Detailed description page of ThPDB2
This page displays user query in tabular form. |
Th1434 details |
Primary information | |
---|---|
ID | 13781 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Amino Acids, Peptides, and Proteins |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | Evenity |
Company | Ucb Pharma S.A. |
Brand Description | Ucb Pharma S.A. |
Prescribed For | Subcutaneous |
Chemical Name | 105 mg |
Formulation | EVENITY is contraindicated in patients with: Hypocalcemia. Pre-existing hypocalcemia must be corrected prior to initiating therapy with EVENITY [see WARNINGS AND PRECAUTIONS, ADVERSE REACTIONS and Use In Specific Populations]. A history of systemic hypersensitivity to romosozumab or to any component of the product formulation. Reactions have included angioedema, erythema multiforme, and urticaria [see WARNINGS AND PRECAUTIONS and ADVERSE REACTIONS]. |
Physical Appearance | joint pain, headache, muscle spasms, swelling of extremities, weakness, neck pain, insomnia, numbness and tingling sensation |
Route of Administration | Evenity is a sclerostin inhibitor. Sclerostin suppresses bone formation. Evenity is a prescription medicine used to treat osteoporosis in postmenopausal women with a high risk of bone fracture who cannot use other osteoporosis medications (or when other medications did not work). It is not known if Evenity... |
Recommended Dosage | Evenity is a prescription medicine used to treat the symptoms of Osteoporosis. Evenity may be used alone or with other medications. |
Contraindication | NA |
Side Effects | EVENITY (romosozumab-aqqg) injection is supplied as a sterile, preservative-free, clear to opalescent, colorless to light yellow solution for subcutaneous injection in a single-use prefilled syringe. |
Useful Link 1 | Link |
Useful Link 2 | Link |
Remarks | NA |
Primary information | |
---|---|
ID | 13782 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Antibodies |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | Evenity |
Company | Amgen |
Brand Description | Amgen |
Prescribed For | Subcutaneous |
Chemical Name | 105 mg / 1.17 mL |
Formulation | EVENITY is contraindicated in patients with: Hypocalcemia. Pre-existing hypocalcemia must be corrected prior to initiating therapy with EVENITY [see WARNINGS AND PRECAUTIONS, ADVERSE REACTIONS and Use In Specific Populations]. A history of systemic hypersensitivity to romosozumab or to any component of the product formulation. Reactions have included angioedema, erythema multiforme, and urticaria [see WARNINGS AND PRECAUTIONS and ADVERSE REACTIONS]. |
Physical Appearance | joint pain, headache, muscle spasms, swelling of extremities, weakness, neck pain, insomnia, numbness and tingling sensation |
Route of Administration | Evenity is a sclerostin inhibitor. Sclerostin suppresses bone formation. Evenity is a prescription medicine used to treat osteoporosis in postmenopausal women with a high risk of bone fracture who cannot use other osteoporosis medications (or when other medications did not work). It is not known if Evenity... |
Recommended Dosage | Evenity is a prescription medicine used to treat the symptoms of Osteoporosis. Evenity may be used alone or with other medications. |
Contraindication | NA |
Side Effects | EVENITY (romosozumab-aqqg) injection is supplied as a sterile, preservative-free, clear to opalescent, colorless to light yellow solution for subcutaneous injection in a single-use prefilled syringe. |
Useful Link 1 | Link |
Useful Link 2 | Link |
Remarks | NA |
Primary information | |
---|---|
ID | 13783 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Antibodies, Monoclonal |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | Evenity |
Company | AMGEN INC |
Brand Description | AMGEN INC |
Prescribed For | Subcutaneous |
Chemical Name | 105 mg/1.17mL |
Formulation | EVENITY is contraindicated in patients with: Hypocalcemia. Pre-existing hypocalcemia must be corrected prior to initiating therapy with EVENITY [see WARNINGS AND PRECAUTIONS, ADVERSE REACTIONS and Use In Specific Populations]. A history of systemic hypersensitivity to romosozumab or to any component of the product formulation. Reactions have included angioedema, erythema multiforme, and urticaria [see WARNINGS AND PRECAUTIONS and ADVERSE REACTIONS]. |
Physical Appearance | joint pain, headache, muscle spasms, swelling of extremities, weakness, neck pain, insomnia, numbness and tingling sensation |
Route of Administration | Evenity is a sclerostin inhibitor. Sclerostin suppresses bone formation. Evenity is a prescription medicine used to treat osteoporosis in postmenopausal women with a high risk of bone fracture who cannot use other osteoporosis medications (or when other medications did not work). It is not known if Evenity... |
Recommended Dosage | Evenity is a prescription medicine used to treat the symptoms of Osteoporosis. Evenity may be used alone or with other medications. |
Contraindication | NA |
Side Effects | EVENITY (romosozumab-aqqg) injection is supplied as a sterile, preservative-free, clear to opalescent, colorless to light yellow solution for subcutaneous injection in a single-use prefilled syringe. |
Useful Link 1 | Link |
Useful Link 2 | Link |
Remarks | NA |
Primary information | |
---|---|
ID | 13784 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Antibodies, Monoclonal, Humanized |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | NA |
Company | NA |
Brand Description | NA |
Prescribed For | NA |
Chemical Name | NA |
Formulation | NA |
Physical Appearance | NA |
Route of Administration | NA |
Recommended Dosage | NA |
Contraindication | NA |
Side Effects | NA |
Useful Link 1 | Link |
Useful Link 2 | NA |
Remarks | NA |
Primary information | |
---|---|
ID | 13785 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Blood Proteins |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | NA |
Company | NA |
Brand Description | NA |
Prescribed For | NA |
Chemical Name | NA |
Formulation | NA |
Physical Appearance | NA |
Route of Administration | NA |
Recommended Dosage | NA |
Contraindication | NA |
Side Effects | NA |
Useful Link 1 | Link |
Useful Link 2 | NA |
Remarks | NA |
Primary information | |
---|---|
ID | 13786 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Bone Anabolic Agents |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | NA |
Company | NA |
Brand Description | NA |
Prescribed For | NA |
Chemical Name | NA |
Formulation | NA |
Physical Appearance | NA |
Route of Administration | NA |
Recommended Dosage | NA |
Contraindication | NA |
Side Effects | NA |
Useful Link 1 | Link |
Useful Link 2 | NA |
Remarks | NA |
Primary information | |
---|---|
ID | 13787 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Drugs Affecting Bone Structure and Mineralization |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | NA |
Company | NA |
Brand Description | NA |
Prescribed For | NA |
Chemical Name | NA |
Formulation | NA |
Physical Appearance | NA |
Route of Administration | NA |
Recommended Dosage | NA |
Contraindication | NA |
Side Effects | NA |
Useful Link 1 | Link |
Useful Link 2 | NA |
Remarks | NA |
Primary information | |
---|---|
ID | 13788 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Drugs for Treatment of Bone Diseases |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | NA |
Company | NA |
Brand Description | NA |
Prescribed For | NA |
Chemical Name | NA |
Formulation | NA |
Physical Appearance | NA |
Route of Administration | NA |
Recommended Dosage | NA |
Contraindication | NA |
Side Effects | NA |
Useful Link 1 | Link |
Useful Link 2 | NA |
Remarks | NA |
Primary information | |
---|---|
ID | 13789 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Globulins |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | NA |
Company | NA |
Brand Description | NA |
Prescribed For | NA |
Chemical Name | NA |
Formulation | NA |
Physical Appearance | NA |
Route of Administration | NA |
Recommended Dosage | NA |
Contraindication | NA |
Side Effects | NA |
Useful Link 1 | Link |
Useful Link 2 | NA |
Remarks | NA |
Primary information | |
---|---|
ID | 13790 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Immunoglobulins |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | NA |
Company | NA |
Brand Description | NA |
Prescribed For | NA |
Chemical Name | NA |
Formulation | NA |
Physical Appearance | NA |
Route of Administration | NA |
Recommended Dosage | NA |
Contraindication | NA |
Side Effects | NA |
Useful Link 1 | Link |
Useful Link 2 | NA |
Remarks | NA |
Primary information | |
---|---|
ID | 13791 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Immunoproteins |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | NA |
Company | NA |
Brand Description | NA |
Prescribed For | NA |
Chemical Name | NA |
Formulation | NA |
Physical Appearance | NA |
Route of Administration | NA |
Recommended Dosage | NA |
Contraindication | NA |
Side Effects | NA |
Useful Link 1 | Link |
Useful Link 2 | NA |
Remarks | NA |
Primary information | |
---|---|
ID | 13792 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Musculo-Skeletal System |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | NA |
Company | NA |
Brand Description | NA |
Prescribed For | NA |
Chemical Name | NA |
Formulation | NA |
Physical Appearance | NA |
Route of Administration | NA |
Recommended Dosage | NA |
Contraindication | NA |
Side Effects | NA |
Useful Link 1 | Link |
Useful Link 2 | NA |
Remarks | NA |
Primary information | |
---|---|
ID | 13793 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Proteins |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | NA |
Company | NA |
Brand Description | NA |
Prescribed For | NA |
Chemical Name | NA |
Formulation | NA |
Physical Appearance | NA |
Route of Administration | NA |
Recommended Dosage | NA |
Contraindication | NA |
Side Effects | NA |
Useful Link 1 | Link |
Useful Link 2 | NA |
Remarks | NA |
Primary information | |
---|---|
ID | 13794 |
Therapeutic ID | Th1434 |
Protein Name | Romosozumab |
Sequence | NA |
Molecular Weight | 145805 |
Chemical Formula | NA |
Isoelectric Point | NA |
Hydrophobicity | NA |
Melting point | NA |
Half-life | 12.8 days[L9554]. |
Description | Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies[L9554]. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study[L5921,L5924]. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months[A177071]. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide[A177050]. Romosozumab is marketed in the United States by Amgen under the brand name Evinity[L5921]. Romosozumab was granted FDA approval on April 9,2019[L5921]. |
Indication/Disease | Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments[L9554]. |
Pharmacodynamics | Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin[L9554]. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts[A177056,A177062]. |
Mechanism of Action | Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway[A177056]. Romosozumab targets and inhibits the protein sclerostin, thereby preventing inhibition of bone formation by allowing Wnt to bind to LDL receptor-related proteins 5 and 6[A177056,A177062]. Activation of the Wnt pathways leads to downstream signalling, translocation of beta catenin to the osteoblast nucleus where it promotes survival and proliferation of osteoblasts[A177062]. Sclerostin also promotes bone resorption through increasing production of receptor activator of nuclear factor kappa-beta-ligand (RANKL)[A177062]. Romosozumab's inhibition of sclerostin also inhibits the increase in RANKL dependant increases in osteoclast activity and bone resorption[A177056,A177062]. Both effects from the same therapy have not been seen in other osteoporosis treatments to date[A177056]. |
Toxicity | There are no significant differences in pharmacokinetics cross age, sex, race, progression of osteoporosis, past history of alendronic acid prescribing, and all stages of renal impairment[L9554]. However, patients with severe renal impairment or who are on dialysis are at an increased risk of hypocalcemia[L9554]. A patient's weight will affect their level of romosozumab exposure[L9554]. Romosozumab has not been shown to be associated with carcinogenicity or impairment of fertility, and is not expected to be mutagenic[L9554]. Romosozumab is not indicated in pregnancy, lactation, or pedatric patients[L9554]. Romosozumab is associated with skeletal defects in the offspring of rats given romosozumab and is detected in the excreted milk[L9554]. Romosozumab is currently undergoing post marketing surveillance to ensure the risk of major adverse cardiac events is not being underestimated[L5924]. There is currently an expected hazard ratio of 1.30 compared to current treatments for osteoporosis, though hip and vertebral fractures may have an equal impact on overall quality of life[L5924]. |
Metabolism | The metabolism of romosozumab has not been clarified, however it is expected to be degraded into small peptides and amino acids like other protein drugs[L9554]. |
Absorption | Romosozumab reaches peak concentration within 2 to 7 days with a median time of 5 days[L9554]. Subcutaneous bioavailability is 50 to 70%[A177056,A177062]. |
3.92L[L9554]. | |
Clearance | 0.38mL/hr/kg[L9554]. |
Categories | Serum Globulins |
Patents Number | NA |
Date of Issue | NA |
Date of Expiry | NA |
Drug Interaction | NA |
Target | Sclerostin |
Brand Name | NA |
Company | NA |
Brand Description | NA |
Prescribed For | NA |
Chemical Name | NA |
Formulation | NA |
Physical Appearance | NA |
Route of Administration | NA |
Recommended Dosage | NA |
Contraindication | NA |
Side Effects | NA |
Useful Link 1 | Link |
Useful Link 2 | NA |
Remarks | NA |