3.6378 mg) insulin glargine. The 10 mL vial presentation contains the following inactive ingredients per mL: 30 mcg zinc, 2.7 mg m-cresol | Solution | Subcutaneous Injection | LANTUS may be administered at any time during the day. LANTUS should be administered subcutaneously once a day at the same time every day. The dose of LANTUS must be individualized based on clinical response. | Hypersensitivity | Low blood sugar (headache, hunger, weakness, sweating, confusion, irritability, dizziness, fast heart rate, or feeling jittery). Sign of insulin allergy include itching skin rash over the entire body, wheezing, trouble breathing, fast heart rate, sweating. | Link | NA | NA |
| 10284 | Th1041 | Insulin Glargine | >Th1041_Insulin_Glargine GIVEQCCTSICSLYQLENYCG | 6063 | C267H404N72O78S6 | 6.88 | 0.098 | 81 | Not reported in humans; 30 hours in mammalian reticulocytes. | Insulin glargine is produced by recombinant DNA technology using a non-pathogenic laboratory strain of Escherichia coli (K12). It is an analogue of human insulin made by replacing the asparagine residue at position A21 of the A-chain with glycine and adding two arginines to the C-terminus (positions B31 and 32) of the B-chain. The resulting protein is soluble at pH 4 and forms microprecipitates at physiological pH 7.4. Small amounts of insulin glargine are slowly released from microprecipitates giving the drug a long duration of action (up to 24 hours) and no pronounced peak concentration. | To treat Type 1 or 2 diabetes mellitus in patients over 17 years old who require a long-acting (basal) insulin for the control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for glycemic control. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin glargine binds to the insulin receptor, a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism. Insulin glargine is completely soluble at pH 4, the pH of administered solution, and has low solubility at physiological pH 7.4. Upon subcuteous injection, the solution is neutralized resulting in the formation of microprecipitates. Small amounts of insulin glargine are released from microprecipitates giving the drug a relatively constant concentration over time profile over 24 hours with no pronounced peak. This release mechanism allows the drug to mimic basal insulin levels within the body. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Partly metabolized to two active metabolites with similar in vitro activity to insulin: A21-Gly-insulin and A21-Gly-des-B30-Thr-insulin. | Due to the modifications in the A and B chain, the isoelectric point shifts towards a neutral pH and insulin glargine is more stable in acidic conditions than regular insulin. As insulin glargine is less soluble at neutral pH, once injected, forms micro-p | NA | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Antimetabolites, Biological Products, Blood Glucose Lowering Agents, Complex Mixtures, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Hypolipidemic Agents, Insulin, Insulin Analog, Insulin, Long-Acting, Lipid Regulating Agents, Pancreatic Hormones, Peptide Hormones, Peptides | US6100376 | 8-Aug-2000 | 6-Nov-2009 | The beta-blocker, Timolol, Sotalol, Propranolol, Practolol, Acebutolol, Atenolol, Betaxolol, Bevantolol, Bisoprolol, Carteolol, Carvedilol, Esmolol | NA | Lantus R / Lusduna Nexvue / Optisulin / Semglee | (Mylan Pharmaceuticals Inc) | (Mylan Pharmaceuticals Inc) | to control high blood sugar in adults with diabetes mellitus. | NA | NA | clear aqueous fluid | Injection | NA | LANTUS is contraindicated: during episodes of hypoglycemia in patients with hypersensitivity to LANTUS or one of its excipients | NA | Link | NA | NA |
| 10285 | Th1041 | Insulin Glargine | >Th1041_Insulin_Glargine GIVEQCCTSICSLYQLENYCG | 6063 | C267H404N72O78S6 | 6.88 | 0.098 | 81 | Not reported in humans; 30 hours in mammalian reticulocytes. | Insulin glargine is produced by recombinant DNA technology using a non-pathogenic laboratory strain of Escherichia coli (K12). It is an analogue of human insulin made by replacing the asparagine residue at position A21 of the A-chain with glycine and adding two arginines to the C-terminus (positions B31 and 32) of the B-chain. The resulting protein is soluble at pH 4 and forms microprecipitates at physiological pH 7.4. Small amounts of insulin glargine are slowly released from microprecipitates giving the drug a long duration of action (up to 24 hours) and no pronounced peak concentration. | To treat Type 1 or 2 diabetes mellitus in patients over 17 years old who require a long-acting (basal) insulin for the control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for glycemic control. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin glargine binds to the insulin receptor, a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism. Insulin glargine is completely soluble at pH 4, the pH of administered solution, and has low solubility at physiological pH 7.4. Upon subcuteous injection, the solution is neutralized resulting in the formation of microprecipitates. Small amounts of insulin glargine are released from microprecipitates giving the drug a relatively constant concentration over time profile over 24 hours with no pronounced peak. This release mechanism allows the drug to mimic basal insulin levels within the body. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Partly metabolized to two active metabolites with similar in vitro activity to insulin: A21-Gly-insulin and A21-Gly-des-B30-Thr-insulin. | Due to the modifications in the A and B chain, the isoelectric point shifts towards a neutral pH and insulin glargine is more stable in acidic conditions than regular insulin. As insulin glargine is less soluble at neutral pH, once injected, forms micro-p | NA | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Antimetabolites, Biological Products, Blood Glucose Lowering Agents, Complex Mixtures, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Hypolipidemic Agents, Insulin, Insulin Analog, Insulin, Long-Acting, Lipid Regulating Agents, Pancreatic Hormones, Peptide Hormones, Peptides | CA1339044 | 1-Apr-1997 | 1-Apr-2014 | NA | NA | Abasaglar/Basaglar | Eli Lilly Nederland B.V | Eli Lilly Nederland B.V | to control high blood sugar in adults and children with type 1 diabetes mellitus and adults with type 2 diabetes mellitus. | NA | BASAGLAR is produced by recombinant DNA technology utilizing a non-pathogenic laboratory strain of Escherichia coli (K12) as the production organism. Insulin glargine differs from human insulin in that the amino acid asparagine at position A21 is replaced by glycine and two arginines are added to the C-terminus of the B-chain. | clear, colorless, sterile aqueous solution | subcutaneously into the abdominal area, thigh, or deltoid, and rotate injection sites within the same region from one injection to the next | Inject between 1 and 80 units per injection. | BASAGLAR is contraindicated: During episodes of hypoglycemia. In patients with hypersensitivity to insulin glargine or one of its excipients | low blood sugar (hypoglycemia), allergic reactions, injection site reactions, body fat redistribution, itching, rash, swelling, weight gain, upper respiratory tract infection, runny or stuffy nose, back pain, cough, urinary tract infection, diarrhea, depression, or headache. | Link | NA | NA |
| 10286 | Th1041 | Insulin Glargine | >Th1041_Insulin_Glargine GIVEQCCTSICSLYQLENYCG | 6063 | C267H404N72O78S6 | 6.88 | 0.098 | 81 | Not reported in humans; 30 hours in mammalian reticulocytes. | Insulin glargine is produced by recombinant DNA technology using a non-pathogenic laboratory strain of Escherichia coli (K12). It is an analogue of human insulin made by replacing the asparagine residue at position A21 of the A-chain with glycine and adding two arginines to the C-terminus (positions B31 and 32) of the B-chain. The resulting protein is soluble at pH 4 and forms microprecipitates at physiological pH 7.4. Small amounts of insulin glargine are slowly released from microprecipitates giving the drug a long duration of action (up to 24 hours) and no pronounced peak concentration. | To treat Type 1 or 2 diabetes mellitus in patients over 17 years old who require a long-acting (basal) insulin for the control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for glycemic control. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin glargine binds to the insulin receptor, a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism. Insulin glargine is completely soluble at pH 4, the pH of administered solution, and has low solubility at physiological pH 7.4. Upon subcuteous injection, the solution is neutralized resulting in the formation of microprecipitates. Small amounts of insulin glargine are released from microprecipitates giving the drug a relatively constant concentration over time profile over 24 hours with no pronounced peak. This release mechanism allows the drug to mimic basal insulin levels within the body. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Partly metabolized to two active metabolites with similar in vitro activity to insulin: A21-Gly-insulin and A21-Gly-des-B30-Thr-insulin. | Due to the modifications in the A and B chain, the isoelectric point shifts towards a neutral pH and insulin glargine is more stable in acidic conditions than regular insulin. As insulin glargine is less soluble at neutral pH, once injected, forms micro-p | NA | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Antimetabolites, Biological Products, Blood Glucose Lowering Agents, Complex Mixtures, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Hypolipidemic Agents, Insulin, Insulin Analog, Insulin, Long-Acting, Lipid Regulating Agents, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | NA | NA | Lantus OptiSet | NA | NA | Its used to reduce high blood sugar in adults, adolescents and children of 6 years or above with diabetes mellitus. | NA | NA | Solution | Subcutaneous Injection | Patients need one injection of Lantus every day, at the same time of the day. In children, only evening injection has been studied.OptiSet delivers insulin in increments of 2 units up to a maximum single dose of 40 units. The dosage may vary from person tto person. | Hypersensitivity | Hypoglycemia, skin changes at the injection site, allergic reactions, large-scale skin reactions (rash and itching all over the body), severe swelling of skin or mucous membranes (angio-oedema), shortness of breath, a fall in blood pressure with rapid headache. | Link | NA | NA |
| 10287 | Th1041 | Insulin Glargine | >Th1041_Insulin_Glargine GIVEQCCTSICSLYQLENYCG | 6063 | C267H404N72O78S6 | 6.88 | 0.098 | 81 | Not reported in humans; 30 hours in mammalian reticulocytes. | Insulin glargine is produced by recombinant DNA technology using a non-pathogenic laboratory strain of Escherichia coli (K12). It is an analogue of human insulin made by replacing the asparagine residue at position A21 of the A-chain with glycine and adding two arginines to the C-terminus (positions B31 and 32) of the B-chain. The resulting protein is soluble at pH 4 and forms microprecipitates at physiological pH 7.4. Small amounts of insulin glargine are slowly released from microprecipitates giving the drug a long duration of action (up to 24 hours) and no pronounced peak concentration. | To treat Type 1 or 2 diabetes mellitus in patients over 17 years old who require a long-acting (basal) insulin for the control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for control of hyperglycemia. May be used in pediatric patients with Type 1 diabetes mellitus who require a long-acting (basal) insulin for glycemic control. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis. | Insulin glargine binds to the insulin receptor, a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism. Insulin glargine is completely soluble at pH 4, the pH of administered solution, and has low solubility at physiological pH 7.4. Upon subcuteous injection, the solution is neutralized resulting in the formation of microprecipitates. Small amounts of insulin glargine are released from microprecipitates giving the drug a relatively constant concentration over time profile over 24 hours with no pronounced peak. This release mechanism allows the drug to mimic basal insulin levels within the body. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweat | Partly metabolized to two active metabolites with similar in vitro activity to insulin: A21-Gly-insulin and A21-Gly-des-B30-Thr-insulin. | Due to the modifications in the A and B chain, the isoelectric point shifts towards a neutral pH and insulin glargine is more stable in acidic conditions than regular insulin. As insulin glargine is less soluble at neutral pH, once injected, forms micro-p | NA | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Antimetabolites, Biological Products, Blood Glucose Lowering Agents, Complex Mixtures, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Hypolipidemic Agents, Insulin, Insulin Analog, Insulin, Long-Acting, Lipid Regulating Agents, Pancreatic Hormones, Peptide Hormones, Peptides | NA | NA | NA | NA | NA | Lantus SoloStar | NA | NA | It works by helping your body to use sugar properly. This lowers the amount of glucose in the blood, which helps to treat diabetes. | NA | NA | Solution | Subcutaneous Injection | NA | Hypersensitivity | Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); changes in vision; chills; confusion; dizziness; drowsiness; fainting; fast heartbeat; fast, shallow breathing. | Link | NA | NA |
| 10372 | Th1055 | Follitropin beta | >Th1055_Follitropin_beta APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Follitropin beta is a human follicle stimulating hormone (FSH) preparation of recombinant DNA origin, which consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Follitropin beta is produced in genetically engineered Chinese hamster cell lines (CHO). The nomenclature “beta†differentiates it from another recombinant human FSH product that was marketed earlier as follitropin alpha. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels. Structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | For treatment of female infertility | Used for the treatment of female infertility, Follitropin beta or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of Follitropin beta is the primary hormone responsible for follicular recruitment and development. | Follitropin alpha is a recombinant form of endogenous follicle stimulating hormone (FSH). FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | Headaches, ovarian cysts, nausea and upper respiratory tract infections occurred in more than 10% of women in clinical trials. In men, the most serious adverse events reported were testicular surgery for cryptorchidism which existed prestudy, hemoptysis, an infected pilonidal cyst, and lymphadenopathy associated with an Epstein-Barr viral infection. Other concerns include overstimulation of the ovaries, pulmonary and vascular complications and multiple births. Post-marketing reports revealed hypersensitivity reactions including anaphylactoid reactions and asthma. Follitropin is contraindicated in pregnant women. | NA | bioavailability is approximately 66-76%. | 8 L [female subjects following intravenous administration of a 300 IU dose] | 0.011 /h/kg [European women with a single intramuscular dose of 300 IU] 0.011 /h/kg [Japanese women with a single intramuscular dose of 300 IU] | Amino Acids, Peptides, and Proteins, Follicle Stimulating Hormone, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Proteins, Sex Hormones and Modulators of the Genital System, Thyroid Products | US7741268 | 22-Jun-2010 | 2-Apr-2024 | NA | Follicle-stimulating hormone receptor | Follistim AQ | Merck | Merck | Follistim AQ (follitropin beta injection) is indicated for the development of multiple follicles in ovulatory patients participating in an Assisted Reproductive Technology (ART) program. Follistim AQ (follitropin beta) is also indicated for the induction of ovulation and pregnancy in anovulatory infertile patients in whom the cause of infertility is functional and not due to primary ovarian failure. | NA | Each single-use vial of Follistim AQ (follitropin beta) contains the following per 0.5 mL: 75 IU or 150 IU of FSH activity; 25 mg sucrose, NF; 7.35 mg sodium citrate (dihydrate), USP; 0.25 mg L-methionine, USP; 0.1 mg polysorbate 20, NF; and water for injection, USP. Hydrochloric acid, NF and/or sodium hydroxide, NF are used to adjust the pHto 7. | Follistim AQ (follitropin beta) is presented as a Sterile aqueous solution | for Subcutaneous or INTRAMUSubcutaneousULAR admini | starting dose of 150 to 225 IU of Follistim AQ (follitropin beta injection) is recommended for at least the first four days of treatment. After this, the dose may be adjusted for the individual patient based upon their ovarian response. | Tumor of the ovary, breast, uterus, hypothalamus or pituitary gland; Pregnancy; Uncontrolled thyroid or adrenal dysfunction; High levels of FSH indicating primary ovarian failure; | The following adverse events have been reported in women treated with gonado tropins: pulmonary and vascular complications, hemoperitoneum, adnexal torsion (as a complication of ovarian enlargement), dizziness, tachycardia, dyspnea, tachypnea, febrile reactions, flu-like symptoms including fever, chills, mus culoskeletal aches, joint pains, nausea, headache and malaise, breast tenderness, and dermatological symptoms | Link | NA | NA |
| 10373 | Th1055 | Follitropin beta | >Th1055_Follitropin_beta APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Follitropin beta is a human follicle stimulating hormone (FSH) preparation of recombinant DNA origin, which consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Follitropin beta is produced in genetically engineered Chinese hamster cell lines (CHO). The nomenclature “beta†differentiates it from another recombinant human FSH product that was marketed earlier as follitropin alpha. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels. Structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | For treatment of female infertility | Used for the treatment of female infertility, Follitropin beta or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of Follitropin beta is the primary hormone responsible for follicular recruitment and development. | Follitropin alpha is a recombinant form of endogenous follicle stimulating hormone (FSH). FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | Headaches, ovarian cysts, nausea and upper respiratory tract infections occurred in more than 10% of women in clinical trials. In men, the most serious adverse events reported were testicular surgery for cryptorchidism which existed prestudy, hemoptysis, an infected pilonidal cyst, and lymphadenopathy associated with an Epstein-Barr viral infection. Other concerns include overstimulation of the ovaries, pulmonary and vascular complications and multiple births. Post-marketing reports revealed hypersensitivity reactions including anaphylactoid reactions and asthma. Follitropin is contraindicated in pregnant women. | NA | bioavailability is approximately 66-76%. | 8 L [female subjects following intravenous administration of a 300 IU dose] | 0.011 /h/kg [European women with a single intramuscular dose of 300 IU] 0.011 /h/kg [Japanese women with a single intramuscular dose of 300 IU] | Amino Acids, Peptides, and Proteins, Follicle Stimulating Hormone, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Proteins, Sex Hormones and Modulators of the Genital System, Thyroid Products | US5270057 | 14-Dec-1993 | 14-Dec-2010 | NA | NA | Bemfola | Gedeon Richter Plc | Gedeon Richter Plc | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10374 | Th1055 | Follitropin beta | >Th1055_Follitropin_beta APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Follitropin beta is a human follicle stimulating hormone (FSH) preparation of recombinant DNA origin, which consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Follitropin beta is produced in genetically engineered Chinese hamster cell lines (CHO). The nomenclature “beta†differentiates it from another recombinant human FSH product that was marketed earlier as follitropin alpha. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels. Structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | For treatment of female infertility | Used for the treatment of female infertility, Follitropin beta or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of Follitropin beta is the primary hormone responsible for follicular recruitment and development. | Follitropin alpha is a recombinant form of endogenous follicle stimulating hormone (FSH). FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | Headaches, ovarian cysts, nausea and upper respiratory tract infections occurred in more than 10% of women in clinical trials. In men, the most serious adverse events reported were testicular surgery for cryptorchidism which existed prestudy, hemoptysis, an infected pilonidal cyst, and lymphadenopathy associated with an Epstein-Barr viral infection. Other concerns include overstimulation of the ovaries, pulmonary and vascular complications and multiple births. Post-marketing reports revealed hypersensitivity reactions including anaphylactoid reactions and asthma. Follitropin is contraindicated in pregnant women. | NA | bioavailability is approximately 66-76%. | 8 L [female subjects following intravenous administration of a 300 IU dose] | 0.011 /h/kg [European women with a single intramuscular dose of 300 IU] 0.011 /h/kg [Japanese women with a single intramuscular dose of 300 IU] | Amino Acids, Peptides, and Proteins, Follicle Stimulating Hormone, Genito Urinary System and Sex Hormones, Gonadotropins, Gonadotropins and Antigonadotropins, Gonadotropins, Pituitary, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Peptide Hormones, Peptides, Pituitary Hormones, Pituitary Hormones, Anterior, Proteins, Sex Hormones and Modulators of the Genital System, Thyroid Products | CA2037884 | 21-Oct-2003 | 8-Mar-2011 | NA | NA | Fertavid | Merck Sharp & Dohme B.V. | Merck Sharp & Dohme B.V. | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10375 | Th1056 | Vasopressin | >Th1056_Vasopressin CYFQNCPRG | 2140.46 | C92H130N28O24S4 | NA | -4.9 | NA | 10-20 minutes | Antidiuretic hormone, also known as vasopressin, is a nine amino acid peptide secreted from the posterior pituitary. Antidiuretic hormone binds to receptors in the distal or collecting tubules of the kidney and promotes reabsorbtion of water back into the circulation. | For the treatment of enuresis, polyuria, diabetes insipidus, polydipsia and oesophageal varices with bleeding | Vasopressin is an antidiuretic hormone indicated for the prevention and treatment of postoperative abdominal distention, in abdominal roentgenography to dispel interfering gas shadows, and in diabetes insipidus. Vasopressin can cause contraction of smooth muscle of the gastrointestinal tract and of all parts of the vascular bed, especially the capillaries, small arterioles and venules. It has less effect on the smooth musculature of the large veins. Vasopressin may also be used to control bleeding in some forms of von Willebrand disease and to treat extreme cases of bed wetting in children. It may also play a role in memory formation although the mechanism is unknown. | Vasopressin acts on three different receptors, vasopressin receptor V1a (which initiates vasoconstriction, liver gluconeogenesis, platelet aggregation and release of factor VIII), vasopressin receptor V1b (which mediates corticotrophin secretion from the pituitary) and vasopressin receptor V2 which controls free water reabsorption in the renal medullar. The binding of vasopressin to the V2 receptor activates adenylate cyclase which causes the release of aquaporin 2 channels into the cells lining the renal medullar duct. This allows water to be reabsorbed down an osmotic gradient so the urine is more concentrated. | Vasopressin overdose is expected to present with consequences related to excessive vasoconstriction of peripheral, mesenteric, coronary vascular beds, hyponatremia, and possibly with ventricular tachyarrhythmias, rhabdomyolysis, and gastrointestinal symptoms. As vasopressin is rapidly metabolized and cleared, symptoms will resolve with cessation of vasopressin administration. | The majority of a dose of vasopressin is metabolized and rapidly destroyed in the liver and kidneys. | NA | NA | Vasopressin has a clearance of 9-25 mL/min/kg in patients with vasodilatory shock receiving 0.01-0.1 U/min of vasopressin. | Amino Acids, Peptides, and Proteins, Antidiuretic Agents, Arginine Vasopressin, Arginine Vasopressin, analogs & derivatives, Cardiovascular Agents, Coagulants, Decreased Diuresis, Hematologic Agents, Hemostatics, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Natriuretic Agents, Nerve Tissue Proteins, Neuropeptides, Oligopeptides, Peptide Hormones, Peptides, Pituitary, Pituitary Hormones, Pituitary Hormones, Posterior, Proteins, Vasoconstriction, Vasoconstrictor Agents, Vasopressin and Analogues, Vasopressins | NA | NA | NA | NA | Vasopressin V2 receptor,Vasopressin V1a receptor,Vasopressin V1b receptor, Oxytocin receptor | Pitressin | JHP Pharmaceuticals | JHP Pharmaceuticals | Vasopressin is indicated for prevention and treatment of postoperative abdominal distention, in abdominal roentgenography to dispel interfering gas shadows, and in diabetes insipidus. | NA | Vasopressin 20 units, Sodium Chloride 9 mg, Chlorobutanol 0.5% (as a preservative), Water for Injection q.s. pH (range 2.5 - 4.5) adjusted with Acetic Acid. | Vasopressin Injection, USP is a Sterile, aqueous solution of synthetic vasopressin (8-L-arginine vasopressin) of the posterior pituitary gland | intramuSubcutaneousular or Subcutaneous use | For Abdominal Distention, Abdominal Roentgenography, Diabetes Insipidus: Ten units of vassopressin (0.5mL) will usually elicit full physiologic response in adult patients. | Anaphylaxis or hypersensitivity to the drug or its components. | anaphylaxia (cardiac arrest), circumoral pallor, arrhythmias, decreased cardiac output, angina, myocardial ischemia, peripheral vasoconstruction and gangrene, nausea, vomiting, tremor, vertigo, bronchial constriction | Link | NA | NA |
| 10382 | Th1060 | Insulin, porcine | >Th1060_Insulin,_porcine GIVEQCCTSICSLYQLENYCN | 5795.6 | C257H387N65O76S6 | 5.39 | 0.218 | NA | 0.03 hours | Insulin isolated from pig pancreas. Composed of alpha and beta chains, processed from pro-insulin. Forms a hexameric structure. | For the treatment of type I and II diabetes mellitus. | Insulin is used in the treatment of type I and type II diabetes. The primary activity of insulin is the regulation of glucose metabolism. In muscle and other tissues (except the brain), insulin causes rapid transport of glucose and amino acids intracellularly. It also promotes anabolism, and inhibits protein catabolism. In the liver, insulin promotes the uptake and storage of glucose in the form of glycogen, inhibits gluconeogenesis, and promotes the conversion of excess glucose into fat. | Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism. | NA | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | NA | NA | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Insulin, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides, Proteins | NA | NA | NA | NA | Interferon alpha/beta receptor 2,Interferon alpha/beta receptor 1 | vetsulin | Intervet Inc (Merck Animal Health) | Intervet Inc (Merck Animal Health) | vetsulin (porcine insulin zinc suspension) is indicated for the reduction of hyperglycemia and hyperglycemia-associated clinical signs in dogs and cats with diabetes mellitus | NA | purified porcine insulin 40 IU (35% amorphous and 65% crystalline), Zinc (as chloride) 0.08 mg, Sodium acetate trihydrate 1.36 mg, Sodium chloride 7.0 mg, Methylparaben (preservative) 1.0 mg, pH is adjusted with hydrochloric acid and/or sodium hydroxide. | Vetsulin is supplied as a sterile injectable suspension in multidose vials containing 10 mL of 40 IU/mL porcine insulin zinc suspension. Vials are supplied in cartons of one, 10 mL vial. | Subcutaneous Injection | In dogs: The initial recommended vetsulin dose is 0.5 IU insulin/kg body weight. Initially, this dose should be given once daily concurrently with, or right after a meal; In Cats:The initial recommended dose in cats is 1 to 2 IU per injection. The injections should be given twice daily at approximately 12 hour intervals. | Dogs and cats known to have a systemic allergy to pork or pork products should not be treated with vetsulin. vetsulin is contraindicated during periods of hypoglycemia. | In dogs: Clinical signs of hypoglycemia were generally mild in nature (described as weakness, lethargy, stumbling, falling down, and/or depression, hematuria, vomiting, diarrhea, pancreatitis, non-specific hepatopathy/pancreatitis, development of cataracts, and urinary tract infections. In Cats: omiting, lethargy, diarrhea, decreased appetite/anorexia, pancreatitis, dermal events, respiratory disease, urinary tract disorder, renal disease, dehydration, weight loss, polydipsia, polyuria, behavioral change, and ocular discharge/conjunctivitis. | Link | NA | NA |
| 10383 | Th1060 | Insulin, porcine | >Th1060_Insulin,_porcine GIVEQCCTSICSLYQLENYCN | 5795.6 | C257H387N65O76S6 | 5.39 | 0.218 | NA | 0.03 hours | Insulin isolated from pig pancreas. Composed of alpha and beta chains, processed from pro-insulin. Forms a hexameric structure. | For the treatment of type I and II diabetes mellitus. | Insulin is used in the treatment of type I and type II diabetes. The primary activity of insulin is the regulation of glucose metabolism. In muscle and other tissues (except the brain), insulin causes rapid transport of glucose and amino acids intracellularly. It also promotes anabolism, and inhibits protein catabolism. In the liver, insulin promotes the uptake and storage of glucose in the form of glycogen, inhibits gluconeogenesis, and promotes the conversion of excess glucose into fat. | Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism. | NA | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | NA | NA | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Insulin, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides, Proteins | NA | NA | NA | NA | Insulin-like growth factor 1 receptor, Insulin receptor | Hypurin | Wockhardt Uk Ltd | Wockhardt Uk Ltd | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10384 | Th1060 | Insulin, porcine | >Th1060_Insulin,_porcine GIVEQCCTSICSLYQLENYCN | 5795.6 | C257H387N65O76S6 | 5.39 | 0.218 | NA | 0.03 hours | Insulin isolated from pig pancreas. Composed of alpha and beta chains, processed from pro-insulin. Forms a hexameric structure. | For the treatment of type I and II diabetes mellitus. | Insulin is used in the treatment of type I and type II diabetes. The primary activity of insulin is the regulation of glucose metabolism. In muscle and other tissues (except the brain), insulin causes rapid transport of glucose and amino acids intracellularly. It also promotes anabolism, and inhibits protein catabolism. In the liver, insulin promotes the uptake and storage of glucose in the form of glycogen, inhibits gluconeogenesis, and promotes the conversion of excess glucose into fat. | Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism. | NA | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | NA | NA | NA | Alimentary Tract and Metabolism, Amino Acids, Peptides, and Proteins, Blood Glucose Lowering Agents, Cytochrome P-450 CYP1A2 Inducers, Cytochrome P-450 CYP1A2 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Drugs Used in Diabetes, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Insulin, Insulin, Short-Acting, Insulins and Analogues for Injection, Fast-Acting, Pancreatic Hormones, Peptide Hormones, Peptides, Proteins | NA | NA | NA | NA | Hyaluronan,Transforming growth factor beta-1 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10415 | Th1069 | Pegvisomant | >Th1069_Pegvisomant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 | 6 days | Pegvisomant is a highly selective growth hormone (GH) receptor antagonist. It is used to treat acromegaly. Unlike dopamine or somatostatin analogs (which inhibit growth hormone secretion), this drug actually blocks the hepatic (GH-mediated) production of insulin like growth factor (IGF-1), which is the main mediator of growth hormone activity. | Pegvisomant is a growth hormone receptor antagonist used for the treatment of acromegaly. | Somavert is used for the treatment of acromegaly, which arises from excessive IGF-1 levels. Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH, and thus interferes with GH signal transduction. Inhibition of GH action results in decreased serum concentrations of insulin-like growth factor-I (IGF-I), and IGF binding protein-3 (IGFBP-3). This reduces the symptoms of acromegaly. | Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH. This leads to the normalization of serum IGF-1 levels. | NA | NA | NA | 7 L | 36 ± 28 mL/h [SC doses ranging from 10 to 20 mg/day] | Acromegaly, Amino Acids, Peptides, and Proteins, Anterior Pituitary Lobe Hormones and Analogues, Cholinesterase Inhibitors, Cytochrome P-450 CYP3A Inducers, Cytochrome P-450 CYP3A4 Inducers, Cytochrome P-450 CYP3A4 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Growth Hormone Receptor Antagonist, Growth Hormone Receptor Antagonists, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Pegylated agents, Peptide Hormones, Peptides, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Somatotropin Antagonists, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | US5849535 | 15-Dec-1998 | 25-Mar-2017 | Dihydrocodeine opioids may diminish the therapeutic effect of pegvisomant. It is recommended to monitor therapy | Growth hormone receptor | SOMAVERT | Pfizer | Pfizer | SOMAVERT is indicated for the treatment of acromegaly in patients who have had an inadequate response to surgery or radiation therapy, or for whom these therapies are not appropriate. The goal of treatment is to normalize serum insulin-like growth factor-I (IGF-I) levels. | NA | SOMAVERT is available in single-dose sterile vials containing 10, 15, or 20 mg of pegvisomant protein (approximately 10, 15, and 20 U activity, respectively). Each vial also contains 1.36 mg of glycine, 36.0 mg of mannitol, 1.04 mg of sodium phosphate dibasic anhydrous, and 0.36 mg of sodium phosphate monobasic monohydrate | SOMAVERT for injection is supplied as a Sterile, white lyophilized powder | Subcutaneous Injection | The recommended loading dose of SOMAVERT is 40 mg given subcutaneously, under healthcare provider supervision. Increase the dosage by 5 mg increments every 4-6 weeks if IGF-I concentrations are elevated.Decrease the dosage by 5 mg decrements every 4-6 weeks if IGF-I concentrations are below the normal range. | None. | Hypoglycemia associated with GH lowering in patients with Diabetes Mellitus, Liver test elevations, Cross-reactivity with GH assay, Lipohypertrophy, Systemic hypersensitivity, pain, nausea ,diarrhea, dizziness, Sinusitis | Link | NA | NA |
| 10416 | Th1069 | Pegvisomant | >Th1069_Pegvisomant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 | 6 days | Pegvisomant is a highly selective growth hormone (GH) receptor antagonist. It is used to treat acromegaly. Unlike dopamine or somatostatin analogs (which inhibit growth hormone secretion), this drug actually blocks the hepatic (GH-mediated) production of insulin like growth factor (IGF-1), which is the main mediator of growth hormone activity. | Pegvisomant is a growth hormone receptor antagonist used for the treatment of acromegaly. | Somavert is used for the treatment of acromegaly, which arises from excessive IGF-1 levels. Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH, and thus interferes with GH signal transduction. Inhibition of GH action results in decreased serum concentrations of insulin-like growth factor-I (IGF-I), and IGF binding protein-3 (IGFBP-3). This reduces the symptoms of acromegaly. | Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH. This leads to the normalization of serum IGF-1 levels. | NA | NA | NA | 7 L | 36 ± 28 mL/h [SC doses ranging from 10 to 20 mg/day] | Acromegaly, Amino Acids, Peptides, and Proteins, Anterior Pituitary Lobe Hormones and Analogues, Cholinesterase Inhibitors, Cytochrome P-450 CYP3A Inducers, Cytochrome P-450 CYP3A4 Inducers, Cytochrome P-450 CYP3A4 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Growth Hormone Receptor Antagonist, Growth Hormone Receptor Antagonists, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Pegylated agents, Peptide Hormones, Peptides, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Somatotropin Antagonists, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | US5350836 | 27-Sep-1994 | 27-Sep-2011 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10417 | Th1069 | Pegvisomant | >Th1069_Pegvisomant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 | 6 days | Pegvisomant is a highly selective growth hormone (GH) receptor antagonist. It is used to treat acromegaly. Unlike dopamine or somatostatin analogs (which inhibit growth hormone secretion), this drug actually blocks the hepatic (GH-mediated) production of insulin like growth factor (IGF-1), which is the main mediator of growth hormone activity. | Pegvisomant is a growth hormone receptor antagonist used for the treatment of acromegaly. | Somavert is used for the treatment of acromegaly, which arises from excessive IGF-1 levels. Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH, and thus interferes with GH signal transduction. Inhibition of GH action results in decreased serum concentrations of insulin-like growth factor-I (IGF-I), and IGF binding protein-3 (IGFBP-3). This reduces the symptoms of acromegaly. | Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH. This leads to the normalization of serum IGF-1 levels. | NA | NA | NA | 7 L | 36 ± 28 mL/h [SC doses ranging from 10 to 20 mg/day] | Acromegaly, Amino Acids, Peptides, and Proteins, Anterior Pituitary Lobe Hormones and Analogues, Cholinesterase Inhibitors, Cytochrome P-450 CYP3A Inducers, Cytochrome P-450 CYP3A4 Inducers, Cytochrome P-450 CYP3A4 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Growth Hormone Receptor Antagonist, Growth Hormone Receptor Antagonists, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Pegylated agents, Peptide Hormones, Peptides, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Somatotropin Antagonists, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | CA2230492 | 26-May-2009 | 20-Sep-2016 | NA | B-lymphocyte antigen CD20,Low affinity immunoglobulin gamma Fc region receptor III-B,Complement C1r subcomponent,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10418 | Th1069 | Pegvisomant | >Th1069_Pegvisomant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 | 6 days | Pegvisomant is a highly selective growth hormone (GH) receptor antagonist. It is used to treat acromegaly. Unlike dopamine or somatostatin analogs (which inhibit growth hormone secretion), this drug actually blocks the hepatic (GH-mediated) production of insulin like growth factor (IGF-1), which is the main mediator of growth hormone activity. | Pegvisomant is a growth hormone receptor antagonist used for the treatment of acromegaly. | Somavert is used for the treatment of acromegaly, which arises from excessive IGF-1 levels. Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH, and thus interferes with GH signal transduction. Inhibition of GH action results in decreased serum concentrations of insulin-like growth factor-I (IGF-I), and IGF binding protein-3 (IGFBP-3). This reduces the symptoms of acromegaly. | Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH. This leads to the normalization of serum IGF-1 levels. | NA | NA | NA | 7 L | 36 ± 28 mL/h [SC doses ranging from 10 to 20 mg/day] | Acromegaly, Amino Acids, Peptides, and Proteins, Anterior Pituitary Lobe Hormones and Analogues, Cholinesterase Inhibitors, Cytochrome P-450 CYP3A Inducers, Cytochrome P-450 CYP3A4 Inducers, Cytochrome P-450 CYP3A4 Inducers (strength unknown), Cytochrome P-450 Enzyme Inducers, Growth Hormone Receptor Antagonist, Growth Hormone Receptor Antagonists, Hormones, Hormones, Hormone Substitutes, and Hormone Antagonists, Hypoglycemia-Associated Agents, Pegylated agents, Peptide Hormones, Peptides, Pituitary and Hypothalamic Hormones and Analogues, Pituitary Hormones, Pituitary Hormones, Anterior, Somatotropin Antagonists, Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | CA2102129 | 1-Apr-2003 | 1-May-2012 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10448 | Th1080 | Choriogonadotropin alfa | >Th1080_Choriogonadotropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25719.7 | C1105H1770N318O336S26 | 8.61 | -0.258 | 55 | Mean terminal half-life 29 ± 6 hr (initial half-life is 4.5± 0.5 hr) | Recombinant human chorionic gonadotropin with a 92-residue alpha subunit and a 145 residue beta subunit. Glycosylation consists of N-and O-linked carbohydrate moieties linked to N-52 and N-78 (on alpha subunit) and N13 and 30, S121, 127, 132 and 138 (on beta subunit). The primary structure of the alpha-chain of r-hCG is identical to that of the alpha-chain of hCG, FSH and LH. | For the treatment of female infertility | Choriogonadotropin alfa is used to treat female infertility, Choriogonadotropin alfa stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Ovidrel is an analogue of Luteinizing Hormone (LH) and binds to the LH/hCG receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Choriogonadotropin alfa binds to the Follicle stimulating hormone receptor which results in ovulation in the absence of sufficient endogenous Luteinizing hormone. | NA | NA | The mean absolute bioavailability following a single subcutaneous injection to healthy female volunteers is about 40%. | 5.9 ± 1.0 L | 0.29 ± 0.04 L/h [healthy down-regulated females] | Genito Urinary System and Sex Hormones,Gonadotropins,Gonadotropins and Antigonadotropins,Sex Hormones and Modulators of the Genital System | US6706681 | 16-Mar-2004 | 16-Mar-2021 | NA | Lutropin-choriogonadotropic hormone receptor,Follicle-stimulating hormone receptor | Choriogonadotropin alfa | Emd serono inc, Ferring pharmaceuticals inc, App pharmaceuticals llc, Bel mar laboratories inc, Bris | Emd serono inc, Ferring pharmaceuticals inc, App pharmaceuticals llc, Bel mar laboratories inc, Bris | NA | NA | Chorionic Gonadotropin for Injection, USP is available in multiple dose vials containing 10,000 USP Units with accompanying Bacteriostatic Water for Injection for reconstitution. When reconstituted with 10 mL of the accompanying diluent each vial contains: Chorionic Gonadotropin 10,000 Units, Mannitol 100 mg, Benzyl alcohol 0.9%, Water for Injection q.s. Buffered with dibasic sodium phosphate and monobasic sodium phosphate. Hydrochloric acid and/or sodium hydroxide may have been used for pH adjustment (6.0-8.0). Nitrogen gas is used in the freeze drying process. | NA | NA | Adult Dose for Ovulation Induction: Ovulation Induction (if the cause of anovulation is secondary and not due to primary ovarian failure): chorionic gonadotropin: 5000 to 10,000 units IM one day following last day of menotropins. recombinant chorionic gonadotropin: 250 mcg subcutaneously one day following last dose of follicle-stimulating agent. Usual Adult Dose for Hypogonadism - Male hypogonadotropic hypogonadism (secondary to a pituitary deficiency):500 to 1000 units IM three times a week for 3 weeks followed by the same dose twice a week for 3 weeks or, 4000 units IM three times a week for 6 to 9 months followed by 2000 units three times a week for an additional 3 months. | Nausea; pain, swelling, bruising, or redness at the injection site; vomiting. Severe allergic reactions, bloating or swelling in the stomach or pelvic area; breast pain; calf or leg pain, redness, swelling, or tenderness; chest pain; decreased urination; irregular heartbeat; persistent or severe nausea, vomiting, or diarrhea; severe pelvic pain; severe stomach pain or bloating; sudden shortness of breath; sudden, unexpected weight gain. The principal serious adverse reactions are: (1) Ovarian hyperstimulation, a syndrome of sudden ovarian enlargement, ascites with or without pain and/or pleural effusion, (2) Rupture of ovarian cysts with resultant hemoperitoneum, (3) Multiple births and (4) Arterial thromboembolism. Anaphylaxis and other hypersensitivity reactions have been reported with urinary-derived HCG products. | NA | NA | NA | NA |
| 10449 | Th1080 | Choriogonadotropin alfa | >Th1080_Choriogonadotropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25719.7 | C1105H1770N318O336S26 | 8.61 | -0.258 | 55 | Mean terminal half-life 29 ± 6 hr (initial half-life is 4.5± 0.5 hr) | Recombinant human chorionic gonadotropin with a 92-residue alpha subunit and a 145 residue beta subunit. Glycosylation consists of N-and O-linked carbohydrate moieties linked to N-52 and N-78 (on alpha subunit) and N13 and 30, S121, 127, 132 and 138 (on beta subunit). The primary structure of the alpha-chain of r-hCG is identical to that of the alpha-chain of hCG, FSH and LH. | For the treatment of female infertility | Choriogonadotropin alfa is used to treat female infertility, Choriogonadotropin alfa stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Ovidrel is an analogue of Luteinizing Hormone (LH) and binds to the LH/hCG receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Choriogonadotropin alfa binds to the Follicle stimulating hormone receptor which results in ovulation in the absence of sufficient endogenous Luteinizing hormone. | NA | NA | The mean absolute bioavailability following a single subcutaneous injection to healthy female volunteers is about 40%. | 5.9 ± 1.0 L | 0.29 ± 0.04 L/h [healthy down-regulated females] | Genito Urinary System and Sex Hormones,Gonadotropins,Gonadotropins and Antigonadotropins,Sex Hormones and Modulators of the Genital System | US5767251 | 16-Jun-1998 | 16-Jun-2015 | NA | Lutropin-choriogonadotropic hormone receptor,Follicle-stimulating hormone receptor | Ovitrelle | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10450 | Th1080 | Choriogonadotropin alfa | >Th1080_Choriogonadotropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25719.7 | C1105H1770N318O336S26 | 8.61 | -0.258 | 55 | Mean terminal half-life 29 ± 6 hr (initial half-life is 4.5± 0.5 hr) | Recombinant human chorionic gonadotropin with a 92-residue alpha subunit and a 145 residue beta subunit. Glycosylation consists of N-and O-linked carbohydrate moieties linked to N-52 and N-78 (on alpha subunit) and N13 and 30, S121, 127, 132 and 138 (on beta subunit). The primary structure of the alpha-chain of r-hCG is identical to that of the alpha-chain of hCG, FSH and LH. | For the treatment of female infertility | Choriogonadotropin alfa is used to treat female infertility, Choriogonadotropin alfa stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Ovidrel is an analogue of Luteinizing Hormone (LH) and binds to the LH/hCG receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Choriogonadotropin alfa binds to the Follicle stimulating hormone receptor which results in ovulation in the absence of sufficient endogenous Luteinizing hormone. | NA | NA | The mean absolute bioavailability following a single subcutaneous injection to healthy female volunteers is about 40%. | 5.9 ± 1.0 L | 0.29 ± 0.04 L/h [healthy down-regulated females] | Genito Urinary System and Sex Hormones,Gonadotropins,Gonadotropins and Antigonadotropins,Sex Hormones and Modulators of the Genital System | US5767251 | 16-Jun-1998 | 16-Jun-2015 | NA | Lutropin-choriogonadotropic hormone receptor,Follicle-stimulating hormone receptor | Ovidrel | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10451 | Th1080 | Choriogonadotropin alfa | >Th1080_Choriogonadotropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25719.7 | C1105H1770N318O336S26 | 8.61 | -0.258 | 55 | Mean terminal half-life 29 ± 6 hr (initial half-life is 4.5± 0.5 hr) | Recombinant human chorionic gonadotropin with a 92-residue alpha subunit and a 145 residue beta subunit. Glycosylation consists of N-and O-linked carbohydrate moieties linked to N-52 and N-78 (on alpha subunit) and N13 and 30, S121, 127, 132 and 138 (on beta subunit). The primary structure of the alpha-chain of r-hCG is identical to that of the alpha-chain of hCG, FSH and LH. | For the treatment of female infertility | Choriogonadotropin alfa is used to treat female infertility, Choriogonadotropin alfa stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Ovidrel is an analogue of Luteinizing Hormone (LH) and binds to the LH/hCG receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Choriogonadotropin alfa binds to the Follicle stimulating hormone receptor which results in ovulation in the absence of sufficient endogenous Luteinizing hormone. | NA | NA | The mean absolute bioavailability following a single subcutaneous injection to healthy female volunteers is about 40%. | 5.9 ± 1.0 L | 0.29 ± 0.04 L/h [healthy down-regulated females] | Genito Urinary System and Sex Hormones,Gonadotropins,Gonadotropins and Antigonadotropins,Sex Hormones and Modulators of the Genital System | US5767251 | 16-Jun-1998 | 16-Jun-2015 | NA | Lutropin-choriogonadotropic hormone receptor,Follicle-stimulating hormone receptor | Pregnyl | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10452 | Th1080 | Choriogonadotropin alfa | >Th1080_Choriogonadotropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25719.7 | C1105H1770N318O336S26 | 8.61 | -0.258 | 55 | Mean terminal half-life 29 ± 6 hr (initial half-life is 4.5± 0.5 hr) | Recombinant human chorionic gonadotropin with a 92-residue alpha subunit and a 145 residue beta subunit. Glycosylation consists of N-and O-linked carbohydrate moieties linked to N-52 and N-78 (on alpha subunit) and N13 and 30, S121, 127, 132 and 138 (on beta subunit). The primary structure of the alpha-chain of r-hCG is identical to that of the alpha-chain of hCG, FSH and LH. | For the treatment of female infertility | Choriogonadotropin alfa is used to treat female infertility, Choriogonadotropin alfa stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Ovidrel is an analogue of Luteinizing Hormone (LH) and binds to the LH/hCG receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Choriogonadotropin alfa binds to the Follicle stimulating hormone receptor which results in ovulation in the absence of sufficient endogenous Luteinizing hormone. | NA | NA | The mean absolute bioavailability following a single subcutaneous injection to healthy female volunteers is about 40%. | 5.9 ± 1.0 L | 0.29 ± 0.04 L/h [healthy down-regulated females] | Genito Urinary System and Sex Hormones,Gonadotropins,Gonadotropins and Antigonadotropins,Sex Hormones and Modulators of the Genital System | US5767251 | 16-Jun-1998 | 16-Jun-2015 | NA | Lutropin-choriogonadotropic hormone receptor,Follicle-stimulating hormone receptor | Chorionic Gonadotropin | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10507 | Th1099 | Mecasermin | >Th1099_Mecasermin GPETLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSA | 7649 | C331H518N94O101S7 | NA | NA | NA | 5.8 hours | E. coli derived, recombinant human insulin-like growth factor-1 (rhIGF-1). It has 70 amino acids in a single chain (identical to the endogenous human protein), with three intramolecular disulfide bridges and a molecular weight of 7649 daltons. | For the long-term treatment of growth failure in pediatric patients with Primary IGFD or with GH gene deletion who have developed neutralizing antibodies to GH. It is not indicated to treat Secondary IGFD resulting from GH deficiency, malnutrition, hypothyroidism or other causes; it is not a substitute for GH therapy. | Mecasermin is a biosynthetic (recombinant DNA origin) form of human insulin growth factor 1 (IGF-1) designed to replace natural IGF-1 in pediatric patients who are deficient, promoting normalized statural growth. Growth hormones (GH) bind to growth hormone receptors (GHR) in the liver and other tissues, which stimulates the synthesis of IGF-1. In target tissues, IGF-1 activates the IGF-1 receptor, resulting in intracellular signals that stimulate growth. Although many actions of the GH are mediated through IGF-1, the precise roles of GH and IGF-1 have not been fully elucidated. Patients with severe primary IGF-1 deficiency (Primary IGFD) fail to produce adequate levels of IGF-1, due to disruption of the GH pathway used to promote IGF-1 release (possible GH pathway disruptions include mutations in the GHR, post-GHR signaling pathway, and IGF-1 gene defects). | Mecasermin supplies recombinant-DNA-origin IGF-1, which binds to the Type I IGF-1 receptor. This receptor exerts intra-cellular signaling activity in a number of processes involved in statural growth, including mitogenesis in multiple tissue types, chondrocyte growth and division along cartilage growth plates, and increases in organ growth. | Overdosage of Mecasermin leads to hypoglycemia . One case of acute overdose was treated with IV glucose. Long-term overdosage may result in signs and symptoms of acromegaly. The effects of Mecasermin in human pregnancy has not been studied, however effects on fetal development in animal studies were only seen at doses higher than the maximum recommended human dose based on body surface area. Studies on excretion of the drug in human milk, use in patients under 2 years, use in patients over 65 years, or use in patients with renal or hepatic impairment have not been performed. | Information on the metabolism of Mecasermin is not readily available, however it is likely to be metabolized by the liver and kidney like other injectable peptide drugs | While the bioavailability of rhIGF-1 after subcutaneous administration in healthy subjects has been reported to be close to 100%, the absolute bioavailability of mecasermin given subcutaneously to subjects with primary insulin-like growth factor-1 deficiency (Primary IGFD) has not been determined. | 0.257 ± 0.073 L/kg [subjects with severe Primary IGFD] | Clearance of Mecasermin is inversely proportional to IGF binding protein 3 (IGFBP-3) * Clearance is estimated to be 0.04L/hr/kg at 0.5 micrograms/mL of IGFBP-3 * Clearance is estimated to be 0.01L/hr/kg at 3 micrograms/mL of IGFBP-3 (the median level of IGFBP-3 for patients with normal IGF-1 levels) | Amino Acids, Peptides, and Proteins,Anterior Pituitary Lobe Hormones and Analogues,Biological Factors,Blood Glucose Lowering Agents,Blood Proteins,Growth Substances,Hypoglycemia-Associated Agents,Intercellular Signaling Peptides and Proteins,Peptides,Pituitary and Hypothalamic Hormones and Analogues,Proteins,Somatomedins,Somatotropin Agonists,Somatropin and Somatropin Agonists,Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | US5681814 | 28-Oct-1997 | 18-Sep-2017 | NA | Insulin-like growth factor 1 receptor,Insulin-like growth factor-binding protein 3,Insulin receptor,Cation-independent mannose-6-phosphate receptor | Increlex | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10508 | Th1099 | Mecasermin | >Th1099_Mecasermin GPETLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSA | 7649 | C331H518N94O101S8 | NA | NA | NA | 5.8 hours | E. coli derived, recombinant human insulin-like growth factor-1 (rhIGF-1). It has 70 amino acids in a single chain (identical to the endogenous human protein), with three intramolecular disulfide bridges and a molecular weight of 7649 daltons. | For the long-term treatment of growth failure in pediatric patients with Primary IGFD or with GH gene deletion who have developed neutralizing antibodies to GH. It is not indicated to treat Secondary IGFD resulting from GH deficiency, malnutrition, hypothyroidism or other causes; it is not a substitute for GH therapy. | Mecasermin is a biosynthetic (recombinant DNA origin) form of human insulin growth factor 1 (IGF-1) designed to replace natural IGF-1 in pediatric patients who are deficient, promoting normalized statural growth. Growth hormones (GH) bind to growth hormone receptors (GHR) in the liver and other tissues, which stimulates the synthesis of IGF-1. In target tissues, IGF-1 activates the IGF-1 receptor, resulting in intracellular signals that stimulate growth. Although many actions of the GH are mediated through IGF-1, the precise roles of GH and IGF-1 have not been fully elucidated. Patients with severe primary IGF-1 deficiency (Primary IGFD) fail to produce adequate levels of IGF-1, due to disruption of the GH pathway used to promote IGF-1 release (possible GH pathway disruptions include mutations in the GHR, post-GHR signaling pathway, and IGF-1 gene defects). | Mecasermin supplies recombinant-DNA-origin IGF-1, which binds to the Type I IGF-1 receptor. This receptor exerts intra-cellular signaling activity in a number of processes involved in statural growth, including mitogenesis in multiple tissue types, chondrocyte growth and division along cartilage growth plates, and increases in organ growth. | Overdosage of Mecasermin leads to hypoglycemia . One case of acute overdose was treated with IV glucose. Long-term overdosage may result in signs and symptoms of acromegaly. The effects of Mecasermin in human pregnancy has not been studied, however effects on fetal development in animal studies were only seen at doses higher than the maximum recommended human dose based on body surface area. Studies on excretion of the drug in human milk, use in patients under 2 years, use in patients over 65 years, or use in patients with renal or hepatic impairment have not been performed. | Information on the metabolism of Mecasermin is not readily available, however it is likely to be metabolized by the liver and kidney like other injectable peptide drugs | While the bioavailability of rhIGF-1 after subcutaneous administration in healthy subjects has been reported to be close to 100%, the absolute bioavailability of mecasermin given subcutaneously to subjects with primary insulin-like growth factor-1 deficiency (Primary IGFD) has not been determined. | 0.257 ± 0.073 L/kg [subjects with severe Primary IGFD] | Clearance of Mecasermin is inversely proportional to IGF binding protein 3 (IGFBP-3) * Clearance is estimated to be 0.04L/hr/kg at 0.5 micrograms/mL of IGFBP-3 * Clearance is estimated to be 0.01L/hr/kg at 3 micrograms/mL of IGFBP-3 (the median level of IGFBP-3 for patients with normal IGF-1 levels) | Amino Acids, Peptides, and Proteins,Anterior Pituitary Lobe Hormones and Analogues,Biological Factors,Blood Glucose Lowering Agents,Blood Proteins,Growth Substances,Hypoglycemia-Associated Agents,Intercellular Signaling Peptides and Proteins,Peptides,Pituitary and Hypothalamic Hormones and Analogues,Proteins,Somatomedins,Somatotropin Agonists,Somatropin and Somatropin Agonists,Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | US5200509 | 6-Apr-1993 | 6-Apr-2010 | NA | Insulin-like growth factor 1 receptor,Insulin-like growth factor-binding protein 3,Insulin receptor,Cation-independent mannose-6-phosphate receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10527 | Th1103 | Cosyntropin | >Th1103_Cosyntropin SYSMEHFRWGKPVGKKRRPVKVYP | 2933.437 | C136H210N40O31S | NA | NA | NA | 15 minutes (IV adminstration) | A synthetic peptide identical to the 24-amino acid N-terminal segment of adrenocorticotropic hormone. ACTH. This segment is similar in all species and responsible for biological activity. | For use as a diagnostic agent in the screening of patients presumed to have adrenocortical insufficiency. | Cosyntropin exhibits the full corticosteroidogenic activity of natural ACTH. Various studies have shown that the biologic activity of ACTH resides in the N- terminal portion of the molecule and that the 1-20 amino acid residue is the minimal sequence retaining full activity. Partial or complete loss of activity is noted with progressive shortening of the chain beyond 20 amino acid residue. For example, the decrement from 20 to 19 results in a 70% loss of potency. The pharmacologic profile of Cosyntropin is similar to that of purified natural ACTH. It has been established that 0.25 mg of Cosyntropin will stimulate the adrenal cortex maximally and to the same extent as 25 units of natural ACTH. Cosyntropin has less immunogenic activity than ACTH because the amino acid sequence having most of the antigenic activity of ACTH, i.e., amino acids 25-39, is not present in cosyntropin. The extra-adrenal effects which natural ACTH and Cosyntropin have in common include increased melanotropic activity, increased growth hormone secretion and an adipokinetic effect. These are considered to be without physiological or clinical significance. | Cosyntropin combines with a specific receptor in the adrenal cell plasma membrane and, in patients with normal adrenocortical function, stimulates the initial reaction involved in the synthesis of adrenal steroids (including cortisol, cortisone, weak androgenic substances, and a limited quantity of aldosterone) from cholesterol by increasing the quantity of the substrate within the mitochondria. Cosyntropin does not significantly increase plasma cortisol concentration in patients with primary or secondary adrenocortical insufficiency. | NA | NA | Rapidly absorbed following intramuscular administration. | NA | NA | Hormones and Diagnostic Agents | NA | NA | NA | NA | Adrenocorticotropic hormone receptor | Cortrosyn | Amphastar Pharmaceuticals | Amphastar Pharmaceuticals | CORTROSYN (cosyntropin) for Injection is intended for use as a diagnostic agent in the screening of patients presumed to have ad-renocortical insufficiency. Because of its rapid effect on the adrenal cortex it may be utilized to perform a 30-minute test of adrenal func-tion (plasma cortisol response) as an office or outpatient procedure, using only 2 venipuncture | NA | Box of 10 vials of CORTROSYN (cosyntropin) for Injection 0.25 mg without antimicrobial preservatives | NA | Intravenous, Intravenous infusion, Intramuscular | CORTROSYN (cosyntropin) for Injection may be administered intramuscularly or as a direct Intravenous infusion when used as a rapid screening test of adrenal function. It may also be given as an Intravenous infusion over a 4 to 8 hour period to provide a greater stimulus to the adrenal glands. Doses of CORTROSYN (cosyntropin) 0.25 to 0.75 mg have been used in clinical studies and a maximal response noted with the smallest dose. | The only contraindication to CORTROSYN (cosyntropin) for Injec-tion is a history of a previous adverse reaction to it. | Since CORTROSYN (cosyntropin) for Injection is intended for diag-nostic and not therapeutic use. A rare hypersensitivity reaction usually associated with a pre-existing allergic disease and/or a previous reaction to natural ACTH is possible. Symptoms may include slight whealing with splotchy erythema at the injection site. The other effects such as bradycardia, tachycardia, hypertension, peripheral edema. | NA | NA | NA |
| 10538 | Th1106 | Insulin detemir | >Th1106_Insulin_detemir GIVEQCCTSICSLYQLENYCN | 5916.9 | C267H402N64O76S6 | NA | NA | NA | 5 to 7 hours | Recombinant (from yeast cells), long-acting human insulin analogue. It has a myristic acid (14-C fatty acid), bound to lysine at position B29, which increases self-association and albumin binding. Coupled with its slow systemic absorption from the injection site, prolongs its distribution into tissues enabling it to act for a longer time than native insulin. | For the treatment of type 1 or 2 diabetes mellitus. May be used in combination with oral anti-diabetic agents in type 2 diabetic patients who are not in adequate metabolic control with oral anti-diabetic agents alone. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin detemir is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals. The onset of action of insulin detemir is 1 to 2 hours and its duration of action is up to 24 hours. Interestingly, it has a lower affinity (30%) for the insulin receptor than human insulin. | Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. Insulin detemir's long duration of action appears to be a result of slow systemic absorption from the injection site and delayed distribution to target tissues. The myristic acid side chain on insulin detemir increases self-association and gives it a high binding affinity to serum albumin. These features slows its distribution into target tissues and prolongs its duration of action. | Hypoglycemia may occur with inappropriately high doses. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. Injection site reactions may also occur. Symptoms include: redness, inflammation, bruising, swelling and itching at the injection site. | As with natural insulin, all metabolites formed are inactive. | Maximum serum concentrations are reached 6 to 8 hours following subcutaneous injection. When single dose of 0.5 units/kg of insulin detemir was given to adult type 1 diabetes patients, the maximum serum concentration (Cmax) was 4,641 ± 2,299 pmol/L. Absorption is also dependent on the site of injection. When injected into the thigh, the AUC was lower than when injected into the deltoid and abdominal regions. Bioavailability is approximately 60%. | 0.1 L/kg | Apparent clearance (CL/F), type 1 diabetes adult patients = 3.41 ± 1.00 L/min·kg | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Long-Acting,Pancreatic Hormones,Peptide Hormones,Peptides | US5750497 | 12-May-1998 | 16-Jun-2019 | NA | Insulin receptor,Insulin-like growth factor 1 receptor | LEVEMIR | Novo Nordisk | Novo Nordisk | LEVEMIR is indicated to improve glycemic control in adults and children with diabetes mellitus. | NA | Each milliliter of LEVEMIR contains 100 units (14.2 mg/mL) insulin detemir, 65.4 meg inc, 2.06 mg m-cresol, 16.0 mg glycerol, 1.80 mg phenol, 0.89 mg disodium phosphate dihydrate, 1.17 mg sodium chloride, and water for injection. Hydrochloric acid and/or sodium hydroxide may be added to adjust pH. LEVEMIR has a pH of approximately 7.4 | Clear, colorless, aqueous, neutral Sterile solution | Subcutaneous | Patients who require twice-daily dosing can administer the evening dose with the evening meal, at bedtime, or 12 hours after the morning dose. The dose of LEVEMIR must be individualized based on clinical response. Blood glucose monitoring is essential in all patients receiving insulin therapy. | LEVEMIR is not recommended for the treatment of diabetic ketoacidosis. Intravenous rapid-acting or short-acting insulin is the preferred treatment for this condition. LEVEMIR is contraindicated in patients with hypersensitivity to LEVEMIR or any of its excipients. Reactions have included anaphylaxis. | Hypoglycemia, upper respiratory tract infection, Headache, Pharyngitis, Influenza-like illness, Abdominal Pain | Link | NA | NA |
| 10539 | Th1106 | Insulin detemir | >Th1106_Insulin_detemir GIVEQCCTSICSLYQLENYCN | 5916.9 | C267H402N64O76S6 | NA | NA | NA | 5 to 7 hours | Recombinant (from yeast cells), long-acting human insulin analogue. It has a myristic acid (14-C fatty acid), bound to lysine at position B29, which increases self-association and albumin binding. Coupled with its slow systemic absorption from the injection site, prolongs its distribution into tissues enabling it to act for a longer time than native insulin. LEVEMIR | For the treatment of type 1 or 2 diabetes mellitus. May be used in combination with oral anti-diabetic agents in type 2 diabetic patients who are not in adequate metabolic control with oral anti-diabetic agents alone. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin detemir is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals. The onset of action of insulin detemir is 1 to 2 hours and its duration of action is up to 24 hours. Interestingly, it has a lower affinity (30%) for the insulin receptor than human insulin. | Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. Insulin detemir's long duration of action appears to be a result of slow systemic absorption from the injection site and delayed distribution to target tissues. The myristic acid side chain on insulin detemir increases self-association and gives it a high binding affinity to serum albumin. These features slows its distribution into target tissues and prolongs its duration of action. | Hypoglycemia may occur with inappropriately high doses. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. Injection site reactions may also occur. Symptoms include: redness, inflammation, bruising, swelling and itching at the injection site. | As with natural insulin, all metabolites formed are inactive. | Maximum serum concentrations are reached 6 to 8 hours following subcutaneous injection. When single dose of 0.5 units/kg of insulin detemir was given to adult type 1 diabetes patients, the maximum serum concentration (Cmax) was 4,641 ± 2,299 pmol/L. Absorption is also dependent on the site of injection. When injected into the thigh, the AUC was lower than when injected into the deltoid and abdominal regions. Bioavailability is approximately 60%. | 0.1 L/kg | Apparent clearance (CL/F), type 1 diabetes adult patients = 3.41 ± 1.00 L/min·kg | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Long-Acting,Pancreatic Hormones,Peptide Hormones,Peptides | US6011007 | 1-Apr-2000 | 2-Feb-2014 | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10540 | Th1106 | Insulin detemir | >Th1106_Insulin_detemir GIVEQCCTSICSLYQLENYCN | 5916.9 | C267H402N64O76S6 | NA | NA | NA | 5 to 7 hours | Recombinant (from yeast cells), long-acting human insulin analogue. It has a myristic acid (14-C fatty acid), bound to lysine at position B29, which increases self-association and albumin binding. Coupled with its slow systemic absorption from the injection site, prolongs its distribution into tissues enabling it to act for a longer time than native insulin. LEVEMIR | For the treatment of type 1 or 2 diabetes mellitus. May be used in combination with oral anti-diabetic agents in type 2 diabetic patients who are not in adequate metabolic control with oral anti-diabetic agents alone. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin detemir is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals. The onset of action of insulin detemir is 1 to 2 hours and its duration of action is up to 24 hours. Interestingly, it has a lower affinity (30%) for the insulin receptor than human insulin. | Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. Insulin detemir's long duration of action appears to be a result of slow systemic absorption from the injection site and delayed distribution to target tissues. The myristic acid side chain on insulin detemir increases self-association and gives it a high binding affinity to serum albumin. These features slows its distribution into target tissues and prolongs its duration of action. | Hypoglycemia may occur with inappropriately high doses. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. Injection site reactions may also occur. Symptoms include: redness, inflammation, bruising, swelling and itching at the injection site. | As with natural insulin, all metabolites formed are inactive. | Maximum serum concentrations are reached 6 to 8 hours following subcutaneous injection. When single dose of 0.5 units/kg of insulin detemir was given to adult type 1 diabetes patients, the maximum serum concentration (Cmax) was 4,641 ± 2,299 pmol/L. Absorption is also dependent on the site of injection. When injected into the thigh, the AUC was lower than when injected into the deltoid and abdominal regions. Bioavailability is approximately 60%. | 0.1 L/kg | Apparent clearance (CL/F), type 1 diabetes adult patients = 3.41 ± 1.00 L/min·kg | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Long-Acting,Pancreatic Hormones,Peptide Hormones,Peptides | CA2171424 | 6-Apr-2002 | 16-09-2014 | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10541 | Th1106 | Insulin detemir | >Th1106_Insulin_detemir GIVEQCCTSICSLYQLENYCN | 5916.9 | C267H402N64O76S6 | NA | NA | NA | 5 to 7 hours | Recombinant (from yeast cells), long-acting human insulin analogue. It has a myristic acid (14-C fatty acid), bound to lysine at position B29, which increases self-association and albumin binding. Coupled with its slow systemic absorption from the injection site, prolongs its distribution into tissues enabling it to act for a longer time than native insulin. LEVEMIR | For the treatment of type 1 or 2 diabetes mellitus. May be used in combination with oral anti-diabetic agents in type 2 diabetic patients who are not in adequate metabolic control with oral anti-diabetic agents alone. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin detemir is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals. The onset of action of insulin detemir is 1 to 2 hours and its duration of action is up to 24 hours. Interestingly, it has a lower affinity (30%) for the insulin receptor than human insulin. | Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. Insulin detemir's long duration of action appears to be a result of slow systemic absorption from the injection site and delayed distribution to target tissues. The myristic acid side chain on insulin detemir increases self-association and gives it a high binding affinity to serum albumin. These features slows its distribution into target tissues and prolongs its duration of action. | Hypoglycemia may occur with inappropriately high doses. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. Injection site reactions may also occur. Symptoms include: redness, inflammation, bruising, swelling and itching at the injection site. | As with natural insulin, all metabolites formed are inactive. | Maximum serum concentrations are reached 6 to 8 hours following subcutaneous injection. When single dose of 0.5 units/kg of insulin detemir was given to adult type 1 diabetes patients, the maximum serum concentration (Cmax) was 4,641 ± 2,299 pmol/L. Absorption is also dependent on the site of injection. When injected into the thigh, the AUC was lower than when injected into the deltoid and abdominal regions. Bioavailability is approximately 60%. | 0.1 L/kg | Apparent clearance (CL/F), type 1 diabetes adult patients = 3.41 ± 1.00 L/min·kg | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Long-Acting,Pancreatic Hormones,Peptide Hormones,Peptides | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10542 | Th1106 | Insulin detemir | >Th1106_Insulin_detemir GIVEQCCTSICSLYQLENYCN | 5916.9 | C267H402N64O76S6 | NA | NA | NA | 5 to 7 hours | Recombinant (from yeast cells), long-acting human insulin analogue. It has a myristic acid (14-C fatty acid), bound to lysine at position B29, which increases self-association and albumin binding. Coupled with its slow systemic absorption from the injection site, prolongs its distribution into tissues enabling it to act for a longer time than native insulin. LEVEMIR | For the treatment of type 1 or 2 diabetes mellitus. May be used in combination with oral anti-diabetic agents in type 2 diabetic patients who are not in adequate metabolic control with oral anti-diabetic agents alone. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin detemir is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals. The onset of action of insulin detemir is 1 to 2 hours and its duration of action is up to 24 hours. Interestingly, it has a lower affinity (30%) for the insulin receptor than human insulin. | Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. Insulin detemir's long duration of action appears to be a result of slow systemic absorption from the injection site and delayed distribution to target tissues. The myristic acid side chain on insulin detemir increases self-association and gives it a high binding affinity to serum albumin. These features slows its distribution into target tissues and prolongs its duration of action. | Hypoglycemia may occur with inappropriately high doses. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. Injection site reactions may also occur. Symptoms include: redness, inflammation, bruising, swelling and itching at the injection site. | As with natural insulin, all metabolites formed are inactive. | Maximum serum concentrations are reached 6 to 8 hours following subcutaneous injection. When single dose of 0.5 units/kg of insulin detemir was given to adult type 1 diabetes patients, the maximum serum concentration (Cmax) was 4,641 ± 2,299 pmol/L. Absorption is also dependent on the site of injection. When injected into the thigh, the AUC was lower than when injected into the deltoid and abdominal regions. Bioavailability is approximately 60%. | 0.1 L/kg | Apparent clearance (CL/F), type 1 diabetes adult patients = 3.41 ± 1.00 L/min·kg | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Long-Acting,Pancreatic Hormones,Peptide Hormones,Peptides | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10543 | Th1106 | Insulin detemir | >Th1106_Insulin_detemir GIVEQCCTSICSLYQLENYCN | 5916.9 | C267H402N64O76S6 | NA | NA | NA | 5 to 7 hours | Recombinant (from yeast cells), long-acting human insulin analogue. It has a myristic acid (14-C fatty acid), bound to lysine at position B29, which increases self-association and albumin binding. Coupled with its slow systemic absorption from the injection site, prolongs its distribution into tissues enabling it to act for a longer time than native insulin. LEVEMIR | For the treatment of type 1 or 2 diabetes mellitus. May be used in combination with oral anti-diabetic agents in type 2 diabetic patients who are not in adequate metabolic control with oral anti-diabetic agents alone. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin detemir is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals. The onset of action of insulin detemir is 1 to 2 hours and its duration of action is up to 24 hours. Interestingly, it has a lower affinity (30%) for the insulin receptor than human insulin. | Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. Insulin detemir's long duration of action appears to be a result of slow systemic absorption from the injection site and delayed distribution to target tissues. The myristic acid side chain on insulin detemir increases self-association and gives it a high binding affinity to serum albumin. These features slows its distribution into target tissues and prolongs its duration of action. | Hypoglycemia may occur with inappropriately high doses. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. Injection site reactions may also occur. Symptoms include: redness, inflammation, bruising, swelling and itching at the injection site. | As with natural insulin, all metabolites formed are inactive. | Maximum serum concentrations are reached 6 to 8 hours following subcutaneous injection. When single dose of 0.5 units/kg of insulin detemir was given to adult type 1 diabetes patients, the maximum serum concentration (Cmax) was 4,641 ± 2,299 pmol/L. Absorption is also dependent on the site of injection. When injected into the thigh, the AUC was lower than when injected into the deltoid and abdominal regions. Bioavailability is approximately 60%. | 0.1 L/kg | Apparent clearance (CL/F), type 1 diabetes adult patients = 3.41 ± 1.00 L/min·kg | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Long-Acting,Pancreatic Hormones,Peptide Hormones,Peptides | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10544 | Th1106 | Insulin detemir | >Th1106_Insulin_detemir GIVEQCCTSICSLYQLENYCN | 5916.9 | C267H402N64O76S6 | NA | NA | NA | 5 to 7 hours | Recombinant (from yeast cells), long-acting human insulin analogue. It has a myristic acid (14-C fatty acid), bound to lysine at position B29, which increases self-association and albumin binding. Coupled with its slow systemic absorption from the injection site, prolongs its distribution into tissues enabling it to act for a longer time than native insulin. LEVEMIR | For the treatment of type 1 or 2 diabetes mellitus. May be used in combination with oral anti-diabetic agents in type 2 diabetic patients who are not in adequate metabolic control with oral anti-diabetic agents alone. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin detemir is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals. The onset of action of insulin detemir is 1 to 2 hours and its duration of action is up to 24 hours. Interestingly, it has a lower affinity (30%) for the insulin receptor than human insulin. | Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. Insulin detemir's long duration of action appears to be a result of slow systemic absorption from the injection site and delayed distribution to target tissues. The myristic acid side chain on insulin detemir increases self-association and gives it a high binding affinity to serum albumin. These features slows its distribution into target tissues and prolongs its duration of action. | Hypoglycemia may occur with inappropriately high doses. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. Injection site reactions may also occur. Symptoms include: redness, inflammation, bruising, swelling and itching at the injection site. | As with natural insulin, all metabolites formed are inactive. | Maximum serum concentrations are reached 6 to 8 hours following subcutaneous injection. When single dose of 0.5 units/kg of insulin detemir was given to adult type 1 diabetes patients, the maximum serum concentration (Cmax) was 4,641 ± 2,299 pmol/L. Absorption is also dependent on the site of injection. When injected into the thigh, the AUC was lower than when injected into the deltoid and abdominal regions. Bioavailability is approximately 60%. | 0.1 L/kg | Apparent clearance (CL/F), type 1 diabetes adult patients = 3.41 ± 1.00 L/min·kg | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Long-Acting,Pancreatic Hormones,Peptide Hormones,Peptides | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10545 | Th1106 | Insulin detemir | >Th1106_Insulin_detemir GIVEQCCTSICSLYQLENYCN | 5916.9 | C267H402N64O76S6 | NA | NA | NA | 5 to 7 hours | Recombinant (from yeast cells), long-acting human insulin analogue. It has a myristic acid (14-C fatty acid), bound to lysine at position B29, which increases self-association and albumin binding. Coupled with its slow systemic absorption from the injection site, prolongs its distribution into tissues enabling it to act for a longer time than native insulin. LEVEMIR | For the treatment of type 1 or 2 diabetes mellitus. May be used in combination with oral anti-diabetic agents in type 2 diabetic patients who are not in adequate metabolic control with oral anti-diabetic agents alone. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin detemir is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals. The onset of action of insulin detemir is 1 to 2 hours and its duration of action is up to 24 hours. Interestingly, it has a lower affinity (30%) for the insulin receptor than human insulin. | Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. Insulin detemir's long duration of action appears to be a result of slow systemic absorption from the injection site and delayed distribution to target tissues. The myristic acid side chain on insulin detemir increases self-association and gives it a high binding affinity to serum albumin. These features slows its distribution into target tissues and prolongs its duration of action. | Hypoglycemia may occur with inappropriately high doses. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. Injection site reactions may also occur. Symptoms include: redness, inflammation, bruising, swelling and itching at the injection site. | As with natural insulin, all metabolites formed are inactive. | Maximum serum concentrations are reached 6 to 8 hours following subcutaneous injection. When single dose of 0.5 units/kg of insulin detemir was given to adult type 1 diabetes patients, the maximum serum concentration (Cmax) was 4,641 ± 2,299 pmol/L. Absorption is also dependent on the site of injection. When injected into the thigh, the AUC was lower than when injected into the deltoid and abdominal regions. Bioavailability is approximately 60%. | 0.1 L/kg | Apparent clearance (CL/F), type 1 diabetes adult patients = 3.41 ± 1.00 L/min·kg | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Long-Acting,Pancreatic Hormones,Peptide Hormones,Peptides | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10546 | Th1106 | Insulin detemir | >Th1106_Insulin_detemir GIVEQCCTSICSLYQLENYCN | 5916.9 | C267H402N64O76S6 | NA | NA | NA | 5 to 7 hours | Recombinant (from yeast cells), long-acting human insulin analogue. It has a myristic acid (14-C fatty acid), bound to lysine at position B29, which increases self-association and albumin binding. Coupled with its slow systemic absorption from the injection site, prolongs its distribution into tissues enabling it to act for a longer time than native insulin. LEVEMIR | For the treatment of type 1 or 2 diabetes mellitus. May be used in combination with oral anti-diabetic agents in type 2 diabetic patients who are not in adequate metabolic control with oral anti-diabetic agents alone. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin detemir is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals. The onset of action of insulin detemir is 1 to 2 hours and its duration of action is up to 24 hours. Interestingly, it has a lower affinity (30%) for the insulin receptor than human insulin. | Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. Insulin detemir's long duration of action appears to be a result of slow systemic absorption from the injection site and delayed distribution to target tissues. The myristic acid side chain on insulin detemir increases self-association and gives it a high binding affinity to serum albumin. These features slows its distribution into target tissues and prolongs its duration of action. | Hypoglycemia may occur with inappropriately high doses. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. Injection site reactions may also occur. Symptoms include: redness, inflammation, bruising, swelling and itching at the injection site. | As with natural insulin, all metabolites formed are inactive. | Maximum serum concentrations are reached 6 to 8 hours following subcutaneous injection. When single dose of 0.5 units/kg of insulin detemir was given to adult type 1 diabetes patients, the maximum serum concentration (Cmax) was 4,641 ± 2,299 pmol/L. Absorption is also dependent on the site of injection. When injected into the thigh, the AUC was lower than when injected into the deltoid and abdominal regions. Bioavailability is approximately 60%. | 0.1 L/kg | Apparent clearance (CL/F), type 1 diabetes adult patients = 3.41 ± 1.00 L/min·kg | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Long-Acting,Pancreatic Hormones,Peptide Hormones,Peptides | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10547 | Th1107 | Insulin glulisine | >Th1107_Insulin_glulisine GIVEQCCTSICSLYQLENYCN | 5823 | C258H384N64O78S6 | NA | NA | NA | Elimination half life= 42 minutes (SC injection) | Insulin glulisine is a recombinant (E. Coli derived), rapid-acting analog of human insulin. It contains two mutations, one at position B3, where R is replaced by K and the other at position B29, where K is replaced by E. This results in decrease hexamer formation and increased stability of the monomer, thus increasing the rate of absorption and quicker action as compared to native insulin. | For the treatment of Type 1 and 2 diabetes mellitus. Should be used in regimens including a long-acting or basal insulin analogue unless it is used in a continuous infusion pump. May be used with oral antidiabetic agents. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin glulisine is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin glulisine is approximately 15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 2-4 hours. | Insulin glulisine binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the arginine at position B3 for lysine and replacement of the B29 lysine with glutamic acid decreases the propensity to form hexamers, stabilizes the hormone in monomeric form and results in a rapid rate of absorption and short duration of action. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. | NA | Compared to regular human insulin, insulin glulisine is faster absorbed. When 0.15 units/kg was subcutaneously administered to type 1 diabetes patients, the pharmacokinetic parameters are as follows: Tmax = 60 minutes (range of 40 - 120 minutes); Cmax = 83 microUnits/mL (range of 40 - 131 microUnits/mL). Absolute bioavailability following subcutaneous administration is approximately 70%, regardless of site of injection. | 13 L | NA | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Short-Acting,Insulins and Analogues for Injection, Fast-Acting,Pancreatic Hormones,Peptide Hormones,Peptides,Proteins | US6960561 | 11-Jan-2005 | 25-01-2023 | NA | Insulin receptor,Insulin-like growth factor 1 receptor | APIDRA | sanofi-aventis | sanofi-aventis | APIDRA is indicated to improve glycemic control in adults and children with diabetes mellitus. | NA | Each milliliter of APIDRA contains 100 units (3.49 mg) insulin glulisine, 3.15 mg metacresol, 6 mg tromethamine, 5 mg sodium chloride, 0.01 mg polysorbate 20, and water for injection. APIDRA has a pH of approximately 7.3. The pH is adjusted by addition of aqueous solutions of hydrochloric acid and/or sodium hydroxide | Sterile, aqueous, clear, and colorless solution | NA | APIDRA is a recombinant insulin analog that is equipotent to human insulin (i.e. one unit of APIDRA has the same glucose-lowering effect as one unit of regular human insulin) when given intravenously. When given subcutaneously, APIDRA has a more rapid onset of action and a shorter duration of action than regular human insulin. The dosage of APIDRA must be individualized. Blood glucose monitoring is essential in all patients receiving insulin therapy. The total daily insulin requirement may vary and is usually between 0.5 to 1 Unit/kg/day. Insulin requirements may be altered during stress, major illness, or with changes in exercise, meal patterns, or coadministered drugs. | APIDRA is contraindicated: during episodes of hypoglycemia, in patients who are hypersensitive to APIDRA or to any of its excipients When used in patients with known hypersensitivity to APIDRA or its excipients, patients may develop localized or generalized hypersensitivity reactions. | Hypoglycemia, Hypokalemia | Link | NA | NA |
| 10548 | Th1107 | Insulin glulisine | >Th1107_Insulin_glulisine GIVEQCCTSICSLYQLENYCN | 5823 | C258H384N64O78S6 | NA | NA | NA | Elimination half life= 42 minutes (SC injection) | Insulin glulisine is a recombinant (E. Coli derived), rapid-acting analog of human insulin. It contains two mutations, one at position B3, where R is replaced by K and the other at position B29, where K is replaced by E. This results in decrease hexamer formation and increased stability of the monomer, thus increasing the rate of absorption and quicker action as compared to native insulin. | For the treatment of Type 1 and 2 diabetes mellitus. Should be used in regimens including a long-acting or basal insulin analogue unless it is used in a continuous infusion pump. May be used with oral antidiabetic agents. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin glulisine is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin glulisine is approximately 15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 2-4 hours. | Insulin glulisine binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the arginine at position B3 for lysine and replacement of the B29 lysine with glutamic acid decreases the propensity to form hexamers, stabilizes the hormone in monomeric form and results in a rapid rate of absorption and short duration of action. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. | NA | Compared to regular human insulin, insulin glulisine is faster absorbed. When 0.15 units/kg was subcutaneously administered to type 1 diabetes patients, the pharmacokinetic parameters are as follows: Tmax = 60 minutes (range of 40 - 120 minutes); Cmax = 83 microUnits/mL (range of 40 - 131 microUnits/mL). Absolute bioavailability following subcutaneous administration is approximately 70%, regardless of site of injection. | 13 L | NA | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Short-Acting,Insulins and Analogues for Injection, Fast-Acting,Pancreatic Hormones,Peptide Hormones,Peptides,Proteins | US6221633 | 24-04-2001 | 18-06-2018 | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10549 | Th1107 | Insulin glulisine | >Th1107_Insulin_glulisine GIVEQCCTSICSLYQLENYCN | 5823 | C258H384N64O78S6 | NA | NA | NA | Elimination half life= 42 minutes (SC injection) | Insulin glulisine is a recombinant (E. Coli derived), rapid-acting analog of human insulin. It contains two mutations, one at position B3, where R is replaced by K and the other at position B29, where K is replaced by E. This results in decrease hexamer formation and increased stability of the monomer, thus increasing the rate of absorption and quicker action as compared to native insulin. | For the treatment of Type 1 and 2 diabetes mellitus. Should be used in regimens including a long-acting or basal insulin analogue unless it is used in a continuous infusion pump. May be used with oral antidiabetic agents. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin glulisine is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin glulisine is approximately 15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 2-4 hours. | Insulin glulisine binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the arginine at position B3 for lysine and replacement of the B29 lysine with glutamic acid decreases the propensity to form hexamers, stabilizes the hormone in monomeric form and results in a rapid rate of absorption and short duration of action. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. | NA | Compared to regular human insulin, insulin glulisine is faster absorbed. When 0.15 units/kg was subcutaneously administered to type 1 diabetes patients, the pharmacokinetic parameters are as follows: Tmax = 60 minutes (range of 40 - 120 minutes); Cmax = 83 microUnits/mL (range of 40 - 131 microUnits/mL). Absolute bioavailability following subcutaneous administration is approximately 70%, regardless of site of injection. | 13 L | NA | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Short-Acting,Insulins and Analogues for Injection, Fast-Acting,Pancreatic Hormones,Peptide Hormones,Peptides,Proteins | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10550 | Th1107 | Insulin glulisine | >Th1107_Insulin_glulisine GIVEQCCTSICSLYQLENYCN | 5823 | C258H384N64O78S6 | NA | NA | NA | Elimination half life= 42 minutes (SC injection) | Insulin glulisine is a recombinant (E. Coli derived), rapid-acting analog of human insulin. It contains two mutations, one at position B3, where R is replaced by K and the other at position B29, where K is replaced by E. This results in decrease hexamer formation and increased stability of the monomer, thus increasing the rate of absorption and quicker action as compared to native insulin. | For the treatment of Type 1 and 2 diabetes mellitus. Should be used in regimens including a long-acting or basal insulin analogue unless it is used in a continuous infusion pump. May be used with oral antidiabetic agents. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin glulisine is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin glulisine is approximately 15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 2-4 hours. | Insulin glulisine binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the arginine at position B3 for lysine and replacement of the B29 lysine with glutamic acid decreases the propensity to form hexamers, stabilizes the hormone in monomeric form and results in a rapid rate of absorption and short duration of action. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. | NA | Compared to regular human insulin, insulin glulisine is faster absorbed. When 0.15 units/kg was subcutaneously administered to type 1 diabetes patients, the pharmacokinetic parameters are as follows: Tmax = 60 minutes (range of 40 - 120 minutes); Cmax = 83 microUnits/mL (range of 40 - 131 microUnits/mL). Absolute bioavailability following subcutaneous administration is approximately 70%, regardless of site of injection. | 13 L | NA | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Short-Acting,Insulins and Analogues for Injection, Fast-Acting,Pancreatic Hormones,Peptide Hormones,Peptides,Proteins | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10551 | Th1107 | Insulin glulisine | >Th1107_Insulin_glulisine GIVEQCCTSICSLYQLENYCN | 5823 | C258H384N64O78S6 | NA | NA | NA | Elimination half life= 42 minutes (SC injection) | Insulin glulisine is a recombinant (E. Coli derived), rapid-acting analog of human insulin. It contains two mutations, one at position B3, where R is replaced by K and the other at position B29, where K is replaced by E. This results in decrease hexamer formation and increased stability of the monomer, thus increasing the rate of absorption and quicker action as compared to native insulin. | For the treatment of Type 1 and 2 diabetes mellitus. Should be used in regimens including a long-acting or basal insulin analogue unless it is used in a continuous infusion pump. May be used with oral antidiabetic agents. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin glulisine is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin glulisine is approximately 15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 2-4 hours. | Insulin glulisine binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the arginine at position B3 for lysine and replacement of the B29 lysine with glutamic acid decreases the propensity to form hexamers, stabilizes the hormone in monomeric form and results in a rapid rate of absorption and short duration of action. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. | NA | Compared to regular human insulin, insulin glulisine is faster absorbed. When 0.15 units/kg was subcutaneously administered to type 1 diabetes patients, the pharmacokinetic parameters are as follows: Tmax = 60 minutes (range of 40 - 120 minutes); Cmax = 83 microUnits/mL (range of 40 - 131 microUnits/mL). Absolute bioavailability following subcutaneous administration is approximately 70%, regardless of site of injection. | 13 L | NA | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Short-Acting,Insulins and Analogues for Injection, Fast-Acting,Pancreatic Hormones,Peptide Hormones,Peptides,Proteins | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10552 | Th1107 | Insulin glulisine | >Th1107_Insulin_glulisine GIVEQCCTSICSLYQLENYCN | 5823 | C258H384N64O78S6 | NA | NA | NA | Elimination half life= 42 minutes (SC injection) | Insulin glulisine is a recombinant (E. Coli derived), rapid-acting analog of human insulin. It contains two mutations, one at position B3, where R is replaced by K and the other at position B29, where K is replaced by E. This results in decrease hexamer formation and increased stability of the monomer, thus increasing the rate of absorption and quicker action as compared to native insulin. | For the treatment of Type 1 and 2 diabetes mellitus. Should be used in regimens including a long-acting or basal insulin analogue unless it is used in a continuous infusion pump. May be used with oral antidiabetic agents. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin glulisine is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin glulisine is approximately 15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 2-4 hours. | Insulin glulisine binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the arginine at position B3 for lysine and replacement of the B29 lysine with glutamic acid decreases the propensity to form hexamers, stabilizes the hormone in monomeric form and results in a rapid rate of absorption and short duration of action. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. | NA | Compared to regular human insulin, insulin glulisine is faster absorbed. When 0.15 units/kg was subcutaneously administered to type 1 diabetes patients, the pharmacokinetic parameters are as follows: Tmax = 60 minutes (range of 40 - 120 minutes); Cmax = 83 microUnits/mL (range of 40 - 131 microUnits/mL). Absolute bioavailability following subcutaneous administration is approximately 70%, regardless of site of injection. | 13 L | NA | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Short-Acting,Insulins and Analogues for Injection, Fast-Acting,Pancreatic Hormones,Peptide Hormones,Peptides,Proteins | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10553 | Th1107 | Insulin glulisine | >Th1107_Insulin_glulisine GIVEQCCTSICSLYQLENYCN | 5823 | C258H384N64O78S6 | NA | NA | NA | Elimination half life= 42 minutes (SC injection) | Insulin glulisine is a recombinant (E. Coli derived), rapid-acting analog of human insulin. It contains two mutations, one at position B3, where R is replaced by K and the other at position B29, where K is replaced by E. This results in decrease hexamer formation and increased stability of the monomer, thus increasing the rate of absorption and quicker action as compared to native insulin. | For the treatment of Type 1 and 2 diabetes mellitus. Should be used in regimens including a long-acting or basal insulin analogue unless it is used in a continuous infusion pump. May be used with oral antidiabetic agents. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin glulisine is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin glulisine is approximately 15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 2-4 hours. | Insulin glulisine binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the arginine at position B3 for lysine and replacement of the B29 lysine with glutamic acid decreases the propensity to form hexamers, stabilizes the hormone in monomeric form and results in a rapid rate of absorption and short duration of action. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. | NA | Compared to regular human insulin, insulin glulisine is faster absorbed. When 0.15 units/kg was subcutaneously administered to type 1 diabetes patients, the pharmacokinetic parameters are as follows: Tmax = 60 minutes (range of 40 - 120 minutes); Cmax = 83 microUnits/mL (range of 40 - 131 microUnits/mL). Absolute bioavailability following subcutaneous administration is approximately 70%, regardless of site of injection. | 13 L | NA | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Short-Acting,Insulins and Analogues for Injection, Fast-Acting,Pancreatic Hormones,Peptide Hormones,Peptides,Proteins | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10554 | Th1107 | Insulin glulisine | >Th1107_Insulin_glulisine GIVEQCCTSICSLYQLENYCN | 5823 | C258H384N64O78S6 | NA | NA | NA | Elimination half life= 42 minutes (SC injection) | Insulin glulisine is a recombinant (E. Coli derived), rapid-acting analog of human insulin. It contains two mutations, one at position B3, where R is replaced by K and the other at position B29, where K is replaced by E. This results in decrease hexamer formation and increased stability of the monomer, thus increasing the rate of absorption and quicker action as compared to native insulin. | For the treatment of Type 1 and 2 diabetes mellitus. Should be used in regimens including a long-acting or basal insulin analogue unless it is used in a continuous infusion pump. May be used with oral antidiabetic agents. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin glulisine is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin glulisine is approximately 15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 2-4 hours. | Insulin glulisine binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the arginine at position B3 for lysine and replacement of the B29 lysine with glutamic acid decreases the propensity to form hexamers, stabilizes the hormone in monomeric form and results in a rapid rate of absorption and short duration of action. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. | NA | Compared to regular human insulin, insulin glulisine is faster absorbed. When 0.15 units/kg was subcutaneously administered to type 1 diabetes patients, the pharmacokinetic parameters are as follows: Tmax = 60 minutes (range of 40 - 120 minutes); Cmax = 83 microUnits/mL (range of 40 - 131 microUnits/mL). Absolute bioavailability following subcutaneous administration is approximately 70%, regardless of site of injection. | 13 L | NA | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Short-Acting,Insulins and Analogues for Injection, Fast-Acting,Pancreatic Hormones,Peptide Hormones,Peptides,Proteins | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10555 | Th1107 | Insulin glulisine | >Th1107_Insulin_glulisine GIVEQCCTSICSLYQLENYCN | 5823 | C258H384N64O78S6 | NA | NA | NA | Elimination half life= 42 minutes (SC injection) | Insulin glulisine is a recombinant (E. Coli derived), rapid-acting analog of human insulin. It contains two mutations, one at position B3, where R is replaced by K and the other at position B29, where K is replaced by E. This results in decrease hexamer formation and increased stability of the monomer, thus increasing the rate of absorption and quicker action as compared to native insulin. | For the treatment of Type 1 and 2 diabetes mellitus. Should be used in regimens including a long-acting or basal insulin analogue unless it is used in a continuous infusion pump. May be used with oral antidiabetic agents. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin glulisine is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin glulisine is approximately 15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 2-4 hours. | Insulin glulisine binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the arginine at position B3 for lysine and replacement of the B29 lysine with glutamic acid decreases the propensity to form hexamers, stabilizes the hormone in monomeric form and results in a rapid rate of absorption and short duration of action. | Inappropriately high dosages relative to food intake and/or energy expenditure may result in severe and sometimes prolonged and life-threatening hypoglycemia. Neurogenic (autonomic) signs and symptoms of hypoglycemia include trembling, palpitations, sweating, anxiety, hunger, nausea and tingling. Neuroglycopenic signs and symptoms of hypoglycemia include difficulty concentrating, lethargy/weakness, confusion, drowsiness, vision changes, difficulty speaking, headache, and dizziness. Mild hypoglycemia is characterized by the presence of autonomic symptoms. Moderate hypoglycemia is characterized by the presence of autonomic and neuroglycopenic symptoms. Individuals may become unconscious in severe cases of hypoglycemia. | NA | Compared to regular human insulin, insulin glulisine is faster absorbed. When 0.15 units/kg was subcutaneously administered to type 1 diabetes patients, the pharmacokinetic parameters are as follows: Tmax = 60 minutes (range of 40 - 120 minutes); Cmax = 83 microUnits/mL (range of 40 - 131 microUnits/mL). Absolute bioavailability following subcutaneous administration is approximately 70%, regardless of site of injection. | 13 L | NA | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypoglycemia-Associated Agents,Insulin,Insulin Analog,Insulin, Short-Acting,Insulins and Analogues for Injection, Fast-Acting,Pancreatic Hormones,Peptide Hormones,Peptides,Proteins | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10558 | Th1110 | Thymalfasin | >Th1110_Thymalfasin SDAAVDTSSEITTKDLKEKKEVVEEAEN | 3108.276 | C129H215N33O55 | NA | NA | NA | Approx. 2 hrs | Chemically synthesized version identicle to human acetylated polypeptide , thymosin alpha 1. It is now approved in 35 developing countries for the treatment of Hepatitis B and C and in boosting immunity against other diseases. | Indicated as an adjuvant for influenza vaccine in elderly patients and as an adjuvant for both influenza and hepatitis B vaccines in chronic hemodialysis patients who failed to achieve adequate antibody titers from previous immunization. | Thymalfasin is a 28-amino acid polypeptide produced synthetically but originally isolated from thymosin fraction 5, a bovine thymus extract containing a number of immunologically active peptides. In vitro studies have shown that Thymalfasin can influence T-cell production and maturation, stimulate production of Th1 cytokines such as interferon-gamma and interleukin-2, and activate natural killer cell-mediated cytotoxicity. | The mechanism of action of thymalfasin is not completely understood but is thought to be related to its immunomodulating activities, centered primarily around augmentation of T-cell function. In various in vitro assays, thymosin alpha 1 has been shown to promote T-cell differentiation and maturation; for example, CD4+, CD8+, and CD3+ cells have all been shown to be increased. Thymosin alpha 1 has also been shown to increase production of IFN-g, IL-2, IL-3, and expression of IL-2 receptor following activation by mitogens or antigens, increase NK cell activity, increase production of migratory inhibitory factor (MIF), and increase antibody response to T-cell dependent antigens. Thymosin alpha 1 has also been shown to antagonize dexamethasone-induced apoptosis of thymocytes in vitro. In vivo administration of thymosin alpha 1 to animals immunosuppressed by chemotherapy, tumor burden, or irradiation showed that thymosin alpha 1 protects against cytotoxic damage to bone marrow, tumor progression and opportunistic infections, thereby increasing survival time and number of survivors. Many of the in vitro and in vivo effects of thymosin alpha 1 have been interpreted as influences on either differentiation of pluripotent stem cells to thymocytes or activation of thymocytes into activated T-cells. Thymalfasin also has been shown in vitro to upregulate expression of toll like receptors (TLR) including TLR2 and TLR9 in mouse and human dendritic cells, as well as activate NF-kB and JNK/P38/AP1 pathways. Thymalfasin's activation of dendritic cells provides another possible pathway explaining thymalfasin's immunomodulatory and antiviral effects. | There are no reported instances of deliberate or accidental overdosage in humans. Animal toxicology studies have shown no adverse reactions in single doses up to 20 mg/kg and in repeated doses up to 6 mg/kg/day for 13 weeks, which were the highest doses studied. The highest single dose tested in animals represents 800-times the clinical dose. | NA | Rapidly absorbed with peak serum levels achieved at approximately 2 hours. | NA | NA | Adjuvants, Immunologic,Amino Acids, Peptides, and Proteins,Antineoplastic Agents,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunologic Factors,Peptide Hormones,Peptides,Proteins,Thymus Hormones | NA | NA | NA | NA | NA | Zadaxin | SciClone Pharmaceuticals (SCLN) | SciClone Pharmaceuticals (SCLN) | ZADAXIN thymosin alpha 1 (thymalfasin) is indicated as a monotherapy or combination therapy with interferon for the treatment of chronic hepatitis B. | NA | lyophilized preparation contains 1.6 mg thymosin alpha 1, 50 mg mannitol, and sodium phosphate buffer to adjust the pH to 6.8 | N. A. | Subcutaneous | The recommend-ed dose of ZADAXIN (thymalfasin) for chronic hepatitis B when used as a monotherapy or in combination with interferon (at the labeled dose and schedule for interferon) is 1.6 mg (900 µg/m2) administered subcutaneously twice a week for 6 to 12 months. Patients weighing less than 40 kg should receive a ZADAXIN (thymalfasin) dose of 40 µg/kg. | ZADAXIN (thymalfasin) is contraindicated in patients with a history of hypersensitivity to thymosin alpha 1 or any component of the injection. Because ZADAXIN (thymalfasin) therapy appears to work by enhancing the immune system, it should be considered contraindicated in patients who are being deliberately immunosuppressed, such as organ transplant patients, unless the potential benefits of the therapy clearly outweigh the potential risks. | Adverse experiences have been infrequent and mild, consisting primarily of local discomfort at the injection site, and rare instances of erythema, transient muscle atrophy, polyarthralgia combined with hand edema, and rash. | Link | NA | NA |
| 10694 | Th1157 | Sermorelin | >Th1157_Sermorelin YADAIFTNSYRKVLGQLSARKLLQDIMSRQ | 3357.882 | C149H246N44O42S | 9.99 | -0.33 | NA | 11-12 minutes | Sermorelin acetate is the acetate salt of an amidated synthetic 29-amino acid peptide (GRF 1-29 NH 2 ) that corresponds to the amino-terminal segment of the naturally occurring human growth hormone-releasing hormone (GHRH or GRF) consisting of 44 amino acid residues. | For the treatment of dwarfism, prevention of HIV-induced weight loss | Sermorelin is used in the treatment of children with growth hormone deficiency or growth failure. Geref increases plasma growth hormone (GH) concentration by stimulating the pituitary gland to release GH. Geref is similar to the full-length native hormone (44 residues) in its ability to stimulate GH secretion in humans. | Sermorelin binds to the growth hormone releasing hormone receptor and mimics native GRF in its ability to stimulate growth hormone secretion. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins,Anterior Pituitary Lobe Hormones and Analogues,Diagnostic Agents,Growth Hormone-Releasing Hormone,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Hypothalamic Hormones,Nerve Tissue Proteins,Neuropeptides,Peptide Hormones,Peptides,Pituitary and Hypothalamic Hormones and Analogues,Pituitary Hormone-Releasing Hormones,Somatropin and Somatropin Agonists,Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins,Tests for Pituitary Function | NA | NA | NA | NA | Growth hormone-releasing hormone receptor | Sermorelin acetate | Emd serono inc | Emd serono inc | Sermorelin is approved for diagnostic evaluation of pituitary function and also for increasing growth in children. Off label usage may include acute or age-related growth hormone insufficiency | NA | Two vial presentations are available, Each vial contains 0.5 mg sermorelin (as the acetate) and 5 mg mannitol. The pH is adjusted with dibasic sodium phosphate and monobasic sodium phosphate buffer. Each vial contains 3.0 mg sermorelin (as the acetate) and 5 mg mannitol. The pH is adjusted with dibasic sodium phosphate and monobasic sodium phosphate buffer. | Sermorelin is a sterile, non-pyrogenic, lyophilized powder | Subcutaneous Injection | A dosage of 0.2 - 0.3 mcg once daily at bedtime by subcutaneous injection is recommended. It is also recommended that subcutaneous injection sites be periodically rotated. | Sermorelin should not be used by patients with a known sensitivity to sermorelin or any of the excipients | The most common treatment-related adverse event (occurring in about 1 patient in 6) is local injection reaction characterized by pain, swelling or redness. Other treatment-related adverse events had individual occurrence rates of less than 1% and include: headache, flushing, dysphagia, dizziness, hyperactivity, somnolence and urticaria. | Link | NA | NA |
| 10756 | Th1176 | Dulaglutide | >Th1176_Dulaglutide HGEGTFTSDVSSYLEEQAAKEFIAWLVKGGGGGGGSGGGGSGGGGSAESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 59669.81 | C2646H4044N704O836S18 | NA | NA | NA | Approximately 5 days. | Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicityâ„¢. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. | Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying. | LD50 information for dulaglutide is not readily available in the literature.[L34685] Cases of overdose with dulaglutide have resulted in gastrointestinal disturbance. Appropriate supportive treatment is recommended to manage signs and symptoms.[L34670] Additionally, hypoglycemia has been observed after an overdose with dulaglutide; frequent plasma glucose monitoring should be performed.[L30380] | Dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.[L30380] | Dulaglutide is slowly absorbed after subcutaneous injection.[L34670] In a pharmacokinetic study of 20 healthy adults, Cmax occurred within 24-48 hours after dosing.[A234419] The average absolute bioavailability of dulaglutide after subcutaneous injections of single 0.75 mg and 1.5 mg doses was 65% and 47%, respectively.[L30380] | The apparent volume of distribution of dulaglutide was 3.09 L in a pharmacokinetic study; the apparent population mean peripheral volume of distribution was approximately 6 L.[L30380] | The apparent population mean clearance of dulaglutide was 0.142 L/h in a pharmacokinetic study.[L30380] | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Blood Proteins,Drugs Used in Diabetes,Gastrointestinal Hormones,Globulins,GLP-1 Agonists,Glucagon-like peptide-1 (GLP-1) analogues,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunoglobulin Fragments,Immunoglobulins,Immunoproteins,Incretin Mimetics,Pancreatic Hormones,Peptide Fragments,Peptide Hormones,Peptides,Proglucagon,Protein Precursors,Proteins,Recombinant Proteins,Serum Globulins | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Insulin Regular; Dulaglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Dulaglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Dulaglutide; Oxandrolone may increase the hypoglycemic activities of Dulaglutide; Paroxetine may increase the hypoglycemic activities of Dulaglutide; Pegvisomant may increase the hypoglycemic activities of Dulaglutide. | Glucagon-like peptide 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA |
| 10757 | Th1176 | Dulaglutide | >Th1176_Dulaglutide HGEGTFTSDVSSYLEEQAAKEFIAWLVKGGGGGGGSGGGGSGGGGSAESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 59669.81 | C2646H4044N704O836S19 | NA | NA | NA | Approximately 5 days. | Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicityâ„¢. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. | Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying. | LD50 information for dulaglutide is not readily available in the literature.[L34685] Cases of overdose with dulaglutide have resulted in gastrointestinal disturbance. Appropriate supportive treatment is recommended to manage signs and symptoms.[L34670] Additionally, hypoglycemia has been observed after an overdose with dulaglutide; frequent plasma glucose monitoring should be performed.[L30380] | Dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.[L30380] | Dulaglutide is slowly absorbed after subcutaneous injection.[L34670] In a pharmacokinetic study of 20 healthy adults, Cmax occurred within 24-48 hours after dosing.[A234419] The average absolute bioavailability of dulaglutide after subcutaneous injections of single 0.75 mg and 1.5 mg doses was 65% and 47%, respectively.[L30380] | The apparent volume of distribution of dulaglutide was 3.09 L in a pharmacokinetic study; the apparent population mean peripheral volume of distribution was approximately 6 L.[L30380] | The apparent population mean clearance of dulaglutide was 0.142 L/h in a pharmacokinetic study.[L30380] | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Blood Proteins,Drugs Used in Diabetes,Gastrointestinal Hormones,Globulins,GLP-1 Agonists,Glucagon-like peptide-1 (GLP-1) analogues,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunoglobulin Fragments,Immunoglobulins,Immunoproteins,Incretin Mimetics,Pancreatic Hormones,Peptide Fragments,Peptide Hormones,Peptides,Proglucagon,Protein Precursors,Proteins,Recombinant Proteins,Serum Globulins | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Insulin Regular; Dulaglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Dulaglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Dulaglutide; Oxandrolone may increase the hypoglycemic activities of Dulaglutide; Paroxetine may increase the hypoglycemic activities of Dulaglutide; Pegvisomant may increase the hypoglycemic activities of Dulaglutide. | Glucagon-like peptide 1 receptor | Trulicity | Eli Lilly and Company | Eli Lilly and Company | TRULICITYâ„¢ is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | NA | TRULICITY solution contains 0.75 mg or 1.5 mg of dulaglutide. Each single-dose pen or prefilled syringe contains 0.5 mL of solution and the following excipients: citric acid anhydrous (0.07 mg), mannitol (23.2 mg), polysorbate 80 (0.10 mg), trisodium citrate dihydrate (1.37 mg), in water for injection. | Solution, Injection | Subcutaneous | The recommended initiating dose of TRULICITY is 0.75 mg once weekly. The dose may be increased to 1.5 mg once weekly for additional glycemic control. The maximum recommended dose is 1.5 mg once weekly. Administer TRULICITY once weekly, any time of day, with or without food. TRULICITY should be injected subcutaneously in the abdomen, thigh, or upper arm. If a dose is missed, instruct patients to administer as soon as possible if there are at least 3 days (72 hours) until the next scheduled dose. If less than 3 days remain before the next scheduled dose, skip the missed dose and administer the next dose on the regularly scheduled day. In each case, patients can then resume their regular once weekly dosing schedule. The day of weekly administration can be changed if necessary as long as the last dose was administered 3 or more days before. | TRULICITY is contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); TRULICITY is also contraindicated in patients with a prior serious hypersensitivity reaction to dulaglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin; Hypersensitivity reactions; Renal impairment; Severe Gastrointestinal Disease. | Link | NA | NA |
| 10758 | Th1176 | Dulaglutide | >Th1176_Dulaglutide HGEGTFTSDVSSYLEEQAAKEFIAWLVKGGGGGGGSGGGGSGGGGSAESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 59669.81 | C2646H4044N704O836S20 | NA | NA | NA | Approximately 5 days. | Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicityâ„¢. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. | Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying. | LD50 information for dulaglutide is not readily available in the literature.[L34685] Cases of overdose with dulaglutide have resulted in gastrointestinal disturbance. Appropriate supportive treatment is recommended to manage signs and symptoms.[L34670] Additionally, hypoglycemia has been observed after an overdose with dulaglutide; frequent plasma glucose monitoring should be performed.[L30380] | Dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.[L30380] | Dulaglutide is slowly absorbed after subcutaneous injection.[L34670] In a pharmacokinetic study of 20 healthy adults, Cmax occurred within 24-48 hours after dosing.[A234419] The average absolute bioavailability of dulaglutide after subcutaneous injections of single 0.75 mg and 1.5 mg doses was 65% and 47%, respectively.[L30380] | The apparent volume of distribution of dulaglutide was 3.09 L in a pharmacokinetic study; the apparent population mean peripheral volume of distribution was approximately 6 L.[L30380] | The apparent population mean clearance of dulaglutide was 0.142 L/h in a pharmacokinetic study.[L30380] | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Blood Proteins,Drugs Used in Diabetes,Gastrointestinal Hormones,Globulins,GLP-1 Agonists,Glucagon-like peptide-1 (GLP-1) analogues,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunoglobulin Fragments,Immunoglobulins,Immunoproteins,Incretin Mimetics,Pancreatic Hormones,Peptide Fragments,Peptide Hormones,Peptides,Proglucagon,Protein Precursors,Proteins,Recombinant Proteins,Serum Globulins | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Insulin Regular; Dulaglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Dulaglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Dulaglutide; Oxandrolone may increase the hypoglycemic activities of Dulaglutide; Paroxetine may increase the hypoglycemic activities of Dulaglutide; Pegvisomant may increase the hypoglycemic activities of Dulaglutide. | Glucagon-like peptide 1 receptor | Trulicity | Eli Lilly Canada Inc | Eli Lilly Canada Inc | TRULICITYâ„¢ is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | NA | TRULICITY solution contains 0.75 mg or 1.5 mg of dulaglutide. Each single-dose pen or prefilled syringe contains 0.5 mL of solution and the following excipients: citric acid anhydrous (0.07 mg), mannitol (23.2 mg), polysorbate 80 (0.10 mg), trisodium citrate dihydrate (1.37 mg), in water for injection. | Solution | Subcutaneous | The recommended initiating dose of TRULICITY is 0.75 mg once weekly. The dose may be increased to 1.5 mg once weekly for additional glycemic control. The maximum recommended dose is 1.5 mg once weekly. Administer TRULICITY once weekly, any time of day, with or without food. TRULICITY should be injected subcutaneously in the abdomen, thigh, or upper arm. If a dose is missed, instruct patients to administer as soon as possible if there are at least 3 days (72 hours) until the next scheduled dose. If less than 3 days remain before the next scheduled dose, skip the missed dose and administer the next dose on the regularly scheduled day. In each case, patients can then resume their regular once weekly dosing schedule. The day of weekly administration can be changed if necessary as long as the last dose was administered 3 or more days before. | TRULICITY is contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); TRULICITY is also contraindicated in patients with a prior serious hypersensitivity reaction to dulaglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin; Hypersensitivity reactions; Renal impairment; Severe Gastrointestinal Disease. | Link | NA | NA |
| 10759 | Th1176 | Dulaglutide | >Th1176_Dulaglutide HGEGTFTSDVSSYLEEQAAKEFIAWLVKGGGGGGGSGGGGSGGGGSAESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 59669.81 | C2646H4044N704O836S21 | NA | NA | NA | Approximately 5 days. | Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicityâ„¢. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. | Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying. | LD50 information for dulaglutide is not readily available in the literature.[L34685] Cases of overdose with dulaglutide have resulted in gastrointestinal disturbance. Appropriate supportive treatment is recommended to manage signs and symptoms.[L34670] Additionally, hypoglycemia has been observed after an overdose with dulaglutide; frequent plasma glucose monitoring should be performed.[L30380] | Dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.[L30380] | Dulaglutide is slowly absorbed after subcutaneous injection.[L34670] In a pharmacokinetic study of 20 healthy adults, Cmax occurred within 24-48 hours after dosing.[A234419] The average absolute bioavailability of dulaglutide after subcutaneous injections of single 0.75 mg and 1.5 mg doses was 65% and 47%, respectively.[L30380] | The apparent volume of distribution of dulaglutide was 3.09 L in a pharmacokinetic study; the apparent population mean peripheral volume of distribution was approximately 6 L.[L30380] | The apparent population mean clearance of dulaglutide was 0.142 L/h in a pharmacokinetic study.[L30380] | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Blood Proteins,Drugs Used in Diabetes,Gastrointestinal Hormones,Globulins,GLP-1 Agonists,Glucagon-like peptide-1 (GLP-1) analogues,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunoglobulin Fragments,Immunoglobulins,Immunoproteins,Incretin Mimetics,Pancreatic Hormones,Peptide Fragments,Peptide Hormones,Peptides,Proglucagon,Protein Precursors,Proteins,Recombinant Proteins,Serum Globulins | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Insulin Regular; Dulaglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Dulaglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Dulaglutide; Oxandrolone may increase the hypoglycemic activities of Dulaglutide; Paroxetine may increase the hypoglycemic activities of Dulaglutide; Pegvisomant may increase the hypoglycemic activities of Dulaglutide. | Glucagon-like peptide 1 receptor | Trulicity | Eli Lilly Canada Inc | Eli Lilly Canada Inc | TRULICITYâ„¢ is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | NA | TRULICITY solution contains 0.75 mg or 1.5 mg of dulaglutide. Each single-dose pen or prefilled syringe contains 0.5 mL of solution and the following excipients: citric acid anhydrous (0.07 mg), mannitol (23.2 mg), polysorbate 80 (0.10 mg), trisodium citrate dihydrate (1.37 mg), in water for injection. | Solution | Subcutaneous | The recommended initiating dose of TRULICITY is 0.75 mg once weekly. The dose may be increased to 1.5 mg once weekly for additional glycemic control. The maximum recommended dose is 1.5 mg once weekly. Administer TRULICITY once weekly, any time of day, with or without food. TRULICITY should be injected subcutaneously in the abdomen, thigh, or upper arm. If a dose is missed, instruct patients to administer as soon as possible if there are at least 3 days (72 hours) until the next scheduled dose. If less than 3 days remain before the next scheduled dose, skip the missed dose and administer the next dose on the regularly scheduled day. In each case, patients can then resume their regular once weekly dosing schedule. The day of weekly administration can be changed if necessary as long as the last dose was administered 3 or more days before. | TRULICITY is contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); TRULICITY is also contraindicated in patients with a prior serious hypersensitivity reaction to dulaglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin; Hypersensitivity reactions; Renal impairment; Severe Gastrointestinal Disease. | Link | NA | NA |
| 10760 | Th1176 | Dulaglutide | >Th1176_Dulaglutide HGEGTFTSDVSSYLEEQAAKEFIAWLVKGGGGGGGSGGGGSGGGGSAESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 59669.81 | C2646H4044N704O836S22 | NA | NA | NA | Approximately 5 days. | Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicityâ„¢. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. | Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying. | LD50 information for dulaglutide is not readily available in the literature.[L34685] Cases of overdose with dulaglutide have resulted in gastrointestinal disturbance. Appropriate supportive treatment is recommended to manage signs and symptoms.[L34670] Additionally, hypoglycemia has been observed after an overdose with dulaglutide; frequent plasma glucose monitoring should be performed.[L30380] | Dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.[L30380] | Dulaglutide is slowly absorbed after subcutaneous injection.[L34670] In a pharmacokinetic study of 20 healthy adults, Cmax occurred within 24-48 hours after dosing.[A234419] The average absolute bioavailability of dulaglutide after subcutaneous injections of single 0.75 mg and 1.5 mg doses was 65% and 47%, respectively.[L30380] | The apparent volume of distribution of dulaglutide was 3.09 L in a pharmacokinetic study; the apparent population mean peripheral volume of distribution was approximately 6 L.[L30380] | The apparent population mean clearance of dulaglutide was 0.142 L/h in a pharmacokinetic study.[L30380] | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Blood Proteins,Drugs Used in Diabetes,Gastrointestinal Hormones,Globulins,GLP-1 Agonists,Glucagon-like peptide-1 (GLP-1) analogues,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunoglobulin Fragments,Immunoglobulins,Immunoproteins,Incretin Mimetics,Pancreatic Hormones,Peptide Fragments,Peptide Hormones,Peptides,Proglucagon,Protein Precursors,Proteins,Recombinant Proteins,Serum Globulins | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Insulin Regular; Dulaglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Dulaglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Dulaglutide; Oxandrolone may increase the hypoglycemic activities of Dulaglutide; Paroxetine may increase the hypoglycemic activities of Dulaglutide; Pegvisomant may increase the hypoglycemic activities of Dulaglutide. | Glucagon-like peptide 1 receptor | Trulicity | Eli Lilly Canada Inc | Eli Lilly Canada Inc | TRULICITYâ„¢ is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | NA | TRULICITY solution contains 0.75 mg or 1.5 mg of dulaglutide. Each single-dose pen or prefilled syringe contains 0.5 mL of solution and the following excipients: citric acid anhydrous (0.07 mg), mannitol (23.2 mg), polysorbate 80 (0.10 mg), trisodium citrate dihydrate (1.37 mg), in water for injection. | Solution | Subcutaneous | The recommended initiating dose of TRULICITY is 0.75 mg once weekly. The dose may be increased to 1.5 mg once weekly for additional glycemic control. The maximum recommended dose is 1.5 mg once weekly. Administer TRULICITY once weekly, any time of day, with or without food. TRULICITY should be injected subcutaneously in the abdomen, thigh, or upper arm. If a dose is missed, instruct patients to administer as soon as possible if there are at least 3 days (72 hours) until the next scheduled dose. If less than 3 days remain before the next scheduled dose, skip the missed dose and administer the next dose on the regularly scheduled day. In each case, patients can then resume their regular once weekly dosing schedule. The day of weekly administration can be changed if necessary as long as the last dose was administered 3 or more days before. | TRULICITY is contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); TRULICITY is also contraindicated in patients with a prior serious hypersensitivity reaction to dulaglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin; Hypersensitivity reactions; Renal impairment; Severe Gastrointestinal Disease. | Link | NA | NA |
| 10761 | Th1176 | Dulaglutide | >Th1176_Dulaglutide HGEGTFTSDVSSYLEEQAAKEFIAWLVKGGGGGGGSGGGGSGGGGSAESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 59669.81 | C2646H4044N704O836S23 | NA | NA | NA | Approximately 5 days. | Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicityâ„¢. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. | Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying. | LD50 information for dulaglutide is not readily available in the literature.[L34685] Cases of overdose with dulaglutide have resulted in gastrointestinal disturbance. Appropriate supportive treatment is recommended to manage signs and symptoms.[L34670] Additionally, hypoglycemia has been observed after an overdose with dulaglutide; frequent plasma glucose monitoring should be performed.[L30380] | Dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.[L30380] | Dulaglutide is slowly absorbed after subcutaneous injection.[L34670] In a pharmacokinetic study of 20 healthy adults, Cmax occurred within 24-48 hours after dosing.[A234419] The average absolute bioavailability of dulaglutide after subcutaneous injections of single 0.75 mg and 1.5 mg doses was 65% and 47%, respectively.[L30380] | The apparent volume of distribution of dulaglutide was 3.09 L in a pharmacokinetic study; the apparent population mean peripheral volume of distribution was approximately 6 L.[L30380] | The apparent population mean clearance of dulaglutide was 0.142 L/h in a pharmacokinetic study.[L30380] | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Blood Proteins,Drugs Used in Diabetes,Gastrointestinal Hormones,Globulins,GLP-1 Agonists,Glucagon-like peptide-1 (GLP-1) analogues,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunoglobulin Fragments,Immunoglobulins,Immunoproteins,Incretin Mimetics,Pancreatic Hormones,Peptide Fragments,Peptide Hormones,Peptides,Proglucagon,Protein Precursors,Proteins,Recombinant Proteins,Serum Globulins | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Insulin Regular; Dulaglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Dulaglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Dulaglutide; Oxandrolone may increase the hypoglycemic activities of Dulaglutide; Paroxetine may increase the hypoglycemic activities of Dulaglutide; Pegvisomant may increase the hypoglycemic activities of Dulaglutide. | Glucagon-like peptide 1 receptor | Trulicity | Eli Lilly Canada Inc | Eli Lilly Canada Inc | TRULICITYâ„¢ is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | NA | TRULICITY solution contains 0.75 mg or 1.5 mg of dulaglutide. Each single-dose pen or prefilled syringe contains 0.5 mL of solution and the following excipients: citric acid anhydrous (0.07 mg), mannitol (23.2 mg), polysorbate 80 (0.10 mg), trisodium citrate dihydrate (1.37 mg), in water for injection. | Solution | Subcutaneous | The recommended initiating dose of TRULICITY is 0.75 mg once weekly. The dose may be increased to 1.5 mg once weekly for additional glycemic control. The maximum recommended dose is 1.5 mg once weekly. Administer TRULICITY once weekly, any time of day, with or without food. TRULICITY should be injected subcutaneously in the abdomen, thigh, or upper arm. If a dose is missed, instruct patients to administer as soon as possible if there are at least 3 days (72 hours) until the next scheduled dose. If less than 3 days remain before the next scheduled dose, skip the missed dose and administer the next dose on the regularly scheduled day. In each case, patients can then resume their regular once weekly dosing schedule. The day of weekly administration can be changed if necessary as long as the last dose was administered 3 or more days before. | TRULICITY is contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); TRULICITY is also contraindicated in patients with a prior serious hypersensitivity reaction to dulaglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin; Hypersensitivity reactions; Renal impairment; Severe Gastrointestinal Disease. | Link | NA | NA |
| 10762 | Th1176 | Dulaglutide | >Th1176_Dulaglutide HGEGTFTSDVSSYLEEQAAKEFIAWLVKGGGGGGGSGGGGSGGGGSAESKYGPPCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSQEDPEVQFNWYVDGVEVHNAKTKPREEQFNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKGLPSSIEKTISKAKGQPREPQVYTLPPSQEEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSRLTVDKSRWQEGNVFSCSVMHEALHNHYTQKSLSLSLG | 59670.81 | C2646H4044N704O836S24 | NA | NA | NA | Approximately 5 days. | Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicityâ„¢. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. | Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. | Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying. | LD50 information for dulaglutide is not readily available in the literature.[L34685] Cases of overdose with dulaglutide have resulted in gastrointestinal disturbance. Appropriate supportive treatment is recommended to manage signs and symptoms.[L34670] Additionally, hypoglycemia has been observed after an overdose with dulaglutide; frequent plasma glucose monitoring should be performed.[L30380] | Dulaglutide is presumed to be degraded into its component amino acids by general protein catabolism pathways.[L30380] | Dulaglutide is slowly absorbed after subcutaneous injection.[L34670] In a pharmacokinetic study of 20 healthy adults, Cmax occurred within 24-48 hours after dosing.[A234419] The average absolute bioavailability of dulaglutide after subcutaneous injections of single 0.75 mg and 1.5 mg doses was 65% and 47%, respectively.[L30380] | The apparent volume of distribution of dulaglutide was 3.09 L in a pharmacokinetic study; the apparent population mean peripheral volume of distribution was approximately 6 L.[L30380] | The apparent population mean clearance of dulaglutide was 0.142 L/h in a pharmacokinetic study.[L30380] | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Blood Proteins,Drugs Used in Diabetes,Gastrointestinal Hormones,Globulins,GLP-1 Agonists,Glucagon-like peptide-1 (GLP-1) analogues,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Immunoglobulin Fragments,Immunoglobulins,Immunoproteins,Incretin Mimetics,Pancreatic Hormones,Peptide Fragments,Peptide Hormones,Peptides,Proglucagon,Protein Precursors,Proteins,Recombinant Proteins,Serum Globulins | NA | NA | NA | Acetylsalicylic acid may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Chlorpropamide; Dihydrotestosterone may increase the hypoglycemic activities of Dulaglutide; Dulaglutide may increase the hypoglycemic activities of Insulin Regular; Dulaglutide may increase the hypoglycemic activities of Insulin Lispro; The therapeutic efficacy of Dulaglutide can be decreased when used in combination with Leuprolide; Lipoic Acid may increase the hypoglycemic activities of Dulaglutide; Oxandrolone may increase the hypoglycemic activities of Dulaglutide; Paroxetine may increase the hypoglycemic activities of Dulaglutide; Pegvisomant may increase the hypoglycemic activities of Dulaglutide. | Glucagon-like peptide 1 receptor | Trulicity | Eli Lilly and Company | Eli Lilly and Company | TRULICITYâ„¢ is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. | NA | TRULICITY solution contains 0.75 mg or 1.5 mg of dulaglutide. Each single-dose pen or prefilled syringe contains 0.5 mL of solution and the following excipients: citric acid anhydrous (0.07 mg), mannitol (23.2 mg), polysorbate 80 (0.10 mg), trisodium citrate dihydrate (1.37 mg), in water for injection. | Solution, Injection | Subcutaneous | The recommended initiating dose of TRULICITY is 0.75 mg once weekly. The dose may be increased to 1.5 mg once weekly for additional glycemic control. The maximum recommended dose is 1.5 mg once weekly. Administer TRULICITY once weekly, any time of day, with or without food. TRULICITY should be injected subcutaneously in the abdomen, thigh, or upper arm. If a dose is missed, instruct patients to administer as soon as possible if there are at least 3 days (72 hours) until the next scheduled dose. If less than 3 days remain before the next scheduled dose, skip the missed dose and administer the next dose on the regularly scheduled day. In each case, patients can then resume their regular once weekly dosing schedule. The day of weekly administration can be changed if necessary as long as the last dose was administered 3 or more days before. | TRULICITY is contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2); TRULICITY is also contraindicated in patients with a prior serious hypersensitivity reaction to dulaglutide or to any of the product components | Risk of Thyroid C-cell Tumors; Pancreatitis; Hypoglycemia with Concomitant Use of Insulin Secretagogues or Insulin; Hypersensitivity reactions; Renal impairment; Severe Gastrointestinal Disease. | Link | NA | NA |
| 10845 | Th1208 | Metreleptin | >Th1208_Metreleptin MVPIQKVQDDTKTLIKTIVTRINDISHTQSVSSKQKVTGLDFIPGLHPILTLSKMDQTLAVYQQILTSMPSRNVIQISNDLENLRDLLHVLAFSKSCHLPWASGLETLDSLGGVLEASGYSTEVVALSRLQGSLQDMLWQLDLSPGC | 16155.44 | C714H1167N191O221S6 | NA | NA | NA | 3.8 to 4.7 hours | Metreleptin, a recombinant analog of the human hormone leptin, is an orphan drug used to treat complications of leptin deficiency in people with congenital or acquired lipodystrophy. Affecting less than 500 people worldwide, lipodystrophy is characterized by a lack of adipose tissue, fat deposition in the muscles and liver, and metabolic complications such as hypertriglyceridemia, insulin resistance, diabetes mellitus, and fatty liver disease. These metabolic abnormalities are often aggravated by excessive food intake, which is further aggravated by leptin deficiency, a protein secreted by adipose tissue. Administration of Metreleptin results in improvement of metabolic symptoms including improvements in insulin resistance, reduced HbA1c and fasting glucose, reduced triglycerides, and reductions in food intake. Metreleptin is produced in E. coli and differs from native human leptin by the addition of a methionine residue at its amino terminus. It is administered as a once daily subcutaneous injection. On Feb. 24, 2014, Metreleptin was approved by the FDA for the treatment of complications of leptin deficiency, in addition to diet, in patients with congenital generalized or acquired generalized lipodystrophy. Metreleptin is marketed under the brand Myalept® by Aegerion Pharmaceuticals, Inc. | It is indicated as an adjunct to diet as replacement therapy to treat the complications of leptin deficiency in patients with congenital or acquired generalized lipodystrophy. | In patients with leptin deficiency, clinical trials demonstrated that exogenous leptin administration results in weight loss, reduction in mean HbA1c and fasting glucose levels, reduced blood insulin, and reduced triglyceride levels leading to improved insulin sensitivity and reductions in food intake. | Metreleptin functions by binding to and activating the human leptin receptor (ObR), which belongs to the Class I cytokine family of receptors that signals through the JAK/STAT transduction pathway. | The most common adverse events reported for metreleptin use have been headache, hypoglycemia, weight loss, and abdominal pain. A boxed warning states that anti-metreleptin antibodies, serious infections, and worsening metabolic control have been reported in patients taking the drug, and that some patients with acquired generalized lipodystrophy taking metreleptin have developed T-cell lymphoma. Anti-metreleptin antibodies with neutralizing activity have been identified in patients treated with metreleptin which can lead to inhibition of endogenous leptin action and loss of drug efficacy. As part of a Risk Evaluation and Mitigation Strategy (REMS), the FDA has required healthcare providers to be trained in the use of metreleptin before prescribing it and to attest that patients for whom they prescribe metreleptin have a labeled indication for the drug. Metreleptin is classified as category C (no adequate studies in women) for use during pregnancy. Two-year carcinogenicity studies in rodents have not been conducted with metreleptin. No proliferative or preneoplastic lesions were observed in mice or dogs following treatment up to six months. However, leptin is reported in the literature to promote cell proliferation in vitro and tumor progression in some mouse models of cancer. Metreleptin was not mutagenic in the Ames bacterial mutagenicity assay or clastogenic in an in vitro chromosomal aberration assay in Chinese hamster ovary cells and human peripheral blood lymphocytes. Metreleptin was not mutagenic or clastogenic in an in vivo mouse micronucleus assay. In a fertility study in mice, metreleptin had no adverse effects on mating, fertility, or early embryonic development at doses ranging between 7 and 15 times the maximum recommended clinical dose based on body surface area of a 20- and 60-kg patient, respectively. | No formal metabolism studies have been conducted with metreleptin. Nonclinical data indicate renal clearance is the major route of metreleptin elimination, with no apparent contribution of systemic metabolism or degradation. | Peak serum leptin concentration (Cmax) occurred approximately 4.0 to 4.3 hours after subcutaneous administration of single doses ranging from 0.1 to 0.3 mg/kg in healthy subjects. | Following intravenous administration of metreleptin, leptin volume of distribution was approximately 4 to 5 times plasma volume; volumes (mean ± SD) were 370 ± 184 mL/kg, 398 ± 92 mL/kg, and 463 ± 116 mL/kg for 0.3, 1.0, and 3.0 mg/kg/day doses, respectively. | The clearance of metreleptin is expected to be delayed in the presence of leptin antibodies. | Adipokines,Alimentary Tract and Metabolism,Amino Acids and Derivatives,Amino Acids, Peptides, and Proteins,Analogs/Derivatives,Biological Factors,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Intercellular Signaling Peptides and Proteins,Leptin Analog,Obesity, drug therapy,Peptide Hormones,Peptides,Proteins | US20070099836 | 29-11-2006 | 29-11-2026 | Chlorotrianisene, Chlorpropamide, Cyclosporine, Dienogest, Etonogestrel, Gliclazide, Glimepiride, Glipizide, Glyburide, Insulin Aspart, Insulin Degludec, Insulin Detemir, Insulin Glargine, Insulin Glulisine, Insulin Human, Insulin Lispro, Levonorgestrel, Medroxyprogesterone acetate, Norethisterone, Theophylline, Tolazamide, Tolbutamide, Warfarin | Leptin receptor | Myalept | Amylin Pharmaceuticals, LLC | Amylin Pharmaceuticals, LLC | MYALEPT (metreleptin) for injection is indicated as an adjunct to diet as replacement therapy to treat the complications of leptin deficiency in patients with congenital or acquired generalized lipodystrophy. | NA | NA | Lyophilized powder for solution | subcutaneous | The starting daily dose (injection volume) should be 0.06 mg/kg for a baseline weight of less than 40kg. For a weight greater than 40 kg, the starting dose should be 2.5 mg (0.5 mL) for males and 5 mg (1 mL) for females. | MYALEPT is contraindicated in patients with general obesity not associated with congenital leptin deficiency. MYALEPT has not been shown to be effective in treating general obesity, and the development of anti-metreleptin antibodies with neutralizing activity has been reported in obese patients treated with MYALEPT; Also, is contraindicated in patients with prior severe hypersensitivity reactions to metreleptin or to any of the product components. Known hypersensitivity reactions have included urticaria and generalized rash. | As observed from an open-lable single-arm study the most frequesnt reactions were headache, hypoglycaemia, decreased weight, abdominal pain, athralgia, dizziness, ear infection, fatigue, nausea, ovarian cyst, upper respiratory tract infection, anaemia, diarrhea, back pain, paresthesia, proteinuria, pyrexia. | Link | NA | NA |
| 10849 | Th1212 | Insulin Pork | >Th1212_Insulin_Pork GIVEQCCTSICSLYQLENYCN | 5795.6 | C257H387N65O76S6 | 5.39 | 0.218 | NA | NA | Insulin isolated from pig pancreas. Composed of alpha and beta chains, processed from pro-insulin. Forms a hexameric structure. | For the treatment of type I and II diabetes mellitus. | Insulin is used in the treatment of type I and type II diabetes. The primary activity of insulin is the regulation of glucose metabolism. In muscle and other tissues (except the brain), insulin causes rapid transport of glucose and amino acids intracellularly. It also promotes anabolism, and inhibits protein catabolism. In the liver, insulin promotes the uptake and storage of glucose in the form of glycogen, inhibits gluconeogenesis, and promotes the conversion of excess glucose into fat. | Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism. | NA | Insulin is predominantly cleared by metabolic degradation via a receptor-mediated process. | NA | NA | NA | Alimentary Tract and Metabolism,Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Cytochrome P-450 CYP1A2 Inducers,Cytochrome P-450 CYP1A2 Inducers (strength unknown),Cytochrome P-450 Enzyme Inducers,Drugs Used in Diabetes,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Insulin,Insulin, Short-Acting,Insulins and Analogues for Injection, Fast-Acting,Pancreatic Hormones,Peptide Hormones,Peptides,Protein Precursors,Proteins | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | Iletin II | Lilly | Lilly | NA | NA | 100 units/mL (U-100) | sterile suspension | Subcutaneous | NA | NA | NA | Link | NA | NA |
| 10861 | Th1223 | Chorionic Gonadotropin (Human) | >Th1223_Chorionic_Gonadotropin_(Human) APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | NA | NA | NA | NA | NA | NA | Human chorionic gonadotropin (HCG), a polypeptide hormone produced by the human placenta. Endogenously produced HCG interacts with the LHCG receptor of the ovary and promotes the maintenance of the corpus luteum during the beginning of pregnancy. This allows the corpus luteum to continuously secrete the hormone progesterone during the first trimester, which is required for maintenance of the uterus and prevents menstruation. In males, HCG also stimulates the production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testis to produce androgens. HCG is composed of an alpha and a beta sub-unit. The alpha sub-unit is essentially identical to the alpha sub units of the human pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), as well as to the alpha sub-unit of human thyroid-stimulating hormone (TSH), while the beta sub units of these hormones differ in amino acid sequence. As a drug product, chorionic gonadotropin is a highly purified pyrogen-free preparation obtained from the urine of pregnant females. | For the treatment of prepubertal cryptorchidism (not due to anatomical obstruction), for the treatment of selected cases of hypogonadotropic hypogonadism (hypogonadism secondary to a pituitary deficiency) in males and for the induction of ovulation and pregnancy in the anovulatory, infertile woman in whom the cause of anovulation is secondary and not due to primary ovarian failure, and who has been appropriately pretreated with human menotropins. | he action of HCG is virtually identical to that of pituitary LH, although HCG appears to have a small degree of FSH activity as well. It stimulates production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testis to produce androgens and the corpus luteum of the ovary to produce progesterone. | NA | NA | NA | NA | NA | NA | Hormones | US6706681 | 16-03-2004 | 16-03-2021 | NA | Lutropin-choriogonadotropic hormone receptor | Ovidrel | Emd Serono | Emd Serono | It is indicated for the induction of final follicular maturation and early luteinization in infertile women who have undergone pituitary desensitization and who have been appropriately pretreated with follicle stimulating hormones as part of an Assisted Reproductive Technology (ART) program such as in vitro fertilization and embryo transfer. It is also indicated for the induction of ovulation (OI) and pregnancy in anovulatory infertile patients in whom the cause of infertility is functional and not due to primary ovarian failure. | NA | Each Ovidrel® PreFilled Syringe is filled with 0.515 mL containing 257.5 μg of choriogonadotropin alfa, 28.1 mg mannitol, 505 μg 85% O-phosphoric acid, 103 μg L-methionine, 51.5 μg Poloxamer 188, Sodium Hydroxide (for pH adjustment), and Water for Injection to deliver 250 μg of choriogonadotropin alfa in 0.5 mL. The pH of the solution is 6.5 to 7.5. | Injection, solution | Subcutaneous | Ovidrel® PreFilled Syringe 250 μg should be administered one day following the last dose of the follicle stimulating agent. Ovidrel® PreFilled Syringe should not be administered until adequate follicular development is indicated by serum estradiol and vaginal ultrasonography. | Ovidrel® PreFilled Syringe (choriogonadotropin alfa injection) is contraindicated in women who exhibit:Prior hypersensitivity to hCG preparations or one of their excipients.Primary ovarian failure.Uncontrolled thyroid or adrenal dysfunction.An uncontrolled organic intracranial lesion such as a pituitary tumor.Abnormal uterine bleeding of undetermined origin (see “Selection of Patientsâ€Â).Ovarian cyst or enlargement of undetermined origin (see “Selection of Patientsâ€Â).Sex hormone dependent tumors of the reproductive tract and accessory organs.Pregnancy. | Redness or pain at the injection site, mild abdominal pain, mood changes, or mild nausea/vomiting may occur. | Link | NA | NA |
| 10862 | Th1223 | Chorionic Gonadotropin (Human) | >Th1223_Chorionic_Gonadotropin_(Human) APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | NA | NA | NA | NA | NA | NA | Human chorionic gonadotropin (HCG), a polypeptide hormone produced by the human placenta. Endogenously produced HCG interacts with the LHCG receptor of the ovary and promotes the maintenance of the corpus luteum during the beginning of pregnancy. This allows the corpus luteum to continuously secrete the hormone progesterone during the first trimester, which is required for maintenance of the uterus and prevents menstruation. In males, HCG also stimulates the production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testis to produce androgens. HCG is composed of an alpha and a beta sub-unit. The alpha sub-unit is essentially identical to the alpha sub units of the human pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), as well as to the alpha sub-unit of human thyroid-stimulating hormone (TSH), while the beta sub units of these hormones differ in amino acid sequence. As a drug product, chorionic gonadotropin is a highly purified pyrogen-free preparation obtained from the urine of pregnant females. | For the treatment of prepubertal cryptorchidism (not due to anatomical obstruction), for the treatment of selected cases of hypogonadotropic hypogonadism (hypogonadism secondary to a pituitary deficiency) in males and for the induction of ovulation and pregnancy in the anovulatory, infertile woman in whom the cause of anovulation is secondary and not due to primary ovarian failure, and who has been appropriately pretreated with human menotropins. | he action of HCG is virtually identical to that of pituitary LH, although HCG appears to have a small degree of FSH activity as well. It stimulates production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testis to produce androgens and the corpus luteum of the ovary to produce progesterone. | NA | NA | NA | NA | NA | NA | Hormones | US6706681 | 16-03-2004 | 16-03-2021 | NA | Lutropin-choriogonadotropic hormone receptor | Pregnyl | Physicians Total Care, Inc. | Physicians Total Care, Inc. | It is used for treating fertility problems in certain women who have not gone through menopause. Treating certain testicular development problems and stimulating the development of secondary sexual characteristics in certain patients. It is also used to treat boys 4 to 9 years old who have testicles that have not moved into the scrotum. | NA | Available in vials containing 10,000 USP units of sterile dried powder with 5 mg monobasic sodium phosphate and 4.4 mg dibasic sodium phosphate. If required, pH is adjusted with sodium hydroxide and/or phosphoric acid. Each package also contains a 10-mL vial of solvent containing: water for injection with 0.56% sodium chloride and 0.9% BENZYL ALCOHOL, WHICH IS NOT FOR USE IN NEWBORNS. If required, pH is adjusted with sodium hydroxide and/or hydrochloric acid. | Injection, Solution | Intramuscular, Subcutaneous | 4000 USP units 3 times weekly for 3 weeks. | Precocious puberty, prostatic carcinoma or other androgen-dependent neoplasm, prior allergic reaction to HCG. | Headache, irritability, restlessness, depression, fatigue, edema, precocious puberty, gynecomastia, pain at the site of injection. | Link | NA | NA |
| 10863 | Th1224 | Chorionic Gonadotropin (Recombinant) | >Th1224_Chorionic_Gonadotropin_(Recombinant) APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25719.7 | C1105H1770N318O336S26 | 8.61 | -0.258 | 55 °C | The mean terminal half-life is about 29 ± 6 hours (initial half-life is 4.5 ± 0.5 hours). | Recombinant human chorionic gonadotropin with 2 subunits, alpha = 92 residues, beta = 145 residues, each with N-and O-linked carbohydrate moieties linked to ASN-52 and ASN-78 (on alpha subunit) and ASN-13, ASN-30, SER-121, SER-127, SER-132 and SER-138 (on beta subunit). The primary structure of the alpha-chain of r-hCG is identical to that of the alpha-chain of hCG, FSH and LH. | For the treatment of female infertility | Choriogonadotropin alfa is used to treat female infertility, Choriogonadotropin alfa stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Ovidrel is an analogue of Luteinizing Hormone (LH) and binds to the LH/hCG receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. | Choriogonadotropin alfa binds to the Follicle stimulating hormone receptor which results in ovulation in the absence of sufficient endogenous Luteinizing hormone. | NA | NA | NA | NA | NA | Hormones | US5767251 | 16-06-1998 | 16-06-2015 | NA | Lutropin-choriogonadotropic hormone receptor, Follicle-stimulating hormone receptor | Ovitrelle | Merck Serono Europe Limited | Merck Serono Europe Limited | Ovitrelle is indicated in the treatment of:women undergoing superovulation prior to assisted reproductive techniques such as in vitro fertilisation (IVF): Ovitrelle is administered to trigger final follicular maturation and luteinisation after stimulation of follicular growth;anovulatory or oligo-ovulatory women: Ovitrelle is administered to trigger ovulation and luteinisation in anovulatory or oligo-ovulatory patients after stimulation of follicular growth. | NA | Each pre-filled syringe contains 250 micrograms choriogonadotropin alfa* (equivalent to approximately 6,500 IU) in 0.5 mL solution | powder and solvent to be made up into a solution | Subcutaneous | One pre-filled syringe of Ovitrelle (250 micrograms) is administered 24 to 48 hours after the last administration of a follicle stimulating hormone (FSH) or human menopausal gonadotropin (hMG) preparation, i.e. when optimal stimulation of follicular growth is achieved. | hypersensitive (allergic) to choriogonadotropin alfa or any of the other ingredients. | The most common side effects with Ovitrelle (seen in between 1 and 10 patients in 100) are reactions at the injection site, headache, tiredness, vomiting, nausea (feeling sick), abdominal pain (stomach ache) and ovarian hyperstimulation syndrome (such as feeling sick, weight gain and diarrhoea). Ovarian hyperstimulation syndrome occurs when the ovaries over respond to treatment, especially when medicines to trigger ovulation have been used. | Link | NA | NA |
| 10877 | Th1237 | Somatropin recombinant | >Th1237_Somatropin_recombinant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 °C at pH 3.5 | 21.1 (±5.1) minutes | Recombinant human growth hormone (somatotropin) 191 residues, MW 22.1 kD, synthesized in E. coli | For treatment of dwarfism, acromegaly and prevention of HIV-induced weight loss | Used in the treatment of dwarfism and growth failure, growth hormone (hGH) stimulates skeletal growth in pediatric patients with growth failure due to a lack of adequate secretion of endogenous GH. Skeletal growth is accomplished at the epiphyseal plates at the ends of a growing bone. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and one of its mediators, IGF-I (insulin-like growth factor). | hGH binds to the human growth hormone receptor (GHR). Upon binding, hGH causes dimerization of GHR, activation of the GHR-associated JAK2 tyrosine kinase, and tyrosyl phosphorylation of both JAK2 and GHR. These events recruit and/or activate a variety of signaling molecules, including MAP kinases, insulin receptor substrates, phosphatidylinositol 3' phosphate kinase, diacylglycerol, protein kinase C, intracellular calcium, and Stat transcription factors. These signaling molecules contribute to the GH-induced changes in enzymatic activity, transport function, and gene expression that ultimately culminate in changes in growth and metabolism. | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | CA1326439,CA2252535 | Mostly fro | Mostly 202 | The therapeutic efficacy of Somatropin recombinant can be decreased when used in combination with Bazedoxifene, Chlorotrianisene, Conjugated Equine Estrogens, Cortisone acetate, Dienestrol, Diethylstilbestrol, Estradiol, Estriol, Estrone, Ethinyl Estradiol. | Growth hormone receptor, Prolactin receptor | BioTropin | Biotech General | Biotech General | It is indicate dfor short stature due to pitutary growth hormone deficency, turner Syndorme, Children suffering from renal insuuficiency. | NA | NA | Powder and Solvent for Solution | Subcutaneous | The reequired dose is 10mg/ml | children with closed epiphyses. | may lead to loss or increase of adipose tissue as well as punctual haemorrhage and bruising at the injection site. | Link | NA | NA |
| 10878 | Th1237 | Somatropin recombinant | >Th1237_Somatropin_recombinant FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 °C at pH 3.5 | 21.1 (±5.1) minutes | Recombinant human growth hormone (somatotropin) 191 residues, MW 22.1 kD, synthesized in E. coli | For treatment of dwarfism, acromegaly and prevention of HIV-induced weight loss | Used in the treatment of dwarfism and growth failure, growth hormone (hGH) stimulates skeletal growth in pediatric patients with growth failure due to a lack of adequate secretion of endogenous GH. Skeletal growth is accomplished at the epiphyseal plates at the ends of a growing bone. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and one of its mediators, IGF-I (insulin-like growth factor). | hGH binds to the human growth hormone receptor (GHR). Upon binding, hGH causes dimerization of GHR, activation of the GHR-associated JAK2 tyrosine kinase, and tyrosyl phosphorylation of both JAK2 and GHR. These events recruit and/or activate a variety of signaling molecules, including MAP kinases, insulin receptor substrates, phosphatidylinositol 3' phosphate kinase, diacylglycerol, protein kinase C, intracellular calcium, and Stat transcription factors. These signaling molecules contribute to the GH-induced changes in enzymatic activity, transport function, and gene expression that ultimately culminate in changes in growth and metabolism. | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | CA1326439,CA2252535 | Mostly fro | Mostly 202 | The therapeutic efficacy of Somatropin recombinant can be decreased when used in combination with Bazedoxifene, Chlorotrianisene, Conjugated Equine Estrogens, Cortisone acetate, Dienestrol, Diethylstilbestrol, Estradiol, Estriol, Estrone, Ethinyl Estradiol. | Growth hormone receptor, Prolactin receptor | NutropinAQ | Genentech Inc. | Genentech Inc. | Treating certain children or adults when the body does not produce enough growth hormone. It is also used to treat certain children who are not growing normally due to Turner syndrome or other conditions (eg, chronic kidney problems, idiopathic short stature). | NA | Each pen cartridge or NuSpin contain either 5 mg, 10 mg or 20 mg of somatropin formulated in 17.4 mg sodium chloride, 5 mg phenol, 4 mg polysorbate 20, and 10 mM sodium citrate | Sterile liquid | Subcutaneous | A weekly dosage of up to 0.3 mg/kg of body weight divided into daily subcutaneous injections is recommended for Idiopathic Short Stature (ISS) | Acute Critical Illness, Prader-Willi Syndrome (PWS) In Children, Active Malignancy, Diabetic Retinopathy, Hypersensitivity, Closed Epiphysis | Abnormal or decreased touch sensation, bleeding, blistering, burning, coldness, discoloration of the skin, feeling of pressure, hives, infection, inflammation, itching, lumps, numbness, pain, rash, redness, scarring, soreness, stinging, swelling, tenderness, tingling, ulceration, or warmth at the injection site | Link | NA | NA |
| 11242 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | Hormones | 6582728 | 24-06-2003 | 24-06-2020 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Actrapid | Novo Nordisk | Novo Nordisk | Intravenous; Subcutaneous | 40 iu/ml | NA | The most common side effect with Actrapid (seen in more than 1 patient in 10) is hypoglycaemia (low blood glucose levels). | Actrapid is a solution for injection that contains the active substance human insulin. It is available as vials, cartridges (Penfill) or prefilled pens (NovoLet, InnoLet or FlexPen). | Actrapid is used to treat diabetes. | NA | NA | Link | Link | NA |
| 11243 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | 8912193 | 16-12-2014 | 12-06-2029 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Actrapid | Novo Nordisk | Novo Nordisk | Intravenous; Subcutaneous | 100 iu/ml | NA | The most common side effect with Actrapid (seen in more than 1 patient in 10) is hypoglycaemia (low blood glucose levels). | Actrapid is a solution for injection that contains the active substance human insulin. It is available as vials, cartridges (Penfill) or prefilled pens (NovoLet, InnoLet or FlexPen). | Actrapid is used to treat diabetes. | NA | NA | Link | Link | NA |
| 11249 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | Pancreatic Hormones | 7943572 | 17-05-2011 | 10-08-2026 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Afrezza | Mannkind Corporation | Mannkind Corporation | Respiratory (inhalation) | NA | AFREZZA is contraindicated in patients with the following: During episodes of hypoglycemia Chronic lung disease, such as asthma or chronic obstructive pulmonary disease (COPD), because of the risk of acute bronchospasm. Hypersensitivity to regular human insulin or any of the AFREZZA excipients. | low blood sugar (hypoglycemia), cough, sore throat, headache, diarrhea, fatigue, nausea, bronchitis, urinary tract infection, and weight gain. | Afrezza is a man-made insulin that is breathed-in through your lungs (inhaled) and is used to control high blood sugar in adults with diabetes mellitus. Afrezza is not for use in place of long-acting insulin. Afrezza must be used with long-acting insulin in people who have type 1 diabetes mellitus. Afrezza... | Afrezza is a prescription medicine used to treat the symptoms of Type 2 Diabetes Mellitus. Afrezza may be used alone or with other medications. | NA | AFREZZA consists of single-use plastic cartridges filled with a white powder containing insulin (human), which is administered via oral inhalation using the AFREZZA Inhaler only. | Link | Link | NA |
| 11250 | Th1244 | Insulin human | >Th1244_Insulin_human GIVEQCCTSICSLYQLENYCN | 5808 | C257H383N65O77S6 | NA | NA | 81 °C | Systemic insulin disposition (apparent terminal half-life) following oral inhalation of 4 to 48 units of human insulin was 120-206 minutes. | Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin is an important treatment in the management of Type 1 Diabetes (T1D) which is caused by an autoimmune reaction that destroys the beta cells of the pancreas, resulting in the body not being able to produce or synthesize the insulin needed to manage circulating blood sugar levels. As a result, people with T1D rely primarily on exogenous forms of insulin to lower glucose levels in the blood. Insulin is also used in the treatment of Type 2 Diabetes (T2D), another form of diabetes mellitus that is a slowly progressing metabolic disorder caused by a combination of genetic and lifestyle factors that promote chronically elevated blood sugar levels. Without treatment or improvement in non-pharmacological measures such as diet and exercise to lower blood glucose, high blood sugar eventually causes cellular resistance to endogenous insulin, and in the long term, damage to pancreatic islet cells. Insulin is typically prescribed later in the course of T2D, after trying several oral medications such as [DB00331], [DB01120], or [DB01261] have been tried, when sufficient damage has been caused to pancreatic cells that the body is no longer able to produce insulin on its own. Marketed as the brand name product Humulin R or Novolin R, human insulin begins to exert its effects within 30 minutes of subcutaneous administration, while peak levels occur 3-4 hours after administration. Due to its quick onset of action, human insulin is considered "bolus insulin" as it provides high levels of insulin in a short period of time to mimic the release of endogenous insulin from the pancreas after meals. Bolus insulin is often combined with once daily, long-acting "basal insulin" such as [DB01307], [DB09564], and [DB00047] to provide low concentrations of background insulin that can keep blood sugar stable between meals or overnight. Use of basal and bolus insulin together is intended to mimic the pancreas' production of endogenous insulin, with a goal of avoiding any periods of hypoglycemia. Human insulin is also available in an inhalable form, intended to be used as a bolus meal-time insulin. Exubera was the first inhaled insulin available on the market and was developed by Inhale Therapeutics (later named Nektar Therapeutics). Unfortunately, limited uptake by physicians and patients, poor sales, bulky packaging, and concerns over the possible impact on lung cancer development resulted in Exubera products being withdrawn from the US markets [A176005]. Exubera was followed by Afrezza, a monomeric inhaled insulin developed by Mannkind Corporation, which received FDA approval in 2016. While still available in the US, Afrezza has had similar concerns associated with its use, and had an FDA "black box" warning added to it to warn about use in patients with chronic lung disease. Afrezza does not currently have Health Canada or European Medicines Agency approval for marketing in Canada or the EU. Human Insulin is a 51 residue peptide hormone produced by recombinant DNA technology by inserting the human insulin gene into Escherichia coli bacteria or Saccharomyces cerevisiae. The structure is identical to native human insulin, with two amino acid chains covalently linked by disulfide bonds. Human insulin is also available in an intermediate-acting form as NPH (Neutral Protamine Hagedorn) as the marketed products Novolin N and Humulin N. NPH insulin is provided as a crystalline suspension of insulin with protamine and zinc, resulting in an onset of action in 1 to 3 hours, duration of action up to 24 hours, and peak action from 6 to 8 hours. Due to the added crystals, NPH insulin is typically cloudy when compared to other forms of insulin and has a neutral pH. Without an adequate supply of insulin to promote absorption of glucose from the bloodstream, blood sugar levels can climb to dangerously high levels and can result in symptoms such as fatigue, headache, blurred vision, and increased thirst. If left untreated, the body starts to break down fat, instead of glucose, for energy which results in a build-up of ketone acids in the blood and a syndrome called ketoacidosis, which is a life-threatening medical emergency. In the long term, elevated blood sugar levels increase the risk of heart attack, stroke, and diabetic neuropathy. | Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. | Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). | The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism. | NA | The metabolism and elimination of orally inhaled human insulin are comparable to regular human insulin. | When injected subcutaneously, the glucose-lowering effect of human insulin begins approximately 30 minutes post-dose. After a single subcutaneous administration of 0.1 unit/kg of human insulin to healthy subjects, peak insulin concentrations occurred between 1.5 to 2.5 hours post-dose. When administered in an inhaled form (as the product Afrezza), the time to maximum serum insulin concentration ranges from 10-20 minutes after oral inhalation of 4 to 48 units of human insulin. Serum insulin concentrations declined to baseline by approximately 60-240 minutes for these dose levels. Intrapatient variability in insulin exposure measured by AUC and Cmax is approximately 16% (95% CI 12-23%) and 21% (95% CI 16-30%), respectively. | NA | NA | Peptide Hormones | 8119593 | 21-02-2012 | 11-08-2029 | NA | Insulin receptor,Insulin-like growth factor 1 receptor,Carboxypeptidase E,Protein NOV homolog,Low-density lipoprotein receptor-related protein 2,Insulin-like growth factor-binding protein 7 | Afrezza | Sanofi Aventis | Sanofi Aventis | Respiratory (inhalation) | 5 | AFREZZA is contraindicated in patients with the following: During episodes of hypoglycemia Chronic lung disease, such as asthma or chronic obstructive pulmonary disease (COPD), because of the risk of acute bronchospasm. Hypersensitivity to regular human insulin or any of the AFREZZA excipients. | low blood sugar (hypoglycemia), cough, sore throat, headache, diarrhea, fatigue, nausea, bronchitis, urinary tract infection, and weight gain. | Afrezza is a man-made insulin that is breathed-in through your lungs (inhaled) and is used to control high blood sugar in adults with diabetes mellitus. Afrezza is not for use in place of long-acting insulin. Afrezza must be used with long-acting insulin in people who have type 1 diabetes mellitus. Afrezza... | Afrezza is a prescription medicine used to treat the symptoms of Type 2 Diabetes Mellitus. Afrezza may be used alone or with other medications. | NA | AFREZZA consists of single-use plastic cartridges filled with a white powder containing insulin (human), which is administered via oral inhalation using the AFREZZA Inhaler only. | Link | Link | NA |
| 11411 | Th1247 | Glucagon | >Th1247_Glucagon HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | NA | NA | The half life of glucagon is 26 minutes for an intramuscular dose.[L7634] The half life of glucagon nasal powder is approximately 35 minutes.[L7643] The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.[L8519] | Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon was granted FDA approval on 14 November 1960.[L7631] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia.[A19402,L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon has a short duration of action.[L7634,L7637,L7640,L7643] Glucagon may cause hyperglycemia in diabetic patients.[L7634,L7637,L7640,L7643] | Glucagon binds to the glucagon receptor activating Gsa and Gq.[A19402] This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A.[A19402] Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium.[A19402] Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.[A19402] Glucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.[L7634,L7643] | Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium.[L7634,L7637,L7640,L7643] Phentolamine may be given to control blood pressure.[L7634,L7637,L7640,L7643] Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.[L7637] The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.[L7637] | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma.[L7634,L7643] | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.[L7637] An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes.[L7637] A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.[L7643] | The volume of distribution of glucagon is 0.25L/kg.[L7637] The apparent volume of distribution is 885L.[L7643] | A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.[L7637] | Gastrointestinal Hormones | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | GlucaGen | Boehringer Ingelheim Pharmaceuticals, Inc. | Boehringer Ingelheim Pharmaceuticals, Inc. | Intramuscular; Intravenous; Subcutaneous | 1 mg/1mL | GlucaGen is contraindicated in patients with: Known hypersensitivity to glucagon, lactose or any other constituent in GlucaGen Pheochromocytoma [see WARNINGS AND PRECAUTIONS] Insulinoma [see WARNINGS AND PRECAUTIONS] | Severe side effects are very rare, although nausea and vomiting may occur occasionally especially with doses above 1 mg or with rapid injection (less than 1 minute). You may also have rapid heart beat for a short while. | GlucaGen is a hormone that increases blood sugar levels. It also slows involuntary muscle movements of the stomach and intestines that aid in digestion. GlucaGen is used to treat hypoglycemia (low blood sugar). This medicine is also used during a radiologic (x-ray) examination to help diagnose certain... | NA | (3S)-3-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-oxopentanoyl]amino]-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | Link | NA |
| 11415 | Th1247 | Glucagon | >Th1247_Glucagon HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | NA | NA | The half life of glucagon is 26 minutes for an intramuscular dose.[L7634] The half life of glucagon nasal powder is approximately 35 minutes.[L7643] The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.[L8519] | Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon was granted FDA approval on 14 November 1960.[L7631] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia.[A19402,L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon has a short duration of action.[L7634,L7637,L7640,L7643] Glucagon may cause hyperglycemia in diabetic patients.[L7634,L7637,L7640,L7643] | Glucagon binds to the glucagon receptor activating Gsa and Gq.[A19402] This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A.[A19402] Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium.[A19402] Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.[A19402] Glucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.[L7634,L7643] | Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium.[L7634,L7637,L7640,L7643] Phentolamine may be given to control blood pressure.[L7634,L7637,L7640,L7643] Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.[L7637] The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.[L7637] | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma.[L7634,L7643] | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.[L7637] An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes.[L7637] A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.[L7643] | The volume of distribution of glucagon is 0.25L/kg.[L7637] The apparent volume of distribution is 885L.[L7643] | A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.[L7637] | Glycogenolytic Hormones | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | Glucagon | Physicians Total Care, Inc. | Physicians Total Care, Inc. | Intramuscular; Intravenous; Subcutaneous | 1 mg/1mL | Glucagon is contraindicated in patients with known hypersensitivity to it or in patients with known pheochromocytoma. | temporary changes in blood pressure, increase in heart rate, allergic reactions, nausea, vomiting, and low blood sugar (hypoglycemia) | Glucagon is a hormone that increases blood sugar levels. It also slows involuntary muscle movements of the stomach and intestines that aid in digestion. Glucagon is a prescription medicine used to treat very low blood sugar (hypoglycemia). Glucagon is also used to stop stomach movement during radiologic... | GlucaGon for injection is a gastrointestinal motility inhibitor indicated for use as a diagnostic aid during radiologic examinations to temporarily inhibit movement of the gastrointestinal (GI) tract. | (3S)-3-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-oxopentanoyl]amino]-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | Link | NA |
| 11416 | Th1247 | Glucagon | >Th1247_Glucagon HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | NA | NA | The half life of glucagon is 26 minutes for an intramuscular dose.[L7634] The half life of glucagon nasal powder is approximately 35 minutes.[L7643] The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.[L8519] | Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon was granted FDA approval on 14 November 1960.[L7631] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia.[A19402,L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon has a short duration of action.[L7634,L7637,L7640,L7643] Glucagon may cause hyperglycemia in diabetic patients.[L7634,L7637,L7640,L7643] | Glucagon binds to the glucagon receptor activating Gsa and Gq.[A19402] This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A.[A19402] Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium.[A19402] Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.[A19402] Glucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.[L7634,L7643] | Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium.[L7634,L7637,L7640,L7643] Phentolamine may be given to control blood pressure.[L7634,L7637,L7640,L7643] Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.[L7637] The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.[L7637] | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma.[L7634,L7643] | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.[L7637] An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes.[L7637] A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.[L7643] | The volume of distribution of glucagon is 0.25L/kg.[L7637] The apparent volume of distribution is 885L.[L7643] | A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.[L7637] | Hormones | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | Glucagon | TYA Pharmaceuticals | TYA Pharmaceuticals | Intramuscular; Intravenous; Subcutaneous | 1 mg/1mL | Glucagon is contraindicated in patients with known hypersensitivity to it or in patients with known pheochromocytoma. | temporary changes in blood pressure, increase in heart rate, allergic reactions, nausea, vomiting, and low blood sugar (hypoglycemia) | Glucagon is a hormone that increases blood sugar levels. It also slows involuntary muscle movements of the stomach and intestines that aid in digestion. Glucagon is a prescription medicine used to treat very low blood sugar (hypoglycemia). Glucagon is also used to stop stomach movement during radiologic... | GlucaGon for injection is a gastrointestinal motility inhibitor indicated for use as a diagnostic aid during radiologic examinations to temporarily inhibit movement of the gastrointestinal (GI) tract. | (3S)-3-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-oxopentanoyl]amino]-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | Link | NA |
| 11417 | Th1247 | Glucagon | >Th1247_Glucagon HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | NA | NA | The half life of glucagon is 26 minutes for an intramuscular dose.[L7634] The half life of glucagon nasal powder is approximately 35 minutes.[L7643] The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.[L8519] | Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon was granted FDA approval on 14 November 1960.[L7631] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia.[A19402,L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon has a short duration of action.[L7634,L7637,L7640,L7643] Glucagon may cause hyperglycemia in diabetic patients.[L7634,L7637,L7640,L7643] | Glucagon binds to the glucagon receptor activating Gsa and Gq.[A19402] This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A.[A19402] Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium.[A19402] Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.[A19402] Glucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.[L7634,L7643] | Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium.[L7634,L7637,L7640,L7643] Phentolamine may be given to control blood pressure.[L7634,L7637,L7640,L7643] Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.[L7637] The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.[L7637] | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma.[L7634,L7643] | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.[L7637] An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes.[L7637] A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.[L7643] | The volume of distribution of glucagon is 0.25L/kg.[L7637] The apparent volume of distribution is 885L.[L7643] | A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.[L7637] | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | Glucagon | A-S Medication Solutions | A-S Medication Solutions | Intramuscular; Intravenous; Subcutaneous | 1 mg/1mL | Glucagon is contraindicated in patients with known hypersensitivity to it or in patients with known pheochromocytoma. | temporary changes in blood pressure, increase in heart rate, allergic reactions, nausea, vomiting, and low blood sugar (hypoglycemia) | Glucagon is a hormone that increases blood sugar levels. It also slows involuntary muscle movements of the stomach and intestines that aid in digestion. Glucagon is a prescription medicine used to treat very low blood sugar (hypoglycemia). Glucagon is also used to stop stomach movement during radiologic... | GlucaGon for injection is a gastrointestinal motility inhibitor indicated for use as a diagnostic aid during radiologic examinations to temporarily inhibit movement of the gastrointestinal (GI) tract. | (3S)-3-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-oxopentanoyl]amino]-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | Link | NA |
| 11420 | Th1247 | Glucagon | >Th1247_Glucagon HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | NA | NA | The half life of glucagon is 26 minutes for an intramuscular dose.[L7634] The half life of glucagon nasal powder is approximately 35 minutes.[L7643] The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.[L8519] | Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon was granted FDA approval on 14 November 1960.[L7631] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia.[A19402,L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon has a short duration of action.[L7634,L7637,L7640,L7643] Glucagon may cause hyperglycemia in diabetic patients.[L7634,L7637,L7640,L7643] | Glucagon binds to the glucagon receptor activating Gsa and Gq.[A19402] This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A.[A19402] Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium.[A19402] Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.[A19402] Glucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.[L7634,L7643] | Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium.[L7634,L7637,L7640,L7643] Phentolamine may be given to control blood pressure.[L7634,L7637,L7640,L7643] Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.[L7637] The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.[L7637] | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma.[L7634,L7643] | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.[L7637] An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes.[L7637] A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.[L7643] | The volume of distribution of glucagon is 0.25L/kg.[L7637] The apparent volume of distribution is 885L.[L7643] | A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.[L7637] | Pancreatic Hormones | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | Glucagon | HF Acquisition Co LLC, DBA HealthFirst | HF Acquisition Co LLC, DBA HealthFirst | Intramuscular; Intravenous | NA | Glucagon is contraindicated in patients with known hypersensitivity to it or in patients with known pheochromocytoma. | temporary changes in blood pressure, increase in heart rate, allergic reactions, nausea, vomiting, and low blood sugar (hypoglycemia) | Glucagon is a hormone that increases blood sugar levels. It also slows involuntary muscle movements of the stomach and intestines that aid in digestion. Glucagon is a prescription medicine used to treat very low blood sugar (hypoglycemia). Glucagon is also used to stop stomach movement during radiologic... | GlucaGon for injection is a gastrointestinal motility inhibitor indicated for use as a diagnostic aid during radiologic examinations to temporarily inhibit movement of the gastrointestinal (GI) tract. | (3S)-3-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-oxopentanoyl]amino]-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | Link | NA |
| 11421 | Th1247 | Glucagon | >Th1247_Glucagon HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | NA | NA | The half life of glucagon is 26 minutes for an intramuscular dose.[L7634] The half life of glucagon nasal powder is approximately 35 minutes.[L7643] The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.[L8519] | Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon was granted FDA approval on 14 November 1960.[L7631] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia.[A19402,L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon has a short duration of action.[L7634,L7637,L7640,L7643] Glucagon may cause hyperglycemia in diabetic patients.[L7634,L7637,L7640,L7643] | Glucagon binds to the glucagon receptor activating Gsa and Gq.[A19402] This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A.[A19402] Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium.[A19402] Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.[A19402] Glucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.[L7634,L7643] | Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium.[L7634,L7637,L7640,L7643] Phentolamine may be given to control blood pressure.[L7634,L7637,L7640,L7643] Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.[L7637] The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.[L7637] | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma.[L7634,L7643] | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.[L7637] An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes.[L7637] A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.[L7643] | The volume of distribution of glucagon is 0.25L/kg.[L7637] The apparent volume of distribution is 885L.[L7643] | A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.[L7637] | Peptide Hormones | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | Glucagon | Eli Lilly and Company | Eli Lilly and Company | Intramuscular; Intravenous; Subcutaneous | 1 mg/1mL | Glucagon is contraindicated in patients with known hypersensitivity to it or in patients with known pheochromocytoma. | temporary changes in blood pressure, increase in heart rate, allergic reactions, nausea, vomiting, and low blood sugar (hypoglycemia) | Glucagon is a hormone that increases blood sugar levels. It also slows involuntary muscle movements of the stomach and intestines that aid in digestion. Glucagon is a prescription medicine used to treat very low blood sugar (hypoglycemia). Glucagon is also used to stop stomach movement during radiologic... | GlucaGon for injection is a gastrointestinal motility inhibitor indicated for use as a diagnostic aid during radiologic examinations to temporarily inhibit movement of the gastrointestinal (GI) tract. | (3S)-3-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-oxopentanoyl]amino]-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | Link | NA |
| 11426 | Th1247 | Glucagon | >Th1247_Glucagon HSQGTFTSDYSKYLDSRRAQDFVQWLMNT | 3767.1 | C165H249N49O51S1 | 7.1 | NA | NA | The half life of glucagon is 26 minutes for an intramuscular dose.[L7634] The half life of glucagon nasal powder is approximately 35 minutes.[L7643] The half life of glucagon by a subcutaneous auto-injector or pre-filled syringe is 32 minutes.[L8519] | Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon was granted FDA approval on 14 November 1960.[L7631] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia.[L7634,L7637,L7640,L7643,L8519] | Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia.[A19402,L7634,L7637,L7640,L7643,L8519] Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose.[L7640,L7643] Glucagon has a short duration of action.[L7634,L7637,L7640,L7643] Glucagon may cause hyperglycemia in diabetic patients.[L7634,L7637,L7640,L7643] | Glucagon binds to the glucagon receptor activating Gsa and Gq.[A19402] This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A.[A19402] Activating Gq activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium.[A19402] Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.[A19402] Glucagon also relaxes smooth muscle of the stomach, duodenum, small bowel, and colon.[L7634,L7643] | Patients experiencing an overdose may present with nausea, vomiting, inhibition of GI tract motility, increased blood pressure and heart rate, and decreased serum potassium.[L7634,L7637,L7640,L7643] Phentolamine may be given to control blood pressure.[L7634,L7637,L7640,L7643] Treatment of glucagon overdose is largely symptomatic for nausea, vomiting, and hypokalemia.[L7637] The LD50 for intravenous glucagon in mice is 300mg/kg and in rats is 38.6mg/kg.[L7637] | Glucagon is a protein and so it is metabolized into smaller polypeptides and amino acids in the liver, kidney, and plasma.[L7634,L7643] | A 1mg intravenous dose of glucagon reaches a Cmax of 7.9ng/mL with a Tmax of 20 minutes.[L7637] An intramuscular dose reaches a Cmax of 6.9ng/mL with a Tmax of 13 minutes.[L7637] A 3mg dose of glucagon nasal powder reaches a Cmax of 6130pg/mL with a Tmax of 15 minutes.[L7643] | The volume of distribution of glucagon is 0.25L/kg.[L7637] The apparent volume of distribution is 885L.[L7643] | A 1mg intravenous dose of glucagon has a clearance of 13.5mL/min/kg.[L7637] | Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | NA | Glucagon receptor,Glucagon-like peptide 2 receptor,Glucagon-like peptide 1 receptor | Gvoke HypoPen 1 mg Auto-Injector | Xeris Pharmaceuticals, Inc. | Xeris Pharmaceuticals, Inc. | Subcutaneous | 1 mg/0.2mL | GVOKE is contraindicated in patients with: Pheochromocytoma Insulinoma [ see WARNINGS AND PRECAUTIONS] because of the risk of hypoglycemia Known hypersensitivity to glucagon or to any of the excipients in GVOKE. Allergic reactions have been reported with glucagon and include anaphylactic shock with breathing difficulties and hypotension. | nausea vomiting hives injection site swelling or redness headache fast heartbeat | Glucagon comes as a solution (liquid) in a prefilled syringe and an auto-injector device to inject subcutaneously (just under the skin). It also comes as a powder to be mixed with a provided liquid to be injected subcutaneously, intramuscularly (into the muscle), or intravenously (into a vein). It is usually injected as needed at the first sign of severe hypoglycemia. | Glucagon is used along with emergency medical treatment to treat very low blood sugar. Glucagon is also used in diagnostic testing of the stomach and other digestive organs. Glucagon is in a class of medications called glycogenolytic agents. It works by causing the liver to release stored sugar to the blood. It also works by relaxing smooth muscles of the stomach and other digestive organs for diagnostic testing. | (3S)-3-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-oxopentanoyl]amino]-4-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-amino-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-1,4-dioxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | Link | NA |
| 11449 | Th1249 | Somatotropin | >Th1249_Somatotropin FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 °C at pH 3.5 | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the mean apparent terminal half-life was Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the terminal elimination half-life was approximately 21.1 (±5.1) minutes.[L10971] | Human growth hormone (HGH), also known as somatotropin, is a peptide hormone that is synthesized and secreted by the somatotropic cells of the anterior pituitary gland.[A228183] Growth hormone plays an essential role in growth regulation during childhood as well as other basal metabolic functions, muscle and fat mass regulation, blood glucose level regulation, and lipid regulation in both children and adults.[A228183, L31508] Synthesized in a strain of _Escherichia coli_, recombinant HGH is a polypeptide hormone that contains 191 amino acid residues with a molecular weight of 22 kDa. It has an identical primary protein structure to endogenous human growth hormone.[A228188] Recombinant HGH has been commercially available since 1985 after its development by Genentech. [Somatrem] was the first available recombinant HGH and was largely replaced by somatropin, another form of recombinant HGH.[A228183] Growth hormone therapy is approved for various disorders of growth hormone deficiency, growth failure, or short stature including Turner syndrome, chronic renal insufficiency before transplantation, Prader-Willi syndrome, a history of fetal growth restriction, short stature homeobox (SHOX) haploinsufficiency, Noonan syndrome, idiopathic short stature, and adult- or childhood-onset growth hormone deficiency.[A228188] Recombinant growth hormone is available as a subcutaneous injection for children and adults under a wide variety of brand names. | Somatotropin is indicated for the treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone, short stature associated with Turner syndrome, Prader-Willi syndrome (PWS), idiopathic short stature (ISS), short stature or growth failure in short stature homeobox-containing gene (SHOX) deficiency, and short stature born small for gestational age (SGA).[L31513, L31518] It is indicated for the treatment of growth failure in children associated with chronic kidney disease up to the time of renal transplantation.[L31523] It is also indicated for adults with adult-onset growth hormone deficiency, either alone or associated with multiple hormone deficiencies (hypopituitarism), as a result of pituitary disease, hypothalamic disease, surgery, radiation therapy, or trauma. It is also used to treat childhood-onset growth hormone deficiency in adults due to congenital, genetic, acquired, or idiopathic causes.[L31518] Somatotropin is indicated for the treatment of wasting or cachexia in patients with human immunodeficiency virus (HIV) who are receiving antiretroviral therapy to increase lean body mass and body weight and improve physical endurance.[L31498] Somatotropin is indicated for the treatment of short bowel syndrome in adult patients receiving specialized nutritional support.[L31493] | Somatotropin induces growth in nearly every tissue and organ in the body.[L31508] It stimulates linear growth and cartilaginous growth of long bones. In children with short stature, growth hormone increases both the number and size of muscle cells. It also promotes the growth of internal organs, and it also increases red cell mass. By promoting nitrogen retention, growth hormone increases cellular protein synthesis. Growth hormone also retains potassium and phosphorus in the serum, which may be the result of cell growth. Growth hormone stimulates the synthesis of chondroitin sulfate and collagen and increases the urinary excretion of hydroxyproline. It has negligible effects on serum calcium levels. Although increased calcium excretion in the urine is observed, calcium absorption from the intestine is simultaneously enhanced.[L10971] In end-stage renal disease, growth hormone was shown to improve several nutritional parameters, such as increases in serum insulin-like growth factor-I (IGF-I), serum albumin, and transferrin, as well as a reduction in blood urea nitrogen.[A228403] The metabolic effects of growth hormone are caused by the upregulation of insulin-like growth factor-1. Generally, growth hormone leads cells to enter an anabolic protein state with increased amino acid uptake, protein synthesis, and decreased catabolism of proteins.[L31508] The diabetogenic effect of larger doses of growth hormone is well documented in the literature: somatotropin antagonizes insulin action _in vivo_, causing insulin resistance and glucose intolerance. It increases glucose production through gluconeogenesis and glycogenolysis from the liver and kidney [A228398] and suppresses glucose uptake in the adipose tissue.[A228388] In mice, growth hormone increased mRNA expression of 2 major gluconeogenic genes, phosphoenolpyruvate carboxy-kinase and glucose-6-phosphatase.[A228398] The risk for impaired glucose tolerance and reduced insulin sensitivity may be increased in susceptible patients, especially in those with risk factors for diabetes mellitus, such as obesity, Turner syndrome, or a family history of diabetes mellitus. The development of new-onset type 2 Diabetes Mellitus was observed in patients receiving somatotropin treatment.[L10971] Growth hormone stimulates lipolysis via activation of the hormone-sensitive lipase in the adipose tissue, thereby increasing circulating levels of free fatty acids and triglycerides in the plasma. It also leads to a reduction of fat stores and decreased serum levels of low-density lipoprotein (LDL) cholesterol.[L10971] In contrast to the effects seen in the adipose tissue, growth hormone promotes cellular uptake of free fatty acids in skeletal muscle by increasing the activity of lipoprotein lipase. Growth hormone may cause hyperinsulinism following beta-cell compensation for insulin resistance; however, there is some evidence that growth hormone directly promotes beta-cell proliferation and glucose-stimulated insulin secretion.[A228398] | In conditions of growth failure, growth hormone deficiency, low body mass, and malnutrition, somatotropin treatment acts to mimic and restore the actions of endogenous growth hormone of stimulating linear bone growth, increasing bone mass, increasing muscle and reduced fat mass, and regulating blood glucose and lipid levels.[A228183] Somatotropin mediates its effects both directly by somatotropin and indirectly by insulin-like growth factor-1 (IGF-1), which is upregulated by growth hormone. It binds to the human growth hormone receptor (GHR), which is a dimeric receptor expressed in target cells in the liver and cartilage.[L10971] Upon binding of growth hormone, GHR dimerizes and interacts with Janus kinase 2 (JAK2), subsequently leading to tyrosine phosphorylation of JAK2 and the GH receptor. The signal transducer activator of transcription (STAT) pathway is initiated, where transcription factors such as STAT1, STAT3, and STAT5 are translocated into the nucleus to stimulate target gene transcription.[L31508] At the epiphysis or growth plate, growth hormone increases linear growth by promoting differentiation of prechondrocytes and expansion of osteoblasts. Growth hormone binding to its receptor in the liver and cartilage promotes the production of IGF-1, which acts on type 1 IGF receptors to also stimulate linear growth. In the liver, activated growth hormone receptor signalling leads to increased production of IGF binding protein-3 (IGFBP-3) and acid-labile subunit (ALS), which are proteins that bind to IGF-1 in a ternary complex to increase its half-life.[A228183] | The oral LD50 is 242 mg/kg in rats and 828 mg/kg in mice. The inhalatory LD50 is 710 mg/m3 and dermal LD50 is 1100 mg/kg in rats. The intraperitoneal LD50 in mice is 828 mg/kg.[L31528] Hypoglycemia followed by hyperglycemia, possibly with fluid retention, can be observed in somatropin overdose. Long-term or excessive use of growth hormone can lead to the signs and symptoms of gigantism and acromegaly.[L10971] | Information is unavailable. | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the Cmax ranged from 13.8 (±5.8) to 17.1 (±10.0) ng/mL and the Tmax was four to five hours. Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the mean steady-state serum levels of approximately 23.1 (±15.0) ng/mL were reached at 150 minutes.[L10971] | NA | NA | Anterior Pituitary Lobe Hormones and Analogues | 1326439 | 25-01-1994 | 25-01-2011 | NA | Growth hormone receptor,Prolactin receptor | Genotropin | Physicians Total Care, Inc. | Physicians Total Care, Inc. | Subcutaneous | 0.4 mg/0.25mL | Acute Critical Illness Treatment with pharmacologic amounts of somatropin is contraindicated in patients with acute critical illness due to complications following open heart surgery, abdominal surgery or multiple accidental trauma, or those with acute respiratory failure [see WARNINGS AND PRECAUTIONS]. Prader-Willi Syndrome In Children Somatropin is contraindicated in patients with Prader-Willi syndrome who are severely obese, have a history of upper airway obstruction or sleep apnea, or have severe respiratory impairment. There have been reports of sudden death when somatropin was used in such patients [see WARNINGS AND PRECAUTIONS]. Active Malignancy In general, somatropin is contraindicated in the presence of active malignancy. Any preexisting malignancy should be inactive and its treatment complete prior to instituting therapy with somatropin. Somatropin should be discontinued if there is evidence of recurrent activity. Since growth hormone deficiency may be an early sign of the presence of a pituitary tumor (or, rarely, other brain tumors), the presence of such tumors should be ruled out prior to initiation of treatment. Somatropin should not be used in patients with any evidence of progression or recurrence of an underlying intracranial tumor. Hypersensitivity GENOTROPIN is contraindicated in patients with a known hypersensitivity to somatropin or any of its excipients. The 5 mg and 12 mg presentations of GENOTROPIN lyophilized powder contain m-cresol as a preservative. Systemic hypersensitivity reactions have been reported with post-marketing use of somatropin products [see WARNINGS AND PRECAUTIONS] . Diabetic Retinopathy Somatropin is contraindicated in patients with active proliferative or severe non-proliferative diabetic retinopathy. Closed Epiphyses Somatropin should not be used for growth promotion in pediatric patients with closed epiphyses. | growth failure in children and adults who lack natural growth hormone, and in those with chronic kidney failure, Noonan syndrome, Turner syndrome, short stature at birth with no catch-up growth, and other causes | Genotropin is a form of human growth hormone important for the growth of bones and muscles. Genotropin is used to treat growth failure in children and adults who lack natural growth hormone. This includes people with short stature due to Noonan syndrome, Turner syndrome, Prader-Willi syndrome, short... | NA | NA | NA | Link | Link | NA |
| 11459 | Th1249 | Somatotropin | >Th1249_Somatotropin FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 °C at pH 3.5 | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the mean apparent terminal half-life was Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the terminal elimination half-life was approximately 21.1 (±5.1) minutes.[L10971] | Human growth hormone (HGH), also known as somatotropin, is a peptide hormone that is synthesized and secreted by the somatotropic cells of the anterior pituitary gland.[A228183] Growth hormone plays an essential role in growth regulation during childhood as well as other basal metabolic functions, muscle and fat mass regulation, blood glucose level regulation, and lipid regulation in both children and adults.[A228183, L31508] Synthesized in a strain of _Escherichia coli_, recombinant HGH is a polypeptide hormone that contains 191 amino acid residues with a molecular weight of 22 kDa. It has an identical primary protein structure to endogenous human growth hormone.[A228188] Recombinant HGH has been commercially available since 1985 after its development by Genentech. [Somatrem] was the first available recombinant HGH and was largely replaced by somatropin, another form of recombinant HGH.[A228183] Growth hormone therapy is approved for various disorders of growth hormone deficiency, growth failure, or short stature including Turner syndrome, chronic renal insufficiency before transplantation, Prader-Willi syndrome, a history of fetal growth restriction, short stature homeobox (SHOX) haploinsufficiency, Noonan syndrome, idiopathic short stature, and adult- or childhood-onset growth hormone deficiency.[A228188] Recombinant growth hormone is available as a subcutaneous injection for children and adults under a wide variety of brand names. | Somatotropin is indicated for the treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone, short stature associated with Turner syndrome, Prader-Willi syndrome (PWS), idiopathic short stature (ISS), short stature or growth failure in short stature homeobox-containing gene (SHOX) deficiency, and short stature born small for gestational age (SGA).[L31513, L31518] It is indicated for the treatment of growth failure in children associated with chronic kidney disease up to the time of renal transplantation.[L31523] It is also indicated for adults with adult-onset growth hormone deficiency, either alone or associated with multiple hormone deficiencies (hypopituitarism), as a result of pituitary disease, hypothalamic disease, surgery, radiation therapy, or trauma. It is also used to treat childhood-onset growth hormone deficiency in adults due to congenital, genetic, acquired, or idiopathic causes.[L31518] Somatotropin is indicated for the treatment of wasting or cachexia in patients with human immunodeficiency virus (HIV) who are receiving antiretroviral therapy to increase lean body mass and body weight and improve physical endurance.[L31498] Somatotropin is indicated for the treatment of short bowel syndrome in adult patients receiving specialized nutritional support.[L31493] | Somatotropin induces growth in nearly every tissue and organ in the body.[L31508] It stimulates linear growth and cartilaginous growth of long bones. In children with short stature, growth hormone increases both the number and size of muscle cells. It also promotes the growth of internal organs, and it also increases red cell mass. By promoting nitrogen retention, growth hormone increases cellular protein synthesis. Growth hormone also retains potassium and phosphorus in the serum, which may be the result of cell growth. Growth hormone stimulates the synthesis of chondroitin sulfate and collagen and increases the urinary excretion of hydroxyproline. It has negligible effects on serum calcium levels. Although increased calcium excretion in the urine is observed, calcium absorption from the intestine is simultaneously enhanced.[L10971] In end-stage renal disease, growth hormone was shown to improve several nutritional parameters, such as increases in serum insulin-like growth factor-I (IGF-I), serum albumin, and transferrin, as well as a reduction in blood urea nitrogen.[A228403] The metabolic effects of growth hormone are caused by the upregulation of insulin-like growth factor-1. Generally, growth hormone leads cells to enter an anabolic protein state with increased amino acid uptake, protein synthesis, and decreased catabolism of proteins.[L31508] The diabetogenic effect of larger doses of growth hormone is well documented in the literature: somatotropin antagonizes insulin action _in vivo_, causing insulin resistance and glucose intolerance. It increases glucose production through gluconeogenesis and glycogenolysis from the liver and kidney [A228398] and suppresses glucose uptake in the adipose tissue.[A228388] In mice, growth hormone increased mRNA expression of 2 major gluconeogenic genes, phosphoenolpyruvate carboxy-kinase and glucose-6-phosphatase.[A228398] The risk for impaired glucose tolerance and reduced insulin sensitivity may be increased in susceptible patients, especially in those with risk factors for diabetes mellitus, such as obesity, Turner syndrome, or a family history of diabetes mellitus. The development of new-onset type 2 Diabetes Mellitus was observed in patients receiving somatotropin treatment.[L10971] Growth hormone stimulates lipolysis via activation of the hormone-sensitive lipase in the adipose tissue, thereby increasing circulating levels of free fatty acids and triglycerides in the plasma. It also leads to a reduction of fat stores and decreased serum levels of low-density lipoprotein (LDL) cholesterol.[L10971] In contrast to the effects seen in the adipose tissue, growth hormone promotes cellular uptake of free fatty acids in skeletal muscle by increasing the activity of lipoprotein lipase. Growth hormone may cause hyperinsulinism following beta-cell compensation for insulin resistance; however, there is some evidence that growth hormone directly promotes beta-cell proliferation and glucose-stimulated insulin secretion.[A228398] | In conditions of growth failure, growth hormone deficiency, low body mass, and malnutrition, somatotropin treatment acts to mimic and restore the actions of endogenous growth hormone of stimulating linear bone growth, increasing bone mass, increasing muscle and reduced fat mass, and regulating blood glucose and lipid levels.[A228183] Somatotropin mediates its effects both directly by somatotropin and indirectly by insulin-like growth factor-1 (IGF-1), which is upregulated by growth hormone. It binds to the human growth hormone receptor (GHR), which is a dimeric receptor expressed in target cells in the liver and cartilage.[L10971] Upon binding of growth hormone, GHR dimerizes and interacts with Janus kinase 2 (JAK2), subsequently leading to tyrosine phosphorylation of JAK2 and the GH receptor. The signal transducer activator of transcription (STAT) pathway is initiated, where transcription factors such as STAT1, STAT3, and STAT5 are translocated into the nucleus to stimulate target gene transcription.[L31508] At the epiphysis or growth plate, growth hormone increases linear growth by promoting differentiation of prechondrocytes and expansion of osteoblasts. Growth hormone binding to its receptor in the liver and cartilage promotes the production of IGF-1, which acts on type 1 IGF receptors to also stimulate linear growth. In the liver, activated growth hormone receptor signalling leads to increased production of IGF binding protein-3 (IGFBP-3) and acid-labile subunit (ALS), which are proteins that bind to IGF-1 in a ternary complex to increase its half-life.[A228183] | The oral LD50 is 242 mg/kg in rats and 828 mg/kg in mice. The inhalatory LD50 is 710 mg/m3 and dermal LD50 is 1100 mg/kg in rats. The intraperitoneal LD50 in mice is 828 mg/kg.[L31528] Hypoglycemia followed by hyperglycemia, possibly with fluid retention, can be observed in somatropin overdose. Long-term or excessive use of growth hormone can lead to the signs and symptoms of gigantism and acromegaly.[L10971] | Information is unavailable. | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the Cmax ranged from 13.8 (±5.8) to 17.1 (±10.0) ng/mL and the Tmax was four to five hours. Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the mean steady-state serum levels of approximately 23.1 (±15.0) ng/mL were reached at 150 minutes.[L10971] | NA | NA | Hormones | RE41956 | 23-11-2010 | 21-07-2021 | NA | Growth hormone receptor,Prolactin receptor | Genotropin | Pharmacia and Upjohn Company LLC | Pharmacia and Upjohn Company LLC | Subcutaneous | 1.2 mg/0.25mL | Acute Critical Illness Treatment with pharmacologic amounts of somatropin is contraindicated in patients with acute critical illness due to complications following open heart surgery, abdominal surgery or multiple accidental trauma, or those with acute respiratory failure [see WARNINGS AND PRECAUTIONS]. Prader-Willi Syndrome In Children Somatropin is contraindicated in patients with Prader-Willi syndrome who are severely obese, have a history of upper airway obstruction or sleep apnea, or have severe respiratory impairment. There have been reports of sudden death when somatropin was used in such patients [see WARNINGS AND PRECAUTIONS]. Active Malignancy In general, somatropin is contraindicated in the presence of active malignancy. Any preexisting malignancy should be inactive and its treatment complete prior to instituting therapy with somatropin. Somatropin should be discontinued if there is evidence of recurrent activity. Since growth hormone deficiency may be an early sign of the presence of a pituitary tumor (or, rarely, other brain tumors), the presence of such tumors should be ruled out prior to initiation of treatment. Somatropin should not be used in patients with any evidence of progression or recurrence of an underlying intracranial tumor. Hypersensitivity GENOTROPIN is contraindicated in patients with a known hypersensitivity to somatropin or any of its excipients. The 5 mg and 12 mg presentations of GENOTROPIN lyophilized powder contain m-cresol as a preservative. Systemic hypersensitivity reactions have been reported with post-marketing use of somatropin products [see WARNINGS AND PRECAUTIONS] . Diabetic Retinopathy Somatropin is contraindicated in patients with active proliferative or severe non-proliferative diabetic retinopathy. Closed Epiphyses Somatropin should not be used for growth promotion in pediatric patients with closed epiphyses. | growth failure in children and adults who lack natural growth hormone, and in those with chronic kidney failure, Noonan syndrome, Turner syndrome, short stature at birth with no catch-up growth, and other causes | Genotropin is a form of human growth hormone important for the growth of bones and muscles. Genotropin is used to treat growth failure in children and adults who lack natural growth hormone. This includes people with short stature due to Noonan syndrome, Turner syndrome, Prader-Willi syndrome, short... | NA | NA | NA | Link | Link | NA |
| 11460 | Th1249 | Somatotropin | >Th1249_Somatotropin FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 °C at pH 3.5 | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the mean apparent terminal half-life was Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the terminal elimination half-life was approximately 21.1 (±5.1) minutes.[L10971] | Human growth hormone (HGH), also known as somatotropin, is a peptide hormone that is synthesized and secreted by the somatotropic cells of the anterior pituitary gland.[A228183] Growth hormone plays an essential role in growth regulation during childhood as well as other basal metabolic functions, muscle and fat mass regulation, blood glucose level regulation, and lipid regulation in both children and adults.[A228183, L31508] Synthesized in a strain of _Escherichia coli_, recombinant HGH is a polypeptide hormone that contains 191 amino acid residues with a molecular weight of 22 kDa. It has an identical primary protein structure to endogenous human growth hormone.[A228188] Recombinant HGH has been commercially available since 1985 after its development by Genentech. [Somatrem] was the first available recombinant HGH and was largely replaced by somatropin, another form of recombinant HGH.[A228183] Growth hormone therapy is approved for various disorders of growth hormone deficiency, growth failure, or short stature including Turner syndrome, chronic renal insufficiency before transplantation, Prader-Willi syndrome, a history of fetal growth restriction, short stature homeobox (SHOX) haploinsufficiency, Noonan syndrome, idiopathic short stature, and adult- or childhood-onset growth hormone deficiency.[A228188] Recombinant growth hormone is available as a subcutaneous injection for children and adults under a wide variety of brand names. | Somatotropin is indicated for the treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone, short stature associated with Turner syndrome, Prader-Willi syndrome (PWS), idiopathic short stature (ISS), short stature or growth failure in short stature homeobox-containing gene (SHOX) deficiency, and short stature born small for gestational age (SGA).[L31513, L31518] It is indicated for the treatment of growth failure in children associated with chronic kidney disease up to the time of renal transplantation.[L31523] It is also indicated for adults with adult-onset growth hormone deficiency, either alone or associated with multiple hormone deficiencies (hypopituitarism), as a result of pituitary disease, hypothalamic disease, surgery, radiation therapy, or trauma. It is also used to treat childhood-onset growth hormone deficiency in adults due to congenital, genetic, acquired, or idiopathic causes.[L31518] Somatotropin is indicated for the treatment of wasting or cachexia in patients with human immunodeficiency virus (HIV) who are receiving antiretroviral therapy to increase lean body mass and body weight and improve physical endurance.[L31498] Somatotropin is indicated for the treatment of short bowel syndrome in adult patients receiving specialized nutritional support.[L31493] | Somatotropin induces growth in nearly every tissue and organ in the body.[L31508] It stimulates linear growth and cartilaginous growth of long bones. In children with short stature, growth hormone increases both the number and size of muscle cells. It also promotes the growth of internal organs, and it also increases red cell mass. By promoting nitrogen retention, growth hormone increases cellular protein synthesis. Growth hormone also retains potassium and phosphorus in the serum, which may be the result of cell growth. Growth hormone stimulates the synthesis of chondroitin sulfate and collagen and increases the urinary excretion of hydroxyproline. It has negligible effects on serum calcium levels. Although increased calcium excretion in the urine is observed, calcium absorption from the intestine is simultaneously enhanced.[L10971] In end-stage renal disease, growth hormone was shown to improve several nutritional parameters, such as increases in serum insulin-like growth factor-I (IGF-I), serum albumin, and transferrin, as well as a reduction in blood urea nitrogen.[A228403] The metabolic effects of growth hormone are caused by the upregulation of insulin-like growth factor-1. Generally, growth hormone leads cells to enter an anabolic protein state with increased amino acid uptake, protein synthesis, and decreased catabolism of proteins.[L31508] The diabetogenic effect of larger doses of growth hormone is well documented in the literature: somatotropin antagonizes insulin action _in vivo_, causing insulin resistance and glucose intolerance. It increases glucose production through gluconeogenesis and glycogenolysis from the liver and kidney [A228398] and suppresses glucose uptake in the adipose tissue.[A228388] In mice, growth hormone increased mRNA expression of 2 major gluconeogenic genes, phosphoenolpyruvate carboxy-kinase and glucose-6-phosphatase.[A228398] The risk for impaired glucose tolerance and reduced insulin sensitivity may be increased in susceptible patients, especially in those with risk factors for diabetes mellitus, such as obesity, Turner syndrome, or a family history of diabetes mellitus. The development of new-onset type 2 Diabetes Mellitus was observed in patients receiving somatotropin treatment.[L10971] Growth hormone stimulates lipolysis via activation of the hormone-sensitive lipase in the adipose tissue, thereby increasing circulating levels of free fatty acids and triglycerides in the plasma. It also leads to a reduction of fat stores and decreased serum levels of low-density lipoprotein (LDL) cholesterol.[L10971] In contrast to the effects seen in the adipose tissue, growth hormone promotes cellular uptake of free fatty acids in skeletal muscle by increasing the activity of lipoprotein lipase. Growth hormone may cause hyperinsulinism following beta-cell compensation for insulin resistance; however, there is some evidence that growth hormone directly promotes beta-cell proliferation and glucose-stimulated insulin secretion.[A228398] | In conditions of growth failure, growth hormone deficiency, low body mass, and malnutrition, somatotropin treatment acts to mimic and restore the actions of endogenous growth hormone of stimulating linear bone growth, increasing bone mass, increasing muscle and reduced fat mass, and regulating blood glucose and lipid levels.[A228183] Somatotropin mediates its effects both directly by somatotropin and indirectly by insulin-like growth factor-1 (IGF-1), which is upregulated by growth hormone. It binds to the human growth hormone receptor (GHR), which is a dimeric receptor expressed in target cells in the liver and cartilage.[L10971] Upon binding of growth hormone, GHR dimerizes and interacts with Janus kinase 2 (JAK2), subsequently leading to tyrosine phosphorylation of JAK2 and the GH receptor. The signal transducer activator of transcription (STAT) pathway is initiated, where transcription factors such as STAT1, STAT3, and STAT5 are translocated into the nucleus to stimulate target gene transcription.[L31508] At the epiphysis or growth plate, growth hormone increases linear growth by promoting differentiation of prechondrocytes and expansion of osteoblasts. Growth hormone binding to its receptor in the liver and cartilage promotes the production of IGF-1, which acts on type 1 IGF receptors to also stimulate linear growth. In the liver, activated growth hormone receptor signalling leads to increased production of IGF binding protein-3 (IGFBP-3) and acid-labile subunit (ALS), which are proteins that bind to IGF-1 in a ternary complex to increase its half-life.[A228183] | The oral LD50 is 242 mg/kg in rats and 828 mg/kg in mice. The inhalatory LD50 is 710 mg/m3 and dermal LD50 is 1100 mg/kg in rats. The intraperitoneal LD50 in mice is 828 mg/kg.[L31528] Hypoglycemia followed by hyperglycemia, possibly with fluid retention, can be observed in somatropin overdose. Long-term or excessive use of growth hormone can lead to the signs and symptoms of gigantism and acromegaly.[L10971] | Information is unavailable. | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the Cmax ranged from 13.8 (±5.8) to 17.1 (±10.0) ng/mL and the Tmax was four to five hours. Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the mean steady-state serum levels of approximately 23.1 (±15.0) ng/mL were reached at 150 minutes.[L10971] | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | 6004297 | 21-12-1999 | 28-07-2019 | NA | Growth hormone receptor,Prolactin receptor | Genotropin | Pharmacia and Upjohn Company LLC | Pharmacia and Upjohn Company LLC | Subcutaneous | 1.4 mg/0.25mL | Acute Critical Illness Treatment with pharmacologic amounts of somatropin is contraindicated in patients with acute critical illness due to complications following open heart surgery, abdominal surgery or multiple accidental trauma, or those with acute respiratory failure [see WARNINGS AND PRECAUTIONS]. Prader-Willi Syndrome In Children Somatropin is contraindicated in patients with Prader-Willi syndrome who are severely obese, have a history of upper airway obstruction or sleep apnea, or have severe respiratory impairment. There have been reports of sudden death when somatropin was used in such patients [see WARNINGS AND PRECAUTIONS]. Active Malignancy In general, somatropin is contraindicated in the presence of active malignancy. Any preexisting malignancy should be inactive and its treatment complete prior to instituting therapy with somatropin. Somatropin should be discontinued if there is evidence of recurrent activity. Since growth hormone deficiency may be an early sign of the presence of a pituitary tumor (or, rarely, other brain tumors), the presence of such tumors should be ruled out prior to initiation of treatment. Somatropin should not be used in patients with any evidence of progression or recurrence of an underlying intracranial tumor. Hypersensitivity GENOTROPIN is contraindicated in patients with a known hypersensitivity to somatropin or any of its excipients. The 5 mg and 12 mg presentations of GENOTROPIN lyophilized powder contain m-cresol as a preservative. Systemic hypersensitivity reactions have been reported with post-marketing use of somatropin products [see WARNINGS AND PRECAUTIONS] . Diabetic Retinopathy Somatropin is contraindicated in patients with active proliferative or severe non-proliferative diabetic retinopathy. Closed Epiphyses Somatropin should not be used for growth promotion in pediatric patients with closed epiphyses. | growth failure in children and adults who lack natural growth hormone, and in those with chronic kidney failure, Noonan syndrome, Turner syndrome, short stature at birth with no catch-up growth, and other causes | Genotropin is a form of human growth hormone important for the growth of bones and muscles. Genotropin is used to treat growth failure in children and adults who lack natural growth hormone. This includes people with short stature due to Noonan syndrome, Turner syndrome, Prader-Willi syndrome, short... | NA | NA | NA | Link | Link | NA |
| 11463 | Th1249 | Somatotropin | >Th1249_Somatotropin FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 °C at pH 3.5 | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the mean apparent terminal half-life was Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the terminal elimination half-life was approximately 21.1 (±5.1) minutes.[L10971] | Human growth hormone (HGH), also known as somatotropin, is a peptide hormone that is synthesized and secreted by the somatotropic cells of the anterior pituitary gland.[A228183] Growth hormone plays an essential role in growth regulation during childhood as well as other basal metabolic functions, muscle and fat mass regulation, blood glucose level regulation, and lipid regulation in both children and adults.[A228183, L31508] Synthesized in a strain of _Escherichia coli_, recombinant HGH is a polypeptide hormone that contains 191 amino acid residues with a molecular weight of 22 kDa. It has an identical primary protein structure to endogenous human growth hormone.[A228188] Recombinant HGH has been commercially available since 1985 after its development by Genentech. [Somatrem] was the first available recombinant HGH and was largely replaced by somatropin, another form of recombinant HGH.[A228183] Growth hormone therapy is approved for various disorders of growth hormone deficiency, growth failure, or short stature including Turner syndrome, chronic renal insufficiency before transplantation, Prader-Willi syndrome, a history of fetal growth restriction, short stature homeobox (SHOX) haploinsufficiency, Noonan syndrome, idiopathic short stature, and adult- or childhood-onset growth hormone deficiency.[A228188] Recombinant growth hormone is available as a subcutaneous injection for children and adults under a wide variety of brand names. | Somatotropin is indicated for the treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone, short stature associated with Turner syndrome, Prader-Willi syndrome (PWS), idiopathic short stature (ISS), short stature or growth failure in short stature homeobox-containing gene (SHOX) deficiency, and short stature born small for gestational age (SGA).[L31513, L31518] It is indicated for the treatment of growth failure in children associated with chronic kidney disease up to the time of renal transplantation.[L31523] It is also indicated for adults with adult-onset growth hormone deficiency, either alone or associated with multiple hormone deficiencies (hypopituitarism), as a result of pituitary disease, hypothalamic disease, surgery, radiation therapy, or trauma. It is also used to treat childhood-onset growth hormone deficiency in adults due to congenital, genetic, acquired, or idiopathic causes.[L31518] Somatotropin is indicated for the treatment of wasting or cachexia in patients with human immunodeficiency virus (HIV) who are receiving antiretroviral therapy to increase lean body mass and body weight and improve physical endurance.[L31498] Somatotropin is indicated for the treatment of short bowel syndrome in adult patients receiving specialized nutritional support.[L31493] | Somatotropin induces growth in nearly every tissue and organ in the body.[L31508] It stimulates linear growth and cartilaginous growth of long bones. In children with short stature, growth hormone increases both the number and size of muscle cells. It also promotes the growth of internal organs, and it also increases red cell mass. By promoting nitrogen retention, growth hormone increases cellular protein synthesis. Growth hormone also retains potassium and phosphorus in the serum, which may be the result of cell growth. Growth hormone stimulates the synthesis of chondroitin sulfate and collagen and increases the urinary excretion of hydroxyproline. It has negligible effects on serum calcium levels. Although increased calcium excretion in the urine is observed, calcium absorption from the intestine is simultaneously enhanced.[L10971] In end-stage renal disease, growth hormone was shown to improve several nutritional parameters, such as increases in serum insulin-like growth factor-I (IGF-I), serum albumin, and transferrin, as well as a reduction in blood urea nitrogen.[A228403] The metabolic effects of growth hormone are caused by the upregulation of insulin-like growth factor-1. Generally, growth hormone leads cells to enter an anabolic protein state with increased amino acid uptake, protein synthesis, and decreased catabolism of proteins.[L31508] The diabetogenic effect of larger doses of growth hormone is well documented in the literature: somatotropin antagonizes insulin action _in vivo_, causing insulin resistance and glucose intolerance. It increases glucose production through gluconeogenesis and glycogenolysis from the liver and kidney [A228398] and suppresses glucose uptake in the adipose tissue.[A228388] In mice, growth hormone increased mRNA expression of 2 major gluconeogenic genes, phosphoenolpyruvate carboxy-kinase and glucose-6-phosphatase.[A228398] The risk for impaired glucose tolerance and reduced insulin sensitivity may be increased in susceptible patients, especially in those with risk factors for diabetes mellitus, such as obesity, Turner syndrome, or a family history of diabetes mellitus. The development of new-onset type 2 Diabetes Mellitus was observed in patients receiving somatotropin treatment.[L10971] Growth hormone stimulates lipolysis via activation of the hormone-sensitive lipase in the adipose tissue, thereby increasing circulating levels of free fatty acids and triglycerides in the plasma. It also leads to a reduction of fat stores and decreased serum levels of low-density lipoprotein (LDL) cholesterol.[L10971] In contrast to the effects seen in the adipose tissue, growth hormone promotes cellular uptake of free fatty acids in skeletal muscle by increasing the activity of lipoprotein lipase. Growth hormone may cause hyperinsulinism following beta-cell compensation for insulin resistance; however, there is some evidence that growth hormone directly promotes beta-cell proliferation and glucose-stimulated insulin secretion.[A228398] | In conditions of growth failure, growth hormone deficiency, low body mass, and malnutrition, somatotropin treatment acts to mimic and restore the actions of endogenous growth hormone of stimulating linear bone growth, increasing bone mass, increasing muscle and reduced fat mass, and regulating blood glucose and lipid levels.[A228183] Somatotropin mediates its effects both directly by somatotropin and indirectly by insulin-like growth factor-1 (IGF-1), which is upregulated by growth hormone. It binds to the human growth hormone receptor (GHR), which is a dimeric receptor expressed in target cells in the liver and cartilage.[L10971] Upon binding of growth hormone, GHR dimerizes and interacts with Janus kinase 2 (JAK2), subsequently leading to tyrosine phosphorylation of JAK2 and the GH receptor. The signal transducer activator of transcription (STAT) pathway is initiated, where transcription factors such as STAT1, STAT3, and STAT5 are translocated into the nucleus to stimulate target gene transcription.[L31508] At the epiphysis or growth plate, growth hormone increases linear growth by promoting differentiation of prechondrocytes and expansion of osteoblasts. Growth hormone binding to its receptor in the liver and cartilage promotes the production of IGF-1, which acts on type 1 IGF receptors to also stimulate linear growth. In the liver, activated growth hormone receptor signalling leads to increased production of IGF binding protein-3 (IGFBP-3) and acid-labile subunit (ALS), which are proteins that bind to IGF-1 in a ternary complex to increase its half-life.[A228183] | The oral LD50 is 242 mg/kg in rats and 828 mg/kg in mice. The inhalatory LD50 is 710 mg/m3 and dermal LD50 is 1100 mg/kg in rats. The intraperitoneal LD50 in mice is 828 mg/kg.[L31528] Hypoglycemia followed by hyperglycemia, possibly with fluid retention, can be observed in somatropin overdose. Long-term or excessive use of growth hormone can lead to the signs and symptoms of gigantism and acromegaly.[L10971] | Information is unavailable. | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the Cmax ranged from 13.8 (±5.8) to 17.1 (±10.0) ng/mL and the Tmax was four to five hours. Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the mean steady-state serum levels of approximately 23.1 (±15.0) ng/mL were reached at 150 minutes.[L10971] | NA | NA | Peptide Hormones | 5849704 | 15-12-1998 | 15-12-2015 | NA | Growth hormone receptor,Prolactin receptor | Genotropin | Pharmacia and Upjohn Company LLC | Pharmacia and Upjohn Company LLC | Subcutaneous | 2 mg/0.25mL | Acute Critical Illness Treatment with pharmacologic amounts of somatropin is contraindicated in patients with acute critical illness due to complications following open heart surgery, abdominal surgery or multiple accidental trauma, or those with acute respiratory failure [see WARNINGS AND PRECAUTIONS]. Prader-Willi Syndrome In Children Somatropin is contraindicated in patients with Prader-Willi syndrome who are severely obese, have a history of upper airway obstruction or sleep apnea, or have severe respiratory impairment. There have been reports of sudden death when somatropin was used in such patients [see WARNINGS AND PRECAUTIONS]. Active Malignancy In general, somatropin is contraindicated in the presence of active malignancy. Any preexisting malignancy should be inactive and its treatment complete prior to instituting therapy with somatropin. Somatropin should be discontinued if there is evidence of recurrent activity. Since growth hormone deficiency may be an early sign of the presence of a pituitary tumor (or, rarely, other brain tumors), the presence of such tumors should be ruled out prior to initiation of treatment. Somatropin should not be used in patients with any evidence of progression or recurrence of an underlying intracranial tumor. Hypersensitivity GENOTROPIN is contraindicated in patients with a known hypersensitivity to somatropin or any of its excipients. The 5 mg and 12 mg presentations of GENOTROPIN lyophilized powder contain m-cresol as a preservative. Systemic hypersensitivity reactions have been reported with post-marketing use of somatropin products [see WARNINGS AND PRECAUTIONS] . Diabetic Retinopathy Somatropin is contraindicated in patients with active proliferative or severe non-proliferative diabetic retinopathy. Closed Epiphyses Somatropin should not be used for growth promotion in pediatric patients with closed epiphyses. | growth failure in children and adults who lack natural growth hormone, and in those with chronic kidney failure, Noonan syndrome, Turner syndrome, short stature at birth with no catch-up growth, and other causes | Genotropin is a form of human growth hormone important for the growth of bones and muscles. Genotropin is used to treat growth failure in children and adults who lack natural growth hormone. This includes people with short stature due to Noonan syndrome, Turner syndrome, Prader-Willi syndrome, short... | NA | NA | NA | Link | Link | NA |
| 11466 | Th1249 | Somatotropin | >Th1249_Somatotropin FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 °C at pH 3.5 | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the mean apparent terminal half-life was Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the terminal elimination half-life was approximately 21.1 (±5.1) minutes.[L10971] | Human growth hormone (HGH), also known as somatotropin, is a peptide hormone that is synthesized and secreted by the somatotropic cells of the anterior pituitary gland.[A228183] Growth hormone plays an essential role in growth regulation during childhood as well as other basal metabolic functions, muscle and fat mass regulation, blood glucose level regulation, and lipid regulation in both children and adults.[A228183, L31508] Synthesized in a strain of _Escherichia coli_, recombinant HGH is a polypeptide hormone that contains 191 amino acid residues with a molecular weight of 22 kDa. It has an identical primary protein structure to endogenous human growth hormone.[A228188] Recombinant HGH has been commercially available since 1985 after its development by Genentech. [Somatrem] was the first available recombinant HGH and was largely replaced by somatropin, another form of recombinant HGH.[A228183] Growth hormone therapy is approved for various disorders of growth hormone deficiency, growth failure, or short stature including Turner syndrome, chronic renal insufficiency before transplantation, Prader-Willi syndrome, a history of fetal growth restriction, short stature homeobox (SHOX) haploinsufficiency, Noonan syndrome, idiopathic short stature, and adult- or childhood-onset growth hormone deficiency.[A228188] Recombinant growth hormone is available as a subcutaneous injection for children and adults under a wide variety of brand names. | Somatotropin is indicated for the treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone, short stature associated with Turner syndrome, Prader-Willi syndrome (PWS), idiopathic short stature (ISS), short stature or growth failure in short stature homeobox-containing gene (SHOX) deficiency, and short stature born small for gestational age (SGA).[L31513, L31518] It is indicated for the treatment of growth failure in children associated with chronic kidney disease up to the time of renal transplantation.[L31523] It is also indicated for adults with adult-onset growth hormone deficiency, either alone or associated with multiple hormone deficiencies (hypopituitarism), as a result of pituitary disease, hypothalamic disease, surgery, radiation therapy, or trauma. It is also used to treat childhood-onset growth hormone deficiency in adults due to congenital, genetic, acquired, or idiopathic causes.[L31518] Somatotropin is indicated for the treatment of wasting or cachexia in patients with human immunodeficiency virus (HIV) who are receiving antiretroviral therapy to increase lean body mass and body weight and improve physical endurance.[L31498] Somatotropin is indicated for the treatment of short bowel syndrome in adult patients receiving specialized nutritional support.[L31493] | Somatotropin induces growth in nearly every tissue and organ in the body.[L31508] It stimulates linear growth and cartilaginous growth of long bones. In children with short stature, growth hormone increases both the number and size of muscle cells. It also promotes the growth of internal organs, and it also increases red cell mass. By promoting nitrogen retention, growth hormone increases cellular protein synthesis. Growth hormone also retains potassium and phosphorus in the serum, which may be the result of cell growth. Growth hormone stimulates the synthesis of chondroitin sulfate and collagen and increases the urinary excretion of hydroxyproline. It has negligible effects on serum calcium levels. Although increased calcium excretion in the urine is observed, calcium absorption from the intestine is simultaneously enhanced.[L10971] In end-stage renal disease, growth hormone was shown to improve several nutritional parameters, such as increases in serum insulin-like growth factor-I (IGF-I), serum albumin, and transferrin, as well as a reduction in blood urea nitrogen.[A228403] The metabolic effects of growth hormone are caused by the upregulation of insulin-like growth factor-1. Generally, growth hormone leads cells to enter an anabolic protein state with increased amino acid uptake, protein synthesis, and decreased catabolism of proteins.[L31508] The diabetogenic effect of larger doses of growth hormone is well documented in the literature: somatotropin antagonizes insulin action _in vivo_, causing insulin resistance and glucose intolerance. It increases glucose production through gluconeogenesis and glycogenolysis from the liver and kidney [A228398] and suppresses glucose uptake in the adipose tissue.[A228388] In mice, growth hormone increased mRNA expression of 2 major gluconeogenic genes, phosphoenolpyruvate carboxy-kinase and glucose-6-phosphatase.[A228398] The risk for impaired glucose tolerance and reduced insulin sensitivity may be increased in susceptible patients, especially in those with risk factors for diabetes mellitus, such as obesity, Turner syndrome, or a family history of diabetes mellitus. The development of new-onset type 2 Diabetes Mellitus was observed in patients receiving somatotropin treatment.[L10971] Growth hormone stimulates lipolysis via activation of the hormone-sensitive lipase in the adipose tissue, thereby increasing circulating levels of free fatty acids and triglycerides in the plasma. It also leads to a reduction of fat stores and decreased serum levels of low-density lipoprotein (LDL) cholesterol.[L10971] In contrast to the effects seen in the adipose tissue, growth hormone promotes cellular uptake of free fatty acids in skeletal muscle by increasing the activity of lipoprotein lipase. Growth hormone may cause hyperinsulinism following beta-cell compensation for insulin resistance; however, there is some evidence that growth hormone directly promotes beta-cell proliferation and glucose-stimulated insulin secretion.[A228398] | In conditions of growth failure, growth hormone deficiency, low body mass, and malnutrition, somatotropin treatment acts to mimic and restore the actions of endogenous growth hormone of stimulating linear bone growth, increasing bone mass, increasing muscle and reduced fat mass, and regulating blood glucose and lipid levels.[A228183] Somatotropin mediates its effects both directly by somatotropin and indirectly by insulin-like growth factor-1 (IGF-1), which is upregulated by growth hormone. It binds to the human growth hormone receptor (GHR), which is a dimeric receptor expressed in target cells in the liver and cartilage.[L10971] Upon binding of growth hormone, GHR dimerizes and interacts with Janus kinase 2 (JAK2), subsequently leading to tyrosine phosphorylation of JAK2 and the GH receptor. The signal transducer activator of transcription (STAT) pathway is initiated, where transcription factors such as STAT1, STAT3, and STAT5 are translocated into the nucleus to stimulate target gene transcription.[L31508] At the epiphysis or growth plate, growth hormone increases linear growth by promoting differentiation of prechondrocytes and expansion of osteoblasts. Growth hormone binding to its receptor in the liver and cartilage promotes the production of IGF-1, which acts on type 1 IGF receptors to also stimulate linear growth. In the liver, activated growth hormone receptor signalling leads to increased production of IGF binding protein-3 (IGFBP-3) and acid-labile subunit (ALS), which are proteins that bind to IGF-1 in a ternary complex to increase its half-life.[A228183] | The oral LD50 is 242 mg/kg in rats and 828 mg/kg in mice. The inhalatory LD50 is 710 mg/m3 and dermal LD50 is 1100 mg/kg in rats. The intraperitoneal LD50 in mice is 828 mg/kg.[L31528] Hypoglycemia followed by hyperglycemia, possibly with fluid retention, can be observed in somatropin overdose. Long-term or excessive use of growth hormone can lead to the signs and symptoms of gigantism and acromegaly.[L10971] | Information is unavailable. | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the Cmax ranged from 13.8 (±5.8) to 17.1 (±10.0) ng/mL and the Tmax was four to five hours. Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the mean steady-state serum levels of approximately 23.1 (±15.0) ng/mL were reached at 150 minutes.[L10971] | NA | NA | Pituitary and Hypothalamic Hormones and Analogues | 9486588 | 08-11-2016 | 02-07-2022 | NA | Growth hormone receptor,Prolactin receptor | Genotropin | Pfizer Canada Ulc | Pfizer Canada Ulc | Subcutaneous | 0.6 mg / syr | Acute Critical Illness Treatment with pharmacologic amounts of somatropin is contraindicated in patients with acute critical illness due to complications following open heart surgery, abdominal surgery or multiple accidental trauma, or those with acute respiratory failure [see WARNINGS AND PRECAUTIONS]. Prader-Willi Syndrome In Children Somatropin is contraindicated in patients with Prader-Willi syndrome who are severely obese, have a history of upper airway obstruction or sleep apnea, or have severe respiratory impairment. There have been reports of sudden death when somatropin was used in such patients [see WARNINGS AND PRECAUTIONS]. Active Malignancy In general, somatropin is contraindicated in the presence of active malignancy. Any preexisting malignancy should be inactive and its treatment complete prior to instituting therapy with somatropin. Somatropin should be discontinued if there is evidence of recurrent activity. Since growth hormone deficiency may be an early sign of the presence of a pituitary tumor (or, rarely, other brain tumors), the presence of such tumors should be ruled out prior to initiation of treatment. Somatropin should not be used in patients with any evidence of progression or recurrence of an underlying intracranial tumor. Hypersensitivity GENOTROPIN is contraindicated in patients with a known hypersensitivity to somatropin or any of its excipients. The 5 mg and 12 mg presentations of GENOTROPIN lyophilized powder contain m-cresol as a preservative. Systemic hypersensitivity reactions have been reported with post-marketing use of somatropin products [see WARNINGS AND PRECAUTIONS] . Diabetic Retinopathy Somatropin is contraindicated in patients with active proliferative or severe non-proliferative diabetic retinopathy. Closed Epiphyses Somatropin should not be used for growth promotion in pediatric patients with closed epiphyses. | growth failure in children and adults who lack natural growth hormone, and in those with chronic kidney failure, Noonan syndrome, Turner syndrome, short stature at birth with no catch-up growth, and other causes | Genotropin is a form of human growth hormone important for the growth of bones and muscles. Genotropin is used to treat growth failure in children and adults who lack natural growth hormone. This includes people with short stature due to Noonan syndrome, Turner syndrome, Prader-Willi syndrome, short... | NA | NA | NA | Link | Link | NA |
| 11467 | Th1249 | Somatotropin | >Th1249_Somatotropin FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 °C at pH 3.5 | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the mean apparent terminal half-life was Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the terminal elimination half-life was approximately 21.1 (±5.1) minutes.[L10971] | Human growth hormone (HGH), also known as somatotropin, is a peptide hormone that is synthesized and secreted by the somatotropic cells of the anterior pituitary gland.[A228183] Growth hormone plays an essential role in growth regulation during childhood as well as other basal metabolic functions, muscle and fat mass regulation, blood glucose level regulation, and lipid regulation in both children and adults.[A228183, L31508] Synthesized in a strain of _Escherichia coli_, recombinant HGH is a polypeptide hormone that contains 191 amino acid residues with a molecular weight of 22 kDa. It has an identical primary protein structure to endogenous human growth hormone.[A228188] Recombinant HGH has been commercially available since 1985 after its development by Genentech. [Somatrem] was the first available recombinant HGH and was largely replaced by somatropin, another form of recombinant HGH.[A228183] Growth hormone therapy is approved for various disorders of growth hormone deficiency, growth failure, or short stature including Turner syndrome, chronic renal insufficiency before transplantation, Prader-Willi syndrome, a history of fetal growth restriction, short stature homeobox (SHOX) haploinsufficiency, Noonan syndrome, idiopathic short stature, and adult- or childhood-onset growth hormone deficiency.[A228188] Recombinant growth hormone is available as a subcutaneous injection for children and adults under a wide variety of brand names. | Somatotropin is indicated for the treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone, short stature associated with Turner syndrome, Prader-Willi syndrome (PWS), idiopathic short stature (ISS), short stature or growth failure in short stature homeobox-containing gene (SHOX) deficiency, and short stature born small for gestational age (SGA).[L31513, L31518] It is indicated for the treatment of growth failure in children associated with chronic kidney disease up to the time of renal transplantation.[L31523] It is also indicated for adults with adult-onset growth hormone deficiency, either alone or associated with multiple hormone deficiencies (hypopituitarism), as a result of pituitary disease, hypothalamic disease, surgery, radiation therapy, or trauma. It is also used to treat childhood-onset growth hormone deficiency in adults due to congenital, genetic, acquired, or idiopathic causes.[L31518] Somatotropin is indicated for the treatment of wasting or cachexia in patients with human immunodeficiency virus (HIV) who are receiving antiretroviral therapy to increase lean body mass and body weight and improve physical endurance.[L31498] Somatotropin is indicated for the treatment of short bowel syndrome in adult patients receiving specialized nutritional support.[L31493] | Somatotropin induces growth in nearly every tissue and organ in the body.[L31508] It stimulates linear growth and cartilaginous growth of long bones. In children with short stature, growth hormone increases both the number and size of muscle cells. It also promotes the growth of internal organs, and it also increases red cell mass. By promoting nitrogen retention, growth hormone increases cellular protein synthesis. Growth hormone also retains potassium and phosphorus in the serum, which may be the result of cell growth. Growth hormone stimulates the synthesis of chondroitin sulfate and collagen and increases the urinary excretion of hydroxyproline. It has negligible effects on serum calcium levels. Although increased calcium excretion in the urine is observed, calcium absorption from the intestine is simultaneously enhanced.[L10971] In end-stage renal disease, growth hormone was shown to improve several nutritional parameters, such as increases in serum insulin-like growth factor-I (IGF-I), serum albumin, and transferrin, as well as a reduction in blood urea nitrogen.[A228403] The metabolic effects of growth hormone are caused by the upregulation of insulin-like growth factor-1. Generally, growth hormone leads cells to enter an anabolic protein state with increased amino acid uptake, protein synthesis, and decreased catabolism of proteins.[L31508] The diabetogenic effect of larger doses of growth hormone is well documented in the literature: somatotropin antagonizes insulin action _in vivo_, causing insulin resistance and glucose intolerance. It increases glucose production through gluconeogenesis and glycogenolysis from the liver and kidney [A228398] and suppresses glucose uptake in the adipose tissue.[A228388] In mice, growth hormone increased mRNA expression of 2 major gluconeogenic genes, phosphoenolpyruvate carboxy-kinase and glucose-6-phosphatase.[A228398] The risk for impaired glucose tolerance and reduced insulin sensitivity may be increased in susceptible patients, especially in those with risk factors for diabetes mellitus, such as obesity, Turner syndrome, or a family history of diabetes mellitus. The development of new-onset type 2 Diabetes Mellitus was observed in patients receiving somatotropin treatment.[L10971] Growth hormone stimulates lipolysis via activation of the hormone-sensitive lipase in the adipose tissue, thereby increasing circulating levels of free fatty acids and triglycerides in the plasma. It also leads to a reduction of fat stores and decreased serum levels of low-density lipoprotein (LDL) cholesterol.[L10971] In contrast to the effects seen in the adipose tissue, growth hormone promotes cellular uptake of free fatty acids in skeletal muscle by increasing the activity of lipoprotein lipase. Growth hormone may cause hyperinsulinism following beta-cell compensation for insulin resistance; however, there is some evidence that growth hormone directly promotes beta-cell proliferation and glucose-stimulated insulin secretion.[A228398] | In conditions of growth failure, growth hormone deficiency, low body mass, and malnutrition, somatotropin treatment acts to mimic and restore the actions of endogenous growth hormone of stimulating linear bone growth, increasing bone mass, increasing muscle and reduced fat mass, and regulating blood glucose and lipid levels.[A228183] Somatotropin mediates its effects both directly by somatotropin and indirectly by insulin-like growth factor-1 (IGF-1), which is upregulated by growth hormone. It binds to the human growth hormone receptor (GHR), which is a dimeric receptor expressed in target cells in the liver and cartilage.[L10971] Upon binding of growth hormone, GHR dimerizes and interacts with Janus kinase 2 (JAK2), subsequently leading to tyrosine phosphorylation of JAK2 and the GH receptor. The signal transducer activator of transcription (STAT) pathway is initiated, where transcription factors such as STAT1, STAT3, and STAT5 are translocated into the nucleus to stimulate target gene transcription.[L31508] At the epiphysis or growth plate, growth hormone increases linear growth by promoting differentiation of prechondrocytes and expansion of osteoblasts. Growth hormone binding to its receptor in the liver and cartilage promotes the production of IGF-1, which acts on type 1 IGF receptors to also stimulate linear growth. In the liver, activated growth hormone receptor signalling leads to increased production of IGF binding protein-3 (IGFBP-3) and acid-labile subunit (ALS), which are proteins that bind to IGF-1 in a ternary complex to increase its half-life.[A228183] | The oral LD50 is 242 mg/kg in rats and 828 mg/kg in mice. The inhalatory LD50 is 710 mg/m3 and dermal LD50 is 1100 mg/kg in rats. The intraperitoneal LD50 in mice is 828 mg/kg.[L31528] Hypoglycemia followed by hyperglycemia, possibly with fluid retention, can be observed in somatropin overdose. Long-term or excessive use of growth hormone can lead to the signs and symptoms of gigantism and acromegaly.[L10971] | Information is unavailable. | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the Cmax ranged from 13.8 (±5.8) to 17.1 (±10.0) ng/mL and the Tmax was four to five hours. Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the mean steady-state serum levels of approximately 23.1 (±15.0) ng/mL were reached at 150 minutes.[L10971] | NA | NA | Pituitary Hormones | 9457154 | 04-10-2016 | 27-03-2028 | NA | Growth hormone receptor,Prolactin receptor | Genotropin | Pfizer Canada Ulc | Pfizer Canada Ulc | Subcutaneous | 0.8 mg / syr | Acute Critical Illness Treatment with pharmacologic amounts of somatropin is contraindicated in patients with acute critical illness due to complications following open heart surgery, abdominal surgery or multiple accidental trauma, or those with acute respiratory failure [see WARNINGS AND PRECAUTIONS]. Prader-Willi Syndrome In Children Somatropin is contraindicated in patients with Prader-Willi syndrome who are severely obese, have a history of upper airway obstruction or sleep apnea, or have severe respiratory impairment. There have been reports of sudden death when somatropin was used in such patients [see WARNINGS AND PRECAUTIONS]. Active Malignancy In general, somatropin is contraindicated in the presence of active malignancy. Any preexisting malignancy should be inactive and its treatment complete prior to instituting therapy with somatropin. Somatropin should be discontinued if there is evidence of recurrent activity. Since growth hormone deficiency may be an early sign of the presence of a pituitary tumor (or, rarely, other brain tumors), the presence of such tumors should be ruled out prior to initiation of treatment. Somatropin should not be used in patients with any evidence of progression or recurrence of an underlying intracranial tumor. Hypersensitivity GENOTROPIN is contraindicated in patients with a known hypersensitivity to somatropin or any of its excipients. The 5 mg and 12 mg presentations of GENOTROPIN lyophilized powder contain m-cresol as a preservative. Systemic hypersensitivity reactions have been reported with post-marketing use of somatropin products [see WARNINGS AND PRECAUTIONS] . Diabetic Retinopathy Somatropin is contraindicated in patients with active proliferative or severe non-proliferative diabetic retinopathy. Closed Epiphyses Somatropin should not be used for growth promotion in pediatric patients with closed epiphyses. | growth failure in children and adults who lack natural growth hormone, and in those with chronic kidney failure, Noonan syndrome, Turner syndrome, short stature at birth with no catch-up growth, and other causes | Genotropin is a form of human growth hormone important for the growth of bones and muscles. Genotropin is used to treat growth failure in children and adults who lack natural growth hormone. This includes people with short stature due to Noonan syndrome, Turner syndrome, Prader-Willi syndrome, short... | NA | NA | NA | Link | Link | NA |
| 11468 | Th1249 | Somatotropin | >Th1249_Somatotropin FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 °C at pH 3.5 | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the mean apparent terminal half-life was Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the terminal elimination half-life was approximately 21.1 (±5.1) minutes.[L10971] | Human growth hormone (HGH), also known as somatotropin, is a peptide hormone that is synthesized and secreted by the somatotropic cells of the anterior pituitary gland.[A228183] Growth hormone plays an essential role in growth regulation during childhood as well as other basal metabolic functions, muscle and fat mass regulation, blood glucose level regulation, and lipid regulation in both children and adults.[A228183, L31508] Synthesized in a strain of _Escherichia coli_, recombinant HGH is a polypeptide hormone that contains 191 amino acid residues with a molecular weight of 22 kDa. It has an identical primary protein structure to endogenous human growth hormone.[A228188] Recombinant HGH has been commercially available since 1985 after its development by Genentech. [Somatrem] was the first available recombinant HGH and was largely replaced by somatropin, another form of recombinant HGH.[A228183] Growth hormone therapy is approved for various disorders of growth hormone deficiency, growth failure, or short stature including Turner syndrome, chronic renal insufficiency before transplantation, Prader-Willi syndrome, a history of fetal growth restriction, short stature homeobox (SHOX) haploinsufficiency, Noonan syndrome, idiopathic short stature, and adult- or childhood-onset growth hormone deficiency.[A228188] Recombinant growth hormone is available as a subcutaneous injection for children and adults under a wide variety of brand names. | Somatotropin is indicated for the treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone, short stature associated with Turner syndrome, Prader-Willi syndrome (PWS), idiopathic short stature (ISS), short stature or growth failure in short stature homeobox-containing gene (SHOX) deficiency, and short stature born small for gestational age (SGA).[L31513, L31518] It is indicated for the treatment of growth failure in children associated with chronic kidney disease up to the time of renal transplantation.[L31523] It is also indicated for adults with adult-onset growth hormone deficiency, either alone or associated with multiple hormone deficiencies (hypopituitarism), as a result of pituitary disease, hypothalamic disease, surgery, radiation therapy, or trauma. It is also used to treat childhood-onset growth hormone deficiency in adults due to congenital, genetic, acquired, or idiopathic causes.[L31518] Somatotropin is indicated for the treatment of wasting or cachexia in patients with human immunodeficiency virus (HIV) who are receiving antiretroviral therapy to increase lean body mass and body weight and improve physical endurance.[L31498] Somatotropin is indicated for the treatment of short bowel syndrome in adult patients receiving specialized nutritional support.[L31493] | Somatotropin induces growth in nearly every tissue and organ in the body.[L31508] It stimulates linear growth and cartilaginous growth of long bones. In children with short stature, growth hormone increases both the number and size of muscle cells. It also promotes the growth of internal organs, and it also increases red cell mass. By promoting nitrogen retention, growth hormone increases cellular protein synthesis. Growth hormone also retains potassium and phosphorus in the serum, which may be the result of cell growth. Growth hormone stimulates the synthesis of chondroitin sulfate and collagen and increases the urinary excretion of hydroxyproline. It has negligible effects on serum calcium levels. Although increased calcium excretion in the urine is observed, calcium absorption from the intestine is simultaneously enhanced.[L10971] In end-stage renal disease, growth hormone was shown to improve several nutritional parameters, such as increases in serum insulin-like growth factor-I (IGF-I), serum albumin, and transferrin, as well as a reduction in blood urea nitrogen.[A228403] The metabolic effects of growth hormone are caused by the upregulation of insulin-like growth factor-1. Generally, growth hormone leads cells to enter an anabolic protein state with increased amino acid uptake, protein synthesis, and decreased catabolism of proteins.[L31508] The diabetogenic effect of larger doses of growth hormone is well documented in the literature: somatotropin antagonizes insulin action _in vivo_, causing insulin resistance and glucose intolerance. It increases glucose production through gluconeogenesis and glycogenolysis from the liver and kidney [A228398] and suppresses glucose uptake in the adipose tissue.[A228388] In mice, growth hormone increased mRNA expression of 2 major gluconeogenic genes, phosphoenolpyruvate carboxy-kinase and glucose-6-phosphatase.[A228398] The risk for impaired glucose tolerance and reduced insulin sensitivity may be increased in susceptible patients, especially in those with risk factors for diabetes mellitus, such as obesity, Turner syndrome, or a family history of diabetes mellitus. The development of new-onset type 2 Diabetes Mellitus was observed in patients receiving somatotropin treatment.[L10971] Growth hormone stimulates lipolysis via activation of the hormone-sensitive lipase in the adipose tissue, thereby increasing circulating levels of free fatty acids and triglycerides in the plasma. It also leads to a reduction of fat stores and decreased serum levels of low-density lipoprotein (LDL) cholesterol.[L10971] In contrast to the effects seen in the adipose tissue, growth hormone promotes cellular uptake of free fatty acids in skeletal muscle by increasing the activity of lipoprotein lipase. Growth hormone may cause hyperinsulinism following beta-cell compensation for insulin resistance; however, there is some evidence that growth hormone directly promotes beta-cell proliferation and glucose-stimulated insulin secretion.[A228398] | In conditions of growth failure, growth hormone deficiency, low body mass, and malnutrition, somatotropin treatment acts to mimic and restore the actions of endogenous growth hormone of stimulating linear bone growth, increasing bone mass, increasing muscle and reduced fat mass, and regulating blood glucose and lipid levels.[A228183] Somatotropin mediates its effects both directly by somatotropin and indirectly by insulin-like growth factor-1 (IGF-1), which is upregulated by growth hormone. It binds to the human growth hormone receptor (GHR), which is a dimeric receptor expressed in target cells in the liver and cartilage.[L10971] Upon binding of growth hormone, GHR dimerizes and interacts with Janus kinase 2 (JAK2), subsequently leading to tyrosine phosphorylation of JAK2 and the GH receptor. The signal transducer activator of transcription (STAT) pathway is initiated, where transcription factors such as STAT1, STAT3, and STAT5 are translocated into the nucleus to stimulate target gene transcription.[L31508] At the epiphysis or growth plate, growth hormone increases linear growth by promoting differentiation of prechondrocytes and expansion of osteoblasts. Growth hormone binding to its receptor in the liver and cartilage promotes the production of IGF-1, which acts on type 1 IGF receptors to also stimulate linear growth. In the liver, activated growth hormone receptor signalling leads to increased production of IGF binding protein-3 (IGFBP-3) and acid-labile subunit (ALS), which are proteins that bind to IGF-1 in a ternary complex to increase its half-life.[A228183] | The oral LD50 is 242 mg/kg in rats and 828 mg/kg in mice. The inhalatory LD50 is 710 mg/m3 and dermal LD50 is 1100 mg/kg in rats. The intraperitoneal LD50 in mice is 828 mg/kg.[L31528] Hypoglycemia followed by hyperglycemia, possibly with fluid retention, can be observed in somatropin overdose. Long-term or excessive use of growth hormone can lead to the signs and symptoms of gigantism and acromegaly.[L10971] | Information is unavailable. | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the Cmax ranged from 13.8 (±5.8) to 17.1 (±10.0) ng/mL and the Tmax was four to five hours. Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the mean steady-state serum levels of approximately 23.1 (±15.0) ng/mL were reached at 150 minutes.[L10971] | NA | NA | Pituitary Hormones, Anterior | RE46363 | 11-04-2017 | 03-02-2027 | NA | Growth hormone receptor,Prolactin receptor | Genotropin | Pfizer Canada Ulc | Pfizer Canada Ulc | Subcutaneous | 1 mg / syr | Acute Critical Illness Treatment with pharmacologic amounts of somatropin is contraindicated in patients with acute critical illness due to complications following open heart surgery, abdominal surgery or multiple accidental trauma, or those with acute respiratory failure [see WARNINGS AND PRECAUTIONS]. Prader-Willi Syndrome In Children Somatropin is contraindicated in patients with Prader-Willi syndrome who are severely obese, have a history of upper airway obstruction or sleep apnea, or have severe respiratory impairment. There have been reports of sudden death when somatropin was used in such patients [see WARNINGS AND PRECAUTIONS]. Active Malignancy In general, somatropin is contraindicated in the presence of active malignancy. Any preexisting malignancy should be inactive and its treatment complete prior to instituting therapy with somatropin. Somatropin should be discontinued if there is evidence of recurrent activity. Since growth hormone deficiency may be an early sign of the presence of a pituitary tumor (or, rarely, other brain tumors), the presence of such tumors should be ruled out prior to initiation of treatment. Somatropin should not be used in patients with any evidence of progression or recurrence of an underlying intracranial tumor. Hypersensitivity GENOTROPIN is contraindicated in patients with a known hypersensitivity to somatropin or any of its excipients. The 5 mg and 12 mg presentations of GENOTROPIN lyophilized powder contain m-cresol as a preservative. Systemic hypersensitivity reactions have been reported with post-marketing use of somatropin products [see WARNINGS AND PRECAUTIONS] . Diabetic Retinopathy Somatropin is contraindicated in patients with active proliferative or severe non-proliferative diabetic retinopathy. Closed Epiphyses Somatropin should not be used for growth promotion in pediatric patients with closed epiphyses. | growth failure in children and adults who lack natural growth hormone, and in those with chronic kidney failure, Noonan syndrome, Turner syndrome, short stature at birth with no catch-up growth, and other causes | Genotropin is a form of human growth hormone important for the growth of bones and muscles. Genotropin is used to treat growth failure in children and adults who lack natural growth hormone. This includes people with short stature due to Noonan syndrome, Turner syndrome, Prader-Willi syndrome, short... | NA | NA | NA | Link | Link | NA |
| 11472 | Th1249 | Somatotropin | >Th1249_Somatotropin FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | 22129 | C990H1532N262O300S7 | 5.27 | -0.411 | 76 °C at pH 3.5 | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the mean apparent terminal half-life was Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the terminal elimination half-life was approximately 21.1 (±5.1) minutes.[L10971] | Human growth hormone (HGH), also known as somatotropin, is a peptide hormone that is synthesized and secreted by the somatotropic cells of the anterior pituitary gland.[A228183] Growth hormone plays an essential role in growth regulation during childhood as well as other basal metabolic functions, muscle and fat mass regulation, blood glucose level regulation, and lipid regulation in both children and adults.[A228183, L31508] Synthesized in a strain of _Escherichia coli_, recombinant HGH is a polypeptide hormone that contains 191 amino acid residues with a molecular weight of 22 kDa. It has an identical primary protein structure to endogenous human growth hormone.[A228188] Recombinant HGH has been commercially available since 1985 after its development by Genentech. [Somatrem] was the first available recombinant HGH and was largely replaced by somatropin, another form of recombinant HGH.[A228183] Growth hormone therapy is approved for various disorders of growth hormone deficiency, growth failure, or short stature including Turner syndrome, chronic renal insufficiency before transplantation, Prader-Willi syndrome, a history of fetal growth restriction, short stature homeobox (SHOX) haploinsufficiency, Noonan syndrome, idiopathic short stature, and adult- or childhood-onset growth hormone deficiency.[A228188] Recombinant growth hormone is available as a subcutaneous injection for children and adults under a wide variety of brand names. | Somatotropin is indicated for the treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone, short stature associated with Turner syndrome, Prader-Willi syndrome (PWS), idiopathic short stature (ISS), short stature or growth failure in short stature homeobox-containing gene (SHOX) deficiency, and short stature born small for gestational age (SGA).[L31513, L31518] It is indicated for the treatment of growth failure in children associated with chronic kidney disease up to the time of renal transplantation.[L31523] It is also indicated for adults with adult-onset growth hormone deficiency, either alone or associated with multiple hormone deficiencies (hypopituitarism), as a result of pituitary disease, hypothalamic disease, surgery, radiation therapy, or trauma. It is also used to treat childhood-onset growth hormone deficiency in adults due to congenital, genetic, acquired, or idiopathic causes.[L31518] Somatotropin is indicated for the treatment of wasting or cachexia in patients with human immunodeficiency virus (HIV) who are receiving antiretroviral therapy to increase lean body mass and body weight and improve physical endurance.[L31498] Somatotropin is indicated for the treatment of short bowel syndrome in adult patients receiving specialized nutritional support.[L31493] | Somatotropin induces growth in nearly every tissue and organ in the body.[L31508] It stimulates linear growth and cartilaginous growth of long bones. In children with short stature, growth hormone increases both the number and size of muscle cells. It also promotes the growth of internal organs, and it also increases red cell mass. By promoting nitrogen retention, growth hormone increases cellular protein synthesis. Growth hormone also retains potassium and phosphorus in the serum, which may be the result of cell growth. Growth hormone stimulates the synthesis of chondroitin sulfate and collagen and increases the urinary excretion of hydroxyproline. It has negligible effects on serum calcium levels. Although increased calcium excretion in the urine is observed, calcium absorption from the intestine is simultaneously enhanced.[L10971] In end-stage renal disease, growth hormone was shown to improve several nutritional parameters, such as increases in serum insulin-like growth factor-I (IGF-I), serum albumin, and transferrin, as well as a reduction in blood urea nitrogen.[A228403] The metabolic effects of growth hormone are caused by the upregulation of insulin-like growth factor-1. Generally, growth hormone leads cells to enter an anabolic protein state with increased amino acid uptake, protein synthesis, and decreased catabolism of proteins.[L31508] The diabetogenic effect of larger doses of growth hormone is well documented in the literature: somatotropin antagonizes insulin action _in vivo_, causing insulin resistance and glucose intolerance. It increases glucose production through gluconeogenesis and glycogenolysis from the liver and kidney [A228398] and suppresses glucose uptake in the adipose tissue.[A228388] In mice, growth hormone increased mRNA expression of 2 major gluconeogenic genes, phosphoenolpyruvate carboxy-kinase and glucose-6-phosphatase.[A228398] The risk for impaired glucose tolerance and reduced insulin sensitivity may be increased in susceptible patients, especially in those with risk factors for diabetes mellitus, such as obesity, Turner syndrome, or a family history of diabetes mellitus. The development of new-onset type 2 Diabetes Mellitus was observed in patients receiving somatotropin treatment.[L10971] Growth hormone stimulates lipolysis via activation of the hormone-sensitive lipase in the adipose tissue, thereby increasing circulating levels of free fatty acids and triglycerides in the plasma. It also leads to a reduction of fat stores and decreased serum levels of low-density lipoprotein (LDL) cholesterol.[L10971] In contrast to the effects seen in the adipose tissue, growth hormone promotes cellular uptake of free fatty acids in skeletal muscle by increasing the activity of lipoprotein lipase. Growth hormone may cause hyperinsulinism following beta-cell compensation for insulin resistance; however, there is some evidence that growth hormone directly promotes beta-cell proliferation and glucose-stimulated insulin secretion.[A228398] | In conditions of growth failure, growth hormone deficiency, low body mass, and malnutrition, somatotropin treatment acts to mimic and restore the actions of endogenous growth hormone of stimulating linear bone growth, increasing bone mass, increasing muscle and reduced fat mass, and regulating blood glucose and lipid levels.[A228183] Somatotropin mediates its effects both directly by somatotropin and indirectly by insulin-like growth factor-1 (IGF-1), which is upregulated by growth hormone. It binds to the human growth hormone receptor (GHR), which is a dimeric receptor expressed in target cells in the liver and cartilage.[L10971] Upon binding of growth hormone, GHR dimerizes and interacts with Janus kinase 2 (JAK2), subsequently leading to tyrosine phosphorylation of JAK2 and the GH receptor. The signal transducer activator of transcription (STAT) pathway is initiated, where transcription factors such as STAT1, STAT3, and STAT5 are translocated into the nucleus to stimulate target gene transcription.[L31508] At the epiphysis or growth plate, growth hormone increases linear growth by promoting differentiation of prechondrocytes and expansion of osteoblasts. Growth hormone binding to its receptor in the liver and cartilage promotes the production of IGF-1, which acts on type 1 IGF receptors to also stimulate linear growth. In the liver, activated growth hormone receptor signalling leads to increased production of IGF binding protein-3 (IGFBP-3) and acid-labile subunit (ALS), which are proteins that bind to IGF-1 in a ternary complex to increase its half-life.[A228183] | The oral LD50 is 242 mg/kg in rats and 828 mg/kg in mice. The inhalatory LD50 is 710 mg/m3 and dermal LD50 is 1100 mg/kg in rats. The intraperitoneal LD50 in mice is 828 mg/kg.[L31528] Hypoglycemia followed by hyperglycemia, possibly with fluid retention, can be observed in somatropin overdose. Long-term or excessive use of growth hormone can lead to the signs and symptoms of gigantism and acromegaly.[L10971] | Information is unavailable. | When somatotropin was administered subcutaneously at the dose of 0.024 mg/kg or 3 IU/m2, the Cmax ranged from 13.8 (±5.8) to 17.1 (±10.0) ng/mL and the Tmax was four to five hours. Following intravenous infusion of 33 ng/kg/min of somatotropin in patients with growth hormone deficiency, the mean steady-state serum levels of approximately 23.1 (±15.0) ng/mL were reached at 150 minutes.[L10971] | NA | NA | Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | 9616180 | 11-04-2017 | 20-07-2026 | NA | Growth hormone receptor,Prolactin receptor | Genotropin | Pfizer Canada Ulc | Pfizer Canada Ulc | Subcutaneous | 1.8 mg / syr | Acute Critical Illness Treatment with pharmacologic amounts of somatropin is contraindicated in patients with acute critical illness due to complications following open heart surgery, abdominal surgery or multiple accidental trauma, or those with acute respiratory failure [see WARNINGS AND PRECAUTIONS]. Prader-Willi Syndrome In Children Somatropin is contraindicated in patients with Prader-Willi syndrome who are severely obese, have a history of upper airway obstruction or sleep apnea, or have severe respiratory impairment. There have been reports of sudden death when somatropin was used in such patients [see WARNINGS AND PRECAUTIONS]. Active Malignancy In general, somatropin is contraindicated in the presence of active malignancy. Any preexisting malignancy should be inactive and its treatment complete prior to instituting therapy with somatropin. Somatropin should be discontinued if there is evidence of recurrent activity. Since growth hormone deficiency may be an early sign of the presence of a pituitary tumor (or, rarely, other brain tumors), the presence of such tumors should be ruled out prior to initiation of treatment. Somatropin should not be used in patients with any evidence of progression or recurrence of an underlying intracranial tumor. Hypersensitivity GENOTROPIN is contraindicated in patients with a known hypersensitivity to somatropin or any of its excipients. The 5 mg and 12 mg presentations of GENOTROPIN lyophilized powder contain m-cresol as a preservative. Systemic hypersensitivity reactions have been reported with post-marketing use of somatropin products [see WARNINGS AND PRECAUTIONS] . Diabetic Retinopathy Somatropin is contraindicated in patients with active proliferative or severe non-proliferative diabetic retinopathy. Closed Epiphyses Somatropin should not be used for growth promotion in pediatric patients with closed epiphyses. | growth failure in children and adults who lack natural growth hormone, and in those with chronic kidney failure, Noonan syndrome, Turner syndrome, short stature at birth with no catch-up growth, and other causes | Genotropin is a form of human growth hormone important for the growth of bones and muscles. Genotropin is used to treat growth failure in children and adults who lack natural growth hormone. This includes people with short stature due to Noonan syndrome, Turner syndrome, Prader-Willi syndrome, short... | NA | NA | NA | Link | Link | NA |
| 11634 | Th1252 | Follitropin | >Th1252_Follitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 °C | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Follitropin is a human follicle stimulating hormone (FSH) preparation of recombinant DNA origin, which consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Follitropin beta is produced in genetically engineered Chinese hamster cell lines (CHO). The nomenclature “beta” differentiates it from another recombinant human FSH product that was marketed earlier as follitropin alpha. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels. Structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | In women having been diagnosed with primary ovarian failure, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. In men with hypogonadotrophic hypogonadism, it is used to induce spermatogenesis. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | Used for the treatment of female infertility, Follitropin beta or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of Follitropin beta is the primary hormone responsible for follicular recruitment and development. | Follitropin is a recombinant form of endogenous follicle stimulating hormone (FSH). FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | Headaches, ovarian cysts, nausea and upper respiratory tract infections occurred in more than 10% of women in clinical trials. In men, the most serious adverse events reported were testicular surgery for cryptorchidism which existed prestudy, hemoptysis, an infected pilonidal cyst, and lymphadenopathy associated with an Epstein-Barr viral infection. Other concerns include overstimulation of the ovaries, pulmonary and vascular complications and multiple births. Post-marketing reports revealed hypersensitivity reactions including anaphylactoid reactions and asthma. Follitropin is contraindicated in pregnant women. No studies have been done in nursing mothers. | NA | The absorption rate is the main driving force behind the pharmokinetics of Follitropin alpha as the rate of absorption was found to be slower than the elimination rate after administration subcutaneously and intramuscularly. The bioavailability is approximately 66-76%. The time to peak after subcutaneous injection in healthy volunteers was 8-16 hours in females and 11-20 hours in males. | * 8 L [female subjects following intravenous administration of a 300 IU dose] | * 0.01 1*h-1kg-1 [European women with a single intramuscular dose of 300 IU] * 0.01 1*h-1kg-1 [Japanese women with a single intramuscular dose of 300 IU] | Genito Urinary System and Sex Hormones | 5929028 | 27-07-1999 | 14-01-2018 | NA | Follicle-stimulating hormone receptor | Bemfola | Gedeon Richter Plc. | Gedeon Richter Plc. | Subcutaneous | 300 IU/0.50ml | NA | The most common side effects with Bemfola (which may affect more than 1 in 10 people) are reactions at the injection site (pain, redness, bruising, swelling or irritation). In women, ovarian cysts (sacs of fluid within the ovaries) and headache are also seen in more than 1 patient in 10. For the full list of all side effects reported with Bemfola, see the package leaflet. | NA | NA | NA | NA | Link | Link | NA |
| 11638 | Th1252 | Follitropin | >Th1252_Follitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 °C | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Follitropin is a human follicle stimulating hormone (FSH) preparation of recombinant DNA origin, which consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Follitropin beta is produced in genetically engineered Chinese hamster cell lines (CHO). The nomenclature “beta” differentiates it from another recombinant human FSH product that was marketed earlier as follitropin alpha. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels. Structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | In women having been diagnosed with primary ovarian failure, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. In men with hypogonadotrophic hypogonadism, it is used to induce spermatogenesis. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | Used for the treatment of female infertility, Follitropin beta or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of Follitropin beta is the primary hormone responsible for follicular recruitment and development. | Follitropin is a recombinant form of endogenous follicle stimulating hormone (FSH). FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | Headaches, ovarian cysts, nausea and upper respiratory tract infections occurred in more than 10% of women in clinical trials. In men, the most serious adverse events reported were testicular surgery for cryptorchidism which existed prestudy, hemoptysis, an infected pilonidal cyst, and lymphadenopathy associated with an Epstein-Barr viral infection. Other concerns include overstimulation of the ovaries, pulmonary and vascular complications and multiple births. Post-marketing reports revealed hypersensitivity reactions including anaphylactoid reactions and asthma. Follitropin is contraindicated in pregnant women. No studies have been done in nursing mothers. | NA | The absorption rate is the main driving force behind the pharmokinetics of Follitropin alpha as the rate of absorption was found to be slower than the elimination rate after administration subcutaneously and intramuscularly. The bioavailability is approximately 66-76%. The time to peak after subcutaneous injection in healthy volunteers was 8-16 hours in females and 11-20 hours in males. | * 8 L [female subjects following intravenous administration of a 300 IU dose] | * 0.01 1*h-1kg-1 [European women with a single intramuscular dose of 300 IU] * 0.01 1*h-1kg-1 [Japanese women with a single intramuscular dose of 300 IU] | Hormones | NA | NA | NA | NA | Follicle-stimulating hormone receptor | Fertavid | Merck Sharp & Dohme B.V. | Merck Sharp & Dohme B.V. | Intramuscular; Subcutaneous | 50 IU/0.5mL | NA | NA | NA | NA | NA | NA | Link | Link | NA |
| 11639 | Th1252 | Follitropin | >Th1252_Follitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 °C | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Follitropin is a human follicle stimulating hormone (FSH) preparation of recombinant DNA origin, which consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Follitropin beta is produced in genetically engineered Chinese hamster cell lines (CHO). The nomenclature “beta” differentiates it from another recombinant human FSH product that was marketed earlier as follitropin alpha. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels. Structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | In women having been diagnosed with primary ovarian failure, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. In men with hypogonadotrophic hypogonadism, it is used to induce spermatogenesis. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | Used for the treatment of female infertility, Follitropin beta or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of Follitropin beta is the primary hormone responsible for follicular recruitment and development. | Follitropin is a recombinant form of endogenous follicle stimulating hormone (FSH). FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | Headaches, ovarian cysts, nausea and upper respiratory tract infections occurred in more than 10% of women in clinical trials. In men, the most serious adverse events reported were testicular surgery for cryptorchidism which existed prestudy, hemoptysis, an infected pilonidal cyst, and lymphadenopathy associated with an Epstein-Barr viral infection. Other concerns include overstimulation of the ovaries, pulmonary and vascular complications and multiple births. Post-marketing reports revealed hypersensitivity reactions including anaphylactoid reactions and asthma. Follitropin is contraindicated in pregnant women. No studies have been done in nursing mothers. | NA | The absorption rate is the main driving force behind the pharmokinetics of Follitropin alpha as the rate of absorption was found to be slower than the elimination rate after administration subcutaneously and intramuscularly. The bioavailability is approximately 66-76%. The time to peak after subcutaneous injection in healthy volunteers was 8-16 hours in females and 11-20 hours in males. | * 8 L [female subjects following intravenous administration of a 300 IU dose] | * 0.01 1*h-1kg-1 [European women with a single intramuscular dose of 300 IU] * 0.01 1*h-1kg-1 [Japanese women with a single intramuscular dose of 300 IU] | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | Follicle-stimulating hormone receptor | Fertavid | Merck Sharp & Dohme B.V. | Merck Sharp & Dohme B.V. | Intramuscular; Subcutaneous | 75 IU/0.5mL | NA | NA | NA | NA | NA | NA | Link | Link | NA |
| 11640 | Th1252 | Follitropin | >Th1252_Follitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 °C | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Follitropin is a human follicle stimulating hormone (FSH) preparation of recombinant DNA origin, which consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Follitropin beta is produced in genetically engineered Chinese hamster cell lines (CHO). The nomenclature “beta” differentiates it from another recombinant human FSH product that was marketed earlier as follitropin alpha. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels. Structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | In women having been diagnosed with primary ovarian failure, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. In men with hypogonadotrophic hypogonadism, it is used to induce spermatogenesis. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | Used for the treatment of female infertility, Follitropin beta or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of Follitropin beta is the primary hormone responsible for follicular recruitment and development. | Follitropin is a recombinant form of endogenous follicle stimulating hormone (FSH). FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | Headaches, ovarian cysts, nausea and upper respiratory tract infections occurred in more than 10% of women in clinical trials. In men, the most serious adverse events reported were testicular surgery for cryptorchidism which existed prestudy, hemoptysis, an infected pilonidal cyst, and lymphadenopathy associated with an Epstein-Barr viral infection. Other concerns include overstimulation of the ovaries, pulmonary and vascular complications and multiple births. Post-marketing reports revealed hypersensitivity reactions including anaphylactoid reactions and asthma. Follitropin is contraindicated in pregnant women. No studies have been done in nursing mothers. | NA | The absorption rate is the main driving force behind the pharmokinetics of Follitropin alpha as the rate of absorption was found to be slower than the elimination rate after administration subcutaneously and intramuscularly. The bioavailability is approximately 66-76%. The time to peak after subcutaneous injection in healthy volunteers was 8-16 hours in females and 11-20 hours in males. | * 8 L [female subjects following intravenous administration of a 300 IU dose] | * 0.01 1*h-1kg-1 [European women with a single intramuscular dose of 300 IU] * 0.01 1*h-1kg-1 [Japanese women with a single intramuscular dose of 300 IU] | Peptide Hormones | NA | NA | NA | NA | Follicle-stimulating hormone receptor | Fertavid | Merck Sharp & Dohme B.V. | Merck Sharp & Dohme B.V. | Intramuscular; Subcutaneous | 100 IU/0.5mL | NA | NA | NA | NA | NA | NA | Link | Link | NA |
| 11642 | Th1252 | Follitropin | >Th1252_Follitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 °C | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Follitropin is a human follicle stimulating hormone (FSH) preparation of recombinant DNA origin, which consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Follitropin beta is produced in genetically engineered Chinese hamster cell lines (CHO). The nomenclature “beta” differentiates it from another recombinant human FSH product that was marketed earlier as follitropin alpha. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels. Structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | In women having been diagnosed with primary ovarian failure, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. In men with hypogonadotrophic hypogonadism, it is used to induce spermatogenesis. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | Used for the treatment of female infertility, Follitropin beta or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of Follitropin beta is the primary hormone responsible for follicular recruitment and development. | Follitropin is a recombinant form of endogenous follicle stimulating hormone (FSH). FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | Headaches, ovarian cysts, nausea and upper respiratory tract infections occurred in more than 10% of women in clinical trials. In men, the most serious adverse events reported were testicular surgery for cryptorchidism which existed prestudy, hemoptysis, an infected pilonidal cyst, and lymphadenopathy associated with an Epstein-Barr viral infection. Other concerns include overstimulation of the ovaries, pulmonary and vascular complications and multiple births. Post-marketing reports revealed hypersensitivity reactions including anaphylactoid reactions and asthma. Follitropin is contraindicated in pregnant women. No studies have been done in nursing mothers. | NA | The absorption rate is the main driving force behind the pharmokinetics of Follitropin alpha as the rate of absorption was found to be slower than the elimination rate after administration subcutaneously and intramuscularly. The bioavailability is approximately 66-76%. The time to peak after subcutaneous injection in healthy volunteers was 8-16 hours in females and 11-20 hours in males. | * 8 L [female subjects following intravenous administration of a 300 IU dose] | * 0.01 1*h-1kg-1 [European women with a single intramuscular dose of 300 IU] * 0.01 1*h-1kg-1 [Japanese women with a single intramuscular dose of 300 IU] | Pituitary Hormones | NA | NA | NA | NA | Follicle-stimulating hormone receptor | Fertavid | Merck Sharp & Dohme B.V. | Merck Sharp & Dohme B.V. | Intramuscular; Subcutaneous | 200 IU/0.5mL | NA | NA | NA | NA | NA | NA | Link | Link | NA |
| 11643 | Th1252 | Follitropin | >Th1252_Follitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 °C | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Follitropin is a human follicle stimulating hormone (FSH) preparation of recombinant DNA origin, which consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Follitropin beta is produced in genetically engineered Chinese hamster cell lines (CHO). The nomenclature “beta” differentiates it from another recombinant human FSH product that was marketed earlier as follitropin alpha. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels. Structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | In women having been diagnosed with primary ovarian failure, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. In men with hypogonadotrophic hypogonadism, it is used to induce spermatogenesis. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | Used for the treatment of female infertility, Follitropin beta or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of Follitropin beta is the primary hormone responsible for follicular recruitment and development. | Follitropin is a recombinant form of endogenous follicle stimulating hormone (FSH). FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | Headaches, ovarian cysts, nausea and upper respiratory tract infections occurred in more than 10% of women in clinical trials. In men, the most serious adverse events reported were testicular surgery for cryptorchidism which existed prestudy, hemoptysis, an infected pilonidal cyst, and lymphadenopathy associated with an Epstein-Barr viral infection. Other concerns include overstimulation of the ovaries, pulmonary and vascular complications and multiple births. Post-marketing reports revealed hypersensitivity reactions including anaphylactoid reactions and asthma. Follitropin is contraindicated in pregnant women. No studies have been done in nursing mothers. | NA | The absorption rate is the main driving force behind the pharmokinetics of Follitropin alpha as the rate of absorption was found to be slower than the elimination rate after administration subcutaneously and intramuscularly. The bioavailability is approximately 66-76%. The time to peak after subcutaneous injection in healthy volunteers was 8-16 hours in females and 11-20 hours in males. | * 8 L [female subjects following intravenous administration of a 300 IU dose] | * 0.01 1*h-1kg-1 [European women with a single intramuscular dose of 300 IU] * 0.01 1*h-1kg-1 [Japanese women with a single intramuscular dose of 300 IU] | Pituitary Hormones, Anterior | NA | NA | NA | NA | Follicle-stimulating hormone receptor | Fertavid | Merck Sharp & Dohme B.V. | Merck Sharp & Dohme B.V. | Subcutaneous | 150 IU/0.18mL | NA | NA | NA | NA | NA | NA | Link | Link | NA |
| 11644 | Th1252 | Follitropin | >Th1252_Follitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 °C | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Follitropin is a human follicle stimulating hormone (FSH) preparation of recombinant DNA origin, which consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Follitropin beta is produced in genetically engineered Chinese hamster cell lines (CHO). The nomenclature “beta” differentiates it from another recombinant human FSH product that was marketed earlier as follitropin alpha. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels. Structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | In women having been diagnosed with primary ovarian failure, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. In men with hypogonadotrophic hypogonadism, it is used to induce spermatogenesis. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | Used for the treatment of female infertility, Follitropin beta or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of Follitropin beta is the primary hormone responsible for follicular recruitment and development. | Follitropin is a recombinant form of endogenous follicle stimulating hormone (FSH). FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | Headaches, ovarian cysts, nausea and upper respiratory tract infections occurred in more than 10% of women in clinical trials. In men, the most serious adverse events reported were testicular surgery for cryptorchidism which existed prestudy, hemoptysis, an infected pilonidal cyst, and lymphadenopathy associated with an Epstein-Barr viral infection. Other concerns include overstimulation of the ovaries, pulmonary and vascular complications and multiple births. Post-marketing reports revealed hypersensitivity reactions including anaphylactoid reactions and asthma. Follitropin is contraindicated in pregnant women. No studies have been done in nursing mothers. | NA | The absorption rate is the main driving force behind the pharmokinetics of Follitropin alpha as the rate of absorption was found to be slower than the elimination rate after administration subcutaneously and intramuscularly. The bioavailability is approximately 66-76%. The time to peak after subcutaneous injection in healthy volunteers was 8-16 hours in females and 11-20 hours in males. | * 8 L [female subjects following intravenous administration of a 300 IU dose] | * 0.01 1*h-1kg-1 [European women with a single intramuscular dose of 300 IU] * 0.01 1*h-1kg-1 [Japanese women with a single intramuscular dose of 300 IU] | Placental Hormones | NA | NA | NA | NA | Follicle-stimulating hormone receptor | Fertavid | Merck Sharp & Dohme B.V. | Merck Sharp & Dohme B.V. | Subcutaneous | 300 IU/0.36mL | NA | NA | NA | NA | NA | NA | Link | Link | NA |
| 11647 | Th1252 | Follitropin | >Th1252_Follitropin APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 22672.9 | C975H1513N267O304S26 | 7.5 | -0.33 | 55 °C | Circulation half life of 3-4 hours, elimination half life of 35-40 hours | Follitropin is a human follicle stimulating hormone (FSH) preparation of recombinant DNA origin, which consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Follitropin beta is produced in genetically engineered Chinese hamster cell lines (CHO). The nomenclature “beta” differentiates it from another recombinant human FSH product that was marketed earlier as follitropin alpha. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels. Structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. | In women having been diagnosed with primary ovarian failure, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. In men with hypogonadotrophic hypogonadism, it is used to induce spermatogenesis. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). | Used for the treatment of female infertility, Follitropin beta or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of Follitropin beta is the primary hormone responsible for follicular recruitment and development. | Follitropin is a recombinant form of endogenous follicle stimulating hormone (FSH). FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells. | Headaches, ovarian cysts, nausea and upper respiratory tract infections occurred in more than 10% of women in clinical trials. In men, the most serious adverse events reported were testicular surgery for cryptorchidism which existed prestudy, hemoptysis, an infected pilonidal cyst, and lymphadenopathy associated with an Epstein-Barr viral infection. Other concerns include overstimulation of the ovaries, pulmonary and vascular complications and multiple births. Post-marketing reports revealed hypersensitivity reactions including anaphylactoid reactions and asthma. Follitropin is contraindicated in pregnant women. No studies have been done in nursing mothers. | NA | The absorption rate is the main driving force behind the pharmokinetics of Follitropin alpha as the rate of absorption was found to be slower than the elimination rate after administration subcutaneously and intramuscularly. The bioavailability is approximately 66-76%. The time to peak after subcutaneous injection in healthy volunteers was 8-16 hours in females and 11-20 hours in males. | * 8 L [female subjects following intravenous administration of a 300 IU dose] | * 0.01 1*h-1kg-1 [European women with a single intramuscular dose of 300 IU] * 0.01 1*h-1kg-1 [Japanese women with a single intramuscular dose of 300 IU] | Sex Hormones and Modulators of the Genital System | NA | NA | NA | NA | Follicle-stimulating hormone receptor | Follistim | Organon USA, Inc. | Organon USA, Inc. | Intramuscular; Subcutaneous | NA | Follistim® AQ (follitropin beta injection) is contraindicated in women who exhibit: Prior hypersensitivity to recombinant hFSH products. High levels of FSH indicating primary ovarian failure. Uncontrolled thyroid or adrenal dysfunction. Tumor of the ovary, breast, uterus, hypothalamus or pituitary gland. Pregnancy. Heavy or irregular vaginal bleeding of undetermined origin. Ovarian cysts or enlargement not due to polycystic ovary syndrome (PCOS). Hypersensitivity reactions to streptomycin or neomycin. Follistim® AQ (follitropin beta) may contain traces of these antibiotics and may cause hypersensitivity reactions in susceptible persons. | Acid or sour stomach anxiety backache belching bloating chest pain or tightness confusion cough diarrhea difficulty breathing difficulty in speaking dizziness or lightheadedness double vision excess air or gas in the stomach or intestines fainting fast heartbeat fast, weak pulse full feeling headache heartburn inability to move the arms, legs, or facial muscles indigestion loss of appetite noisy breathing passing gas pelvic pain, discomfort, aching, or heaviness rapid weight gain severe nausea slow speech stomach discomfort, upset, or pain, or swelling sudden increase in stomach or shoulder pain sweating trouble breathing unusual or large amount of vaginal bleeding uterine bleeding between menstrual periods vomiting | Follistim AQ is a man-made form of a hormone that occurs naturally in the body. This hormone regulates ovulation, the growth and development of eggs in a woman's ovaries. Follistim AQ is used to treat infertility in women who cannot ovulate. This medicine is not effective in women with primary ovarian... | Follistim is a prescription medicine used to treat infertility in women to induce Ovulation and to stimulate sperm production in men (Spermatogenesis). Follistim may be used alone or with other medications. | NA | FOR SUBCUTANEOUS OR INTRAMUSCULAR USE ONLY | Link | Link | NA |
| 11985 | Th1275 | Abaloparatide | >Th1275_Abaloparatide AVSEHQLLHDKGKSIQDLRRRELLEKLLXKLHTA | 3961 | C174H300N56O49 | NA | NA | NA | The mean (SD) half-life if 1.7 (0.7) hrs. | Abaloparatide is an analog of PTHrP (parathyroid hormone-related protein). It was approved in April 28, 2017 by the FDA (as Tymlos) for the treatment of postmenopausal women with osteoporosis at high risk for fracture. Abaloparatide is a synthetic peptide that is related to hPTHrP and has demonstrated in preclinical testing the potential to widen the anabolic window for bone therapeutics, stimulating bone formation with a limited effect on bone resorption and mineral mobilization. This could enable improved convenience over currently available anabolic therapies, resulting in greater compliance and, ultimately, greater benefit to patients. | Investigated for use/treatment in postmenopausal osteoporosis to reduce vertebral and/or non-vertebral fractures. | Abaloparatide (BA058), a proprietary analog of human parathyroid hormone-related protein (hPTHrP), is currently undergoing clinical trials by the company for the treatment of osteoporosis in postmenopausal women. PTHrP is a critical peptide for promoting new bone formation, with a distinct role from parathyroid hormone, or PTH, which primarily regulates calcium homeostasis and bone resorption. Clinical studies show increased bone mineral density (BMD) and levels of bone formation markers in a dose-response relationship. | In target cells, abaloparatide acts as an agonist on PTH type 1 receptor (PTH1R) and activates both G protein–mediated cAMP signaling and ß-arrestin-mediated ERK-1/2 signaling pathways with similar potency. Abaloparatide binds to RG conformation of PTH1R with greater selectivity that results in more transient cell signalling responses. | Abaloparatide has shown to induce higher incidences of osteosarcoma in a dose-dependent manner in a 2 year carcinogenicity study with female and male rats. This correlation is not known to be reflected in humans, however patients with increased risk of osteosarcoma including Paget's disease, open epiphyses, and skeletal malignancies should avoid this treatment. Abaloparatide may also cause hypercalcemia so should be avoided in patients with pre-existing conditions of primary hyperthyroidism or hypercalcemia. Overdose is commonly associated with hypercalcemia, nausea, vomiting, dizziness, tachycardia, orthostatic hypotension and headache. There is no known antidote for abaloparatide. | Abaloparatide is metabolized into smaller peptide fragments via non-specific proteolytic degradation. | The time it takes to reach peak concentration following subcutaneous administration of 80 mcg abaloparatide ranges from 0.25 to 0.52 hr, with the median time of 0.51hr. The bioavailability in healthy women is 36% following administration. | Vd is approximately 50L. | NA | Hormones | NA | NA | NA | NA | Parathyroid hormone/parathyroid hormone-related peptide receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | 4-[[2-[[2-[[2-[[2-[[2-[[5-amino-2-[[2-[[2-[[6-amino-2-[[2-[[6-amino-2-[[2-[[2-[[2-[[2-[[5-amino-2-[[2-[[2-[[2-[[2-(2-aminopropanoylamino)-3-methylbutanoyl]amino]-3-hydroxypropanoyl]amino]-4-carboxybutanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-5-oxopentanoyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-3-carboxypropanoyl]amino]hexanoyl]amino]acetyl]amino]hexanoyl]amino]-3-hydroxypropanoyl]amino]-3-methylpentanoyl]amino]-5-oxopentanoyl]amino]-3-carboxypropanoyl]amino]-4-methylpentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-[[1-[[1-[[1-[[6-amino-1-[[1-[[1-[[1-[[6-amino-1-[[1-[[1-[[1-[(1-amino-1-oxopropan-2-yl)amino]-3-hydroxy-1-oxobutan-2-yl]amino]-3-(1H-imidazol-5-yl)-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-2-methyl-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 11986 | Th1275 | Abaloparatide | >Th1275_Abaloparatide AVSEHQLLHDKGKSIQDLRRRELLEKLLXKLHTA | 3961 | C174H300N56O49 | NA | NA | NA | The mean (SD) half-life if 1.7 (0.7) hrs. | Abaloparatide is an analog of PTHrP (parathyroid hormone-related protein). It was approved in April 28, 2017 by the FDA (as Tymlos) for the treatment of postmenopausal women with osteoporosis at high risk for fracture. Abaloparatide is a synthetic peptide that is related to hPTHrP and has demonstrated in preclinical testing the potential to widen the anabolic window for bone therapeutics, stimulating bone formation with a limited effect on bone resorption and mineral mobilization. This could enable improved convenience over currently available anabolic therapies, resulting in greater compliance and, ultimately, greater benefit to patients. | Investigated for use/treatment in postmenopausal osteoporosis to reduce vertebral and/or non-vertebral fractures. | Abaloparatide (BA058), a proprietary analog of human parathyroid hormone-related protein (hPTHrP), is currently undergoing clinical trials by the company for the treatment of osteoporosis in postmenopausal women. PTHrP is a critical peptide for promoting new bone formation, with a distinct role from parathyroid hormone, or PTH, which primarily regulates calcium homeostasis and bone resorption. Clinical studies show increased bone mineral density (BMD) and levels of bone formation markers in a dose-response relationship. | In target cells, abaloparatide acts as an agonist on PTH type 1 receptor (PTH1R) and activates both G protein–mediated cAMP signaling and ß-arrestin-mediated ERK-1/2 signaling pathways with similar potency. Abaloparatide binds to RG conformation of PTH1R with greater selectivity that results in more transient cell signalling responses. | Abaloparatide has shown to induce higher incidences of osteosarcoma in a dose-dependent manner in a 2 year carcinogenicity study with female and male rats. This correlation is not known to be reflected in humans, however patients with increased risk of osteosarcoma including Paget's disease, open epiphyses, and skeletal malignancies should avoid this treatment. Abaloparatide may also cause hypercalcemia so should be avoided in patients with pre-existing conditions of primary hyperthyroidism or hypercalcemia. Overdose is commonly associated with hypercalcemia, nausea, vomiting, dizziness, tachycardia, orthostatic hypotension and headache. There is no known antidote for abaloparatide. | Abaloparatide is metabolized into smaller peptide fragments via non-specific proteolytic degradation. | The time it takes to reach peak concentration following subcutaneous administration of 80 mcg abaloparatide ranges from 0.25 to 0.52 hr, with the median time of 0.51hr. The bioavailability in healthy women is 36% following administration. | Vd is approximately 50L. | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | Parathyroid hormone/parathyroid hormone-related peptide receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | 4-[[2-[[2-[[2-[[2-[[2-[[5-amino-2-[[2-[[2-[[6-amino-2-[[2-[[6-amino-2-[[2-[[2-[[2-[[2-[[5-amino-2-[[2-[[2-[[2-[[2-(2-aminopropanoylamino)-3-methylbutanoyl]amino]-3-hydroxypropanoyl]amino]-4-carboxybutanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-5-oxopentanoyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-3-carboxypropanoyl]amino]hexanoyl]amino]acetyl]amino]hexanoyl]amino]-3-hydroxypropanoyl]amino]-3-methylpentanoyl]amino]-5-oxopentanoyl]amino]-3-carboxypropanoyl]amino]-4-methylpentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-[[1-[[1-[[1-[[6-amino-1-[[1-[[1-[[1-[[6-amino-1-[[1-[[1-[[1-[(1-amino-1-oxopropan-2-yl)amino]-3-hydroxy-1-oxobutan-2-yl]amino]-3-(1H-imidazol-5-yl)-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-2-methyl-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 11989 | Th1275 | Abaloparatide | >Th1275_Abaloparatide AVSEHQLLHDKGKSIQDLRRRELLEKLLXKLHTA | 3961 | C174H300N56O49 | NA | NA | NA | The mean (SD) half-life if 1.7 (0.7) hrs. | Abaloparatide is an analog of PTHrP (parathyroid hormone-related protein). It was approved in April 28, 2017 by the FDA (as Tymlos) for the treatment of postmenopausal women with osteoporosis at high risk for fracture. Abaloparatide is a synthetic peptide that is related to hPTHrP and has demonstrated in preclinical testing the potential to widen the anabolic window for bone therapeutics, stimulating bone formation with a limited effect on bone resorption and mineral mobilization. This could enable improved convenience over currently available anabolic therapies, resulting in greater compliance and, ultimately, greater benefit to patients. | Investigated for use/treatment in postmenopausal osteoporosis to reduce vertebral and/or non-vertebral fractures. | Abaloparatide (BA058), a proprietary analog of human parathyroid hormone-related protein (hPTHrP), is currently undergoing clinical trials by the company for the treatment of osteoporosis in postmenopausal women. PTHrP is a critical peptide for promoting new bone formation, with a distinct role from parathyroid hormone, or PTH, which primarily regulates calcium homeostasis and bone resorption. Clinical studies show increased bone mineral density (BMD) and levels of bone formation markers in a dose-response relationship. | In target cells, abaloparatide acts as an agonist on PTH type 1 receptor (PTH1R) and activates both G protein–mediated cAMP signaling and ß-arrestin-mediated ERK-1/2 signaling pathways with similar potency. Abaloparatide binds to RG conformation of PTH1R with greater selectivity that results in more transient cell signalling responses. | Abaloparatide has shown to induce higher incidences of osteosarcoma in a dose-dependent manner in a 2 year carcinogenicity study with female and male rats. This correlation is not known to be reflected in humans, however patients with increased risk of osteosarcoma including Paget's disease, open epiphyses, and skeletal malignancies should avoid this treatment. Abaloparatide may also cause hypercalcemia so should be avoided in patients with pre-existing conditions of primary hyperthyroidism or hypercalcemia. Overdose is commonly associated with hypercalcemia, nausea, vomiting, dizziness, tachycardia, orthostatic hypotension and headache. There is no known antidote for abaloparatide. | Abaloparatide is metabolized into smaller peptide fragments via non-specific proteolytic degradation. | The time it takes to reach peak concentration following subcutaneous administration of 80 mcg abaloparatide ranges from 0.25 to 0.52 hr, with the median time of 0.51hr. The bioavailability in healthy women is 36% following administration. | Vd is approximately 50L. | NA | Parathyroid Hormones and Analogues | NA | NA | NA | NA | Parathyroid hormone/parathyroid hormone-related peptide receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | 4-[[2-[[2-[[2-[[2-[[2-[[5-amino-2-[[2-[[2-[[6-amino-2-[[2-[[6-amino-2-[[2-[[2-[[2-[[2-[[5-amino-2-[[2-[[2-[[2-[[2-(2-aminopropanoylamino)-3-methylbutanoyl]amino]-3-hydroxypropanoyl]amino]-4-carboxybutanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-5-oxopentanoyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-3-carboxypropanoyl]amino]hexanoyl]amino]acetyl]amino]hexanoyl]amino]-3-hydroxypropanoyl]amino]-3-methylpentanoyl]amino]-5-oxopentanoyl]amino]-3-carboxypropanoyl]amino]-4-methylpentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-[[1-[[1-[[1-[[6-amino-1-[[1-[[1-[[1-[[6-amino-1-[[1-[[1-[[1-[(1-amino-1-oxopropan-2-yl)amino]-3-hydroxy-1-oxobutan-2-yl]amino]-3-(1H-imidazol-5-yl)-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-2-methyl-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 11990 | Th1275 | Abaloparatide | >Th1275_Abaloparatide AVSEHQLLHDKGKSIQDLRRRELLEKLLXKLHTA | 3961 | C174H300N56O49 | NA | NA | NA | The mean (SD) half-life if 1.7 (0.7) hrs. | Abaloparatide is an analog of PTHrP (parathyroid hormone-related protein). It was approved in April 28, 2017 by the FDA (as Tymlos) for the treatment of postmenopausal women with osteoporosis at high risk for fracture. Abaloparatide is a synthetic peptide that is related to hPTHrP and has demonstrated in preclinical testing the potential to widen the anabolic window for bone therapeutics, stimulating bone formation with a limited effect on bone resorption and mineral mobilization. This could enable improved convenience over currently available anabolic therapies, resulting in greater compliance and, ultimately, greater benefit to patients. | Investigated for use/treatment in postmenopausal osteoporosis to reduce vertebral and/or non-vertebral fractures. | Abaloparatide (BA058), a proprietary analog of human parathyroid hormone-related protein (hPTHrP), is currently undergoing clinical trials by the company for the treatment of osteoporosis in postmenopausal women. PTHrP is a critical peptide for promoting new bone formation, with a distinct role from parathyroid hormone, or PTH, which primarily regulates calcium homeostasis and bone resorption. Clinical studies show increased bone mineral density (BMD) and levels of bone formation markers in a dose-response relationship. | In target cells, abaloparatide acts as an agonist on PTH type 1 receptor (PTH1R) and activates both G protein–mediated cAMP signaling and ß-arrestin-mediated ERK-1/2 signaling pathways with similar potency. Abaloparatide binds to RG conformation of PTH1R with greater selectivity that results in more transient cell signalling responses. | Abaloparatide has shown to induce higher incidences of osteosarcoma in a dose-dependent manner in a 2 year carcinogenicity study with female and male rats. This correlation is not known to be reflected in humans, however patients with increased risk of osteosarcoma including Paget's disease, open epiphyses, and skeletal malignancies should avoid this treatment. Abaloparatide may also cause hypercalcemia so should be avoided in patients with pre-existing conditions of primary hyperthyroidism or hypercalcemia. Overdose is commonly associated with hypercalcemia, nausea, vomiting, dizziness, tachycardia, orthostatic hypotension and headache. There is no known antidote for abaloparatide. | Abaloparatide is metabolized into smaller peptide fragments via non-specific proteolytic degradation. | The time it takes to reach peak concentration following subcutaneous administration of 80 mcg abaloparatide ranges from 0.25 to 0.52 hr, with the median time of 0.51hr. The bioavailability in healthy women is 36% following administration. | Vd is approximately 50L. | NA | Peptide Hormones | NA | NA | NA | NA | Parathyroid hormone/parathyroid hormone-related peptide receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | 4-[[2-[[2-[[2-[[2-[[2-[[5-amino-2-[[2-[[2-[[6-amino-2-[[2-[[6-amino-2-[[2-[[2-[[2-[[2-[[5-amino-2-[[2-[[2-[[2-[[2-(2-aminopropanoylamino)-3-methylbutanoyl]amino]-3-hydroxypropanoyl]amino]-4-carboxybutanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-5-oxopentanoyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-3-carboxypropanoyl]amino]hexanoyl]amino]acetyl]amino]hexanoyl]amino]-3-hydroxypropanoyl]amino]-3-methylpentanoyl]amino]-5-oxopentanoyl]amino]-3-carboxypropanoyl]amino]-4-methylpentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-[[1-[[1-[[1-[[6-amino-1-[[1-[[1-[[1-[[6-amino-1-[[1-[[1-[[1-[(1-amino-1-oxopropan-2-yl)amino]-3-hydroxy-1-oxobutan-2-yl]amino]-3-(1H-imidazol-5-yl)-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-2-methyl-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 12442 | Th1323 | NBI-6024 | NA | NA | NA | NA | NA | NA | NA | NBI-6024 is an altered peptide ligand that is designed to cause an immune response which result in preservation of beta-cell function and endogenous insulin production. | Investigated for use/treatment in diabetes mellitus type 1 and pediatric indications. | NA | NBI-6024 is designed specifically to generate an immune response that could result in preservation of beta-islet cell function in patients with Type I diabetes or juvenile-onset diabetes. Because there is progressive beta-islet destruction in Type I diabetes, an early intervention strategy with a product like NBI-6024 could delay or prevent insulin dependence. | NA | NA | NA | NA | NA | Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-4-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-3-hydroxypropanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-4-methylpentanoyl]amino]-3-methylbutanoyl]amino]-4-carboxybutanoyl]amino]propanoyl]amino]-4-methylpentanoyl]amino]propanoyl]amino]-4-methylpentanoyl]amino]-3-methylbutanoyl]amino]propanoyl]amino]acetyl]amino]-5-[[(2S)-1-(carboxymethylamino)-5-(diaminomethylideneamino)-1-oxopentan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 12443 | Th1323 | NBI-6024 | NA | NA | NA | NA | NA | NA | NA | NBI-6024 is an altered peptide ligand that is designed to cause an immune response which result in preservation of beta-cell function and endogenous insulin production. | Investigated for use/treatment in diabetes mellitus type 1 and pediatric indications. | NA | NBI-6024 is designed specifically to generate an immune response that could result in preservation of beta-islet cell function in patients with Type I diabetes or juvenile-onset diabetes. Because there is progressive beta-islet destruction in Type I diabetes, an early intervention strategy with a product like NBI-6024 could delay or prevent insulin dependence. | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-4-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-3-hydroxypropanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-4-methylpentanoyl]amino]-3-methylbutanoyl]amino]-4-carboxybutanoyl]amino]propanoyl]amino]-4-methylpentanoyl]amino]propanoyl]amino]-4-methylpentanoyl]amino]-3-methylbutanoyl]amino]propanoyl]amino]acetyl]amino]-5-[[(2S)-1-(carboxymethylamino)-5-(diaminomethylideneamino)-1-oxopentan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 12444 | Th1323 | NBI-6024 | NA | NA | NA | NA | NA | NA | NA | NBI-6024 is an altered peptide ligand that is designed to cause an immune response which result in preservation of beta-cell function and endogenous insulin production. | Investigated for use/treatment in diabetes mellitus type 1 and pediatric indications. | NA | NBI-6024 is designed specifically to generate an immune response that could result in preservation of beta-islet cell function in patients with Type I diabetes or juvenile-onset diabetes. Because there is progressive beta-islet destruction in Type I diabetes, an early intervention strategy with a product like NBI-6024 could delay or prevent insulin dependence. | NA | NA | NA | NA | NA | Pancreatic Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-4-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-3-hydroxypropanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-4-methylpentanoyl]amino]-3-methylbutanoyl]amino]-4-carboxybutanoyl]amino]propanoyl]amino]-4-methylpentanoyl]amino]propanoyl]amino]-4-methylpentanoyl]amino]-3-methylbutanoyl]amino]propanoyl]amino]acetyl]amino]-5-[[(2S)-1-(carboxymethylamino)-5-(diaminomethylideneamino)-1-oxopentan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 12445 | Th1323 | NBI-6024 | NA | NA | NA | NA | NA | NA | NA | NBI-6024 is an altered peptide ligand that is designed to cause an immune response which result in preservation of beta-cell function and endogenous insulin production. | Investigated for use/treatment in diabetes mellitus type 1 and pediatric indications. | NA | NBI-6024 is designed specifically to generate an immune response that could result in preservation of beta-islet cell function in patients with Type I diabetes or juvenile-onset diabetes. Because there is progressive beta-islet destruction in Type I diabetes, an early intervention strategy with a product like NBI-6024 could delay or prevent insulin dependence. | NA | NA | NA | NA | NA | Peptide Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-4-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-3-hydroxypropanoyl]amino]-3-(1H-imidazol-5-yl)propanoyl]amino]-4-methylpentanoyl]amino]-3-methylbutanoyl]amino]-4-carboxybutanoyl]amino]propanoyl]amino]-4-methylpentanoyl]amino]propanoyl]amino]-4-methylpentanoyl]amino]-3-methylbutanoyl]amino]propanoyl]amino]acetyl]amino]-5-[[(2S)-1-(carboxymethylamino)-5-(diaminomethylideneamino)-1-oxopentan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 12451 | Th1324 | Parathyroid hormone | >Th1324_Parathyroid_hormone SVSEIQLMHNLGKHLNSMERVEWLRKKLQDVHNFVALGAPLAPRDAGSQRPRKKEDNVLVESHEKSLGEADKADVNVLTKAKSQ | 9420 | C408H674N126O126S2 | NA | NA | NA | 1.5 hours. | Parathyroid hormone (PTH) is a single-chain polypeptide composed of 84 amino acids. Available as Preotact, it is an identical form of human recombinant hormome which produced as a fusion protein undergoeing post-translational processing involving the cleavage of the OmpA leader sequence, leaving the mature protein as a single-chain 84 amino-acids polypeptide (9.4 kDa). Preotact is used in the treatment of osteoporosis in postmenopausal women at high risk of osteoporotic fractures and is marketed in Europe by Nycomed. Preos is a registered trade mark owned by NPS Pharmaceuticals, Inc. The name Preos and the New Drug Application is pending approval by the U.S. Food and Drug Administration (FDA). | For use/treatment in osteoporosis. | Parathyroid hormone is responsible for the fine regulation of serum calcium concentration on a minute-to-minute basis. This is achieved by the acute effects of the hormone on calcium resorption in bone and calcium reabsorption in the kidney. The phosphate mobilized from bone is excreted into the urine by means of the hormone's influence on renal phosphate handling. Parathyroid hormone also stimulates calcium absorption in the intestine, this being mediated indirectly by 1,25-dihydroxyvitamin D. Thus, a hypocalcemic stimulus of parathyroid hormone secretion results in an increased influx of calcium from three sources (bone, kidney, and intestine), resulting in a normalization of the serum calcium concentration without change in the serum phosphate concentration. | The biological actions of rhPTH are mediated through binding to at least two distinct high- affinity cell-surface receptors specific for the N-terminal and C-terminal regions of the molecule, both of which are required for normal bone metabolism. The N-terminal portion of the molecule is primarily responsible for the bone building effects of parathyroid hormone. The C-terminal portion of the molecule has antiresorptive activity and is necessary for normal regulation of N-terminal fragment activity. | NA | PTH is primarily metabolised in the liver with lesser contributions by the kidney. Amino terminal fragments are metabolised in the liver while carboxyl terminal groups travel to the kidney for metabolism where they are also thought to have a role in regulation of PTH. Only about 30% of circulating hormone is present as the unfragmented form. | The absolute bioavailability after subcutaneous administration in the abdomen is 55% for doses of 100 micrograms. | The volume of distribution at steady-state following intravenous administration is approximately 5.4 liters with an interpatient variability of about 40%. | NA | Calcium-Regulating Hormones and Agents | NA | NA | NA | NA | Parathyroid hormone/parathyroid hormone-related peptide receptor,Parathyroid hormone 2 receptor | Natpar | Takeda Pharmaceuticals International Ag Ireland Branch | Takeda Pharmaceuticals International Ag Ireland Branch | Subcutaneous | 75 ?g | NATPARA is contraindicated in patients with a known hypersensitivity to any component of this product. Hypersensitivity reactions (e.g., anaphylaxis, angioedema, and urticaria) have occurred with NATPARA [see WARNINGS AND PRECAUTIONS, ADVERSE REACTIONS]. | Abdominal or stomach cramps or pain blurred vision confusion constipation convulsions depression difficulty with breathing dizziness dry mouth headache incoherent speech increased urination irregular heartbeats loss of appetite metallic taste muscle cramps in the hands, arms, feet, legs, or face muscle weakness nausea nervousness numbness and tingling around the mouth, fingertips, or feet pounding in the ears slow or fast heartbeat thirst tremor unusual tiredness vomiting weight loss | NA | NA | NA | NA | Link | Link | NA |
| 12452 | Th1324 | Parathyroid hormone | >Th1324_Parathyroid_hormone SVSEIQLMHNLGKHLNSMERVEWLRKKLQDVHNFVALGAPLAPRDAGSQRPRKKEDNVLVESHEKSLGEADKADVNVLTKAKSQ | 9420 | C408H674N126O126S2 | NA | NA | NA | 1.5 hours. | Parathyroid hormone (PTH) is a single-chain polypeptide composed of 84 amino acids. Available as Preotact, it is an identical form of human recombinant hormome which produced as a fusion protein undergoeing post-translational processing involving the cleavage of the OmpA leader sequence, leaving the mature protein as a single-chain 84 amino-acids polypeptide (9.4 kDa). Preotact is used in the treatment of osteoporosis in postmenopausal women at high risk of osteoporotic fractures and is marketed in Europe by Nycomed. Preos is a registered trade mark owned by NPS Pharmaceuticals, Inc. The name Preos and the New Drug Application is pending approval by the U.S. Food and Drug Administration (FDA). | For use/treatment in osteoporosis. | Parathyroid hormone is responsible for the fine regulation of serum calcium concentration on a minute-to-minute basis. This is achieved by the acute effects of the hormone on calcium resorption in bone and calcium reabsorption in the kidney. The phosphate mobilized from bone is excreted into the urine by means of the hormone's influence on renal phosphate handling. Parathyroid hormone also stimulates calcium absorption in the intestine, this being mediated indirectly by 1,25-dihydroxyvitamin D. Thus, a hypocalcemic stimulus of parathyroid hormone secretion results in an increased influx of calcium from three sources (bone, kidney, and intestine), resulting in a normalization of the serum calcium concentration without change in the serum phosphate concentration. | The biological actions of rhPTH are mediated through binding to at least two distinct high- affinity cell-surface receptors specific for the N-terminal and C-terminal regions of the molecule, both of which are required for normal bone metabolism. The N-terminal portion of the molecule is primarily responsible for the bone building effects of parathyroid hormone. The C-terminal portion of the molecule has antiresorptive activity and is necessary for normal regulation of N-terminal fragment activity. | NA | PTH is primarily metabolised in the liver with lesser contributions by the kidney. Amino terminal fragments are metabolised in the liver while carboxyl terminal groups travel to the kidney for metabolism where they are also thought to have a role in regulation of PTH. Only about 30% of circulating hormone is present as the unfragmented form. | The absolute bioavailability after subcutaneous administration in the abdomen is 55% for doses of 100 micrograms. | The volume of distribution at steady-state following intravenous administration is approximately 5.4 liters with an interpatient variability of about 40%. | NA | Hormones | NA | NA | NA | NA | Parathyroid hormone/parathyroid hormone-related peptide receptor,Parathyroid hormone 2 receptor | Natpar | Takeda Pharmaceuticals International Ag Ireland Branch | Takeda Pharmaceuticals International Ag Ireland Branch | Subcutaneous | 100 ?g | NATPARA is contraindicated in patients with a known hypersensitivity to any component of this product. Hypersensitivity reactions (e.g., anaphylaxis, angioedema, and urticaria) have occurred with NATPARA [see WARNINGS AND PRECAUTIONS, ADVERSE REACTIONS]. | Abdominal or stomach cramps or pain blurred vision confusion constipation convulsions depression difficulty with breathing dizziness dry mouth headache incoherent speech increased urination irregular heartbeats loss of appetite metallic taste muscle cramps in the hands, arms, feet, legs, or face muscle weakness nausea nervousness numbness and tingling around the mouth, fingertips, or feet pounding in the ears slow or fast heartbeat thirst tremor unusual tiredness vomiting weight loss | NA | NA | NA | NA | Link | Link | NA |
| 12453 | Th1324 | Parathyroid hormone | >Th1324_Parathyroid_hormone SVSEIQLMHNLGKHLNSMERVEWLRKKLQDVHNFVALGAPLAPRDAGSQRPRKKEDNVLVESHEKSLGEADKADVNVLTKAKSQ | 9420 | C408H674N126O126S2 | NA | NA | NA | 1.5 hours. | Parathyroid hormone (PTH) is a single-chain polypeptide composed of 84 amino acids. Available as Preotact, it is an identical form of human recombinant hormome which produced as a fusion protein undergoeing post-translational processing involving the cleavage of the OmpA leader sequence, leaving the mature protein as a single-chain 84 amino-acids polypeptide (9.4 kDa). Preotact is used in the treatment of osteoporosis in postmenopausal women at high risk of osteoporotic fractures and is marketed in Europe by Nycomed. Preos is a registered trade mark owned by NPS Pharmaceuticals, Inc. The name Preos and the New Drug Application is pending approval by the U.S. Food and Drug Administration (FDA). | For use/treatment in osteoporosis. | Parathyroid hormone is responsible for the fine regulation of serum calcium concentration on a minute-to-minute basis. This is achieved by the acute effects of the hormone on calcium resorption in bone and calcium reabsorption in the kidney. The phosphate mobilized from bone is excreted into the urine by means of the hormone's influence on renal phosphate handling. Parathyroid hormone also stimulates calcium absorption in the intestine, this being mediated indirectly by 1,25-dihydroxyvitamin D. Thus, a hypocalcemic stimulus of parathyroid hormone secretion results in an increased influx of calcium from three sources (bone, kidney, and intestine), resulting in a normalization of the serum calcium concentration without change in the serum phosphate concentration. | The biological actions of rhPTH are mediated through binding to at least two distinct high- affinity cell-surface receptors specific for the N-terminal and C-terminal regions of the molecule, both of which are required for normal bone metabolism. The N-terminal portion of the molecule is primarily responsible for the bone building effects of parathyroid hormone. The C-terminal portion of the molecule has antiresorptive activity and is necessary for normal regulation of N-terminal fragment activity. | NA | PTH is primarily metabolised in the liver with lesser contributions by the kidney. Amino terminal fragments are metabolised in the liver while carboxyl terminal groups travel to the kidney for metabolism where they are also thought to have a role in regulation of PTH. Only about 30% of circulating hormone is present as the unfragmented form. | The absolute bioavailability after subcutaneous administration in the abdomen is 55% for doses of 100 micrograms. | The volume of distribution at steady-state following intravenous administration is approximately 5.4 liters with an interpatient variability of about 40%. | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | Parathyroid hormone/parathyroid hormone-related peptide receptor,Parathyroid hormone 2 receptor | NATPARA (parathyroid hormone) | Shire-NPS Pharmaceuticals, Inc. | Shire-NPS Pharmaceuticals, Inc. | Subcutaneous | 25 ug/0.08mL | NATPARA is contraindicated in patients with a known hypersensitivity to any component of this product. Hypersensitivity reactions (e.g., anaphylaxis, angioedema, and urticaria) have occurred with NATPARA [see WARNINGS AND PRECAUTIONS, ADVERSE REACTIONS]. | Abdominal or stomach cramps or pain blurred vision confusion constipation convulsions depression difficulty with breathing dizziness dry mouth headache incoherent speech increased urination irregular heartbeats loss of appetite metallic taste muscle cramps in the hands, arms, feet, legs, or face muscle weakness nausea nervousness numbness and tingling around the mouth, fingertips, or feet pounding in the ears slow or fast heartbeat thirst tremor unusual tiredness vomiting weight loss | NA | NA | NA | NA | Link | Link | NA |
| 12454 | Th1324 | Parathyroid hormone | >Th1324_Parathyroid_hormone SVSEIQLMHNLGKHLNSMERVEWLRKKLQDVHNFVALGAPLAPRDAGSQRPRKKEDNVLVESHEKSLGEADKADVNVLTKAKSQ | 9420 | C408H674N126O126S2 | NA | NA | NA | 1.5 hours. | Parathyroid hormone (PTH) is a single-chain polypeptide composed of 84 amino acids. Available as Preotact, it is an identical form of human recombinant hormome which produced as a fusion protein undergoeing post-translational processing involving the cleavage of the OmpA leader sequence, leaving the mature protein as a single-chain 84 amino-acids polypeptide (9.4 kDa). Preotact is used in the treatment of osteoporosis in postmenopausal women at high risk of osteoporotic fractures and is marketed in Europe by Nycomed. Preos is a registered trade mark owned by NPS Pharmaceuticals, Inc. The name Preos and the New Drug Application is pending approval by the U.S. Food and Drug Administration (FDA). | For use/treatment in osteoporosis. | Parathyroid hormone is responsible for the fine regulation of serum calcium concentration on a minute-to-minute basis. This is achieved by the acute effects of the hormone on calcium resorption in bone and calcium reabsorption in the kidney. The phosphate mobilized from bone is excreted into the urine by means of the hormone's influence on renal phosphate handling. Parathyroid hormone also stimulates calcium absorption in the intestine, this being mediated indirectly by 1,25-dihydroxyvitamin D. Thus, a hypocalcemic stimulus of parathyroid hormone secretion results in an increased influx of calcium from three sources (bone, kidney, and intestine), resulting in a normalization of the serum calcium concentration without change in the serum phosphate concentration. | The biological actions of rhPTH are mediated through binding to at least two distinct high- affinity cell-surface receptors specific for the N-terminal and C-terminal regions of the molecule, both of which are required for normal bone metabolism. The N-terminal portion of the molecule is primarily responsible for the bone building effects of parathyroid hormone. The C-terminal portion of the molecule has antiresorptive activity and is necessary for normal regulation of N-terminal fragment activity. | NA | PTH is primarily metabolised in the liver with lesser contributions by the kidney. Amino terminal fragments are metabolised in the liver while carboxyl terminal groups travel to the kidney for metabolism where they are also thought to have a role in regulation of PTH. Only about 30% of circulating hormone is present as the unfragmented form. | The absolute bioavailability after subcutaneous administration in the abdomen is 55% for doses of 100 micrograms. | The volume of distribution at steady-state following intravenous administration is approximately 5.4 liters with an interpatient variability of about 40%. | NA | Parathyroid Hormones and Analogues | NA | NA | NA | NA | Parathyroid hormone/parathyroid hormone-related peptide receptor,Parathyroid hormone 2 receptor | NATPARA (parathyroid hormone) | Shire-NPS Pharmaceuticals, Inc. | Shire-NPS Pharmaceuticals, Inc. | Subcutaneous | 50 ug/0.08mL | NATPARA is contraindicated in patients with a known hypersensitivity to any component of this product. Hypersensitivity reactions (e.g., anaphylaxis, angioedema, and urticaria) have occurred with NATPARA [see WARNINGS AND PRECAUTIONS, ADVERSE REACTIONS]. | Abdominal or stomach cramps or pain blurred vision confusion constipation convulsions depression difficulty with breathing dizziness dry mouth headache incoherent speech increased urination irregular heartbeats loss of appetite metallic taste muscle cramps in the hands, arms, feet, legs, or face muscle weakness nausea nervousness numbness and tingling around the mouth, fingertips, or feet pounding in the ears slow or fast heartbeat thirst tremor unusual tiredness vomiting weight loss | NA | NA | NA | NA | Link | Link | NA |
| 12455 | Th1324 | Parathyroid hormone | >Th1324_Parathyroid_hormone SVSEIQLMHNLGKHLNSMERVEWLRKKLQDVHNFVALGAPLAPRDAGSQRPRKKEDNVLVESHEKSLGEADKADVNVLTKAKSQ | 9420 | C408H674N126O126S2 | NA | NA | NA | 1.5 hours. | Parathyroid hormone (PTH) is a single-chain polypeptide composed of 84 amino acids. Available as Preotact, it is an identical form of human recombinant hormome which produced as a fusion protein undergoeing post-translational processing involving the cleavage of the OmpA leader sequence, leaving the mature protein as a single-chain 84 amino-acids polypeptide (9.4 kDa). Preotact is used in the treatment of osteoporosis in postmenopausal women at high risk of osteoporotic fractures and is marketed in Europe by Nycomed. Preos is a registered trade mark owned by NPS Pharmaceuticals, Inc. The name Preos and the New Drug Application is pending approval by the U.S. Food and Drug Administration (FDA). | For use/treatment in osteoporosis. | Parathyroid hormone is responsible for the fine regulation of serum calcium concentration on a minute-to-minute basis. This is achieved by the acute effects of the hormone on calcium resorption in bone and calcium reabsorption in the kidney. The phosphate mobilized from bone is excreted into the urine by means of the hormone's influence on renal phosphate handling. Parathyroid hormone also stimulates calcium absorption in the intestine, this being mediated indirectly by 1,25-dihydroxyvitamin D. Thus, a hypocalcemic stimulus of parathyroid hormone secretion results in an increased influx of calcium from three sources (bone, kidney, and intestine), resulting in a normalization of the serum calcium concentration without change in the serum phosphate concentration. | The biological actions of rhPTH are mediated through binding to at least two distinct high- affinity cell-surface receptors specific for the N-terminal and C-terminal regions of the molecule, both of which are required for normal bone metabolism. The N-terminal portion of the molecule is primarily responsible for the bone building effects of parathyroid hormone. The C-terminal portion of the molecule has antiresorptive activity and is necessary for normal regulation of N-terminal fragment activity. | NA | PTH is primarily metabolised in the liver with lesser contributions by the kidney. Amino terminal fragments are metabolised in the liver while carboxyl terminal groups travel to the kidney for metabolism where they are also thought to have a role in regulation of PTH. Only about 30% of circulating hormone is present as the unfragmented form. | The absolute bioavailability after subcutaneous administration in the abdomen is 55% for doses of 100 micrograms. | The volume of distribution at steady-state following intravenous administration is approximately 5.4 liters with an interpatient variability of about 40%. | NA | Peptide Hormones | NA | NA | NA | NA | Parathyroid hormone/parathyroid hormone-related peptide receptor,Parathyroid hormone 2 receptor | NATPARA (parathyroid hormone) | Shire-NPS Pharmaceuticals, Inc. | Shire-NPS Pharmaceuticals, Inc. | Subcutaneous | 75 ug/0.08mL | NATPARA is contraindicated in patients with a known hypersensitivity to any component of this product. Hypersensitivity reactions (e.g., anaphylaxis, angioedema, and urticaria) have occurred with NATPARA [see WARNINGS AND PRECAUTIONS, ADVERSE REACTIONS]. | Abdominal or stomach cramps or pain blurred vision confusion constipation convulsions depression difficulty with breathing dizziness dry mouth headache incoherent speech increased urination irregular heartbeats loss of appetite metallic taste muscle cramps in the hands, arms, feet, legs, or face muscle weakness nausea nervousness numbness and tingling around the mouth, fingertips, or feet pounding in the ears slow or fast heartbeat thirst tremor unusual tiredness vomiting weight loss | NA | NA | NA | NA | Link | Link | NA |
| 12457 | Th1324 | Parathyroid hormone | >Th1324_Parathyroid_hormone SVSEIQLMHNLGKHLNSMERVEWLRKKLQDVHNFVALGAPLAPRDAGSQRPRKKEDNVLVESHEKSLGEADKADVNVLTKAKSQ | 9420 | C408H674N126O126S2 | NA | NA | NA | 1.5 hours. | Parathyroid hormone (PTH) is a single-chain polypeptide composed of 84 amino acids. Available as Preotact, it is an identical form of human recombinant hormome which produced as a fusion protein undergoeing post-translational processing involving the cleavage of the OmpA leader sequence, leaving the mature protein as a single-chain 84 amino-acids polypeptide (9.4 kDa). Preotact is used in the treatment of osteoporosis in postmenopausal women at high risk of osteoporotic fractures and is marketed in Europe by Nycomed. Preos is a registered trade mark owned by NPS Pharmaceuticals, Inc. The name Preos and the New Drug Application is pending approval by the U.S. Food and Drug Administration (FDA). | For use/treatment in osteoporosis. | Parathyroid hormone is responsible for the fine regulation of serum calcium concentration on a minute-to-minute basis. This is achieved by the acute effects of the hormone on calcium resorption in bone and calcium reabsorption in the kidney. The phosphate mobilized from bone is excreted into the urine by means of the hormone's influence on renal phosphate handling. Parathyroid hormone also stimulates calcium absorption in the intestine, this being mediated indirectly by 1,25-dihydroxyvitamin D. Thus, a hypocalcemic stimulus of parathyroid hormone secretion results in an increased influx of calcium from three sources (bone, kidney, and intestine), resulting in a normalization of the serum calcium concentration without change in the serum phosphate concentration. | The biological actions of rhPTH are mediated through binding to at least two distinct high- affinity cell-surface receptors specific for the N-terminal and C-terminal regions of the molecule, both of which are required for normal bone metabolism. The N-terminal portion of the molecule is primarily responsible for the bone building effects of parathyroid hormone. The C-terminal portion of the molecule has antiresorptive activity and is necessary for normal regulation of N-terminal fragment activity. | NA | PTH is primarily metabolised in the liver with lesser contributions by the kidney. Amino terminal fragments are metabolised in the liver while carboxyl terminal groups travel to the kidney for metabolism where they are also thought to have a role in regulation of PTH. Only about 30% of circulating hormone is present as the unfragmented form. | The absolute bioavailability after subcutaneous administration in the abdomen is 55% for doses of 100 micrograms. | The volume of distribution at steady-state following intravenous administration is approximately 5.4 liters with an interpatient variability of about 40%. | NA | Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | NA | Parathyroid hormone/parathyroid hormone-related peptide receptor,Parathyroid hormone 2 receptor | Preotact | Nps Pharma Holdings Limited | Nps Pharma Holdings Limited | Subcutaneous | 100 µg | NA | The most common side effects reported with Pergoveris (seen in more than 1 patient in 10) are headache, ovarian cysts and injection site reactions (e.g. pain, itching, redness, bruising, swelling or irritation at the site of injection). Treatment can cause overstimulation of the ovaries (known as ovarian hyperstimulation syndrome, OHSS), which can lead to serious medical problems. Mild or moderate OHSS is common, while severe OHSS is uncommon. | Preotact is a medicine that contains the active substance parathyroid hormone. It is available as a powder and solvent, contained within a cartridge, to be made up into a solution for injection using a special injection pen. It is also available as a pre-filled pen incorporating the cartridge containing the powder and solvent Each cartridge contains 14 doses. | Preotact is used for the treatment of osteoporosis (a disease that makes bones fragile) in postmenopausal women who are at high risk of fractures. Preotact has been shown to significantly reduce vertebral (spine) fractures, but not hip fractures. | NA | NA | Link | Link | NA |
| 12996 | Th1375 | Corifollitropin alfa | >Th1375_Corifollitropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25398.0389 | NA | NA | NA | NA | Corifollitropin alfa has a longer half-life compared with FSH and thus requires less frequent dosing [A32516]., Corifollitropin alfa has an elimination half-life of 70 hours (59-82 hours) [L2270]. | Corifollitropin alfa, also known as _Elonva_ is used in women undergoing fertility treatment to stimulate the development of more than one mature egg (oocyte) at a time in the ovaries. This drug used together with _a gonadotropin-releasing hormone (GnRH) antagonist_, a type of medicine also used in fertility treatments. Elonva is available only by prescription [L2270]. In July 2014, Merck announced the receipt of a Complete Response Letter (CRL) from the U.S. FDA for its New Drug Application for this drug. Corifollitropin alfa is marketed as Elonva in more than 75 countries [L2272]. Corifollitropin alfa is produced by a method known as ‘recombinant DNA technology’. This means that it is made by cells into which a DNA has been introduced that makes them able to produce corifollitropin alfa [L2270]. Multiple studies and a meta-analysis suggest that corifollitropin alfa is as efficacious as recombinant FSH in terms of live birth rate, ongoing pregnancy rate, as well as clinical pregnancy rate. The increased in the number of eggs retrieved under corifollitropin alfa regimen represents the elevated effectiveness of this drug, however, warns at the same time against the possibility of an increased risk of ovarian hyperstimulation in the high responder study group of women [L2276], [A32526]. | Controlled ovarian stimulation [L2273] in cases of women who are undergoing fertility treatment to stimulate the development of more than one mature egg simultaneously in the ovaries in combination with a gonadotrophin-releasing hormone (GnRH) antagonist (a type of medicine also used in fertility treatments)[L2270]. | A single dose of corifollitropin alfa could initiate and sustain multi-follicular growth in patients undergoing controlled ovarian stimulation, such as during in vitro fertilization or intracytoplasmic sperm injection [L2274]. This drug is structurally similar to follicle stimulating hormone (FSH), a hormone naturally present in females. FSH stimulates the production of eggs (ova) in the ovaries. In corifollitropin alfa, a peptide is attached to the FSH to prolong its activity. As a result, one single dose of the medicine can be administered to stimulate egg production for seven days, replacing daily injections that are normally needed with other FSH medicines [L2270]. In phase III clinical trials, the number of oocytes retrieved following the administration of corifollitropin alfa was slightly higher compared with the number observed with daily recombinant FSH treatment [L2274]. | Corifollitropin alfa is a long-lasting single injection fusion protein which lacks luteinizing hormone (LH) activity. Only one injection is needed for the first 7 days, which replaces the first 7 daily injections of traditional follicle stimulating hormone (FSH). It is a follicle-stimulation hormone (human a-subunit reduced), a combination of follicle stimulation hormone (human ß-subunit reduced) fusion protein with 118-145-chorionic gonadotropin (human ß-subunit) [L2270]. Frequent, repetitive injections increase stress and error rates, and are often a burden for women, leading to therapy noncompliance [L2277]. The agent comprises an alpha-subunit, which is identical to that of FSH, and a beta-subunit, which is produced by the fusion of the C-terminal peptide from the beta-subunit of chorionic gonadotropin to the beta-subunit of FSH [A32516]. Corifollitropin alfa serves as a sustained follicle stimulant that has similar pharmacological effects to recombinant follicle stimulating hormone (rFSH), however, with a relatively long elimination half-life, resulting in a longer duration of action. This is achieved using site-directed mutagenesis and gene transfer techniques to create a glycoprotein that consists of an a-subunit that is identical to human follicle stimulating hormone (FSH) noncovalently bound to a _ß-subunit_ comprised of a complete _ß-chain_ of human FSH elongated by the carboxyterminal peptide of the ß-subunit of human chorionic gonadotrophin (hCG) [L2271]. This unit interacts with the FSH receptor [A32516] to stimulate the release of oocytes. Corifollitropin alfa does not demonstrate any intrinsic LH/hCG activity [L2270]. | The most common side effects with Elonva (seen in between 1 and 10 patients in 100) include a headache, nausea, fatigue, pelvic pain and/or discomfort, breast tenderness and ovarian hyperstimulation syndrome (OHSS). This syndrome occurs when the ovaries have a heightened response to therapy, leading to abdominal swelling and pain, nausea and diarrhea [L2270]. More than one injection of Elonva within one treatment cycle or an excessively high dose of Elonva and/or (rec)FSH can increase the risk of ovarian hyperstimulation syndrome [L2270], which may cause swollen or painful ovaries, abdominal bloating, nausea, and a weight gain of up to 3kg [L2275]. In severe cases, ovarian hyperstimulation syndrome may cause rapid weight gain ranging from 15 to 20 kilograms in 5-10 days. Severe abdominal pain, severe, persistent nausea, and vomiting, decreased urination, and abdominal bloating, as well as other generalized symptoms, may occur [L2275]. About 1 - 2 % of women undergoing ovarian stimulation develop a severe form of ovarian hyperstimulation syndrome (OHSS). Severe OHSS can be life-threatening. Complications may include: ascites, pulmonary edema, electrolyte disturbances (sodium, potassium, others), thrombosis in large vessels, usually in the lower extremities, renal failure, ovarian torsion, rupture of ovarian cysts. Some of these conditions can lead to hemorrhage, respiratory failure, spontaneous miscarriage or pregnancy termination due to complications, resulting in death [L2270]. | The metabolic fate of corifollitropin alfa highly resembles that of endogenous glycoprotein hormones, which predominantly is comprised of kidney clearance and the urinary excretion of the intact protein in parallel to kidney catabolism [A32519]. | After one single subcutaneous injection of this drug, the maximal serum concentration is 4.24 ng/mL (2.49-7.21 ng/mL1) and is reached 44 hours (35-57 h) post-dose administration. Its absolute bioavailability is 58% (48-70%) [L2270]. | Distribution, metabolism and elimination of corifollitropin alfa are very similar to other gonadotropins, such as FSH, hCG and LH [L2273]. After absorption into the blood, corifollitropin alfa is distributed mainly to the ovaries and the kidneys. The steady-state volume of distribution is 9.2 L [L2273]. Exposure to corifollitropin alfa increases in a linear fashion with the dose within a range of 60 micrograms - 240 micrograms [L2270]. | 0.13 L/h (0.10-0.18 L/h1) [L2270] | Genito Urinary System and Sex Hormones | NA | NA | NA | NA | Follicle-stimulating hormone receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12999 | Th1375 | Corifollitropin alfa | >Th1375_Corifollitropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25398.0389 | NA | NA | NA | NA | Corifollitropin alfa has a longer half-life compared with FSH and thus requires less frequent dosing [A32516]., Corifollitropin alfa has an elimination half-life of 70 hours (59-82 hours) [L2270]. | Corifollitropin alfa, also known as _Elonva_ is used in women undergoing fertility treatment to stimulate the development of more than one mature egg (oocyte) at a time in the ovaries. This drug used together with _a gonadotropin-releasing hormone (GnRH) antagonist_, a type of medicine also used in fertility treatments. Elonva is available only by prescription [L2270]. In July 2014, Merck announced the receipt of a Complete Response Letter (CRL) from the U.S. FDA for its New Drug Application for this drug. Corifollitropin alfa is marketed as Elonva in more than 75 countries [L2272]. Corifollitropin alfa is produced by a method known as ‘recombinant DNA technology’. This means that it is made by cells into which a DNA has been introduced that makes them able to produce corifollitropin alfa [L2270]. Multiple studies and a meta-analysis suggest that corifollitropin alfa is as efficacious as recombinant FSH in terms of live birth rate, ongoing pregnancy rate, as well as clinical pregnancy rate. The increased in the number of eggs retrieved under corifollitropin alfa regimen represents the elevated effectiveness of this drug, however, warns at the same time against the possibility of an increased risk of ovarian hyperstimulation in the high responder study group of women [L2276], [A32526]. | Controlled ovarian stimulation [L2273] in cases of women who are undergoing fertility treatment to stimulate the development of more than one mature egg simultaneously in the ovaries in combination with a gonadotrophin-releasing hormone (GnRH) antagonist (a type of medicine also used in fertility treatments)[L2270]. | A single dose of corifollitropin alfa could initiate and sustain multi-follicular growth in patients undergoing controlled ovarian stimulation, such as during in vitro fertilization or intracytoplasmic sperm injection [L2274]. This drug is structurally similar to follicle stimulating hormone (FSH), a hormone naturally present in females. FSH stimulates the production of eggs (ova) in the ovaries. In corifollitropin alfa, a peptide is attached to the FSH to prolong its activity. As a result, one single dose of the medicine can be administered to stimulate egg production for seven days, replacing daily injections that are normally needed with other FSH medicines [L2270]. In phase III clinical trials, the number of oocytes retrieved following the administration of corifollitropin alfa was slightly higher compared with the number observed with daily recombinant FSH treatment [L2274]. | Corifollitropin alfa is a long-lasting single injection fusion protein which lacks luteinizing hormone (LH) activity. Only one injection is needed for the first 7 days, which replaces the first 7 daily injections of traditional follicle stimulating hormone (FSH). It is a follicle-stimulation hormone (human a-subunit reduced), a combination of follicle stimulation hormone (human ß-subunit reduced) fusion protein with 118-145-chorionic gonadotropin (human ß-subunit) [L2270]. Frequent, repetitive injections increase stress and error rates, and are often a burden for women, leading to therapy noncompliance [L2277]. The agent comprises an alpha-subunit, which is identical to that of FSH, and a beta-subunit, which is produced by the fusion of the C-terminal peptide from the beta-subunit of chorionic gonadotropin to the beta-subunit of FSH [A32516]. Corifollitropin alfa serves as a sustained follicle stimulant that has similar pharmacological effects to recombinant follicle stimulating hormone (rFSH), however, with a relatively long elimination half-life, resulting in a longer duration of action. This is achieved using site-directed mutagenesis and gene transfer techniques to create a glycoprotein that consists of an a-subunit that is identical to human follicle stimulating hormone (FSH) noncovalently bound to a _ß-subunit_ comprised of a complete _ß-chain_ of human FSH elongated by the carboxyterminal peptide of the ß-subunit of human chorionic gonadotrophin (hCG) [L2271]. This unit interacts with the FSH receptor [A32516] to stimulate the release of oocytes. Corifollitropin alfa does not demonstrate any intrinsic LH/hCG activity [L2270]. | The most common side effects with Elonva (seen in between 1 and 10 patients in 100) include a headache, nausea, fatigue, pelvic pain and/or discomfort, breast tenderness and ovarian hyperstimulation syndrome (OHSS). This syndrome occurs when the ovaries have a heightened response to therapy, leading to abdominal swelling and pain, nausea and diarrhea [L2270]. More than one injection of Elonva within one treatment cycle or an excessively high dose of Elonva and/or (rec)FSH can increase the risk of ovarian hyperstimulation syndrome [L2270], which may cause swollen or painful ovaries, abdominal bloating, nausea, and a weight gain of up to 3kg [L2275]. In severe cases, ovarian hyperstimulation syndrome may cause rapid weight gain ranging from 15 to 20 kilograms in 5-10 days. Severe abdominal pain, severe, persistent nausea, and vomiting, decreased urination, and abdominal bloating, as well as other generalized symptoms, may occur [L2275]. About 1 - 2 % of women undergoing ovarian stimulation develop a severe form of ovarian hyperstimulation syndrome (OHSS). Severe OHSS can be life-threatening. Complications may include: ascites, pulmonary edema, electrolyte disturbances (sodium, potassium, others), thrombosis in large vessels, usually in the lower extremities, renal failure, ovarian torsion, rupture of ovarian cysts. Some of these conditions can lead to hemorrhage, respiratory failure, spontaneous miscarriage or pregnancy termination due to complications, resulting in death [L2270]. | The metabolic fate of corifollitropin alfa highly resembles that of endogenous glycoprotein hormones, which predominantly is comprised of kidney clearance and the urinary excretion of the intact protein in parallel to kidney catabolism [A32519]. | After one single subcutaneous injection of this drug, the maximal serum concentration is 4.24 ng/mL (2.49-7.21 ng/mL1) and is reached 44 hours (35-57 h) post-dose administration. Its absolute bioavailability is 58% (48-70%) [L2270]. | Distribution, metabolism and elimination of corifollitropin alfa are very similar to other gonadotropins, such as FSH, hCG and LH [L2273]. After absorption into the blood, corifollitropin alfa is distributed mainly to the ovaries and the kidneys. The steady-state volume of distribution is 9.2 L [L2273]. Exposure to corifollitropin alfa increases in a linear fashion with the dose within a range of 60 micrograms - 240 micrograms [L2270]. | 0.13 L/h (0.10-0.18 L/h1) [L2270] | Hormones | NA | NA | NA | NA | Follicle-stimulating hormone receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13000 | Th1375 | Corifollitropin alfa | >Th1375_Corifollitropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25398.0389 | NA | NA | NA | NA | Corifollitropin alfa has a longer half-life compared with FSH and thus requires less frequent dosing [A32516]., Corifollitropin alfa has an elimination half-life of 70 hours (59-82 hours) [L2270]. | Corifollitropin alfa, also known as _Elonva_ is used in women undergoing fertility treatment to stimulate the development of more than one mature egg (oocyte) at a time in the ovaries. This drug used together with _a gonadotropin-releasing hormone (GnRH) antagonist_, a type of medicine also used in fertility treatments. Elonva is available only by prescription [L2270]. In July 2014, Merck announced the receipt of a Complete Response Letter (CRL) from the U.S. FDA for its New Drug Application for this drug. Corifollitropin alfa is marketed as Elonva in more than 75 countries [L2272]. Corifollitropin alfa is produced by a method known as ‘recombinant DNA technology’. This means that it is made by cells into which a DNA has been introduced that makes them able to produce corifollitropin alfa [L2270]. Multiple studies and a meta-analysis suggest that corifollitropin alfa is as efficacious as recombinant FSH in terms of live birth rate, ongoing pregnancy rate, as well as clinical pregnancy rate. The increased in the number of eggs retrieved under corifollitropin alfa regimen represents the elevated effectiveness of this drug, however, warns at the same time against the possibility of an increased risk of ovarian hyperstimulation in the high responder study group of women [L2276], [A32526]. | Controlled ovarian stimulation [L2273] in cases of women who are undergoing fertility treatment to stimulate the development of more than one mature egg simultaneously in the ovaries in combination with a gonadotrophin-releasing hormone (GnRH) antagonist (a type of medicine also used in fertility treatments)[L2270]. | A single dose of corifollitropin alfa could initiate and sustain multi-follicular growth in patients undergoing controlled ovarian stimulation, such as during in vitro fertilization or intracytoplasmic sperm injection [L2274]. This drug is structurally similar to follicle stimulating hormone (FSH), a hormone naturally present in females. FSH stimulates the production of eggs (ova) in the ovaries. In corifollitropin alfa, a peptide is attached to the FSH to prolong its activity. As a result, one single dose of the medicine can be administered to stimulate egg production for seven days, replacing daily injections that are normally needed with other FSH medicines [L2270]. In phase III clinical trials, the number of oocytes retrieved following the administration of corifollitropin alfa was slightly higher compared with the number observed with daily recombinant FSH treatment [L2274]. | Corifollitropin alfa is a long-lasting single injection fusion protein which lacks luteinizing hormone (LH) activity. Only one injection is needed for the first 7 days, which replaces the first 7 daily injections of traditional follicle stimulating hormone (FSH). It is a follicle-stimulation hormone (human a-subunit reduced), a combination of follicle stimulation hormone (human ß-subunit reduced) fusion protein with 118-145-chorionic gonadotropin (human ß-subunit) [L2270]. Frequent, repetitive injections increase stress and error rates, and are often a burden for women, leading to therapy noncompliance [L2277]. The agent comprises an alpha-subunit, which is identical to that of FSH, and a beta-subunit, which is produced by the fusion of the C-terminal peptide from the beta-subunit of chorionic gonadotropin to the beta-subunit of FSH [A32516]. Corifollitropin alfa serves as a sustained follicle stimulant that has similar pharmacological effects to recombinant follicle stimulating hormone (rFSH), however, with a relatively long elimination half-life, resulting in a longer duration of action. This is achieved using site-directed mutagenesis and gene transfer techniques to create a glycoprotein that consists of an a-subunit that is identical to human follicle stimulating hormone (FSH) noncovalently bound to a _ß-subunit_ comprised of a complete _ß-chain_ of human FSH elongated by the carboxyterminal peptide of the ß-subunit of human chorionic gonadotrophin (hCG) [L2271]. This unit interacts with the FSH receptor [A32516] to stimulate the release of oocytes. Corifollitropin alfa does not demonstrate any intrinsic LH/hCG activity [L2270]. | The most common side effects with Elonva (seen in between 1 and 10 patients in 100) include a headache, nausea, fatigue, pelvic pain and/or discomfort, breast tenderness and ovarian hyperstimulation syndrome (OHSS). This syndrome occurs when the ovaries have a heightened response to therapy, leading to abdominal swelling and pain, nausea and diarrhea [L2270]. More than one injection of Elonva within one treatment cycle or an excessively high dose of Elonva and/or (rec)FSH can increase the risk of ovarian hyperstimulation syndrome [L2270], which may cause swollen or painful ovaries, abdominal bloating, nausea, and a weight gain of up to 3kg [L2275]. In severe cases, ovarian hyperstimulation syndrome may cause rapid weight gain ranging from 15 to 20 kilograms in 5-10 days. Severe abdominal pain, severe, persistent nausea, and vomiting, decreased urination, and abdominal bloating, as well as other generalized symptoms, may occur [L2275]. About 1 - 2 % of women undergoing ovarian stimulation develop a severe form of ovarian hyperstimulation syndrome (OHSS). Severe OHSS can be life-threatening. Complications may include: ascites, pulmonary edema, electrolyte disturbances (sodium, potassium, others), thrombosis in large vessels, usually in the lower extremities, renal failure, ovarian torsion, rupture of ovarian cysts. Some of these conditions can lead to hemorrhage, respiratory failure, spontaneous miscarriage or pregnancy termination due to complications, resulting in death [L2270]. | The metabolic fate of corifollitropin alfa highly resembles that of endogenous glycoprotein hormones, which predominantly is comprised of kidney clearance and the urinary excretion of the intact protein in parallel to kidney catabolism [A32519]. | After one single subcutaneous injection of this drug, the maximal serum concentration is 4.24 ng/mL (2.49-7.21 ng/mL1) and is reached 44 hours (35-57 h) post-dose administration. Its absolute bioavailability is 58% (48-70%) [L2270]. | Distribution, metabolism and elimination of corifollitropin alfa are very similar to other gonadotropins, such as FSH, hCG and LH [L2273]. After absorption into the blood, corifollitropin alfa is distributed mainly to the ovaries and the kidneys. The steady-state volume of distribution is 9.2 L [L2273]. Exposure to corifollitropin alfa increases in a linear fashion with the dose within a range of 60 micrograms - 240 micrograms [L2270]. | 0.13 L/h (0.10-0.18 L/h1) [L2270] | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | Follicle-stimulating hormone receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13001 | Th1375 | Corifollitropin alfa | >Th1375_Corifollitropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25398.0389 | NA | NA | NA | NA | Corifollitropin alfa has a longer half-life compared with FSH and thus requires less frequent dosing [A32516]., Corifollitropin alfa has an elimination half-life of 70 hours (59-82 hours) [L2270]. | Corifollitropin alfa, also known as _Elonva_ is used in women undergoing fertility treatment to stimulate the development of more than one mature egg (oocyte) at a time in the ovaries. This drug used together with _a gonadotropin-releasing hormone (GnRH) antagonist_, a type of medicine also used in fertility treatments. Elonva is available only by prescription [L2270]. In July 2014, Merck announced the receipt of a Complete Response Letter (CRL) from the U.S. FDA for its New Drug Application for this drug. Corifollitropin alfa is marketed as Elonva in more than 75 countries [L2272]. Corifollitropin alfa is produced by a method known as ‘recombinant DNA technology’. This means that it is made by cells into which a DNA has been introduced that makes them able to produce corifollitropin alfa [L2270]. Multiple studies and a meta-analysis suggest that corifollitropin alfa is as efficacious as recombinant FSH in terms of live birth rate, ongoing pregnancy rate, as well as clinical pregnancy rate. The increased in the number of eggs retrieved under corifollitropin alfa regimen represents the elevated effectiveness of this drug, however, warns at the same time against the possibility of an increased risk of ovarian hyperstimulation in the high responder study group of women [L2276], [A32526]. | Controlled ovarian stimulation [L2273] in cases of women who are undergoing fertility treatment to stimulate the development of more than one mature egg simultaneously in the ovaries in combination with a gonadotrophin-releasing hormone (GnRH) antagonist (a type of medicine also used in fertility treatments)[L2270]. | A single dose of corifollitropin alfa could initiate and sustain multi-follicular growth in patients undergoing controlled ovarian stimulation, such as during in vitro fertilization or intracytoplasmic sperm injection [L2274]. This drug is structurally similar to follicle stimulating hormone (FSH), a hormone naturally present in females. FSH stimulates the production of eggs (ova) in the ovaries. In corifollitropin alfa, a peptide is attached to the FSH to prolong its activity. As a result, one single dose of the medicine can be administered to stimulate egg production for seven days, replacing daily injections that are normally needed with other FSH medicines [L2270]. In phase III clinical trials, the number of oocytes retrieved following the administration of corifollitropin alfa was slightly higher compared with the number observed with daily recombinant FSH treatment [L2274]. | Corifollitropin alfa is a long-lasting single injection fusion protein which lacks luteinizing hormone (LH) activity. Only one injection is needed for the first 7 days, which replaces the first 7 daily injections of traditional follicle stimulating hormone (FSH). It is a follicle-stimulation hormone (human a-subunit reduced), a combination of follicle stimulation hormone (human ß-subunit reduced) fusion protein with 118-145-chorionic gonadotropin (human ß-subunit) [L2270]. Frequent, repetitive injections increase stress and error rates, and are often a burden for women, leading to therapy noncompliance [L2277]. The agent comprises an alpha-subunit, which is identical to that of FSH, and a beta-subunit, which is produced by the fusion of the C-terminal peptide from the beta-subunit of chorionic gonadotropin to the beta-subunit of FSH [A32516]. Corifollitropin alfa serves as a sustained follicle stimulant that has similar pharmacological effects to recombinant follicle stimulating hormone (rFSH), however, with a relatively long elimination half-life, resulting in a longer duration of action. This is achieved using site-directed mutagenesis and gene transfer techniques to create a glycoprotein that consists of an a-subunit that is identical to human follicle stimulating hormone (FSH) noncovalently bound to a _ß-subunit_ comprised of a complete _ß-chain_ of human FSH elongated by the carboxyterminal peptide of the ß-subunit of human chorionic gonadotrophin (hCG) [L2271]. This unit interacts with the FSH receptor [A32516] to stimulate the release of oocytes. Corifollitropin alfa does not demonstrate any intrinsic LH/hCG activity [L2270]. | The most common side effects with Elonva (seen in between 1 and 10 patients in 100) include a headache, nausea, fatigue, pelvic pain and/or discomfort, breast tenderness and ovarian hyperstimulation syndrome (OHSS). This syndrome occurs when the ovaries have a heightened response to therapy, leading to abdominal swelling and pain, nausea and diarrhea [L2270]. More than one injection of Elonva within one treatment cycle or an excessively high dose of Elonva and/or (rec)FSH can increase the risk of ovarian hyperstimulation syndrome [L2270], which may cause swollen or painful ovaries, abdominal bloating, nausea, and a weight gain of up to 3kg [L2275]. In severe cases, ovarian hyperstimulation syndrome may cause rapid weight gain ranging from 15 to 20 kilograms in 5-10 days. Severe abdominal pain, severe, persistent nausea, and vomiting, decreased urination, and abdominal bloating, as well as other generalized symptoms, may occur [L2275]. About 1 - 2 % of women undergoing ovarian stimulation develop a severe form of ovarian hyperstimulation syndrome (OHSS). Severe OHSS can be life-threatening. Complications may include: ascites, pulmonary edema, electrolyte disturbances (sodium, potassium, others), thrombosis in large vessels, usually in the lower extremities, renal failure, ovarian torsion, rupture of ovarian cysts. Some of these conditions can lead to hemorrhage, respiratory failure, spontaneous miscarriage or pregnancy termination due to complications, resulting in death [L2270]. | The metabolic fate of corifollitropin alfa highly resembles that of endogenous glycoprotein hormones, which predominantly is comprised of kidney clearance and the urinary excretion of the intact protein in parallel to kidney catabolism [A32519]. | After one single subcutaneous injection of this drug, the maximal serum concentration is 4.24 ng/mL (2.49-7.21 ng/mL1) and is reached 44 hours (35-57 h) post-dose administration. Its absolute bioavailability is 58% (48-70%) [L2270]. | Distribution, metabolism and elimination of corifollitropin alfa are very similar to other gonadotropins, such as FSH, hCG and LH [L2273]. After absorption into the blood, corifollitropin alfa is distributed mainly to the ovaries and the kidneys. The steady-state volume of distribution is 9.2 L [L2273]. Exposure to corifollitropin alfa increases in a linear fashion with the dose within a range of 60 micrograms - 240 micrograms [L2270]. | 0.13 L/h (0.10-0.18 L/h1) [L2270] | Peptide Hormones | NA | NA | NA | NA | Follicle-stimulating hormone receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13003 | Th1375 | Corifollitropin alfa | >Th1375_Corifollitropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25398.0389 | NA | NA | NA | NA | Corifollitropin alfa has a longer half-life compared with FSH and thus requires less frequent dosing [A32516]., Corifollitropin alfa has an elimination half-life of 70 hours (59-82 hours) [L2270]. | Corifollitropin alfa, also known as _Elonva_ is used in women undergoing fertility treatment to stimulate the development of more than one mature egg (oocyte) at a time in the ovaries. This drug used together with _a gonadotropin-releasing hormone (GnRH) antagonist_, a type of medicine also used in fertility treatments. Elonva is available only by prescription [L2270]. In July 2014, Merck announced the receipt of a Complete Response Letter (CRL) from the U.S. FDA for its New Drug Application for this drug. Corifollitropin alfa is marketed as Elonva in more than 75 countries [L2272]. Corifollitropin alfa is produced by a method known as ‘recombinant DNA technology’. This means that it is made by cells into which a DNA has been introduced that makes them able to produce corifollitropin alfa [L2270]. Multiple studies and a meta-analysis suggest that corifollitropin alfa is as efficacious as recombinant FSH in terms of live birth rate, ongoing pregnancy rate, as well as clinical pregnancy rate. The increased in the number of eggs retrieved under corifollitropin alfa regimen represents the elevated effectiveness of this drug, however, warns at the same time against the possibility of an increased risk of ovarian hyperstimulation in the high responder study group of women [L2276], [A32526]. | Controlled ovarian stimulation [L2273] in cases of women who are undergoing fertility treatment to stimulate the development of more than one mature egg simultaneously in the ovaries in combination with a gonadotrophin-releasing hormone (GnRH) antagonist (a type of medicine also used in fertility treatments)[L2270]. | A single dose of corifollitropin alfa could initiate and sustain multi-follicular growth in patients undergoing controlled ovarian stimulation, such as during in vitro fertilization or intracytoplasmic sperm injection [L2274]. This drug is structurally similar to follicle stimulating hormone (FSH), a hormone naturally present in females. FSH stimulates the production of eggs (ova) in the ovaries. In corifollitropin alfa, a peptide is attached to the FSH to prolong its activity. As a result, one single dose of the medicine can be administered to stimulate egg production for seven days, replacing daily injections that are normally needed with other FSH medicines [L2270]. In phase III clinical trials, the number of oocytes retrieved following the administration of corifollitropin alfa was slightly higher compared with the number observed with daily recombinant FSH treatment [L2274]. | Corifollitropin alfa is a long-lasting single injection fusion protein which lacks luteinizing hormone (LH) activity. Only one injection is needed for the first 7 days, which replaces the first 7 daily injections of traditional follicle stimulating hormone (FSH). It is a follicle-stimulation hormone (human a-subunit reduced), a combination of follicle stimulation hormone (human ß-subunit reduced) fusion protein with 118-145-chorionic gonadotropin (human ß-subunit) [L2270]. Frequent, repetitive injections increase stress and error rates, and are often a burden for women, leading to therapy noncompliance [L2277]. The agent comprises an alpha-subunit, which is identical to that of FSH, and a beta-subunit, which is produced by the fusion of the C-terminal peptide from the beta-subunit of chorionic gonadotropin to the beta-subunit of FSH [A32516]. Corifollitropin alfa serves as a sustained follicle stimulant that has similar pharmacological effects to recombinant follicle stimulating hormone (rFSH), however, with a relatively long elimination half-life, resulting in a longer duration of action. This is achieved using site-directed mutagenesis and gene transfer techniques to create a glycoprotein that consists of an a-subunit that is identical to human follicle stimulating hormone (FSH) noncovalently bound to a _ß-subunit_ comprised of a complete _ß-chain_ of human FSH elongated by the carboxyterminal peptide of the ß-subunit of human chorionic gonadotrophin (hCG) [L2271]. This unit interacts with the FSH receptor [A32516] to stimulate the release of oocytes. Corifollitropin alfa does not demonstrate any intrinsic LH/hCG activity [L2270]. | The most common side effects with Elonva (seen in between 1 and 10 patients in 100) include a headache, nausea, fatigue, pelvic pain and/or discomfort, breast tenderness and ovarian hyperstimulation syndrome (OHSS). This syndrome occurs when the ovaries have a heightened response to therapy, leading to abdominal swelling and pain, nausea and diarrhea [L2270]. More than one injection of Elonva within one treatment cycle or an excessively high dose of Elonva and/or (rec)FSH can increase the risk of ovarian hyperstimulation syndrome [L2270], which may cause swollen or painful ovaries, abdominal bloating, nausea, and a weight gain of up to 3kg [L2275]. In severe cases, ovarian hyperstimulation syndrome may cause rapid weight gain ranging from 15 to 20 kilograms in 5-10 days. Severe abdominal pain, severe, persistent nausea, and vomiting, decreased urination, and abdominal bloating, as well as other generalized symptoms, may occur [L2275]. About 1 - 2 % of women undergoing ovarian stimulation develop a severe form of ovarian hyperstimulation syndrome (OHSS). Severe OHSS can be life-threatening. Complications may include: ascites, pulmonary edema, electrolyte disturbances (sodium, potassium, others), thrombosis in large vessels, usually in the lower extremities, renal failure, ovarian torsion, rupture of ovarian cysts. Some of these conditions can lead to hemorrhage, respiratory failure, spontaneous miscarriage or pregnancy termination due to complications, resulting in death [L2270]. | The metabolic fate of corifollitropin alfa highly resembles that of endogenous glycoprotein hormones, which predominantly is comprised of kidney clearance and the urinary excretion of the intact protein in parallel to kidney catabolism [A32519]. | After one single subcutaneous injection of this drug, the maximal serum concentration is 4.24 ng/mL (2.49-7.21 ng/mL1) and is reached 44 hours (35-57 h) post-dose administration. Its absolute bioavailability is 58% (48-70%) [L2270]. | Distribution, metabolism and elimination of corifollitropin alfa are very similar to other gonadotropins, such as FSH, hCG and LH [L2273]. After absorption into the blood, corifollitropin alfa is distributed mainly to the ovaries and the kidneys. The steady-state volume of distribution is 9.2 L [L2273]. Exposure to corifollitropin alfa increases in a linear fashion with the dose within a range of 60 micrograms - 240 micrograms [L2270]. | 0.13 L/h (0.10-0.18 L/h1) [L2270] | Pituitary Hormones | NA | NA | NA | NA | Follicle-stimulating hormone receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13004 | Th1375 | Corifollitropin alfa | >Th1375_Corifollitropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25398.0389 | NA | NA | NA | NA | Corifollitropin alfa has a longer half-life compared with FSH and thus requires less frequent dosing [A32516]., Corifollitropin alfa has an elimination half-life of 70 hours (59-82 hours) [L2270]. | Corifollitropin alfa, also known as _Elonva_ is used in women undergoing fertility treatment to stimulate the development of more than one mature egg (oocyte) at a time in the ovaries. This drug used together with _a gonadotropin-releasing hormone (GnRH) antagonist_, a type of medicine also used in fertility treatments. Elonva is available only by prescription [L2270]. In July 2014, Merck announced the receipt of a Complete Response Letter (CRL) from the U.S. FDA for its New Drug Application for this drug. Corifollitropin alfa is marketed as Elonva in more than 75 countries [L2272]. Corifollitropin alfa is produced by a method known as ‘recombinant DNA technology’. This means that it is made by cells into which a DNA has been introduced that makes them able to produce corifollitropin alfa [L2270]. Multiple studies and a meta-analysis suggest that corifollitropin alfa is as efficacious as recombinant FSH in terms of live birth rate, ongoing pregnancy rate, as well as clinical pregnancy rate. The increased in the number of eggs retrieved under corifollitropin alfa regimen represents the elevated effectiveness of this drug, however, warns at the same time against the possibility of an increased risk of ovarian hyperstimulation in the high responder study group of women [L2276], [A32526]. | Controlled ovarian stimulation [L2273] in cases of women who are undergoing fertility treatment to stimulate the development of more than one mature egg simultaneously in the ovaries in combination with a gonadotrophin-releasing hormone (GnRH) antagonist (a type of medicine also used in fertility treatments)[L2270]. | A single dose of corifollitropin alfa could initiate and sustain multi-follicular growth in patients undergoing controlled ovarian stimulation, such as during in vitro fertilization or intracytoplasmic sperm injection [L2274]. This drug is structurally similar to follicle stimulating hormone (FSH), a hormone naturally present in females. FSH stimulates the production of eggs (ova) in the ovaries. In corifollitropin alfa, a peptide is attached to the FSH to prolong its activity. As a result, one single dose of the medicine can be administered to stimulate egg production for seven days, replacing daily injections that are normally needed with other FSH medicines [L2270]. In phase III clinical trials, the number of oocytes retrieved following the administration of corifollitropin alfa was slightly higher compared with the number observed with daily recombinant FSH treatment [L2274]. | Corifollitropin alfa is a long-lasting single injection fusion protein which lacks luteinizing hormone (LH) activity. Only one injection is needed for the first 7 days, which replaces the first 7 daily injections of traditional follicle stimulating hormone (FSH). It is a follicle-stimulation hormone (human a-subunit reduced), a combination of follicle stimulation hormone (human ß-subunit reduced) fusion protein with 118-145-chorionic gonadotropin (human ß-subunit) [L2270]. Frequent, repetitive injections increase stress and error rates, and are often a burden for women, leading to therapy noncompliance [L2277]. The agent comprises an alpha-subunit, which is identical to that of FSH, and a beta-subunit, which is produced by the fusion of the C-terminal peptide from the beta-subunit of chorionic gonadotropin to the beta-subunit of FSH [A32516]. Corifollitropin alfa serves as a sustained follicle stimulant that has similar pharmacological effects to recombinant follicle stimulating hormone (rFSH), however, with a relatively long elimination half-life, resulting in a longer duration of action. This is achieved using site-directed mutagenesis and gene transfer techniques to create a glycoprotein that consists of an a-subunit that is identical to human follicle stimulating hormone (FSH) noncovalently bound to a _ß-subunit_ comprised of a complete _ß-chain_ of human FSH elongated by the carboxyterminal peptide of the ß-subunit of human chorionic gonadotrophin (hCG) [L2271]. This unit interacts with the FSH receptor [A32516] to stimulate the release of oocytes. Corifollitropin alfa does not demonstrate any intrinsic LH/hCG activity [L2270]. | The most common side effects with Elonva (seen in between 1 and 10 patients in 100) include a headache, nausea, fatigue, pelvic pain and/or discomfort, breast tenderness and ovarian hyperstimulation syndrome (OHSS). This syndrome occurs when the ovaries have a heightened response to therapy, leading to abdominal swelling and pain, nausea and diarrhea [L2270]. More than one injection of Elonva within one treatment cycle or an excessively high dose of Elonva and/or (rec)FSH can increase the risk of ovarian hyperstimulation syndrome [L2270], which may cause swollen or painful ovaries, abdominal bloating, nausea, and a weight gain of up to 3kg [L2275]. In severe cases, ovarian hyperstimulation syndrome may cause rapid weight gain ranging from 15 to 20 kilograms in 5-10 days. Severe abdominal pain, severe, persistent nausea, and vomiting, decreased urination, and abdominal bloating, as well as other generalized symptoms, may occur [L2275]. About 1 - 2 % of women undergoing ovarian stimulation develop a severe form of ovarian hyperstimulation syndrome (OHSS). Severe OHSS can be life-threatening. Complications may include: ascites, pulmonary edema, electrolyte disturbances (sodium, potassium, others), thrombosis in large vessels, usually in the lower extremities, renal failure, ovarian torsion, rupture of ovarian cysts. Some of these conditions can lead to hemorrhage, respiratory failure, spontaneous miscarriage or pregnancy termination due to complications, resulting in death [L2270]. | The metabolic fate of corifollitropin alfa highly resembles that of endogenous glycoprotein hormones, which predominantly is comprised of kidney clearance and the urinary excretion of the intact protein in parallel to kidney catabolism [A32519]. | After one single subcutaneous injection of this drug, the maximal serum concentration is 4.24 ng/mL (2.49-7.21 ng/mL1) and is reached 44 hours (35-57 h) post-dose administration. Its absolute bioavailability is 58% (48-70%) [L2270]. | Distribution, metabolism and elimination of corifollitropin alfa are very similar to other gonadotropins, such as FSH, hCG and LH [L2273]. After absorption into the blood, corifollitropin alfa is distributed mainly to the ovaries and the kidneys. The steady-state volume of distribution is 9.2 L [L2273]. Exposure to corifollitropin alfa increases in a linear fashion with the dose within a range of 60 micrograms - 240 micrograms [L2270]. | 0.13 L/h (0.10-0.18 L/h1) [L2270] | Pituitary Hormones, Anterior | NA | NA | NA | NA | Follicle-stimulating hormone receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13006 | Th1375 | Corifollitropin alfa | >Th1375_Corifollitropin_alfa APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | 25398.0389 | NA | NA | NA | NA | Corifollitropin alfa has a longer half-life compared with FSH and thus requires less frequent dosing [A32516]., Corifollitropin alfa has an elimination half-life of 70 hours (59-82 hours) [L2270]. | Corifollitropin alfa, also known as _Elonva_ is used in women undergoing fertility treatment to stimulate the development of more than one mature egg (oocyte) at a time in the ovaries. This drug used together with _a gonadotropin-releasing hormone (GnRH) antagonist_, a type of medicine also used in fertility treatments. Elonva is available only by prescription [L2270]. In July 2014, Merck announced the receipt of a Complete Response Letter (CRL) from the U.S. FDA for its New Drug Application for this drug. Corifollitropin alfa is marketed as Elonva in more than 75 countries [L2272]. Corifollitropin alfa is produced by a method known as ‘recombinant DNA technology’. This means that it is made by cells into which a DNA has been introduced that makes them able to produce corifollitropin alfa [L2270]. Multiple studies and a meta-analysis suggest that corifollitropin alfa is as efficacious as recombinant FSH in terms of live birth rate, ongoing pregnancy rate, as well as clinical pregnancy rate. The increased in the number of eggs retrieved under corifollitropin alfa regimen represents the elevated effectiveness of this drug, however, warns at the same time against the possibility of an increased risk of ovarian hyperstimulation in the high responder study group of women [L2276], [A32526]. | Controlled ovarian stimulation [L2273] in cases of women who are undergoing fertility treatment to stimulate the development of more than one mature egg simultaneously in the ovaries in combination with a gonadotrophin-releasing hormone (GnRH) antagonist (a type of medicine also used in fertility treatments)[L2270]. | A single dose of corifollitropin alfa could initiate and sustain multi-follicular growth in patients undergoing controlled ovarian stimulation, such as during in vitro fertilization or intracytoplasmic sperm injection [L2274]. This drug is structurally similar to follicle stimulating hormone (FSH), a hormone naturally present in females. FSH stimulates the production of eggs (ova) in the ovaries. In corifollitropin alfa, a peptide is attached to the FSH to prolong its activity. As a result, one single dose of the medicine can be administered to stimulate egg production for seven days, replacing daily injections that are normally needed with other FSH medicines [L2270]. In phase III clinical trials, the number of oocytes retrieved following the administration of corifollitropin alfa was slightly higher compared with the number observed with daily recombinant FSH treatment [L2274]. | Corifollitropin alfa is a long-lasting single injection fusion protein which lacks luteinizing hormone (LH) activity. Only one injection is needed for the first 7 days, which replaces the first 7 daily injections of traditional follicle stimulating hormone (FSH). It is a follicle-stimulation hormone (human a-subunit reduced), a combination of follicle stimulation hormone (human ß-subunit reduced) fusion protein with 118-145-chorionic gonadotropin (human ß-subunit) [L2270]. Frequent, repetitive injections increase stress and error rates, and are often a burden for women, leading to therapy noncompliance [L2277]. The agent comprises an alpha-subunit, which is identical to that of FSH, and a beta-subunit, which is produced by the fusion of the C-terminal peptide from the beta-subunit of chorionic gonadotropin to the beta-subunit of FSH [A32516]. Corifollitropin alfa serves as a sustained follicle stimulant that has similar pharmacological effects to recombinant follicle stimulating hormone (rFSH), however, with a relatively long elimination half-life, resulting in a longer duration of action. This is achieved using site-directed mutagenesis and gene transfer techniques to create a glycoprotein that consists of an a-subunit that is identical to human follicle stimulating hormone (FSH) noncovalently bound to a _ß-subunit_ comprised of a complete _ß-chain_ of human FSH elongated by the carboxyterminal peptide of the ß-subunit of human chorionic gonadotrophin (hCG) [L2271]. This unit interacts with the FSH receptor [A32516] to stimulate the release of oocytes. Corifollitropin alfa does not demonstrate any intrinsic LH/hCG activity [L2270]. | The most common side effects with Elonva (seen in between 1 and 10 patients in 100) include a headache, nausea, fatigue, pelvic pain and/or discomfort, breast tenderness and ovarian hyperstimulation syndrome (OHSS). This syndrome occurs when the ovaries have a heightened response to therapy, leading to abdominal swelling and pain, nausea and diarrhea [L2270]. More than one injection of Elonva within one treatment cycle or an excessively high dose of Elonva and/or (rec)FSH can increase the risk of ovarian hyperstimulation syndrome [L2270], which may cause swollen or painful ovaries, abdominal bloating, nausea, and a weight gain of up to 3kg [L2275]. In severe cases, ovarian hyperstimulation syndrome may cause rapid weight gain ranging from 15 to 20 kilograms in 5-10 days. Severe abdominal pain, severe, persistent nausea, and vomiting, decreased urination, and abdominal bloating, as well as other generalized symptoms, may occur [L2275]. About 1 - 2 % of women undergoing ovarian stimulation develop a severe form of ovarian hyperstimulation syndrome (OHSS). Severe OHSS can be life-threatening. Complications may include: ascites, pulmonary edema, electrolyte disturbances (sodium, potassium, others), thrombosis in large vessels, usually in the lower extremities, renal failure, ovarian torsion, rupture of ovarian cysts. Some of these conditions can lead to hemorrhage, respiratory failure, spontaneous miscarriage or pregnancy termination due to complications, resulting in death [L2270]. | The metabolic fate of corifollitropin alfa highly resembles that of endogenous glycoprotein hormones, which predominantly is comprised of kidney clearance and the urinary excretion of the intact protein in parallel to kidney catabolism [A32519]. | After one single subcutaneous injection of this drug, the maximal serum concentration is 4.24 ng/mL (2.49-7.21 ng/mL1) and is reached 44 hours (35-57 h) post-dose administration. Its absolute bioavailability is 58% (48-70%) [L2270]. | Distribution, metabolism and elimination of corifollitropin alfa are very similar to other gonadotropins, such as FSH, hCG and LH [L2273]. After absorption into the blood, corifollitropin alfa is distributed mainly to the ovaries and the kidneys. The steady-state volume of distribution is 9.2 L [L2273]. Exposure to corifollitropin alfa increases in a linear fashion with the dose within a range of 60 micrograms - 240 micrograms [L2270]. | 0.13 L/h (0.10-0.18 L/h1) [L2270] | Sex Hormones and Modulators of the Genital System | NA | NA | NA | NA | Follicle-stimulating hormone receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13008 | Th1376 | Somatrem | NA | 22255.9518 | C995H1537N263O301S8 | NA | NA | NA | 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]. | 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]. | 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]. | 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]. | 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]. | 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. | 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]. | 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]. | 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]. | Anterior Pituitary Lobe Hormones and Analogues | NA | NA | NA | NA | Growth hormone receptor,Insulin-like growth factor 1 receptor | Protropin - Kit Im Sc 5mg/vial | Hoffmann La Roche | Hoffmann La Roche | Intramuscular; Subcutaneous | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13010 | Th1376 | Somatrem | NA | 22255.9518 | C995H1537N263O301S8 | NA | NA | NA | 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]. | 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]. | 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]. | 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]. | 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]. | 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. | 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]. | 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]. | 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]. | Hormones | NA | NA | NA | NA | Growth hormone receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13011 | Th1376 | Somatrem | NA | 22255.9518 | C995H1537N263O301S8 | NA | NA | NA | 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]. | 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]. | 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]. | 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]. | 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]. | 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. | 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]. | 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]. | 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]. | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | Growth hormone receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13012 | Th1376 | Somatrem | NA | 22255.9518 | C995H1537N263O301S8 | NA | NA | NA | 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]. | 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]. | 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]. | 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]. | 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]. | 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. | 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]. | 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]. | 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]. | Peptide Hormones | NA | NA | NA | NA | Growth hormone receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13014 | Th1376 | Somatrem | NA | 22255.9518 | C995H1537N263O301S8 | NA | NA | NA | 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]. | 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]. | 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]. | 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]. | 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]. | 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. | 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]. | 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]. | 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]. | Pituitary and Hypothalamic Hormones and Analogues | NA | NA | NA | NA | Growth hormone receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13015 | Th1376 | Somatrem | NA | 22255.9518 | C995H1537N263O301S8 | NA | NA | NA | 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]. | 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]. | 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]. | 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]. | 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]. | 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. | 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]. | 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]. | 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]. | Pituitary Hormones | NA | NA | NA | NA | Growth hormone receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13016 | Th1376 | Somatrem | NA | 22255.9518 | C995H1537N263O301S8 | NA | NA | NA | 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]. | 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]. | 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]. | 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]. | 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]. | 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. | 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]. | 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]. | 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]. | Pituitary Hormones, Anterior | NA | NA | NA | NA | Growth hormone receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13018 | Th1376 | Somatrem | NA | 22255.9518 | C995H1537N263O301S8 | NA | NA | NA | 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]. | 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]. | 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]. | 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]. | 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]. | 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. | 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]. | 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]. | 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]. | Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | NA | Growth hormone receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13136 | Th1386 | Secretin porcine | >Th1386_Secretin_porcine MATRALLLLLLLPPLLLLAGCAARPAPPRAPRHSDGTFTSELSRLRDSARLQRLLQGLVGKRSQQDPENNTAWTKSGEDRLCQLWSHMPALQAWMPMKPPVDQAWSPWLPPGLRAGALVSEPAIPAAEGSPMPP | NA | NA | NA | NA | NA | NA | Secretin porcine stimulates pancreatic and gastric secretions to aid in the diagnosis of pancreatic exocrine dysfunction and the diagnosis of gastrinoma. | NA | NA | NA | NA | NA | NA | NA | NA | Gastrointestinal Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13137 | Th1386 | Secretin porcine | >Th1386_Secretin_porcine MATRALLLLLLLPPLLLLAGCAARPAPPRAPRHSDGTFTSELSRLRDSARLQRLLQGLVGKRSQQDPENNTAWTKSGEDRLCQLWSHMPALQAWMPMKPPVDQAWSPWLPPGLRAGALVSEPAIPAAEGSPMPP | NA | NA | NA | NA | NA | NA | Secretin porcine stimulates pancreatic and gastric secretions to aid in the diagnosis of pancreatic exocrine dysfunction and the diagnosis of gastrinoma. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13138 | Th1386 | Secretin porcine | >Th1386_Secretin_porcine MATRALLLLLLLPPLLLLAGCAARPAPPRAPRHSDGTFTSELSRLRDSARLQRLLQGLVGKRSQQDPENNTAWTKSGEDRLCQLWSHMPALQAWMPMKPPVDQAWSPWLPPGLRAGALVSEPAIPAAEGSPMPP | NA | NA | NA | NA | NA | NA | Secretin porcine stimulates pancreatic and gastric secretions to aid in the diagnosis of pancreatic exocrine dysfunction and the diagnosis of gastrinoma. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13141 | Th1386 | Secretin porcine | >Th1386_Secretin_porcine MATRALLLLLLLPPLLLLAGCAARPAPPRAPRHSDGTFTSELSRLRDSARLQRLLQGLVGKRSQQDPENNTAWTKSGEDRLCQLWSHMPALQAWMPMKPPVDQAWSPWLPPGLRAGALVSEPAIPAAEGSPMPP | NA | NA | NA | NA | NA | NA | Secretin porcine stimulates pancreatic and gastric secretions to aid in the diagnosis of pancreatic exocrine dysfunction and the diagnosis of gastrinoma. | NA | NA | NA | NA | NA | NA | NA | NA | Peptide Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13148 | Th1387 | Secretin human | >Th1387_Secretin_human HSDGTFTSELSRLREGARLQRLLQGLV | 3039.44 | C130H220N44O39 | NA | NA | NA | The elimination half life of synthetic human secretin is 45 minutes [FDA Label]. | Human secretin is a gastrointestinal peptide hormone that regulates secretions in the stomach, pancreas, and liver. The hormone is produced from the enterochromaffin cells in the duodenum in response to the duodenal content with the pH less than 4.5 [L1875]. The main action of secretin is to stimulate the pancreas to secrete pancreatic juice for pH regulation in the small intestines. Secretin is also responsible in body fluid homeostasis [A32276] and bile production. Although it is a gastrointestinal hormone, secretin is also considered as a neuropeptide hormone since it is also expressed in the central nervous system [A32275]. Purified synthetic human secretin, also referred to as RG1068, is available as an intravenous injection under the market name ChiRhoStim ® in the U.S.. It contains an amino acid sequence identical to the naturally occurring hormone consisting of 27 amino acids [FDA Label] that supports a-helical formation [A32275]. The carboxyl-terminal amino acid, valine, is amidated. Synthetic human secretin displays equivalent biological activity and properties as naturally-occurring secretin [A32265]. It is indicated for the stimulation of the pancreatic and gastric secretions to aid in the diagnosis of pancreatic exocrine dysfunction and the diagnosis of gastrinoma, and facilitate the identification of the ampulla of Vater and accessory papilla during endoscopic retrograde cholangiopancreatography (ERCP). | Indicated for the stimulation of: - pancreatic secretions, including bicarbonate, to aid in the diagnosis of pancreatic exocrine dysfunction [FDA Label]. - gastrin secretion to aid in the diagnosis of gastrinoma [FDA Label]. - pancreatic secretions to facilitate the identification of the ampulla of Vater and accessory papilla during endoscopic retrograde cholangiopancreatography (ERCP) [FDA Label]. | In clinical trials, intravenous administration of synthetic human secretin stimulated the exocrine pancreas to promote juice and bicarbonate secretion, with variable responses depending on the pancreatic function of the individual [FDA Label]. Having an identical amino acid sequence to the biologically-derived secretin, synthetic human secretin exhibits an equivalent biological activity as the natural hormone. The biological activity of synthetic human secretin was approximately 5.0 CU per mcg [FDA Label]. In patients with suspected or known exocrine pancreatic dysfunction, a volume response of less than 2 mL/kg/hr, peak bicarbonate concentration of less than 80 mEq/L, and a bicarbonate output of less than 0.2 mEq/kg/hr following intravenous synthetic human secretin [FDA Label]. Administration in healthy subjects in three crossover studies led to overall pancreatic secretory response of a mean peak bicarbonate concentration of 100 mEq/L, a mean total volume over one hour of 260.7 mL, and a peak bicarbonate concentrations = 80 mEq/L [FDA Label]. In a baseline-controlled study of patients with acute and acute recurrent pancreatitis undergoing magnetic resonance cholangiopancreatography (MRCP), administration of synthetic human secretin resulted in higher levels of sensitivity with minimal loss in specificity. This indicates that the stimulation of pancreatic secretions by synthetic secretin facilitates the diagnosis and clinical decision making of patients acute, acute recurrent, or chronic pancreatitis [A32267]. | Synthetic human secretin mediates the same biological effects as the naturally-occurring gastrointestinal peptide hormone. Secretin is normally released from enterochromaffin cells and S cells in the intestinal mucosa of duodenum upon exposure of proximal intestinal lumen to the acidic gastric content, or fatty acids and amino acids [FDA Label]. Secretin mediates an inhibitory effect on acid secretion by parietal cells of the stomach, and causes alkalinazation of the duodenal content by stimulating the release of pancreatic juice, which has high amounts of water and bicarbonate ions [L1875]. Bicarbonate ions are released into the duodenum from the centroacinar cells, and epithelia lining the pancreatic and biliary ducts [A32275]. Human secretin is a ligand at G-protein coupled secretin receptors which are expressed in the basolateral domain of several tissue cell types [A32275], including pancreas, stomach, liver, colon and other tissues [FDA Label]. Upon interaction, levels of cAMP increase and initiates the cAMP-mediated signalling cascade that results in phosphorylation of protein kinase A (PKA) and activation of cystic fibrosis transmembrane conductance regulator (CFTR) [A32275]. Activation of CFTR activates Cl-/HCO3- anion exchanger 2 and leads to secretion of bicarbonate-rich-pancreatic fluid [A32275]. Via the same cAMP signalling pathway, secretin promotes the secretion of water and electrolytes in cholangiocytes [A32275]. Secretin may work through vagal-vagal neural pathways since stimulation of the efferent vagus nerve stimulates bicarbonate secretion and atropine blocks secretin-stimulated pancreatic secretion [FDA Label]. Additionally, secretin acts as a diuretic to increase urinary volume and bicarbonate excretion [A32275, A32276]. | In acute toxicity studies with mice and rabbits, a dose of 20 µg/kg of synthetic human secretin was not lethal with no clinical symptoms of toxicity. The no-observed-effect level (NOEL) in rats was 10 µg/kg/day in a 14-day intravenous toxicity study without any evidence of adverse toxicity. The NOEL was 5 µg/kg/day in dogs [L1875]. Studies assessing the carcinogenic potential, mutagenicity, or potential for impairment of fertility have not been conducted with synthetic human secretin [FDA Label]. | NA | Following intravenous bolus administration of 0.4 mcg/kg, synthetic human secretin concentration rapidly declines to baseline secretin levels within 90 to 120 minutes [FDA Label]. | The volume of distribution is 2.7 L [FDA Label]. | The clearance of synthetic human secretin is 580.9 ± 51.3 mL/min [FDA Label]. | Gastrointestinal Hormones | NA | NA | NA | NA | Secretin receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-5-[[2-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[2-[[(2S)-1-[[(2S)-1-amino-3-methyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-2-oxoethyl]amino]-1,5-dioxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-4-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-4-carboxybutanoyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-4-methylpentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 13149 | Th1387 | Secretin human | >Th1387_Secretin_human HSDGTFTSELSRLREGARLQRLLQGLV | 3039.44 | C130H220N44O39 | NA | NA | NA | The elimination half life of synthetic human secretin is 45 minutes [FDA Label]. | Human secretin is a gastrointestinal peptide hormone that regulates secretions in the stomach, pancreas, and liver. The hormone is produced from the enterochromaffin cells in the duodenum in response to the duodenal content with the pH less than 4.5 [L1875]. The main action of secretin is to stimulate the pancreas to secrete pancreatic juice for pH regulation in the small intestines. Secretin is also responsible in body fluid homeostasis [A32276] and bile production. Although it is a gastrointestinal hormone, secretin is also considered as a neuropeptide hormone since it is also expressed in the central nervous system [A32275]. Purified synthetic human secretin, also referred to as RG1068, is available as an intravenous injection under the market name ChiRhoStim ® in the U.S.. It contains an amino acid sequence identical to the naturally occurring hormone consisting of 27 amino acids [FDA Label] that supports a-helical formation [A32275]. The carboxyl-terminal amino acid, valine, is amidated. Synthetic human secretin displays equivalent biological activity and properties as naturally-occurring secretin [A32265]. It is indicated for the stimulation of the pancreatic and gastric secretions to aid in the diagnosis of pancreatic exocrine dysfunction and the diagnosis of gastrinoma, and facilitate the identification of the ampulla of Vater and accessory papilla during endoscopic retrograde cholangiopancreatography (ERCP). | Indicated for the stimulation of: - pancreatic secretions, including bicarbonate, to aid in the diagnosis of pancreatic exocrine dysfunction [FDA Label]. - gastrin secretion to aid in the diagnosis of gastrinoma [FDA Label]. - pancreatic secretions to facilitate the identification of the ampulla of Vater and accessory papilla during endoscopic retrograde cholangiopancreatography (ERCP) [FDA Label]. | In clinical trials, intravenous administration of synthetic human secretin stimulated the exocrine pancreas to promote juice and bicarbonate secretion, with variable responses depending on the pancreatic function of the individual [FDA Label]. Having an identical amino acid sequence to the biologically-derived secretin, synthetic human secretin exhibits an equivalent biological activity as the natural hormone. The biological activity of synthetic human secretin was approximately 5.0 CU per mcg [FDA Label]. In patients with suspected or known exocrine pancreatic dysfunction, a volume response of less than 2 mL/kg/hr, peak bicarbonate concentration of less than 80 mEq/L, and a bicarbonate output of less than 0.2 mEq/kg/hr following intravenous synthetic human secretin [FDA Label]. Administration in healthy subjects in three crossover studies led to overall pancreatic secretory response of a mean peak bicarbonate concentration of 100 mEq/L, a mean total volume over one hour of 260.7 mL, and a peak bicarbonate concentrations = 80 mEq/L [FDA Label]. In a baseline-controlled study of patients with acute and acute recurrent pancreatitis undergoing magnetic resonance cholangiopancreatography (MRCP), administration of synthetic human secretin resulted in higher levels of sensitivity with minimal loss in specificity. This indicates that the stimulation of pancreatic secretions by synthetic secretin facilitates the diagnosis and clinical decision making of patients acute, acute recurrent, or chronic pancreatitis [A32267]. | Synthetic human secretin mediates the same biological effects as the naturally-occurring gastrointestinal peptide hormone. Secretin is normally released from enterochromaffin cells and S cells in the intestinal mucosa of duodenum upon exposure of proximal intestinal lumen to the acidic gastric content, or fatty acids and amino acids [FDA Label]. Secretin mediates an inhibitory effect on acid secretion by parietal cells of the stomach, and causes alkalinazation of the duodenal content by stimulating the release of pancreatic juice, which has high amounts of water and bicarbonate ions [L1875]. Bicarbonate ions are released into the duodenum from the centroacinar cells, and epithelia lining the pancreatic and biliary ducts [A32275]. Human secretin is a ligand at G-protein coupled secretin receptors which are expressed in the basolateral domain of several tissue cell types [A32275], including pancreas, stomach, liver, colon and other tissues [FDA Label]. Upon interaction, levels of cAMP increase and initiates the cAMP-mediated signalling cascade that results in phosphorylation of protein kinase A (PKA) and activation of cystic fibrosis transmembrane conductance regulator (CFTR) [A32275]. Activation of CFTR activates Cl-/HCO3- anion exchanger 2 and leads to secretion of bicarbonate-rich-pancreatic fluid [A32275]. Via the same cAMP signalling pathway, secretin promotes the secretion of water and electrolytes in cholangiocytes [A32275]. Secretin may work through vagal-vagal neural pathways since stimulation of the efferent vagus nerve stimulates bicarbonate secretion and atropine blocks secretin-stimulated pancreatic secretion [FDA Label]. Additionally, secretin acts as a diuretic to increase urinary volume and bicarbonate excretion [A32275, A32276]. | In acute toxicity studies with mice and rabbits, a dose of 20 µg/kg of synthetic human secretin was not lethal with no clinical symptoms of toxicity. The no-observed-effect level (NOEL) in rats was 10 µg/kg/day in a 14-day intravenous toxicity study without any evidence of adverse toxicity. The NOEL was 5 µg/kg/day in dogs [L1875]. Studies assessing the carcinogenic potential, mutagenicity, or potential for impairment of fertility have not been conducted with synthetic human secretin [FDA Label]. | NA | Following intravenous bolus administration of 0.4 mcg/kg, synthetic human secretin concentration rapidly declines to baseline secretin levels within 90 to 120 minutes [FDA Label]. | The volume of distribution is 2.7 L [FDA Label]. | The clearance of synthetic human secretin is 580.9 ± 51.3 mL/min [FDA Label]. | Hormones | NA | NA | NA | NA | Secretin receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-5-[[2-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[2-[[(2S)-1-[[(2S)-1-amino-3-methyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-2-oxoethyl]amino]-1,5-dioxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-4-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-4-carboxybutanoyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-4-methylpentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 13150 | Th1387 | Secretin human | >Th1387_Secretin_human HSDGTFTSELSRLREGARLQRLLQGLV | 3039.44 | C130H220N44O39 | NA | NA | NA | The elimination half life of synthetic human secretin is 45 minutes [FDA Label]. | Human secretin is a gastrointestinal peptide hormone that regulates secretions in the stomach, pancreas, and liver. The hormone is produced from the enterochromaffin cells in the duodenum in response to the duodenal content with the pH less than 4.5 [L1875]. The main action of secretin is to stimulate the pancreas to secrete pancreatic juice for pH regulation in the small intestines. Secretin is also responsible in body fluid homeostasis [A32276] and bile production. Although it is a gastrointestinal hormone, secretin is also considered as a neuropeptide hormone since it is also expressed in the central nervous system [A32275]. Purified synthetic human secretin, also referred to as RG1068, is available as an intravenous injection under the market name ChiRhoStim ® in the U.S.. It contains an amino acid sequence identical to the naturally occurring hormone consisting of 27 amino acids [FDA Label] that supports a-helical formation [A32275]. The carboxyl-terminal amino acid, valine, is amidated. Synthetic human secretin displays equivalent biological activity and properties as naturally-occurring secretin [A32265]. It is indicated for the stimulation of the pancreatic and gastric secretions to aid in the diagnosis of pancreatic exocrine dysfunction and the diagnosis of gastrinoma, and facilitate the identification of the ampulla of Vater and accessory papilla during endoscopic retrograde cholangiopancreatography (ERCP). | Indicated for the stimulation of: - pancreatic secretions, including bicarbonate, to aid in the diagnosis of pancreatic exocrine dysfunction [FDA Label]. - gastrin secretion to aid in the diagnosis of gastrinoma [FDA Label]. - pancreatic secretions to facilitate the identification of the ampulla of Vater and accessory papilla during endoscopic retrograde cholangiopancreatography (ERCP) [FDA Label]. | In clinical trials, intravenous administration of synthetic human secretin stimulated the exocrine pancreas to promote juice and bicarbonate secretion, with variable responses depending on the pancreatic function of the individual [FDA Label]. Having an identical amino acid sequence to the biologically-derived secretin, synthetic human secretin exhibits an equivalent biological activity as the natural hormone. The biological activity of synthetic human secretin was approximately 5.0 CU per mcg [FDA Label]. In patients with suspected or known exocrine pancreatic dysfunction, a volume response of less than 2 mL/kg/hr, peak bicarbonate concentration of less than 80 mEq/L, and a bicarbonate output of less than 0.2 mEq/kg/hr following intravenous synthetic human secretin [FDA Label]. Administration in healthy subjects in three crossover studies led to overall pancreatic secretory response of a mean peak bicarbonate concentration of 100 mEq/L, a mean total volume over one hour of 260.7 mL, and a peak bicarbonate concentrations = 80 mEq/L [FDA Label]. In a baseline-controlled study of patients with acute and acute recurrent pancreatitis undergoing magnetic resonance cholangiopancreatography (MRCP), administration of synthetic human secretin resulted in higher levels of sensitivity with minimal loss in specificity. This indicates that the stimulation of pancreatic secretions by synthetic secretin facilitates the diagnosis and clinical decision making of patients acute, acute recurrent, or chronic pancreatitis [A32267]. | Synthetic human secretin mediates the same biological effects as the naturally-occurring gastrointestinal peptide hormone. Secretin is normally released from enterochromaffin cells and S cells in the intestinal mucosa of duodenum upon exposure of proximal intestinal lumen to the acidic gastric content, or fatty acids and amino acids [FDA Label]. Secretin mediates an inhibitory effect on acid secretion by parietal cells of the stomach, and causes alkalinazation of the duodenal content by stimulating the release of pancreatic juice, which has high amounts of water and bicarbonate ions [L1875]. Bicarbonate ions are released into the duodenum from the centroacinar cells, and epithelia lining the pancreatic and biliary ducts [A32275]. Human secretin is a ligand at G-protein coupled secretin receptors which are expressed in the basolateral domain of several tissue cell types [A32275], including pancreas, stomach, liver, colon and other tissues [FDA Label]. Upon interaction, levels of cAMP increase and initiates the cAMP-mediated signalling cascade that results in phosphorylation of protein kinase A (PKA) and activation of cystic fibrosis transmembrane conductance regulator (CFTR) [A32275]. Activation of CFTR activates Cl-/HCO3- anion exchanger 2 and leads to secretion of bicarbonate-rich-pancreatic fluid [A32275]. Via the same cAMP signalling pathway, secretin promotes the secretion of water and electrolytes in cholangiocytes [A32275]. Secretin may work through vagal-vagal neural pathways since stimulation of the efferent vagus nerve stimulates bicarbonate secretion and atropine blocks secretin-stimulated pancreatic secretion [FDA Label]. Additionally, secretin acts as a diuretic to increase urinary volume and bicarbonate excretion [A32275, A32276]. | In acute toxicity studies with mice and rabbits, a dose of 20 µg/kg of synthetic human secretin was not lethal with no clinical symptoms of toxicity. The no-observed-effect level (NOEL) in rats was 10 µg/kg/day in a 14-day intravenous toxicity study without any evidence of adverse toxicity. The NOEL was 5 µg/kg/day in dogs [L1875]. Studies assessing the carcinogenic potential, mutagenicity, or potential for impairment of fertility have not been conducted with synthetic human secretin [FDA Label]. | NA | Following intravenous bolus administration of 0.4 mcg/kg, synthetic human secretin concentration rapidly declines to baseline secretin levels within 90 to 120 minutes [FDA Label]. | The volume of distribution is 2.7 L [FDA Label]. | The clearance of synthetic human secretin is 580.9 ± 51.3 mL/min [FDA Label]. | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | Secretin receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-5-[[2-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[2-[[(2S)-1-[[(2S)-1-amino-3-methyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-2-oxoethyl]amino]-1,5-dioxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-4-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-4-carboxybutanoyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-4-methylpentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 13153 | Th1387 | Secretin human | >Th1387_Secretin_human HSDGTFTSELSRLREGARLQRLLQGLV | 3039.44 | C130H220N44O39 | NA | NA | NA | The elimination half life of synthetic human secretin is 45 minutes [FDA Label]. | Human secretin is a gastrointestinal peptide hormone that regulates secretions in the stomach, pancreas, and liver. The hormone is produced from the enterochromaffin cells in the duodenum in response to the duodenal content with the pH less than 4.5 [L1875]. The main action of secretin is to stimulate the pancreas to secrete pancreatic juice for pH regulation in the small intestines. Secretin is also responsible in body fluid homeostasis [A32276] and bile production. Although it is a gastrointestinal hormone, secretin is also considered as a neuropeptide hormone since it is also expressed in the central nervous system [A32275]. Purified synthetic human secretin, also referred to as RG1068, is available as an intravenous injection under the market name ChiRhoStim ® in the U.S.. It contains an amino acid sequence identical to the naturally occurring hormone consisting of 27 amino acids [FDA Label] that supports a-helical formation [A32275]. The carboxyl-terminal amino acid, valine, is amidated. Synthetic human secretin displays equivalent biological activity and properties as naturally-occurring secretin [A32265]. It is indicated for the stimulation of the pancreatic and gastric secretions to aid in the diagnosis of pancreatic exocrine dysfunction and the diagnosis of gastrinoma, and facilitate the identification of the ampulla of Vater and accessory papilla during endoscopic retrograde cholangiopancreatography (ERCP). | Indicated for the stimulation of: - pancreatic secretions, including bicarbonate, to aid in the diagnosis of pancreatic exocrine dysfunction [FDA Label]. - gastrin secretion to aid in the diagnosis of gastrinoma [FDA Label]. - pancreatic secretions to facilitate the identification of the ampulla of Vater and accessory papilla during endoscopic retrograde cholangiopancreatography (ERCP) [FDA Label]. | In clinical trials, intravenous administration of synthetic human secretin stimulated the exocrine pancreas to promote juice and bicarbonate secretion, with variable responses depending on the pancreatic function of the individual [FDA Label]. Having an identical amino acid sequence to the biologically-derived secretin, synthetic human secretin exhibits an equivalent biological activity as the natural hormone. The biological activity of synthetic human secretin was approximately 5.0 CU per mcg [FDA Label]. In patients with suspected or known exocrine pancreatic dysfunction, a volume response of less than 2 mL/kg/hr, peak bicarbonate concentration of less than 80 mEq/L, and a bicarbonate output of less than 0.2 mEq/kg/hr following intravenous synthetic human secretin [FDA Label]. Administration in healthy subjects in three crossover studies led to overall pancreatic secretory response of a mean peak bicarbonate concentration of 100 mEq/L, a mean total volume over one hour of 260.7 mL, and a peak bicarbonate concentrations = 80 mEq/L [FDA Label]. In a baseline-controlled study of patients with acute and acute recurrent pancreatitis undergoing magnetic resonance cholangiopancreatography (MRCP), administration of synthetic human secretin resulted in higher levels of sensitivity with minimal loss in specificity. This indicates that the stimulation of pancreatic secretions by synthetic secretin facilitates the diagnosis and clinical decision making of patients acute, acute recurrent, or chronic pancreatitis [A32267]. | Synthetic human secretin mediates the same biological effects as the naturally-occurring gastrointestinal peptide hormone. Secretin is normally released from enterochromaffin cells and S cells in the intestinal mucosa of duodenum upon exposure of proximal intestinal lumen to the acidic gastric content, or fatty acids and amino acids [FDA Label]. Secretin mediates an inhibitory effect on acid secretion by parietal cells of the stomach, and causes alkalinazation of the duodenal content by stimulating the release of pancreatic juice, which has high amounts of water and bicarbonate ions [L1875]. Bicarbonate ions are released into the duodenum from the centroacinar cells, and epithelia lining the pancreatic and biliary ducts [A32275]. Human secretin is a ligand at G-protein coupled secretin receptors which are expressed in the basolateral domain of several tissue cell types [A32275], including pancreas, stomach, liver, colon and other tissues [FDA Label]. Upon interaction, levels of cAMP increase and initiates the cAMP-mediated signalling cascade that results in phosphorylation of protein kinase A (PKA) and activation of cystic fibrosis transmembrane conductance regulator (CFTR) [A32275]. Activation of CFTR activates Cl-/HCO3- anion exchanger 2 and leads to secretion of bicarbonate-rich-pancreatic fluid [A32275]. Via the same cAMP signalling pathway, secretin promotes the secretion of water and electrolytes in cholangiocytes [A32275]. Secretin may work through vagal-vagal neural pathways since stimulation of the efferent vagus nerve stimulates bicarbonate secretion and atropine blocks secretin-stimulated pancreatic secretion [FDA Label]. Additionally, secretin acts as a diuretic to increase urinary volume and bicarbonate excretion [A32275, A32276]. | In acute toxicity studies with mice and rabbits, a dose of 20 µg/kg of synthetic human secretin was not lethal with no clinical symptoms of toxicity. The no-observed-effect level (NOEL) in rats was 10 µg/kg/day in a 14-day intravenous toxicity study without any evidence of adverse toxicity. The NOEL was 5 µg/kg/day in dogs [L1875]. Studies assessing the carcinogenic potential, mutagenicity, or potential for impairment of fertility have not been conducted with synthetic human secretin [FDA Label]. | NA | Following intravenous bolus administration of 0.4 mcg/kg, synthetic human secretin concentration rapidly declines to baseline secretin levels within 90 to 120 minutes [FDA Label]. | The volume of distribution is 2.7 L [FDA Label]. | The clearance of synthetic human secretin is 580.9 ± 51.3 mL/min [FDA Label]. | Peptide Hormones | NA | NA | NA | NA | Secretin receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-5-[[2-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[2-[[(2S)-1-[[(2S)-1-amino-3-methyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-2-oxoethyl]amino]-1,5-dioxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-4-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-4-carboxybutanoyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-4-methylpentanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 13316 | Th1395 | Insulin peglispro | NA | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Hormones | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13317 | Th1395 | Insulin peglispro | NA | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13321 | Th1395 | Insulin peglispro | NA | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Pancreatic Hormones | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13323 | Th1395 | Insulin peglispro | NA | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Peptide Hormones | NA | NA | NA | NA | Insulin receptor,Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13660 | Th1422 | Cenderitide | NA | NA | NA | NA | NA | NA | NA | Cenderitide is under investigation for the treatment of ST Elevation (STEMI) Myocardial Infarction of Anterior Wall. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (3S)-3-[[(2S)-1-[(2S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-1-[(2R)-2-[[2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S,3S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[2-[[(2S)-2-[[(2R)-2-[[2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[(2-aminoacetyl)amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]acetyl]amino]-3-sulfanylpropanoyl]amino]-3-phenylpropanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]hexanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-3-methylpentanoyl]amino]acetyl]amino]-3-hydroxypropanoyl]amino]-4-methylsulfanylbutanoyl]amino]-3-hydroxypropanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]acetyl]amino]-3-sulfanylpropanoyl]pyrrolidine-2-carbonyl]amino]-3-hydroxypropanoyl]amino]-4-methylpentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-3-carboxypropanoyl]pyrrolidine-2-carbonyl]amino]-5-(diaminomethylideneamino)pentanoyl]pyrrolidine-2-carbonyl]amino]-4-[[(2S)-1-[(2S)-2-[[(2S)-1-[[(2S,3R)-1-[[(2S)-1-[[(1S)-1-carboxyethyl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]carbamoyl]pyrrolidin-1-yl]-1-oxopropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | NA | NA |
| 13661 | Th1422 | Cenderitide | NA | NA | NA | NA | NA | NA | NA | Cenderitide is under investigation for the treatment of ST Elevation (STEMI) Myocardial Infarction of Anterior Wall. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (3S)-3-[[(2S)-1-[(2S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-1-[(2R)-2-[[2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S,3S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[2-[[(2S)-2-[[(2R)-2-[[2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[(2-aminoacetyl)amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]acetyl]amino]-3-sulfanylpropanoyl]amino]-3-phenylpropanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]hexanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-3-methylpentanoyl]amino]acetyl]amino]-3-hydroxypropanoyl]amino]-4-methylsulfanylbutanoyl]amino]-3-hydroxypropanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]acetyl]amino]-3-sulfanylpropanoyl]pyrrolidine-2-carbonyl]amino]-3-hydroxypropanoyl]amino]-4-methylpentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-3-carboxypropanoyl]pyrrolidine-2-carbonyl]amino]-5-(diaminomethylideneamino)pentanoyl]pyrrolidine-2-carbonyl]amino]-4-[[(2S)-1-[(2S)-2-[[(2S)-1-[[(2S,3R)-1-[[(2S)-1-[[(1S)-1-carboxyethyl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]carbamoyl]pyrrolidin-1-yl]-1-oxopropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | NA | NA |
| 13662 | Th1422 | Cenderitide | NA | NA | NA | NA | NA | NA | NA | Cenderitide is under investigation for the treatment of ST Elevation (STEMI) Myocardial Infarction of Anterior Wall. | NA | NA | NA | NA | NA | NA | NA | NA | Peptide Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (3S)-3-[[(2S)-1-[(2S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-1-[(2R)-2-[[2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S,3S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[2-[[(2S)-2-[[(2R)-2-[[2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[(2-aminoacetyl)amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]acetyl]amino]-3-sulfanylpropanoyl]amino]-3-phenylpropanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]hexanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-3-methylpentanoyl]amino]acetyl]amino]-3-hydroxypropanoyl]amino]-4-methylsulfanylbutanoyl]amino]-3-hydroxypropanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]acetyl]amino]-3-sulfanylpropanoyl]pyrrolidine-2-carbonyl]amino]-3-hydroxypropanoyl]amino]-4-methylpentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]amino]-3-carboxypropanoyl]pyrrolidine-2-carbonyl]amino]-5-(diaminomethylideneamino)pentanoyl]pyrrolidine-2-carbonyl]amino]-4-[[(2S)-1-[(2S)-2-[[(2S)-1-[[(2S,3R)-1-[[(2S)-1-[[(1S)-1-carboxyethyl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]carbamoyl]pyrrolidin-1-yl]-1-oxopropan-2-yl]amino]-4-oxobutanoic acid | NA | Link | NA | NA |
| 13807 | Th1436 | Lenomorelin | NA | NA | NA | NA | NA | NA | NA | Lenomorelin has been investigated for the treatment and basic science of Cancer, Alcoholism, Metabolism, Hypopituitarism, and Frailty Syndrome, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-4-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[(2-aminoacetyl)amino]-3-octanoyloxypropanoyl]amino]-3-hydroxypropanoyl]amino]-3-phenylpropanoyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]pyrrolidine-2-carbonyl]amino]-5-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-6-amino-1-[(2S)-2-[(2S)-2-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-5-amino-1-[(2S)-2-[[(1S)-4-carbamimidamido-1-carboxybutyl]carbamoyl]pyrrolidin-1-yl]-1,5-dioxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-1-oxopropan-2-yl]carbamoyl]pyrrolidine-1-carbonyl]pyrrolidin-1-yl]-1-oxohexan-2-yl]amino]-1-oxohexan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-1-oxohexan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-(1H-imidazol-4-yl)-1-oxopropan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 13808 | Th1436 | Lenomorelin | NA | NA | NA | NA | NA | NA | NA | Lenomorelin has been investigated for the treatment and basic science of Cancer, Alcoholism, Metabolism, Hypopituitarism, and Frailty Syndrome, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-4-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[(2-aminoacetyl)amino]-3-octanoyloxypropanoyl]amino]-3-hydroxypropanoyl]amino]-3-phenylpropanoyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]pyrrolidine-2-carbonyl]amino]-5-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-6-amino-1-[(2S)-2-[(2S)-2-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-5-amino-1-[(2S)-2-[[(1S)-4-carbamimidamido-1-carboxybutyl]carbamoyl]pyrrolidin-1-yl]-1,5-dioxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-1-oxopropan-2-yl]carbamoyl]pyrrolidine-1-carbonyl]pyrrolidin-1-yl]-1-oxohexan-2-yl]amino]-1-oxohexan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-1-oxohexan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-(1H-imidazol-4-yl)-1-oxopropan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 13809 | Th1436 | Lenomorelin | NA | NA | NA | NA | NA | NA | NA | Lenomorelin has been investigated for the treatment and basic science of Cancer, Alcoholism, Metabolism, Hypopituitarism, and Frailty Syndrome, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Peptide Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-4-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[(2-aminoacetyl)amino]-3-octanoyloxypropanoyl]amino]-3-hydroxypropanoyl]amino]-3-phenylpropanoyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]pyrrolidine-2-carbonyl]amino]-5-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-6-amino-1-[(2S)-2-[(2S)-2-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-5-amino-1-[(2S)-2-[[(1S)-4-carbamimidamido-1-carboxybutyl]carbamoyl]pyrrolidin-1-yl]-1,5-dioxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-1-oxopropan-2-yl]carbamoyl]pyrrolidine-1-carbonyl]pyrrolidin-1-yl]-1-oxohexan-2-yl]amino]-1-oxohexan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-1-oxohexan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-(1H-imidazol-4-yl)-1-oxopropan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 13822 | Th1438 | Vosoritide | >Th1438_Vosoritide PGQEHPNARKYKGANKKGLSKGCFGLKLDRIGSMSGLGC | 4100 | C176H290N56O51S3 | NA | NA | NA | The mean half-life following the subcutaneous administration of 15 mcg/kg of vosoritide ranged from 21.0 to 27.9 minutes.[L39229] | Achondroplasia is an autosomal dominant genetic disease and the most common cause of dwarfism in humans.[A242277] It results from a gain-of-function missense mutation in _FGFR3_ that results in a dramatic suppression of bone growth, both in volume and in length.[A242273,A242277] Treatment for achondroplasia includes both surgical and pharmacological interventions, the latter of which includes C-type natriuretic peptide (CNP) analogs. Endogenous CNP, first described in 1998, is primarily responsible for the stimulation of chondrocytes and long bone growth via activity at the NPR-B receptor, making it an attractive target in the treatment of a condition like achondroplasia.[A242273] While the remarkably short half-life of endogenous CNP - 2 to 3 minutes due to its rapid degradation by endopeptidases - makes it ineffective as a therapeutic intervention,[A242273] the development of a peptidase-resistant formulation has allowed for its use as a viable treatment option in achondroplasia. Vosoritide is an analog of CNP with proline-glycine on its N-terminus to convey resistance to neutral endopeptidase.[L39229] It was approved for use under the brand name Voxzogo (BioMarin Pharmaceutical Inc.) in the EU in August 2021 and the US in November 2021,[L39245,L39241] becoming the first pharmacological intervention approved for the treatment of achondroplasia in both regions. | Vosoritide is indicated for the promotion of linear growth in pediatric patients with achondroplasia who are 5 years of age and older with open epiphyses.[L39229] | Vosoritide is an analog of C-type natriuretic peptide that promotes bone growth to combat growth suppression in children with achondroplasia. Urinary cyclic guanosine monophosphate (cGMP) and serum collagen type X marker (CXM) are both elevated following daily therapy with vosoritide and serve as biomarkers for evidence of increased endochondral bone growth, with cGMP indicative of NPR-B binding activity and CXM indicative of bone metabolism.[L39229] Although relatively well-tolerated, transient episodes of hypotension have been observed in clinical studies. Patients with pre-existing cardiovascular disease and those taking antihypertensive medications were excluded from clinical trials. The risk of hypotension may be reduced by ensuring adequate food and fluid intake prior to the administration of vosoritide.[L39229] The use of vosoritide in patients with an eGFR <60 mL/min/1.73m2 should also be avoided as there are no data on the influence of renal impairment on its pharmacokinetics.[L39229] | Achondroplasia is a congenital disease resulting from a missense mutation in the fibroblast growth factor receptor 3 (_FGFR3_) gene,[A242273] resulting in a gain-of-function that negatively regulates endochondral bone growth.[L39229] Under normal conditions, _FGFR3_ is expressed during both embryonic and postnatal development, but serves a different role in each. During initial development, FGFR3 signaling promotes proliferation of chondrocytes (i.e. growth), whereas postnatal skeletal growth is actually inhibited by FGFR3 - as a result, the pathologic activation of FGFR3 observed in patients with achondroplasia leads to suppressed pre-pubertal skeletal growth.[A242277] Vosoritide is an analog of C-type natriuretic peptide (CNP),[L39229] a signaling molecule that appears primarily responsible for the stimulation of chondrocytes and the growth of long bones.[A242273] The binding of CNP (or vosoritide) with its corresponding receptor, NPR-B, results in a signaling cascade that ultimately inhibits the MAPK/ERK pathway via inhibition of RAF-1 and stimulates the proliferation and differentiation of chondrocytes. This activity serves to antagonize the downstream signaling resulting from FGFR3 and its resultant effects on bone growth.[L39229,A242273] | Doses of two- to three-fold the recommended daily dose of 15 mcg/kg were administered to patients in clinical trials with no evidence of associated adverse reactions.[L39237] If an overdose is suspected, implement supportive measures as clinically indicated. | As with other therapeutic proteins, vosoritide is likely metabolized via catabolic pathways into smaller peptides and amino acids.[L39229] | In patients receiving daily subcutaneous injections of vosoritide 15 mcg/kg, the mean Cmax ranged from 4.71-7.18 ng/mL and the mean AUC0-t ranged from 161-290 ng-min/mL.[L39229] The median Tmax following subcutaneous injection was approximately 15 minutes.[L39229] | The mean apparent volume of distribution following the subcutaneous administration of 15 mcg/kg of vosoritide ranged from 2880 to 3020 mL/kg.[L39229] | The mean apparent clearance following the subcutaneous administration of 15 mcg/kg of vosoritide ranged from 79.4 to 104 mL/min/kg.[L39229] | Hormones | NA | NA | NA | NA | Atrial natriuretic peptide receptor 2 | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13823 | Th1438 | Vosoritide | >Th1438_Vosoritide PGQEHPNARKYKGANKKGLSKGCFGLKLDRIGSMSGLGC | 4100 | C176H290N56O51S3 | NA | NA | NA | The mean half-life following the subcutaneous administration of 15 mcg/kg of vosoritide ranged from 21.0 to 27.9 minutes.[L39229] | Achondroplasia is an autosomal dominant genetic disease and the most common cause of dwarfism in humans.[A242277] It results from a gain-of-function missense mutation in _FGFR3_ that results in a dramatic suppression of bone growth, both in volume and in length.[A242273,A242277] Treatment for achondroplasia includes both surgical and pharmacological interventions, the latter of which includes C-type natriuretic peptide (CNP) analogs. Endogenous CNP, first described in 1998, is primarily responsible for the stimulation of chondrocytes and long bone growth via activity at the NPR-B receptor, making it an attractive target in the treatment of a condition like achondroplasia.[A242273] While the remarkably short half-life of endogenous CNP - 2 to 3 minutes due to its rapid degradation by endopeptidases - makes it ineffective as a therapeutic intervention,[A242273] the development of a peptidase-resistant formulation has allowed for its use as a viable treatment option in achondroplasia. Vosoritide is an analog of CNP with proline-glycine on its N-terminus to convey resistance to neutral endopeptidase.[L39229] It was approved for use under the brand name Voxzogo (BioMarin Pharmaceutical Inc.) in the EU in August 2021 and the US in November 2021,[L39245,L39241] becoming the first pharmacological intervention approved for the treatment of achondroplasia in both regions. | Vosoritide is indicated for the promotion of linear growth in pediatric patients with achondroplasia who are 5 years of age and older with open epiphyses.[L39229] | Vosoritide is an analog of C-type natriuretic peptide that promotes bone growth to combat growth suppression in children with achondroplasia. Urinary cyclic guanosine monophosphate (cGMP) and serum collagen type X marker (CXM) are both elevated following daily therapy with vosoritide and serve as biomarkers for evidence of increased endochondral bone growth, with cGMP indicative of NPR-B binding activity and CXM indicative of bone metabolism.[L39229] Although relatively well-tolerated, transient episodes of hypotension have been observed in clinical studies. Patients with pre-existing cardiovascular disease and those taking antihypertensive medications were excluded from clinical trials. The risk of hypotension may be reduced by ensuring adequate food and fluid intake prior to the administration of vosoritide.[L39229] The use of vosoritide in patients with an eGFR <60 mL/min/1.73m2 should also be avoided as there are no data on the influence of renal impairment on its pharmacokinetics.[L39229] | Achondroplasia is a congenital disease resulting from a missense mutation in the fibroblast growth factor receptor 3 (_FGFR3_) gene,[A242273] resulting in a gain-of-function that negatively regulates endochondral bone growth.[L39229] Under normal conditions, _FGFR3_ is expressed during both embryonic and postnatal development, but serves a different role in each. During initial development, FGFR3 signaling promotes proliferation of chondrocytes (i.e. growth), whereas postnatal skeletal growth is actually inhibited by FGFR3 - as a result, the pathologic activation of FGFR3 observed in patients with achondroplasia leads to suppressed pre-pubertal skeletal growth.[A242277] Vosoritide is an analog of C-type natriuretic peptide (CNP),[L39229] a signaling molecule that appears primarily responsible for the stimulation of chondrocytes and the growth of long bones.[A242273] The binding of CNP (or vosoritide) with its corresponding receptor, NPR-B, results in a signaling cascade that ultimately inhibits the MAPK/ERK pathway via inhibition of RAF-1 and stimulates the proliferation and differentiation of chondrocytes. This activity serves to antagonize the downstream signaling resulting from FGFR3 and its resultant effects on bone growth.[L39229,A242273] | Doses of two- to three-fold the recommended daily dose of 15 mcg/kg were administered to patients in clinical trials with no evidence of associated adverse reactions.[L39237] If an overdose is suspected, implement supportive measures as clinically indicated. | As with other therapeutic proteins, vosoritide is likely metabolized via catabolic pathways into smaller peptides and amino acids.[L39229] | In patients receiving daily subcutaneous injections of vosoritide 15 mcg/kg, the mean Cmax ranged from 4.71-7.18 ng/mL and the mean AUC0-t ranged from 161-290 ng-min/mL.[L39229] The median Tmax following subcutaneous injection was approximately 15 minutes.[L39229] | The mean apparent volume of distribution following the subcutaneous administration of 15 mcg/kg of vosoritide ranged from 2880 to 3020 mL/kg.[L39229] | The mean apparent clearance following the subcutaneous administration of 15 mcg/kg of vosoritide ranged from 79.4 to 104 mL/min/kg.[L39229] | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | Atrial natriuretic peptide receptor 2 | Voxzogo | Biomarin International Limited | Biomarin International Limited | Subcutaneous | 0.4 mg | None. | injection site reactions (redness, swelling, hives), vomiting, joint pain, decreased blood pressure, and gastroenteritis. | Voxzogo is a prescription medicine used to increase linear growth in children with achondroplasia who are 5 years of age and older with open bone growth plates (epiphyses). It is not known if Voxzogo is safe and effective in children with achondroplasia under 5 years of age. Before giving you child Voxzogo... | Voxzogo is a prescription medicine used to treat the symptoms of Achondroplasia in pediatric patients 5 years or older. Voxzogo may be used alone or with other medications. | NA | VOXZOGO contains vosoritide, a human C type natriuretic peptide (CNP) analog. Vosoritide is a 39 amino acid peptide. Its amino acid sequence includes the 37 C terminal amino acids of the human CNP53 sequence plus Pro Gly on the N terminus to convey resistance to neutral endopeptidase (NEP) degradation. Vosoritide is manufactured from Escherichia coli using recombinant DNA technology. Vosoritide has a chemical formula of C176H290N56O51S3 with a molecular weight of 4.1 kDa. | Link | Link | NA |
| 13825 | Th1438 | Vosoritide | >Th1438_Vosoritide PGQEHPNARKYKGANKKGLSKGCFGLKLDRIGSMSGLGC | 4100 | C176H290N56O51S3 | NA | NA | NA | The mean half-life following the subcutaneous administration of 15 mcg/kg of vosoritide ranged from 21.0 to 27.9 minutes.[L39229] | Achondroplasia is an autosomal dominant genetic disease and the most common cause of dwarfism in humans.[A242277] It results from a gain-of-function missense mutation in _FGFR3_ that results in a dramatic suppression of bone growth, both in volume and in length.[A242273,A242277] Treatment for achondroplasia includes both surgical and pharmacological interventions, the latter of which includes C-type natriuretic peptide (CNP) analogs. Endogenous CNP, first described in 1998, is primarily responsible for the stimulation of chondrocytes and long bone growth via activity at the NPR-B receptor, making it an attractive target in the treatment of a condition like achondroplasia.[A242273] While the remarkably short half-life of endogenous CNP - 2 to 3 minutes due to its rapid degradation by endopeptidases - makes it ineffective as a therapeutic intervention,[A242273] the development of a peptidase-resistant formulation has allowed for its use as a viable treatment option in achondroplasia. Vosoritide is an analog of CNP with proline-glycine on its N-terminus to convey resistance to neutral endopeptidase.[L39229] It was approved for use under the brand name Voxzogo (BioMarin Pharmaceutical Inc.) in the EU in August 2021 and the US in November 2021,[L39245,L39241] becoming the first pharmacological intervention approved for the treatment of achondroplasia in both regions. | Vosoritide is indicated for the promotion of linear growth in pediatric patients with achondroplasia who are 5 years of age and older with open epiphyses.[L39229] | Vosoritide is an analog of C-type natriuretic peptide that promotes bone growth to combat growth suppression in children with achondroplasia. Urinary cyclic guanosine monophosphate (cGMP) and serum collagen type X marker (CXM) are both elevated following daily therapy with vosoritide and serve as biomarkers for evidence of increased endochondral bone growth, with cGMP indicative of NPR-B binding activity and CXM indicative of bone metabolism.[L39229] Although relatively well-tolerated, transient episodes of hypotension have been observed in clinical studies. Patients with pre-existing cardiovascular disease and those taking antihypertensive medications were excluded from clinical trials. The risk of hypotension may be reduced by ensuring adequate food and fluid intake prior to the administration of vosoritide.[L39229] The use of vosoritide in patients with an eGFR <60 mL/min/1.73m2 should also be avoided as there are no data on the influence of renal impairment on its pharmacokinetics.[L39229] | Achondroplasia is a congenital disease resulting from a missense mutation in the fibroblast growth factor receptor 3 (_FGFR3_) gene,[A242273] resulting in a gain-of-function that negatively regulates endochondral bone growth.[L39229] Under normal conditions, _FGFR3_ is expressed during both embryonic and postnatal development, but serves a different role in each. During initial development, FGFR3 signaling promotes proliferation of chondrocytes (i.e. growth), whereas postnatal skeletal growth is actually inhibited by FGFR3 - as a result, the pathologic activation of FGFR3 observed in patients with achondroplasia leads to suppressed pre-pubertal skeletal growth.[A242277] Vosoritide is an analog of C-type natriuretic peptide (CNP),[L39229] a signaling molecule that appears primarily responsible for the stimulation of chondrocytes and the growth of long bones.[A242273] The binding of CNP (or vosoritide) with its corresponding receptor, NPR-B, results in a signaling cascade that ultimately inhibits the MAPK/ERK pathway via inhibition of RAF-1 and stimulates the proliferation and differentiation of chondrocytes. This activity serves to antagonize the downstream signaling resulting from FGFR3 and its resultant effects on bone growth.[L39229,A242273] | Doses of two- to three-fold the recommended daily dose of 15 mcg/kg were administered to patients in clinical trials with no evidence of associated adverse reactions.[L39237] If an overdose is suspected, implement supportive measures as clinically indicated. | As with other therapeutic proteins, vosoritide is likely metabolized via catabolic pathways into smaller peptides and amino acids.[L39229] | In patients receiving daily subcutaneous injections of vosoritide 15 mcg/kg, the mean Cmax ranged from 4.71-7.18 ng/mL and the mean AUC0-t ranged from 161-290 ng-min/mL.[L39229] The median Tmax following subcutaneous injection was approximately 15 minutes.[L39229] | The mean apparent volume of distribution following the subcutaneous administration of 15 mcg/kg of vosoritide ranged from 2880 to 3020 mL/kg.[L39229] | The mean apparent clearance following the subcutaneous administration of 15 mcg/kg of vosoritide ranged from 79.4 to 104 mL/min/kg.[L39229] | Peptide Hormones | NA | NA | NA | NA | Atrial natriuretic peptide receptor 2 | Voxzogo | Biomarin International Limited | Biomarin International Limited | Subcutaneous | 1.2 mg | None. | injection site reactions (redness, swelling, hives), vomiting, joint pain, decreased blood pressure, and gastroenteritis. | Voxzogo is a prescription medicine used to increase linear growth in children with achondroplasia who are 5 years of age and older with open bone growth plates (epiphyses). It is not known if Voxzogo is safe and effective in children with achondroplasia under 5 years of age. Before giving you child Voxzogo... | Voxzogo is a prescription medicine used to treat the symptoms of Achondroplasia in pediatric patients 5 years or older. Voxzogo may be used alone or with other medications. | NA | VOXZOGO contains vosoritide, a human C type natriuretic peptide (CNP) analog. Vosoritide is a 39 amino acid peptide. Its amino acid sequence includes the 37 C terminal amino acids of the human CNP53 sequence plus Pro Gly on the N terminus to convey resistance to neutral endopeptidase (NEP) degradation. Vosoritide is manufactured from Escherichia coli using recombinant DNA technology. Vosoritide has a chemical formula of C176H290N56O51S3 with a molecular weight of 4.1 kDa. | Link | Link | NA |
| 13918 | Th1447 | Thymosin beta-4 | >Th1447_Thymosin_beta-4 MSDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGES | NA | NA | NA | NA | NA | NA | Thymosin Beta 4 has been investigated for the treatment of STEMI, Dry Eye, Diabetes, Pressure Ulcers, and Dry Eye Syndrome, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13919 | Th1447 | Thymosin beta-4 | >Th1447_Thymosin_beta-4 MSDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGES | NA | NA | NA | NA | NA | NA | Thymosin Beta 4 has been investigated for the treatment of STEMI, Dry Eye, Diabetes, Pressure Ulcers, and Dry Eye Syndrome, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13921 | Th1447 | Thymosin beta-4 | >Th1447_Thymosin_beta-4 MSDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGES | NA | NA | NA | NA | NA | NA | Thymosin Beta 4 has been investigated for the treatment of STEMI, Dry Eye, Diabetes, Pressure Ulcers, and Dry Eye Syndrome, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Peptide Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 13924 | Th1447 | Thymosin beta-4 | >Th1447_Thymosin_beta-4 MSDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGES | NA | NA | NA | NA | NA | NA | Thymosin Beta 4 has been investigated for the treatment of STEMI, Dry Eye, Diabetes, Pressure Ulcers, and Dry Eye Syndrome, among others. | NA | NA | NA | NA | NA | NA | NA | NA | Thymus Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14779 | Th1537 | Pancreatic Polypeptide | >Th1537_Pancreatic_Polypeptide MAAARLCLSLLLLSTCVALLLQPLLGAQGAPLEPVYPGDNATPEQMAQYAADLRRYINMLTRPRYGKRHKEDTLAFSEWGSPHAAVPRELSPLDL | NA | NA | NA | NA | NA | NA | Pancreatic Polypeptide has been investigated for the treatment of Diabetes Mellitus, Type 1. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-5-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S,3S)-1-[[(2S)-4-amino-1-[[(2S)-1-[[(2S)-1-[[(2S,3R)-1-[[(2S)-1-[(2S)-2-[[(2S)-1-[[(2S)-1-amino-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]carbamoyl]pyrrolidin-1-yl]-5-carbamimidamido-1-oxopentan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-1,4-dioxobutan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-carboxy-1-oxopropan-2-yl]amino]-1-oxopropan-2-yl]amino]-1-oxopropan-2-yl]amino]-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-4-[[(2S)-1-[(2S,3R)-2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-2-[[2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-2-aminopropanoyl]pyrrolidine-2-carbonyl]amino]-4-methylpentanoyl]amino]-4-carboxybutanoyl]pyrrolidine-2-carbonyl]amino]-3-methylbutanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]pyrrolidine-2-carbonyl]amino]acetyl]amino]-3-carboxypropanoyl]amino]-4-oxobutanoyl]amino]propanoyl]amino]-3-hydroxybutanoyl]pyrrolidine-2-carbonyl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 14780 | Th1537 | Pancreatic Polypeptide | >Th1537_Pancreatic_Polypeptide MAAARLCLSLLLLSTCVALLLQPLLGAQGAPLEPVYPGDNATPEQMAQYAADLRRYINMLTRPRYGKRHKEDTLAFSEWGSPHAAVPRELSPLDL | NA | NA | NA | NA | NA | NA | Pancreatic Polypeptide has been investigated for the treatment of Diabetes Mellitus, Type 1. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-5-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S,3S)-1-[[(2S)-4-amino-1-[[(2S)-1-[[(2S)-1-[[(2S,3R)-1-[[(2S)-1-[(2S)-2-[[(2S)-1-[[(2S)-1-amino-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]carbamoyl]pyrrolidin-1-yl]-5-carbamimidamido-1-oxopentan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-1,4-dioxobutan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-carboxy-1-oxopropan-2-yl]amino]-1-oxopropan-2-yl]amino]-1-oxopropan-2-yl]amino]-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-4-[[(2S)-1-[(2S,3R)-2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-2-[[2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-2-aminopropanoyl]pyrrolidine-2-carbonyl]amino]-4-methylpentanoyl]amino]-4-carboxybutanoyl]pyrrolidine-2-carbonyl]amino]-3-methylbutanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]pyrrolidine-2-carbonyl]amino]acetyl]amino]-3-carboxypropanoyl]amino]-4-oxobutanoyl]amino]propanoyl]amino]-3-hydroxybutanoyl]pyrrolidine-2-carbonyl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 14783 | Th1537 | Pancreatic Polypeptide | >Th1537_Pancreatic_Polypeptide MAAARLCLSLLLLSTCVALLLQPLLGAQGAPLEPVYPGDNATPEQMAQYAADLRRYINMLTRPRYGKRHKEDTLAFSEWGSPHAAVPRELSPLDL | NA | NA | NA | NA | NA | NA | Pancreatic Polypeptide has been investigated for the treatment of Diabetes Mellitus, Type 1. | NA | NA | NA | NA | NA | NA | NA | NA | Pancreatic Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-5-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S,3S)-1-[[(2S)-4-amino-1-[[(2S)-1-[[(2S)-1-[[(2S,3R)-1-[[(2S)-1-[(2S)-2-[[(2S)-1-[[(2S)-1-amino-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]carbamoyl]pyrrolidin-1-yl]-5-carbamimidamido-1-oxopentan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-1,4-dioxobutan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-carboxy-1-oxopropan-2-yl]amino]-1-oxopropan-2-yl]amino]-1-oxopropan-2-yl]amino]-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-4-[[(2S)-1-[(2S,3R)-2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-2-[[2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-2-aminopropanoyl]pyrrolidine-2-carbonyl]amino]-4-methylpentanoyl]amino]-4-carboxybutanoyl]pyrrolidine-2-carbonyl]amino]-3-methylbutanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]pyrrolidine-2-carbonyl]amino]acetyl]amino]-3-carboxypropanoyl]amino]-4-oxobutanoyl]amino]propanoyl]amino]-3-hydroxybutanoyl]pyrrolidine-2-carbonyl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 14784 | Th1537 | Pancreatic Polypeptide | >Th1537_Pancreatic_Polypeptide MAAARLCLSLLLLSTCVALLLQPLLGAQGAPLEPVYPGDNATPEQMAQYAADLRRYINMLTRPRYGKRHKEDTLAFSEWGSPHAAVPRELSPLDL | NA | NA | NA | NA | NA | NA | Pancreatic Polypeptide has been investigated for the treatment of Diabetes Mellitus, Type 1. | NA | NA | NA | NA | NA | NA | NA | NA | Peptide Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-5-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S,3S)-1-[[(2S)-4-amino-1-[[(2S)-1-[[(2S)-1-[[(2S,3R)-1-[[(2S)-1-[(2S)-2-[[(2S)-1-[[(2S)-1-amino-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]carbamoyl]pyrrolidin-1-yl]-5-carbamimidamido-1-oxopentan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-1,4-dioxobutan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-carboxy-1-oxopropan-2-yl]amino]-1-oxopropan-2-yl]amino]-1-oxopropan-2-yl]amino]-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-4-[[(2S)-1-[(2S,3R)-2-[[(2S)-2-[[(2S)-4-amino-2-[[(2S)-2-[[2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-2-aminopropanoyl]pyrrolidine-2-carbonyl]amino]-4-methylpentanoyl]amino]-4-carboxybutanoyl]pyrrolidine-2-carbonyl]amino]-3-methylbutanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]pyrrolidine-2-carbonyl]amino]acetyl]amino]-3-carboxypropanoyl]amino]-4-oxobutanoyl]amino]propanoyl]amino]-3-hydroxybutanoyl]pyrrolidine-2-carbonyl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 14922 | Th1552 | Albusomatropin | NA | NA | NA | NA | NA | NA | NA | Albusomatropin has been used in trials studying the treatment of Growth Hormone-Deficiency and Growth Hormone Deficiency. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14923 | Th1552 | Albusomatropin | NA | NA | NA | NA | NA | NA | NA | Albusomatropin has been used in trials studying the treatment of Growth Hormone-Deficiency and Growth Hormone Deficiency. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14924 | Th1552 | Albusomatropin | NA | NA | NA | NA | NA | NA | NA | Albusomatropin has been used in trials studying the treatment of Growth Hormone-Deficiency and Growth Hormone Deficiency. | NA | NA | NA | NA | NA | NA | NA | NA | Peptide Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14926 | Th1552 | Albusomatropin | NA | NA | NA | NA | NA | NA | NA | Albusomatropin has been used in trials studying the treatment of Growth Hormone-Deficiency and Growth Hormone Deficiency. | NA | NA | NA | NA | NA | NA | NA | NA | Pituitary Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14927 | Th1552 | Albusomatropin | NA | NA | NA | NA | NA | NA | NA | Albusomatropin has been used in trials studying the treatment of Growth Hormone-Deficiency and Growth Hormone Deficiency. | NA | NA | NA | NA | NA | NA | NA | NA | Pituitary Hormones, Anterior | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 14968 | Th1556 | Urocortin-2 | >Th1556_Urocortin-2 MTRCALLLLMVLMLGRVLVVPVTPIPTFQLRPQNSPQTTPRPAASESPSAAPTWPWAAQSHCSPTRHPGSRIVLSLDVPIGLLQILLEQARARAAREQATTNARILARVGHC | NA | NA | NA | NA | NA | NA | Urocortin 2 has been investigated for the basic science of Heart Failure and Cardiovascular Disease. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-4-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3S)-2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S,3S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3S)-2-amino-3-methylpentanoyl]amino]-3-methylbutanoyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-methylbutanoyl]pyrrolidine-2-carbonyl]amino]-3-methylpentanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-5-oxopentanoyl]amino]-3-methylpentanoyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-4-carboxybutanoyl]amino]-5-oxopentanoyl]amino]propanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]propanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-[[(2S)-5-amino-1-[[(2S)-1-[[(2S,3R)-1-[[(2S,3R)-1-[[(2S)-4-amino-1-[[(2S)-1-[[(2S)-1-[[(2S,3S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[2-[[(2S)-1-[[(2R)-1-amino-1-oxo-3-sulfanylpropan-2-yl]amino]-3-(1H-imidazol-5-yl)-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-3-methyl-1-oxobutan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-1,4-dioxobutan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 14969 | Th1556 | Urocortin-2 | >Th1556_Urocortin-2 MTRCALLLLMVLMLGRVLVVPVTPIPTFQLRPQNSPQTTPRPAASESPSAAPTWPWAAQSHCSPTRHPGSRIVLSLDVPIGLLQILLEQARARAAREQATTNARILARVGHC | NA | NA | NA | NA | NA | NA | Urocortin 2 has been investigated for the basic science of Heart Failure and Cardiovascular Disease. | NA | NA | NA | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-4-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3S)-2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S,3S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3S)-2-amino-3-methylpentanoyl]amino]-3-methylbutanoyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-methylbutanoyl]pyrrolidine-2-carbonyl]amino]-3-methylpentanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-5-oxopentanoyl]amino]-3-methylpentanoyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-4-carboxybutanoyl]amino]-5-oxopentanoyl]amino]propanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]propanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-[[(2S)-5-amino-1-[[(2S)-1-[[(2S,3R)-1-[[(2S,3R)-1-[[(2S)-4-amino-1-[[(2S)-1-[[(2S)-1-[[(2S,3S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[2-[[(2S)-1-[[(2R)-1-amino-1-oxo-3-sulfanylpropan-2-yl]amino]-3-(1H-imidazol-5-yl)-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-3-methyl-1-oxobutan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-1,4-dioxobutan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 14972 | Th1556 | Urocortin-2 | >Th1556_Urocortin-2 MTRCALLLLMVLMLGRVLVVPVTPIPTFQLRPQNSPQTTPRPAASESPSAAPTWPWAAQSHCSPTRHPGSRIVLSLDVPIGLLQILLEQARARAAREQATTNARILARVGHC | NA | NA | NA | NA | NA | NA | Urocortin 2 has been investigated for the basic science of Heart Failure and Cardiovascular Disease. | NA | NA | NA | NA | NA | NA | NA | NA | Peptide Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-4-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3S)-2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S,3S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3S)-2-amino-3-methylpentanoyl]amino]-3-methylbutanoyl]amino]-4-methylpentanoyl]amino]-3-hydroxypropanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-3-methylbutanoyl]pyrrolidine-2-carbonyl]amino]-3-methylpentanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-5-oxopentanoyl]amino]-3-methylpentanoyl]amino]-4-methylpentanoyl]amino]-4-methylpentanoyl]amino]-4-carboxybutanoyl]amino]-5-oxopentanoyl]amino]propanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]propanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-[[(2S)-5-amino-1-[[(2S)-1-[[(2S,3R)-1-[[(2S,3R)-1-[[(2S)-4-amino-1-[[(2S)-1-[[(2S)-1-[[(2S,3S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[2-[[(2S)-1-[[(2R)-1-amino-1-oxo-3-sulfanylpropan-2-yl]amino]-3-(1H-imidazol-5-yl)-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-3-methyl-1-oxobutan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-1,4-dioxobutan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 15622 | Th1613 | Luteinizing hormone | >Th1613_Luteinizing_hormone APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Hormones | NA | NA | NA | NA | NA | Repronex | Ferring Pharmaceuticals | Ferring Pharmaceuticals | Intramuscular; Subcutaneous | NA | Repronex® (menotropins for injection) is contraindicated in women who have: A high FSH level indicating primary ovarian failure. Uncontrolled thyroid and adrenal dysfunction. An organic intracranial lesion such as a pituitary tumor. The presence of any cause of infertility other than anovulation unless they are candidates for in vitro-fertilization. Abnormal bleeding of undetermined origin. Ovarian cysts or enlargement not due to polycystic ovary syndrome. Prior hypersensitivity to menotropins. Repronex® (menotropins for injection) is not indicated in women who are pregnant. There are limited human data on the effects of menotropins when administered during pregnancy. | headache mild stomach pain bloating injection site reactions (redness, pain, swelling, or irritation) breast tenderness or enlargement dizziness ovarian enlargement (abdominal or pelvic pain, tenderness, pressure, or swelling) nausea vomiting diarrhea shortness of breath pain/warmth/tenderness centralized in an arm or leg fever chills drowsiness weakness or aching of muscles or joints, or rash | Menotropins injection is used to treat infertility in women. Menotropins are a mixture of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) that are produced in the body by the pituitary gland. Menotropins injection is used in women with healthy ovaries who are enrolled in a fertility program... | Repronex is a prescription medicine used to treat the symptoms of Ovulation Induction, Assisted Reproductive Technology (ART), and Spermatogenesis. Repronex may be used alone or with other medications. | NA | FOR SUBCUTANEOUS INJECTION AND INTRAMUSCULAR INJECTION | Link | Link | NA |
| 15623 | Th1613 | Luteinizing hormone | >Th1613_Luteinizing_hormone APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15624 | Th1613 | Luteinizing hormone | >Th1613_Luteinizing_hormone APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Peptide Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15626 | Th1613 | Luteinizing hormone | >Th1613_Luteinizing_hormone APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Pituitary Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15627 | Th1613 | Luteinizing hormone | >Th1613_Luteinizing_hormone APDVQDCPECTLQENPFFSQPGAPILQCMGCCFSRAYPTPLRSKKTMLVQKNVTSESTCCVAKSYNRVTVMGGFKVENHTACHCSTCYYHKS | NA | NA | NA | NA | NA | NA | 0 | NA | NA | NA | NA | NA | NA | NA | NA | Pituitary Hormones, Anterior | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15628 | Th1614 | Mecasermin rinfabate | >Th1614_Mecasermin_rinfabate GPETLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSA | NA | NA | NA | NA | NA | Half life ranges from 10 to 16 hours with a mean of 13 hours[F4054]. Mecasermin rinfabate is said to have a longer half life than [DB01277][A176065]. | Mecasermin rinfabate is approved for severe primary insulin-like growth factor (IGF) deficiency or in patients with GH gene deletion who have developed antibodies to growth hormone (GH)[A176020]. Mecasermin rinfabate is similar to [DB01277] in that both drugs contain recombinant DNA origin insulin-like growth factor 1 (IGF-1). Mecasermin rinfabate however, is already bound to recombinant DNA origin insulin-like growth factor binding protein 3 (IGFBP-3)[A12605]. The binding of IGF-1 to IGFBP-3 is said to extend the half life and reduce the clearance of IGF-1 in patients with growth hormone resistant syndromes and low levels of IGFBP-3 though this may represent <500 patients worldwide[A176065]. Mecasermin rinfabate manufactured by Insmed Incorporated under the brand name Iplex was approved by the FDA in 2005[L5722]. In 2007 Insmed withdrew their application for a marketing authorization with The European Medicines Agency[F4075]. | Mecasermin rinfabate was approved for treatment of severe primary insulin-like growth factor (IGF) deficiency or in patients with GH gene deletion who have developed antibodies to growth hormone (GH)[A176020]. Severe primary IGF-1 deficiency is defined by:[FDA Label] A) height standard deviation (SD) score less than or equal to 3 SD below normal B) basal IGF-1 SD score less than or equal to 3 SD below normal C) normal or above normal levels of growth hormone In 2007, Insmed (Mecasermin rinfabate's manufacturer) made an agreement with Tercica (Mecasermin's manufacturer) that Mecasermin would no longer be available for this indication but could be developed for non short stature conditions such as severe insulin resistance, myotonic muscular dystrophy, and HIV associated adipose redistribution syndrome[A176125]. | Mecasermin rinfabate promotes vertical growth in pediatric patients in a similar fashion to [DB01277][FDA Label]. [DB01277] is a biosynthetic (recombinant DNA origin) form of human insulin-like growth factor 1 (IGF-1) designed to replace natural IGF-1 in pediatric patients who are deficient, promoting normalized statural growth[A2324]. Growth hormones (GH) bind to growth hormone receptors (GHR) in the liver and other tissues, which stimulates the synthesis of IGF-1. In target tissues, IGF-1 activates the IGF-1 receptor, resulting in intracellular signals that stimulate growth [A2323]. Although many actions of the GH are mediated through IGF-1, the precise roles of GH and IGF-1 have not been fully elucidated. Patients with severe primary IGF-1 deficiency (Primary IGFD) fail to produce adequate levels of IGF-1, due to disruption of the GH pathway used to promote IGF-1 release (possible GH pathway disruptions include mutations in the GHR, post-GHR signaling pathway, and IGF-1 gene defects[A176065]. The structure of IGFBP-3 remains unsolved[A176309]. | Mecasermin rinfabate supplies recombinant-DNA-origin IGF-1 (rhIGF-1) bound to recombinant-DNA-origin IGFBP-3. 80% of IGF-1 is naturally bound to IGFBP-3 so the binding of rhIGF-1 to rhIGFBP-3 increases the half life of rhIGF-1 compared to [DB01277]. rhIGF-1 binds to the Type I IGF-1 receptor. This receptor exerts intra-cellular signaling activity in a number of processes involved in statural growth, including mitogenesis in multiple tissue types, chondrocyte growth and division along cartilage growth plates, and increases in organ growth[A2324]. | Studies on carcinogenicity, genotoxicity, animal fertility, fetal development, excretion in breast milk, and use in patients over 65 years have not been performed[FDA Label]. Use in pregnant, breast feeding, or geriatric populations should be avoided as there is a lack of safety data[FDA Label]. Animal reproductive toxicity studies have shown increased incidence of abortion, post implantation loss, fewer viable fetuses, and an increase in fetal skeletal abnormalities[F4054]. Insulin-like growth factor 1 (IGF-1) without insulin-like growth factor binding protein 3 (IGFBP-3) has been shown to not be mutagenic according to the Ames test and have no affect on fertility in rats given 7 times the maximum human recommended dose based on body surface area[FDA Label]. No studies have been performed in patients with impaired renal or hepatic function however these impairments are not expected to significantly affect the pharmacokinetics of Mecasermin rinfabate[F4054]. | There is little published data on the pharmacokinetics of Mecasermin rinfabate[A12605]. Mecasermin rinfabate is expected to degrade into small peptides and amino acids[F4054]. It is suspected that IGFBP-3 in Mecasermin rinfabate is broken down by serine proteases or metalloproteases[A12605]. | There is little published data on the pharmacokinetics of Mecasermin rinfabate[A12605]. Mecasermin rinfabate is injected subcutaneously and distributes rapidly throughout the body, especially in well vascularized tissue[F4054]. | Approximately 1000mL/kg[F4054]. | Clearance ranges from 50 to 56mL/hr/kg with a mean of 53mL/hr/kg[F4054]. Mecasermin rinfabate is said to have lower clearance than [DB01277][A176065] | Anterior Pituitary Lobe Hormones and Analogues | NA | NA | NA | NA | Insulin-like growth factor 1 receptor,Insulin receptor,Cation-independent mannose-6-phosphate receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15629 | Th1614 | Mecasermin rinfabate | >Th1614_Mecasermin_rinfabate GPETLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSA | NA | NA | NA | NA | NA | Half life ranges from 10 to 16 hours with a mean of 13 hours[F4054]. Mecasermin rinfabate is said to have a longer half life than [DB01277][A176065]. | Mecasermin rinfabate is approved for severe primary insulin-like growth factor (IGF) deficiency or in patients with GH gene deletion who have developed antibodies to growth hormone (GH)[A176020]. Mecasermin rinfabate is similar to [DB01277] in that both drugs contain recombinant DNA origin insulin-like growth factor 1 (IGF-1). Mecasermin rinfabate however, is already bound to recombinant DNA origin insulin-like growth factor binding protein 3 (IGFBP-3)[A12605]. The binding of IGF-1 to IGFBP-3 is said to extend the half life and reduce the clearance of IGF-1 in patients with growth hormone resistant syndromes and low levels of IGFBP-3 though this may represent <500 patients worldwide[A176065]. Mecasermin rinfabate manufactured by Insmed Incorporated under the brand name Iplex was approved by the FDA in 2005[L5722]. In 2007 Insmed withdrew their application for a marketing authorization with The European Medicines Agency[F4075]. | Mecasermin rinfabate was approved for treatment of severe primary insulin-like growth factor (IGF) deficiency or in patients with GH gene deletion who have developed antibodies to growth hormone (GH)[A176020]. Severe primary IGF-1 deficiency is defined by:[FDA Label] A) height standard deviation (SD) score less than or equal to 3 SD below normal B) basal IGF-1 SD score less than or equal to 3 SD below normal C) normal or above normal levels of growth hormone In 2007, Insmed (Mecasermin rinfabate's manufacturer) made an agreement with Tercica (Mecasermin's manufacturer) that Mecasermin would no longer be available for this indication but could be developed for non short stature conditions such as severe insulin resistance, myotonic muscular dystrophy, and HIV associated adipose redistribution syndrome[A176125]. | Mecasermin rinfabate promotes vertical growth in pediatric patients in a similar fashion to [DB01277][FDA Label]. [DB01277] is a biosynthetic (recombinant DNA origin) form of human insulin-like growth factor 1 (IGF-1) designed to replace natural IGF-1 in pediatric patients who are deficient, promoting normalized statural growth[A2324]. Growth hormones (GH) bind to growth hormone receptors (GHR) in the liver and other tissues, which stimulates the synthesis of IGF-1. In target tissues, IGF-1 activates the IGF-1 receptor, resulting in intracellular signals that stimulate growth [A2323]. Although many actions of the GH are mediated through IGF-1, the precise roles of GH and IGF-1 have not been fully elucidated. Patients with severe primary IGF-1 deficiency (Primary IGFD) fail to produce adequate levels of IGF-1, due to disruption of the GH pathway used to promote IGF-1 release (possible GH pathway disruptions include mutations in the GHR, post-GHR signaling pathway, and IGF-1 gene defects[A176065]. The structure of IGFBP-3 remains unsolved[A176309]. | Mecasermin rinfabate supplies recombinant-DNA-origin IGF-1 (rhIGF-1) bound to recombinant-DNA-origin IGFBP-3. 80% of IGF-1 is naturally bound to IGFBP-3 so the binding of rhIGF-1 to rhIGFBP-3 increases the half life of rhIGF-1 compared to [DB01277]. rhIGF-1 binds to the Type I IGF-1 receptor. This receptor exerts intra-cellular signaling activity in a number of processes involved in statural growth, including mitogenesis in multiple tissue types, chondrocyte growth and division along cartilage growth plates, and increases in organ growth[A2324]. | Studies on carcinogenicity, genotoxicity, animal fertility, fetal development, excretion in breast milk, and use in patients over 65 years have not been performed[FDA Label]. Use in pregnant, breast feeding, or geriatric populations should be avoided as there is a lack of safety data[FDA Label]. Animal reproductive toxicity studies have shown increased incidence of abortion, post implantation loss, fewer viable fetuses, and an increase in fetal skeletal abnormalities[F4054]. Insulin-like growth factor 1 (IGF-1) without insulin-like growth factor binding protein 3 (IGFBP-3) has been shown to not be mutagenic according to the Ames test and have no affect on fertility in rats given 7 times the maximum human recommended dose based on body surface area[FDA Label]. No studies have been performed in patients with impaired renal or hepatic function however these impairments are not expected to significantly affect the pharmacokinetics of Mecasermin rinfabate[F4054]. | There is little published data on the pharmacokinetics of Mecasermin rinfabate[A12605]. Mecasermin rinfabate is expected to degrade into small peptides and amino acids[F4054]. It is suspected that IGFBP-3 in Mecasermin rinfabate is broken down by serine proteases or metalloproteases[A12605]. | There is little published data on the pharmacokinetics of Mecasermin rinfabate[A12605]. Mecasermin rinfabate is injected subcutaneously and distributes rapidly throughout the body, especially in well vascularized tissue[F4054]. | Approximately 1000mL/kg[F4054]. | Clearance ranges from 50 to 56mL/hr/kg with a mean of 53mL/hr/kg[F4054]. Mecasermin rinfabate is said to have lower clearance than [DB01277][A176065] | Pituitary and Hypothalamic Hormones and Analogues | NA | NA | NA | NA | Insulin-like growth factor 1 receptor,Insulin receptor,Cation-independent mannose-6-phosphate receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15631 | Th1614 | Mecasermin rinfabate | >Th1614_Mecasermin_rinfabate GPETLCGAELVDALQFVCGDRGFYFNKPTGYGSSSRRAPQTGIVDECCFRSCDLRRLEMYCAPLKPAKSA | NA | NA | NA | NA | NA | Half life ranges from 10 to 16 hours with a mean of 13 hours[F4054]. Mecasermin rinfabate is said to have a longer half life than [DB01277][A176065]. | Mecasermin rinfabate is approved for severe primary insulin-like growth factor (IGF) deficiency or in patients with GH gene deletion who have developed antibodies to growth hormone (GH)[A176020]. Mecasermin rinfabate is similar to [DB01277] in that both drugs contain recombinant DNA origin insulin-like growth factor 1 (IGF-1). Mecasermin rinfabate however, is already bound to recombinant DNA origin insulin-like growth factor binding protein 3 (IGFBP-3)[A12605]. The binding of IGF-1 to IGFBP-3 is said to extend the half life and reduce the clearance of IGF-1 in patients with growth hormone resistant syndromes and low levels of IGFBP-3 though this may represent <500 patients worldwide[A176065]. Mecasermin rinfabate manufactured by Insmed Incorporated under the brand name Iplex was approved by the FDA in 2005[L5722]. In 2007 Insmed withdrew their application for a marketing authorization with The European Medicines Agency[F4075]. | Mecasermin rinfabate was approved for treatment of severe primary insulin-like growth factor (IGF) deficiency or in patients with GH gene deletion who have developed antibodies to growth hormone (GH)[A176020]. Severe primary IGF-1 deficiency is defined by:[FDA Label] A) height standard deviation (SD) score less than or equal to 3 SD below normal B) basal IGF-1 SD score less than or equal to 3 SD below normal C) normal or above normal levels of growth hormone In 2007, Insmed (Mecasermin rinfabate's manufacturer) made an agreement with Tercica (Mecasermin's manufacturer) that Mecasermin would no longer be available for this indication but could be developed for non short stature conditions such as severe insulin resistance, myotonic muscular dystrophy, and HIV associated adipose redistribution syndrome[A176125]. | Mecasermin rinfabate promotes vertical growth in pediatric patients in a similar fashion to [DB01277][FDA Label]. [DB01277] is a biosynthetic (recombinant DNA origin) form of human insulin-like growth factor 1 (IGF-1) designed to replace natural IGF-1 in pediatric patients who are deficient, promoting normalized statural growth[A2324]. Growth hormones (GH) bind to growth hormone receptors (GHR) in the liver and other tissues, which stimulates the synthesis of IGF-1. In target tissues, IGF-1 activates the IGF-1 receptor, resulting in intracellular signals that stimulate growth [A2323]. Although many actions of the GH are mediated through IGF-1, the precise roles of GH and IGF-1 have not been fully elucidated. Patients with severe primary IGF-1 deficiency (Primary IGFD) fail to produce adequate levels of IGF-1, due to disruption of the GH pathway used to promote IGF-1 release (possible GH pathway disruptions include mutations in the GHR, post-GHR signaling pathway, and IGF-1 gene defects[A176065]. The structure of IGFBP-3 remains unsolved[A176309]. | Mecasermin rinfabate supplies recombinant-DNA-origin IGF-1 (rhIGF-1) bound to recombinant-DNA-origin IGFBP-3. 80% of IGF-1 is naturally bound to IGFBP-3 so the binding of rhIGF-1 to rhIGFBP-3 increases the half life of rhIGF-1 compared to [DB01277]. rhIGF-1 binds to the Type I IGF-1 receptor. This receptor exerts intra-cellular signaling activity in a number of processes involved in statural growth, including mitogenesis in multiple tissue types, chondrocyte growth and division along cartilage growth plates, and increases in organ growth[A2324]. | Studies on carcinogenicity, genotoxicity, animal fertility, fetal development, excretion in breast milk, and use in patients over 65 years have not been performed[FDA Label]. Use in pregnant, breast feeding, or geriatric populations should be avoided as there is a lack of safety data[FDA Label]. Animal reproductive toxicity studies have shown increased incidence of abortion, post implantation loss, fewer viable fetuses, and an increase in fetal skeletal abnormalities[F4054]. Insulin-like growth factor 1 (IGF-1) without insulin-like growth factor binding protein 3 (IGFBP-3) has been shown to not be mutagenic according to the Ames test and have no affect on fertility in rats given 7 times the maximum human recommended dose based on body surface area[FDA Label]. No studies have been performed in patients with impaired renal or hepatic function however these impairments are not expected to significantly affect the pharmacokinetics of Mecasermin rinfabate[F4054]. | There is little published data on the pharmacokinetics of Mecasermin rinfabate[A12605]. Mecasermin rinfabate is expected to degrade into small peptides and amino acids[F4054]. It is suspected that IGFBP-3 in Mecasermin rinfabate is broken down by serine proteases or metalloproteases[A12605]. | There is little published data on the pharmacokinetics of Mecasermin rinfabate[A12605]. Mecasermin rinfabate is injected subcutaneously and distributes rapidly throughout the body, especially in well vascularized tissue[F4054]. | Approximately 1000mL/kg[F4054]. | Clearance ranges from 50 to 56mL/hr/kg with a mean of 53mL/hr/kg[F4054]. Mecasermin rinfabate is said to have lower clearance than [DB01277][A176065] | Systemic Hormonal Preparations, Excl. Sex Hormones and Insulins | NA | NA | NA | NA | Insulin-like growth factor 1 receptor,Insulin receptor,Cation-independent mannose-6-phosphate receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15683 | Th1618 | Somatrogon | >Th1618_Somatrogon SSSSKAPPPSLPSPSRLPGPSDTPILPQFPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGFSSSSKAPPPSLPSPSRLPGPSDTPILPQSSSSKAPPPSLPSPSRLPGPSDTPILPQ | 30465.1 | C1359H2125N361O420S7 | NA | NA | NA | Following subcutaneous administration of 0.66 mg/kg/wk in pediatric patients with growth hormone deficiency, the half-life was 28.3 hours. Somatrogon was detected in the circulation for about 6 days after the last dose.[L39362] | Somatrogon is a long-acting recombinant human growth hormone. Growth hormone is a peptide hormone secreted by the pituitary gland that plays a crucial role in promoting longitudinal growth during childhood and adolescence and regulating metabolic function in adulthood.[A241515] Recombinant growth hormone therapy for growth hormone deficiency and other conditions has been available since 1985, with daily administration being the standard treatment for many years. More recently, longer-acting forms of growth hormone were developed to improve patient adherence and thus, improve the therapeutic efficacy of treatment.[A241485] Somatrogon was produced in Chinese Hamster Ovary (CHO) cells using recombinant DNA technology. It is a chimeric product generated by fusing three copies of the C-terminal peptide (CTP), or 28 carboxy-terminal residues, from the beta chain of human chorionic gonadotropin (hCG) to the N-terminus and C-terminus of human growth hormone.[A241515,L39362] The glycosylation and the presence of CTPs in the protein sequence prolongs the half-life of somatrogon and allows its once-weekly dosing.[L39362] In October 2021, Health Canada approved somatrogon under the market name NGENLA as the long-term treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone caused by growth hormone deficiency, marking Canada as the first country to approve this drug.[L39060] It is available as a once-weekly subcutaneous injection.[L39080] | Somatrogon is indicated for the long-term treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone (growth hormone deficiency).[L39362] | Somatrogon mimics the physiological actions of endogenous growth hormone, such as cell proliferation, metabolism, and growth. It was also shown to increase the serum concentration of insulin-like growth factor (IGF-1).[L39362] | Growth hormone is a key hormone that promotes body growth and regulates carbohydrate, protein and lipid metabolism.[A243092] Somatrogon is a hormone replacement therapy that aims to restore deficient levels of growth hormone (GH). Like endogenous growth hormone, somatrogon binds to the GH receptor, which leads to the binding of JAK2 to GH receptor and activation of JAK2. Activation of JAK2 and phosphorylation of both JAK2 and GHR initiates the recruits various signalling proteins and facilitates multiple signalling pathways responsible for growth and metabolism.[A243092] One of the activated signalling pathways is the STAT5b signalling pathway, which is critical for the effect of GH on body height.[L39362] | Subcutaneous doses of somatrogon higher than 0.66 mg/kg per week have not been studied. Based on existing clinical data of other growth hormone products, short-term overdosage from somatrogon could lead initially to hypoglycemia and subsequently to hyperglycemia. Long-term overdosage could result in signs and symptoms of gigantism or acromegaly consistent with the effects of excess growth hormone. Overdose with somatrogon should be treated with general supportive measures.[L39362] | Somatrogon is expected to undergo protein catabolism, with subsequent reclamation of the amino acids and return to the systemic circulation.[L39362] | Following subcutaneous administration of 0.66 mg/kg/wk in pediatric patients with growth hormone deficiency, Cmax of somatrogon was 690 ng/mL. Tmax was 8 hours and the AUC was 21800 ng x h/mL. Over the dose range of 0.25-0.66 mg/kg/week, somatrogon exposure increased in a dose-proportional manner.[L39362] | Following subcutaneous administration of 0.66 mg/kg/wk in pediatric patients with growth hormone deficiency, the apparent central volume of distribution (Vc) was 0.812 L/kg and the apparent peripheral volume of distribution (Vt) was 0.169 L/kg. Somatrogon does not accumulate after once-weekly administration.[L39362] | Following subcutaneous administration of 0.66 mg/kg/wk in pediatric patients with growth hormone deficiency, the clearance was 0.0336 L/h/kg.[L39362] | Hormones | NA | NA | NA | NA | NA | Ngenla | Pfizer Canada Ulc | Pfizer Canada Ulc | Subcutaneous | 50 mg / mL | NA | The most common side effects with Ngenla (which may affect more than 1 in 10 people) are reactions at the site of injection, headache, and fever. | Ngenla can only be obtained with a prescription and treatment should be started and monitored by a doctor experienced in the management of children and adolescents with growth hormone deficiency. Ngenla is available as an injection in pre-filled pens of different strengths, to be given under the skin once a week. The recommended dose is 0.66 mg per kilogram of body weight each week, adjusted by the doctor if necessary. For patients over 45 kg who require doses higher than 30 mg the dose is given as two injections. Patients or their caregivers can inject the dose themselves after appropriate training. | Ngenla is a medicine used to treat children and adolescents who are not growing at the normal rate as a result of growth hormone deficiency (lack of natural growth hormone). It is given to patients from 3 years of age. | NA | NA | Link | Link | NA |
| 15684 | Th1618 | Somatrogon | >Th1618_Somatrogon SSSSKAPPPSLPSPSRLPGPSDTPILPQFPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGFSSSSKAPPPSLPSPSRLPGPSDTPILPQSSSSKAPPPSLPSPSRLPGPSDTPILPQ | 30465.1 | C1359H2125N361O420S7 | NA | NA | NA | Following subcutaneous administration of 0.66 mg/kg/wk in pediatric patients with growth hormone deficiency, the half-life was 28.3 hours. Somatrogon was detected in the circulation for about 6 days after the last dose.[L39362] | Somatrogon is a long-acting recombinant human growth hormone. Growth hormone is a peptide hormone secreted by the pituitary gland that plays a crucial role in promoting longitudinal growth during childhood and adolescence and regulating metabolic function in adulthood.[A241515] Recombinant growth hormone therapy for growth hormone deficiency and other conditions has been available since 1985, with daily administration being the standard treatment for many years. More recently, longer-acting forms of growth hormone were developed to improve patient adherence and thus, improve the therapeutic efficacy of treatment.[A241485] Somatrogon was produced in Chinese Hamster Ovary (CHO) cells using recombinant DNA technology. It is a chimeric product generated by fusing three copies of the C-terminal peptide (CTP), or 28 carboxy-terminal residues, from the beta chain of human chorionic gonadotropin (hCG) to the N-terminus and C-terminus of human growth hormone.[A241515,L39362] The glycosylation and the presence of CTPs in the protein sequence prolongs the half-life of somatrogon and allows its once-weekly dosing.[L39362] In October 2021, Health Canada approved somatrogon under the market name NGENLA as the long-term treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone caused by growth hormone deficiency, marking Canada as the first country to approve this drug.[L39060] It is available as a once-weekly subcutaneous injection.[L39080] | Somatrogon is indicated for the long-term treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone (growth hormone deficiency).[L39362] | Somatrogon mimics the physiological actions of endogenous growth hormone, such as cell proliferation, metabolism, and growth. It was also shown to increase the serum concentration of insulin-like growth factor (IGF-1).[L39362] | Growth hormone is a key hormone that promotes body growth and regulates carbohydrate, protein and lipid metabolism.[A243092] Somatrogon is a hormone replacement therapy that aims to restore deficient levels of growth hormone (GH). Like endogenous growth hormone, somatrogon binds to the GH receptor, which leads to the binding of JAK2 to GH receptor and activation of JAK2. Activation of JAK2 and phosphorylation of both JAK2 and GHR initiates the recruits various signalling proteins and facilitates multiple signalling pathways responsible for growth and metabolism.[A243092] One of the activated signalling pathways is the STAT5b signalling pathway, which is critical for the effect of GH on body height.[L39362] | Subcutaneous doses of somatrogon higher than 0.66 mg/kg per week have not been studied. Based on existing clinical data of other growth hormone products, short-term overdosage from somatrogon could lead initially to hypoglycemia and subsequently to hyperglycemia. Long-term overdosage could result in signs and symptoms of gigantism or acromegaly consistent with the effects of excess growth hormone. Overdose with somatrogon should be treated with general supportive measures.[L39362] | Somatrogon is expected to undergo protein catabolism, with subsequent reclamation of the amino acids and return to the systemic circulation.[L39362] | Following subcutaneous administration of 0.66 mg/kg/wk in pediatric patients with growth hormone deficiency, Cmax of somatrogon was 690 ng/mL. Tmax was 8 hours and the AUC was 21800 ng x h/mL. Over the dose range of 0.25-0.66 mg/kg/week, somatrogon exposure increased in a dose-proportional manner.[L39362] | Following subcutaneous administration of 0.66 mg/kg/wk in pediatric patients with growth hormone deficiency, the apparent central volume of distribution (Vc) was 0.812 L/kg and the apparent peripheral volume of distribution (Vt) was 0.169 L/kg. Somatrogon does not accumulate after once-weekly administration.[L39362] | Following subcutaneous administration of 0.66 mg/kg/wk in pediatric patients with growth hormone deficiency, the clearance was 0.0336 L/h/kg.[L39362] | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15685 | Th1618 | Somatrogon | >Th1618_Somatrogon SSSSKAPPPSLPSPSRLPGPSDTPILPQFPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSLVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGFSSSSKAPPPSLPSPSRLPGPSDTPILPQSSSSKAPPPSLPSPSRLPGPSDTPILPQ | 30465.1 | C1359H2125N361O420S7 | NA | NA | NA | Following subcutaneous administration of 0.66 mg/kg/wk in pediatric patients with growth hormone deficiency, the half-life was 28.3 hours. Somatrogon was detected in the circulation for about 6 days after the last dose.[L39362] | Somatrogon is a long-acting recombinant human growth hormone. Growth hormone is a peptide hormone secreted by the pituitary gland that plays a crucial role in promoting longitudinal growth during childhood and adolescence and regulating metabolic function in adulthood.[A241515] Recombinant growth hormone therapy for growth hormone deficiency and other conditions has been available since 1985, with daily administration being the standard treatment for many years. More recently, longer-acting forms of growth hormone were developed to improve patient adherence and thus, improve the therapeutic efficacy of treatment.[A241485] Somatrogon was produced in Chinese Hamster Ovary (CHO) cells using recombinant DNA technology. It is a chimeric product generated by fusing three copies of the C-terminal peptide (CTP), or 28 carboxy-terminal residues, from the beta chain of human chorionic gonadotropin (hCG) to the N-terminus and C-terminus of human growth hormone.[A241515,L39362] The glycosylation and the presence of CTPs in the protein sequence prolongs the half-life of somatrogon and allows its once-weekly dosing.[L39362] In October 2021, Health Canada approved somatrogon under the market name NGENLA as the long-term treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone caused by growth hormone deficiency, marking Canada as the first country to approve this drug.[L39060] It is available as a once-weekly subcutaneous injection.[L39080] | Somatrogon is indicated for the long-term treatment of pediatric patients who have growth failure due to an inadequate secretion of endogenous growth hormone (growth hormone deficiency).[L39362] | Somatrogon mimics the physiological actions of endogenous growth hormone, such as cell proliferation, metabolism, and growth. It was also shown to increase the serum concentration of insulin-like growth factor (IGF-1).[L39362] | Growth hormone is a key hormone that promotes body growth and regulates carbohydrate, protein and lipid metabolism.[A243092] Somatrogon is a hormone replacement therapy that aims to restore deficient levels of growth hormone (GH). Like endogenous growth hormone, somatrogon binds to the GH receptor, which leads to the binding of JAK2 to GH receptor and activation of JAK2. Activation of JAK2 and phosphorylation of both JAK2 and GHR initiates the recruits various signalling proteins and facilitates multiple signalling pathways responsible for growth and metabolism.[A243092] One of the activated signalling pathways is the STAT5b signalling pathway, which is critical for the effect of GH on body height.[L39362] | Subcutaneous doses of somatrogon higher than 0.66 mg/kg per week have not been studied. Based on existing clinical data of other growth hormone products, short-term overdosage from somatrogon could lead initially to hypoglycemia and subsequently to hyperglycemia. Long-term overdosage could result in signs and symptoms of gigantism or acromegaly consistent with the effects of excess growth hormone. Overdose with somatrogon should be treated with general supportive measures.[L39362] | Somatrogon is expected to undergo protein catabolism, with subsequent reclamation of the amino acids and return to the systemic circulation.[L39362] | Following subcutaneous administration of 0.66 mg/kg/wk in pediatric patients with growth hormone deficiency, Cmax of somatrogon was 690 ng/mL. Tmax was 8 hours and the AUC was 21800 ng x h/mL. Over the dose range of 0.25-0.66 mg/kg/week, somatrogon exposure increased in a dose-proportional manner.[L39362] | Following subcutaneous administration of 0.66 mg/kg/wk in pediatric patients with growth hormone deficiency, the apparent central volume of distribution (Vc) was 0.812 L/kg and the apparent peripheral volume of distribution (Vt) was 0.169 L/kg. Somatrogon does not accumulate after once-weekly administration.[L39362] | Following subcutaneous administration of 0.66 mg/kg/wk in pediatric patients with growth hormone deficiency, the clearance was 0.0336 L/h/kg.[L39362] | Peptide Hormones | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 15740 | Th1622 | Somapacitan | >Th1622_Somapacitan FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSCVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | NA | C1038H1609N273O319S9 | NA | NA | NA | The elimination half life of somapacitan is 2-3 days.[L15661] | Somapacitan, also known as NNC0195-0092,[A219136] is a growth hormone analog indicated to treat adults with growth hormone deficiency.[A219126,L15661] This human growth hormone analog differs by the creation of an albumin binding site, and prolonging the effect so that it requires weekly dosing rather than daily.[A219146] Somapacitan was granted FDA approval on 28 August 2020.[L15666] | Somapacitan is indicated as a replacement for growth hormone in adult patients with growth hormone deficiency.[L15661] | Somapacitan stimulates the growth hormone receptor.[L15661] Somapacitan has a long duration of action as it is given once weekly.[L15661] It has a moderately wide therapeutic window as an acute overdose may cause hypoglycemia followed by hyperglycemia.[L15661] Patients should be counselled regarding the risk of increased mortality in patients with critical illness, risk of neoplasms, glucose intolerance in diabetes mellitus, intracranial hypertension, hypersensitivity, fluid retention, hypoadrenalism, hypothyroidism, pancreatitis, lipohypertrophy, and lipoatrophy.[L15661] | Somapacitan binds to the growth hormone receptor and induces intracellular signalling to up-regulate insulin-like growth factor I (IGF-1).[A219096,L15661] IGF-1 causes growth in bones and muscle tissue.[A219096] Growth hormones more directly cause the fusion of myoblasts and myotubes to cause muscle fibre growth, activate neural stem cells, and induce chondrocyte proliferation.[A219096] | Patients experiencing an acute overdose of somapacitan may present with fluid retention.[L15661] Chronic overdose may resemble gigantism or acromegaly.[L15661] Treat patients with symptomatic and supportive measures to minimize the permanent effects.[A219141] | Studies in humans and rats show that somapacitan is metabolized through cleavage of the albumin-binding moiety and linker sidechain before further non-specific mechanisms.[A219096,L15661] | A 0.02mg/kg single dose of somapacitan reaches a Cmax of 14.4 ng/mL, with a Tmax of 11.1 hours, and an AUC of 475 ng | The approximate volume of distribution of somapacitan is 14.6 L.[L15661] | The apparent maximum rate of saturable elimination is estimated to be 0.268 ± 0.03 mg/h.[A219126] | Hormones | NA | NA | NA | NA | Growth hormone receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2S)-5-[2-[2-[2-[[(2S)-1-amino-6-[[2-[(2R)-2-amino-2-carboxyethyl]sulfanylacetyl]amino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]ethoxy]ethylamino]-2-[[(4S)-4-carboxy-4-[[2-[2-[2-[4-[16-(2H-tetrazol-5-yl)hexadecanoylsulfamoyl]butanoylamino]ethoxy]ethoxy]acetyl]amino]butanoyl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 15741 | Th1622 | Somapacitan | >Th1622_Somapacitan FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSCVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | NA | C1038H1609N273O319S9 | NA | NA | NA | The elimination half life of somapacitan is 2-3 days.[L15661] | Somapacitan, also known as NNC0195-0092,[A219136] is a growth hormone analog indicated to treat adults with growth hormone deficiency.[A219126,L15661] This human growth hormone analog differs by the creation of an albumin binding site, and prolonging the effect so that it requires weekly dosing rather than daily.[A219146] Somapacitan was granted FDA approval on 28 August 2020.[L15666] | Somapacitan is indicated as a replacement for growth hormone in adult patients with growth hormone deficiency.[L15661] | Somapacitan stimulates the growth hormone receptor.[L15661] Somapacitan has a long duration of action as it is given once weekly.[L15661] It has a moderately wide therapeutic window as an acute overdose may cause hypoglycemia followed by hyperglycemia.[L15661] Patients should be counselled regarding the risk of increased mortality in patients with critical illness, risk of neoplasms, glucose intolerance in diabetes mellitus, intracranial hypertension, hypersensitivity, fluid retention, hypoadrenalism, hypothyroidism, pancreatitis, lipohypertrophy, and lipoatrophy.[L15661] | Somapacitan binds to the growth hormone receptor and induces intracellular signalling to up-regulate insulin-like growth factor I (IGF-1).[A219096,L15661] IGF-1 causes growth in bones and muscle tissue.[A219096] Growth hormones more directly cause the fusion of myoblasts and myotubes to cause muscle fibre growth, activate neural stem cells, and induce chondrocyte proliferation.[A219096] | Patients experiencing an acute overdose of somapacitan may present with fluid retention.[L15661] Chronic overdose may resemble gigantism or acromegaly.[L15661] Treat patients with symptomatic and supportive measures to minimize the permanent effects.[A219141] | Studies in humans and rats show that somapacitan is metabolized through cleavage of the albumin-binding moiety and linker sidechain before further non-specific mechanisms.[A219096,L15661] | A 0.02mg/kg single dose of somapacitan reaches a Cmax of 14.4 ng/mL, with a Tmax of 11.1 hours, and an AUC of 475 ng | The approximate volume of distribution of somapacitan is 14.6 L.[L15661] | The apparent maximum rate of saturable elimination is estimated to be 0.268 ± 0.03 mg/h.[A219126] | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | Growth hormone receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2S)-5-[2-[2-[2-[[(2S)-1-amino-6-[[2-[(2R)-2-amino-2-carboxyethyl]sulfanylacetyl]amino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]ethoxy]ethylamino]-2-[[(4S)-4-carboxy-4-[[2-[2-[2-[4-[16-(2H-tetrazol-5-yl)hexadecanoylsulfamoyl]butanoylamino]ethoxy]ethoxy]acetyl]amino]butanoyl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 15743 | Th1622 | Somapacitan | >Th1622_Somapacitan FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSCVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | NA | C1038H1609N273O319S9 | NA | NA | NA | The elimination half life of somapacitan is 2-3 days.[L15661] | Somapacitan, also known as NNC0195-0092,[A219136] is a growth hormone analog indicated to treat adults with growth hormone deficiency.[A219126,L15661] This human growth hormone analog differs by the creation of an albumin binding site, and prolonging the effect so that it requires weekly dosing rather than daily.[A219146] Somapacitan was granted FDA approval on 28 August 2020.[L15666] | Somapacitan is indicated as a replacement for growth hormone in adult patients with growth hormone deficiency.[L15661] | Somapacitan stimulates the growth hormone receptor.[L15661] Somapacitan has a long duration of action as it is given once weekly.[L15661] It has a moderately wide therapeutic window as an acute overdose may cause hypoglycemia followed by hyperglycemia.[L15661] Patients should be counselled regarding the risk of increased mortality in patients with critical illness, risk of neoplasms, glucose intolerance in diabetes mellitus, intracranial hypertension, hypersensitivity, fluid retention, hypoadrenalism, hypothyroidism, pancreatitis, lipohypertrophy, and lipoatrophy.[L15661] | Somapacitan binds to the growth hormone receptor and induces intracellular signalling to up-regulate insulin-like growth factor I (IGF-1).[A219096,L15661] IGF-1 causes growth in bones and muscle tissue.[A219096] Growth hormones more directly cause the fusion of myoblasts and myotubes to cause muscle fibre growth, activate neural stem cells, and induce chondrocyte proliferation.[A219096] | Patients experiencing an acute overdose of somapacitan may present with fluid retention.[L15661] Chronic overdose may resemble gigantism or acromegaly.[L15661] Treat patients with symptomatic and supportive measures to minimize the permanent effects.[A219141] | Studies in humans and rats show that somapacitan is metabolized through cleavage of the albumin-binding moiety and linker sidechain before further non-specific mechanisms.[A219096,L15661] | A 0.02mg/kg single dose of somapacitan reaches a Cmax of 14.4 ng/mL, with a Tmax of 11.1 hours, and an AUC of 475 ng | The approximate volume of distribution of somapacitan is 14.6 L.[L15661] | The apparent maximum rate of saturable elimination is estimated to be 0.268 ± 0.03 mg/h.[A219126] | Peptide Hormones | NA | NA | NA | NA | Growth hormone receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2S)-5-[2-[2-[2-[[(2S)-1-amino-6-[[2-[(2R)-2-amino-2-carboxyethyl]sulfanylacetyl]amino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]ethoxy]ethylamino]-2-[[(4S)-4-carboxy-4-[[2-[2-[2-[4-[16-(2H-tetrazol-5-yl)hexadecanoylsulfamoyl]butanoylamino]ethoxy]ethoxy]acetyl]amino]butanoyl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 15745 | Th1622 | Somapacitan | >Th1622_Somapacitan FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSCVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | NA | C1038H1609N273O319S9 | NA | NA | NA | The elimination half life of somapacitan is 2-3 days.[L15661] | Somapacitan, also known as NNC0195-0092,[A219136] is a growth hormone analog indicated to treat adults with growth hormone deficiency.[A219126,L15661] This human growth hormone analog differs by the creation of an albumin binding site, and prolonging the effect so that it requires weekly dosing rather than daily.[A219146] Somapacitan was granted FDA approval on 28 August 2020.[L15666] | Somapacitan is indicated as a replacement for growth hormone in adult patients with growth hormone deficiency.[L15661] | Somapacitan stimulates the growth hormone receptor.[L15661] Somapacitan has a long duration of action as it is given once weekly.[L15661] It has a moderately wide therapeutic window as an acute overdose may cause hypoglycemia followed by hyperglycemia.[L15661] Patients should be counselled regarding the risk of increased mortality in patients with critical illness, risk of neoplasms, glucose intolerance in diabetes mellitus, intracranial hypertension, hypersensitivity, fluid retention, hypoadrenalism, hypothyroidism, pancreatitis, lipohypertrophy, and lipoatrophy.[L15661] | Somapacitan binds to the growth hormone receptor and induces intracellular signalling to up-regulate insulin-like growth factor I (IGF-1).[A219096,L15661] IGF-1 causes growth in bones and muscle tissue.[A219096] Growth hormones more directly cause the fusion of myoblasts and myotubes to cause muscle fibre growth, activate neural stem cells, and induce chondrocyte proliferation.[A219096] | Patients experiencing an acute overdose of somapacitan may present with fluid retention.[L15661] Chronic overdose may resemble gigantism or acromegaly.[L15661] Treat patients with symptomatic and supportive measures to minimize the permanent effects.[A219141] | Studies in humans and rats show that somapacitan is metabolized through cleavage of the albumin-binding moiety and linker sidechain before further non-specific mechanisms.[A219096,L15661] | A 0.02mg/kg single dose of somapacitan reaches a Cmax of 14.4 ng/mL, with a Tmax of 11.1 hours, and an AUC of 475 ng | The approximate volume of distribution of somapacitan is 14.6 L.[L15661] | The apparent maximum rate of saturable elimination is estimated to be 0.268 ± 0.03 mg/h.[A219126] | Pituitary Hormones | NA | NA | NA | NA | Growth hormone receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2S)-5-[2-[2-[2-[[(2S)-1-amino-6-[[2-[(2R)-2-amino-2-carboxyethyl]sulfanylacetyl]amino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]ethoxy]ethylamino]-2-[[(4S)-4-carboxy-4-[[2-[2-[2-[4-[16-(2H-tetrazol-5-yl)hexadecanoylsulfamoyl]butanoylamino]ethoxy]ethoxy]acetyl]amino]butanoyl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 15746 | Th1622 | Somapacitan | >Th1622_Somapacitan FPTIPLSRLFDNAMLRAHRLHQLAFDTYQEFEEAYIPKEQKYSFLQNPQTSLCFSESIPTPSNREETQQKSNLELLRISLLLIQSWLEPVQFLRSVFANSCVYGASDSNVYDLLKDLEEGIQTLMGRLEDGSPRTGQIFKQTYSKFDTNSHNDDALLKNYGLLYCFRKDMDKVETFLRIVQCRSVEGSCGF | NA | C1038H1609N273O319S9 | NA | NA | NA | The elimination half life of somapacitan is 2-3 days.[L15661] | Somapacitan, also known as NNC0195-0092,[A219136] is a growth hormone analog indicated to treat adults with growth hormone deficiency.[A219126,L15661] This human growth hormone analog differs by the creation of an albumin binding site, and prolonging the effect so that it requires weekly dosing rather than daily.[A219146] Somapacitan was granted FDA approval on 28 August 2020.[L15666] | Somapacitan is indicated as a replacement for growth hormone in adult patients with growth hormone deficiency.[L15661] | Somapacitan stimulates the growth hormone receptor.[L15661] Somapacitan has a long duration of action as it is given once weekly.[L15661] It has a moderately wide therapeutic window as an acute overdose may cause hypoglycemia followed by hyperglycemia.[L15661] Patients should be counselled regarding the risk of increased mortality in patients with critical illness, risk of neoplasms, glucose intolerance in diabetes mellitus, intracranial hypertension, hypersensitivity, fluid retention, hypoadrenalism, hypothyroidism, pancreatitis, lipohypertrophy, and lipoatrophy.[L15661] | Somapacitan binds to the growth hormone receptor and induces intracellular signalling to up-regulate insulin-like growth factor I (IGF-1).[A219096,L15661] IGF-1 causes growth in bones and muscle tissue.[A219096] Growth hormones more directly cause the fusion of myoblasts and myotubes to cause muscle fibre growth, activate neural stem cells, and induce chondrocyte proliferation.[A219096] | Patients experiencing an acute overdose of somapacitan may present with fluid retention.[L15661] Chronic overdose may resemble gigantism or acromegaly.[L15661] Treat patients with symptomatic and supportive measures to minimize the permanent effects.[A219141] | Studies in humans and rats show that somapacitan is metabolized through cleavage of the albumin-binding moiety and linker sidechain before further non-specific mechanisms.[A219096,L15661] | A 0.02mg/kg single dose of somapacitan reaches a Cmax of 14.4 ng/mL, with a Tmax of 11.1 hours, and an AUC of 475 ng | The approximate volume of distribution of somapacitan is 14.6 L.[L15661] | The apparent maximum rate of saturable elimination is estimated to be 0.268 ± 0.03 mg/h.[A219126] | Pituitary Hormones, Anterior | NA | NA | NA | NA | Growth hormone receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | (2S)-5-[2-[2-[2-[[(2S)-1-amino-6-[[2-[(2R)-2-amino-2-carboxyethyl]sulfanylacetyl]amino]-1-oxohexan-2-yl]amino]-2-oxoethoxy]ethoxy]ethylamino]-2-[[(4S)-4-carboxy-4-[[2-[2-[2-[4-[16-(2H-tetrazol-5-yl)hexadecanoylsulfamoyl]butanoylamino]ethoxy]ethoxy]acetyl]amino]butanoyl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 15772 | Th1625 | Dasiglucagon | >Th1625_Dasiglucagon HSQGTFTSDYSKYLDXARAEEFVKWLEST | 3382 | C152H222N38O50 | NA | NA | NA | The half-life was approximately 30 minutes following subcutaneous administration.[L39190] Dasiglucagon has a longer plasma elimination half-life than traditional reconstituted glucagon.[A242140] | Dasiglucagon is a glucagon analog that acts to increase blood sugar levels.[L39190] It consists of 29 amino acids similar to endogenous glucagon; however, it contains seven substituted amino acids for improved physical and chemical stability in its drug formulation.[L39195] In March 2021, the FDA approved dasiglucagon to treat severe hypoglycemia in patients six years and older with diabetes. It is available as a subcutaneous injection marketed as ZEGALOGUE.[L39190] Severe hypoglycemia is an acute, life-threatening medical condition resulting from a profound drop in blood glucose levels. It is characterized by neurological impairment, with manifestations like loss of consciousness and seizure. Hypoglycemia is a common side effect of antidiabetic treatments, most notably insulin and sulfonylureas. Although it tends to be more common in type 1 diabetes mellitus, occurring in about 22% to 46% of patients annually, about 7% to 25% of patients with type 2 diabetes mellitus treated with insulin experience severe hypoglycemia a year.[L39195] Even with close monitoring of blood glucose levels, it is not always possible to prevent severe hypoglycemic events in patients with diabetes, and children are particularly at risk for experiencing severe hypoglycemia.[L39200] Treatments for severe hypoglycemia have mostly been limited to intravenous dextrose and different glucagon formulations.[L39195] The approval of dasiglucagon marks the first glucagon analog approved for severe hypoglycemia treatment that does not require administration by a healthcare professional.[L39195] | Dasiglucagon is an antihypoglycemic agent indicated for the treatment of severe hypoglycemia in pediatric and adult patients with diabetes aged 6 years and above.[L39190] | Dasiglucagon works to increase blood glucose levels under normal and hypoglycemic conditions.[A242140] After administration of dasiglucagon in adult patients with type 1 diabetes, the mean glucose increase from baseline at 90 minutes was 168 mg/dL. In pediatric patients with type 1 diabetes aged seven to 17 years, the mean glucose increase at 60 minutes after administration of dasiglucagon was 162 mg/dL.[L39190] | Dasiglucagon is an analog of glucagon, which is a peptide hormone responsible for increasing blood glucose levels. It has the same mechanism of action as endogenous glucagon by acting as an agonist at glucagon receptors, which are G-coupled receptors expressed throughout the body. Dasiglucagon binds to glucagon receptors in the liver, which activates Gsa and Gq, and consequently, adenylate cyclase. Adenyl cyclase increases intracellular cyclic AMP, which stimulates glycogenolysis and glucogenesis in the liver.[A19402,A242145] As glucose is primarily released from liver glycogen stores, hepatic stores of glycogen are crucial for dasiglucagon to exert its antihypoglycemic effects.[L39190] | Overdose may be characterized by nausea, vomiting, inhibition of gastrointestinal tract motility, increased blood pressure, and elevated heart rate. In case of a suspected overdose, serum potassium may decrease so monitoring and correcting of potassium levels may be warranted. A marked increase in blood pressure may be managed by the short-term use of phentolamine mesylate. Appropriate supportive treatment should be initiated.[L39190] | Like endogenous glucagon, dasiglucagon undergoes proteolytic degradation pathways in blood, liver, and kidney.[L39190] | Following subcutaneous administration of 0.6 mg dasiglucagon, the mean peak plasma concentration was 5110 pg/mL (1510 pmol/L). Tmax was 35 minutes. In pediatric patients with type 1 diabetes, the mean peak plasma concentration of 3920 pg/mL occurred at around 21 minutes.[L39190] Dasiglucagon has a higher absorption rate than traditional reconstituted glucagon.[A242140] | The mean apparent volume of distribution ranged from 47 L to 57 L after subcutaneous administration.[L39190] | NA | Hormones | NA | NA | NA | NA | Glucagon receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-4-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-4-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-2-methylpropanoyl]amino]propanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-carboxy-1-[[(2S)-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1-oxohexan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 15773 | Th1625 | Dasiglucagon | >Th1625_Dasiglucagon HSQGTFTSDYSKYLDXARAEEFVKWLEST | 3382 | C152H222N38O50 | NA | NA | NA | The half-life was approximately 30 minutes following subcutaneous administration.[L39190] Dasiglucagon has a longer plasma elimination half-life than traditional reconstituted glucagon.[A242140] | Dasiglucagon is a glucagon analog that acts to increase blood sugar levels.[L39190] It consists of 29 amino acids similar to endogenous glucagon; however, it contains seven substituted amino acids for improved physical and chemical stability in its drug formulation.[L39195] In March 2021, the FDA approved dasiglucagon to treat severe hypoglycemia in patients six years and older with diabetes. It is available as a subcutaneous injection marketed as ZEGALOGUE.[L39190] Severe hypoglycemia is an acute, life-threatening medical condition resulting from a profound drop in blood glucose levels. It is characterized by neurological impairment, with manifestations like loss of consciousness and seizure. Hypoglycemia is a common side effect of antidiabetic treatments, most notably insulin and sulfonylureas. Although it tends to be more common in type 1 diabetes mellitus, occurring in about 22% to 46% of patients annually, about 7% to 25% of patients with type 2 diabetes mellitus treated with insulin experience severe hypoglycemia a year.[L39195] Even with close monitoring of blood glucose levels, it is not always possible to prevent severe hypoglycemic events in patients with diabetes, and children are particularly at risk for experiencing severe hypoglycemia.[L39200] Treatments for severe hypoglycemia have mostly been limited to intravenous dextrose and different glucagon formulations.[L39195] The approval of dasiglucagon marks the first glucagon analog approved for severe hypoglycemia treatment that does not require administration by a healthcare professional.[L39195] | Dasiglucagon is an antihypoglycemic agent indicated for the treatment of severe hypoglycemia in pediatric and adult patients with diabetes aged 6 years and above.[L39190] | Dasiglucagon works to increase blood glucose levels under normal and hypoglycemic conditions.[A242140] After administration of dasiglucagon in adult patients with type 1 diabetes, the mean glucose increase from baseline at 90 minutes was 168 mg/dL. In pediatric patients with type 1 diabetes aged seven to 17 years, the mean glucose increase at 60 minutes after administration of dasiglucagon was 162 mg/dL.[L39190] | Dasiglucagon is an analog of glucagon, which is a peptide hormone responsible for increasing blood glucose levels. It has the same mechanism of action as endogenous glucagon by acting as an agonist at glucagon receptors, which are G-coupled receptors expressed throughout the body. Dasiglucagon binds to glucagon receptors in the liver, which activates Gsa and Gq, and consequently, adenylate cyclase. Adenyl cyclase increases intracellular cyclic AMP, which stimulates glycogenolysis and glucogenesis in the liver.[A19402,A242145] As glucose is primarily released from liver glycogen stores, hepatic stores of glycogen are crucial for dasiglucagon to exert its antihypoglycemic effects.[L39190] | Overdose may be characterized by nausea, vomiting, inhibition of gastrointestinal tract motility, increased blood pressure, and elevated heart rate. In case of a suspected overdose, serum potassium may decrease so monitoring and correcting of potassium levels may be warranted. A marked increase in blood pressure may be managed by the short-term use of phentolamine mesylate. Appropriate supportive treatment should be initiated.[L39190] | Like endogenous glucagon, dasiglucagon undergoes proteolytic degradation pathways in blood, liver, and kidney.[L39190] | Following subcutaneous administration of 0.6 mg dasiglucagon, the mean peak plasma concentration was 5110 pg/mL (1510 pmol/L). Tmax was 35 minutes. In pediatric patients with type 1 diabetes, the mean peak plasma concentration of 3920 pg/mL occurred at around 21 minutes.[L39190] Dasiglucagon has a higher absorption rate than traditional reconstituted glucagon.[A242140] | The mean apparent volume of distribution ranged from 47 L to 57 L after subcutaneous administration.[L39190] | NA | Hormones, Hormone Substitutes, and Hormone Antagonists | NA | NA | NA | NA | Glucagon receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-4-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-4-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-2-methylpropanoyl]amino]propanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-carboxy-1-[[(2S)-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1-oxohexan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 15775 | Th1625 | Dasiglucagon | >Th1625_Dasiglucagon HSQGTFTSDYSKYLDXARAEEFVKWLEST | 3382 | C152H222N38O50 | NA | NA | NA | The half-life was approximately 30 minutes following subcutaneous administration.[L39190] Dasiglucagon has a longer plasma elimination half-life than traditional reconstituted glucagon.[A242140] | Dasiglucagon is a glucagon analog that acts to increase blood sugar levels.[L39190] It consists of 29 amino acids similar to endogenous glucagon; however, it contains seven substituted amino acids for improved physical and chemical stability in its drug formulation.[L39195] In March 2021, the FDA approved dasiglucagon to treat severe hypoglycemia in patients six years and older with diabetes. It is available as a subcutaneous injection marketed as ZEGALOGUE.[L39190] Severe hypoglycemia is an acute, life-threatening medical condition resulting from a profound drop in blood glucose levels. It is characterized by neurological impairment, with manifestations like loss of consciousness and seizure. Hypoglycemia is a common side effect of antidiabetic treatments, most notably insulin and sulfonylureas. Although it tends to be more common in type 1 diabetes mellitus, occurring in about 22% to 46% of patients annually, about 7% to 25% of patients with type 2 diabetes mellitus treated with insulin experience severe hypoglycemia a year.[L39195] Even with close monitoring of blood glucose levels, it is not always possible to prevent severe hypoglycemic events in patients with diabetes, and children are particularly at risk for experiencing severe hypoglycemia.[L39200] Treatments for severe hypoglycemia have mostly been limited to intravenous dextrose and different glucagon formulations.[L39195] The approval of dasiglucagon marks the first glucagon analog approved for severe hypoglycemia treatment that does not require administration by a healthcare professional.[L39195] | Dasiglucagon is an antihypoglycemic agent indicated for the treatment of severe hypoglycemia in pediatric and adult patients with diabetes aged 6 years and above.[L39190] | Dasiglucagon works to increase blood glucose levels under normal and hypoglycemic conditions.[A242140] After administration of dasiglucagon in adult patients with type 1 diabetes, the mean glucose increase from baseline at 90 minutes was 168 mg/dL. In pediatric patients with type 1 diabetes aged seven to 17 years, the mean glucose increase at 60 minutes after administration of dasiglucagon was 162 mg/dL.[L39190] | Dasiglucagon is an analog of glucagon, which is a peptide hormone responsible for increasing blood glucose levels. It has the same mechanism of action as endogenous glucagon by acting as an agonist at glucagon receptors, which are G-coupled receptors expressed throughout the body. Dasiglucagon binds to glucagon receptors in the liver, which activates Gsa and Gq, and consequently, adenylate cyclase. Adenyl cyclase increases intracellular cyclic AMP, which stimulates glycogenolysis and glucogenesis in the liver.[A19402,A242145] As glucose is primarily released from liver glycogen stores, hepatic stores of glycogen are crucial for dasiglucagon to exert its antihypoglycemic effects.[L39190] | Overdose may be characterized by nausea, vomiting, inhibition of gastrointestinal tract motility, increased blood pressure, and elevated heart rate. In case of a suspected overdose, serum potassium may decrease so monitoring and correcting of potassium levels may be warranted. A marked increase in blood pressure may be managed by the short-term use of phentolamine mesylate. Appropriate supportive treatment should be initiated.[L39190] | Like endogenous glucagon, dasiglucagon undergoes proteolytic degradation pathways in blood, liver, and kidney.[L39190] | Following subcutaneous administration of 0.6 mg dasiglucagon, the mean peak plasma concentration was 5110 pg/mL (1510 pmol/L). Tmax was 35 minutes. In pediatric patients with type 1 diabetes, the mean peak plasma concentration of 3920 pg/mL occurred at around 21 minutes.[L39190] Dasiglucagon has a higher absorption rate than traditional reconstituted glucagon.[A242140] | The mean apparent volume of distribution ranged from 47 L to 57 L after subcutaneous administration.[L39190] | NA | Peptide Hormones | NA | NA | NA | NA | Glucagon receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | (4S)-4-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-amino-3-(1H-imidazol-4-yl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-oxopentanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]hexanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-3-carboxypropanoyl]amino]-2-methylpropanoyl]amino]propanoyl]amino]-5-carbamimidamidopentanoyl]amino]propanoyl]amino]-5-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-4-carboxy-1-[[(2S)-1-[[(1S,2R)-1-carboxy-2-hydroxypropyl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1-oxohexan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-5-oxopentanoic acid | NA | Link | NA | NA |
| 16384 | Th1894 | Tirzepatide | >Th1894_Tirzepatide YXEGTFTSDYSIXLDKIAQKAFVQWLIAGGPSSGAPPPS | 4810.52 Da | C225H348N48O68 | NA | NA | NA | ,The half-life is approximately five days. | Tirzepatide is a novel dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist. Dual GIP/GLP-1 agonists gained increasing attention as new therapeutic agents for glycemic and weight control as they demonstrated better glucose control and weight loss compared to selective GLP-1 receptor agonists in preclinical and clinical trials. | Tirzepatide is a dual GIP and GLP-1 receptor agonist used for the treatment of type II diabetes in adults as an adjunct to diet and exercise. | Tirzepatide is a synthetic peptide with glucose-lowering effects. It works to stimulate first- and second-phase insulin secretion, and reduces glucagon levels, both in a glucose-dependent manner. Tirzepatide was also shown to delay gastric emptying, lower fasting and postprandial glucose concentration, decrease food intake,4 and reduce body weight in patients with type 2 diabetes. Tirzepatide can increase insulin sensitivity. | Glucagon-like peptide-1 (GLP-1) receptors (GLP-1R) are expressed throughout the body, including pancreatic beta-cells and the gastrointestinal tract. They have been implicated in the pathophysiology of type II diabetes mellitus as GLP-1R signalling is involved in glucose control by enhancing glucose-stimulated insulin secretion, delaying gastric transit, decreasing plasma glucagon levels, and reducing body weight by activating anorexigenic pathways in the brain. Both glucose-dependent insulinotropic polypeptide (GIP) and GLP-1 are peptide hormones involved in glucose homeostasis: they promote glucose-stimulated insulin secretion from the pancreatic beta-cells. However, GIP is the main incretin hormone that exerts insulinotropic effects in response to food intake. | There is limited information regarding the LD50 and overdose of tirzepatide. In case of an overdosage, appropriate supportive treatment should be initiated with a sufficient amount of time for observation and treatment, as tirzepatide has a long half-life. | Tirzepatide is metabolized by proteolytic cleavage of the peptide backbone, beta-oxidation of the C20 fatty diacid moiety, and amide hydrolysis. | Over the dose range of 1-5 mg, the Cmax of tirzepatide ranged from 108 to 397 ng/mL.The mean absolute bioavailability of tirzepatide following subcutaneous administration is 80%. Following subcutaneous administration, the Tmax ranged from eight to 72 hours. The steady-state plasma concentrations were achieved following four weeks of once-weekly subcutaneous administration. | Following subcutaneous administration, the mean steady-state volume of distribution was 9.5 L. The mean apparent steady-state volume of distribution of tirzepatide following subcutaneous administration in patients with type 2 diabetes mellitus was approximately 10.3 L. | The apparent population mean clearance of tirzepatide is 0.061 L/h.4 The mean steady-state apparent clearance of tirzepatide was 0.056 L/h. | Amino Acids, Peptides, and Proteins,Blood Glucose Lowering Agents,Gastrointestinal Hormones,GLP-1 Agonists,Hormones,Hormones, Hormone Substitutes, and Hormone Antagonists,Incretins,Nerve Tissue Proteins,Neuropeptides,Peptide Hormones,Peptides,Proteins | NA | NA | NA | NA | Glucagon-like peptide 1 receptor, Gastric inhibitory polypeptide | Mounjaro | Eli Lilly and Company | Eli Lilly and Company | Subcutaneous | 12.5 mg/0.5mL | MOUNJARO is contraindicated in patients with: A personal or family history of medullary thyroid carcinoma (MTC) or in patients with Multiple Endocrine Neoplasia syndrome type 2 | hives, difficulty breathing, swelling of your face, lips, tongue, or throat, dizziness, fast heart rate, shaking, sweating, nervousness, anxiety, irritability, confusion, dizziness, hunger, pain in the upper right side of your abdomen, pain spreading to your back or below the shoulder blade, nausea, vomiting, fever, yellowing of the skin and eyes (jaundice), clay-colored stools, and bloating of the abdomen | MOUNJARO (tirzepatide) injection, for subcutaneous use, contains tirzepatide, a once weekly GIP receptor and GLP-1 receptor agonist. It is a 39-amino-acid modified peptide based on the GIP sequence. Tirzepatide contains 2 non-coded amino acids (aminoisobutyric acid, Aib) in positions 2 and 13, a C-terminal amide, and Lys residue at position 20 that is attached to 1,20-eicosanedioic acid via a linker. | Mounjaro (tirzepatide) Injection is a prescription medicine used to treat the symptoms of Type 2 Diabetes Mellitus. | NA | MOUNJARO is a clear, colorless to slightly yellow, sterile, preservative-free solution for subcutaneous use. Each singledose pen contains a 0.5 mL solution of 2.5 mg, 5 mg, 7.5 mg, 10 mg, 12.5 mg, or 15 mg of tirzepatide and the following excipients: sodium chloride (4.1 mg), sodium phosphate dibasic heptahydrate (0.7 mg), and water for injection. Hydrochloric acid solution and/or sodium hydroxide solution may have been added to adjust the pH. MOUNJARO has a pH of 6.5 – 7.5. | Link | Link | NA |