Detailed description page of ThPDB2
| This page displays user query in tabular form. |
Th1480 details |
| Primary information | |
|---|---|
| ID | 14247 |
| Therapeutic ID | Th1480 |
| Protein Name | Aducanumab |
| Sequence | >Th1480_Aducanumab XVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG |
| Molecular Weight | 146000 |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | The terminal half life of aducanumab is 24.8 days.[L34393] |
| Description | Aducanumab, or BIIB037, is a monoclonal IgG1 antibody that targets extracellular amyloid-ß plaques in the brain; similar to [gantenerumab], [bapineuzumab] and [solanezumab].[A235668,A235730] Aducanumab is a recombinant antibody derived from patients with slow or absent cognitive decline, and phase 1b clinical trial data has shown patients treated with aducanumab show a reduction in amyloid-ß plaques.[A235668] Based on Mini-Mental State Examination and Clinical Dementia Rating (CDR), patients taking aducanumab showed signs of slowing progression, however these data are controversial.[A235668,A235720] Clinical trials showed a 23% relative difference between the experimental and placebo groups as determined by CDR, however this is equivalent to an absolute difference of 0.4/18.[A235720] Although aducanumab's approval represents the first drug treatment for Alzheimer's disease, the approval is conditional on further results.[L34420] Biogen enrolled patients in phase 3 clinical trials in 2015, but increased the size of the trials from 1350 patients to 1650 patients to maintain statistical power in the face of a high standard deviation.[A235720] Development of aducanumab was discontinued in March 2019 when two phase 3 clinical trials did not pass futility analysis, however Biogen sought FDA approval in October 2019 after reanalysis of the data.[A235720] Aducanumab was granted accelerated FDA approval on 7 June 2021.[L34393] Continued approval will be based on further trials confirming a clinical benefit over currently available therapy.[L34420] |
| Indication/Disease | Aducanumab is indicated in the treatment of Alzheimer's disease.[L34393] |
| Pharmacodynamics | Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß, reducing amyloid plaques in the brain.[L34393] It has a long duration of action as it is given once every 4 weeks.[L34393] Patients should be counselled regarding the risk of amyloid related imaging abnormalities, including microhemorrhages, and hypersensitivity reactions.[L34393] |
| Mechanism of Action | Alzheimer's disease is a neurodegenerative disease.[A235668] Part of the pathology of Alzheimer's disease is the presence of plaques forming extracellularly in the brain.[A235668] These plaques are mostly composed of amyloid-ß, a peptide of varying length formed by the cleavage of the amyloid precursor protein.[A235668] The "amyloid cascade hypothesis" suggests that the accumulation of amyloid-ß oligopeptides in the brain drives the pathogenesis of Alzheimer's disease.[A235730] Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß at amino acids 3-7.[A235668,L34393] The amyloid-ß residues Phe4, His6, Glu3, and Arg5 are responsible for the majority of the contact between amyloid-ß and aducanumab's Fab region.[A235668] Data from studies in mice and humans shows aducanumab treatment reduces amyloid-ß, however human trials show non-significant changes in amyloid-ß40 and amyloid-ß42 across a dose range of 0.3-30 mg/kg and an increase in amyloid-ß40 and amyloid-ß42 at 60 mg/kg.[A235730] Aducanumab treatment is associated with slowing the rate of progression of Alzheimer's disease, based on Mini-Mental State Examination, Clinical Dementia Rating, and levels of p-tau in the cerebrospinal fluid.[A235715] |
| Toxicity | Patients experiencing dose-limiting toxicity may present with amyloid-related imaging abnormalities including edema or microhemorrhages of the brain.[A235730] Symptoms of dose limiting toxicity were generally transient,[A235730] however patients may need to be treated with symptomatic and supportive measures. |
| Metabolism | Aducanumab is expected to be broken down into smaller oligopeptides and amino acids.[A40006,L34393] |
| Absorption | A 10 mg/kg intravenous dose of aducanumab reached a Cmax of 182.7 µg/mL, with a Tmax of 3.0 hours, and an AUCinf of 31,400 h |
| The volume of distribution of aducanumab is 9.63 L.[L34393] | |
| Clearance | A 10 mg/kg intravenous dose of aducanumab has a clearance of 0.39 mL/h/kg.[A235730] |
| Categories | Alzheimer Disease, drug therapy |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Amyloid beta A4 protein |
| Brand Name | Aduhelm |
| Company | Biogen Inc. |
| Brand Description | Biogen Inc. |
| Prescribed For | Intravenous |
| Chemical Name | 100 mg/1mL |
| Formulation | None. |
| Physical Appearance | amyloid related imaging abnormalities (ARIA) fluid retention (edema), headache, amyloid related imaging abnormalities due to haemosiderin deposition (ARIA-H) microhemorrhage, ARIA-H superficial siderosis, falls, diarrhea, and confusion/delirium/altered mental status/disorientation. |
| Route of Administration | Aduhelm is a prescription medicine used to treat people with Alzheimer’s disease. Treatment with Aduhelm should be initiated in patients with mild cognitive impairment or mild dementia stage of disease, the population in which treatment was initiated in clinical trials. It is not known if this medicine... |
| Recommended Dosage | ADUHELM is indicated for the treatment of Alzheimer’s disease. This indication is approved under accelerated approval based on reduction in amyloid beta plaques observed in patients treated with ADUHELM [see Clinical Studies]. Continued approval for this indication may be contingent upon verification of clinical benefit in confirmatory trial(s). |
| Contraindication | NA |
| Side Effects | ADUHELM (aducanumab-avwa) injection is a preservative-free, sterile, clear to opalescent, and colorless to yellow solution for intravenous infusion after dilution supplied in single-dose vials available in concentrations of 170 mg/1.7 mL (100 mg/mL) or 300 mg/3 mL (100 mg/mL) of ADUHELM. |
| Useful Link 1 | Link |
| Useful Link 2 | Link |
| Remarks | NA |
| Primary information | |
|---|---|
| ID | 14248 |
| Therapeutic ID | Th1480 |
| Protein Name | Aducanumab |
| Sequence | >Th1480_Aducanumab XVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG |
| Molecular Weight | 146000 |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | The terminal half life of aducanumab is 24.8 days.[L34393] |
| Description | Aducanumab, or BIIB037, is a monoclonal IgG1 antibody that targets extracellular amyloid-ß plaques in the brain; similar to [gantenerumab], [bapineuzumab] and [solanezumab].[A235668,A235730] Aducanumab is a recombinant antibody derived from patients with slow or absent cognitive decline, and phase 1b clinical trial data has shown patients treated with aducanumab show a reduction in amyloid-ß plaques.[A235668] Based on Mini-Mental State Examination and Clinical Dementia Rating (CDR), patients taking aducanumab showed signs of slowing progression, however these data are controversial.[A235668,A235720] Clinical trials showed a 23% relative difference between the experimental and placebo groups as determined by CDR, however this is equivalent to an absolute difference of 0.4/18.[A235720] Although aducanumab's approval represents the first drug treatment for Alzheimer's disease, the approval is conditional on further results.[L34420] Biogen enrolled patients in phase 3 clinical trials in 2015, but increased the size of the trials from 1350 patients to 1650 patients to maintain statistical power in the face of a high standard deviation.[A235720] Development of aducanumab was discontinued in March 2019 when two phase 3 clinical trials did not pass futility analysis, however Biogen sought FDA approval in October 2019 after reanalysis of the data.[A235720] Aducanumab was granted accelerated FDA approval on 7 June 2021.[L34393] Continued approval will be based on further trials confirming a clinical benefit over currently available therapy.[L34420] |
| Indication/Disease | Aducanumab is indicated in the treatment of Alzheimer's disease.[L34393] |
| Pharmacodynamics | Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß, reducing amyloid plaques in the brain.[L34393] It has a long duration of action as it is given once every 4 weeks.[L34393] Patients should be counselled regarding the risk of amyloid related imaging abnormalities, including microhemorrhages, and hypersensitivity reactions.[L34393] |
| Mechanism of Action | Alzheimer's disease is a neurodegenerative disease.[A235668] Part of the pathology of Alzheimer's disease is the presence of plaques forming extracellularly in the brain.[A235668] These plaques are mostly composed of amyloid-ß, a peptide of varying length formed by the cleavage of the amyloid precursor protein.[A235668] The "amyloid cascade hypothesis" suggests that the accumulation of amyloid-ß oligopeptides in the brain drives the pathogenesis of Alzheimer's disease.[A235730] Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß at amino acids 3-7.[A235668,L34393] The amyloid-ß residues Phe4, His6, Glu3, and Arg5 are responsible for the majority of the contact between amyloid-ß and aducanumab's Fab region.[A235668] Data from studies in mice and humans shows aducanumab treatment reduces amyloid-ß, however human trials show non-significant changes in amyloid-ß40 and amyloid-ß42 across a dose range of 0.3-30 mg/kg and an increase in amyloid-ß40 and amyloid-ß42 at 60 mg/kg.[A235730] Aducanumab treatment is associated with slowing the rate of progression of Alzheimer's disease, based on Mini-Mental State Examination, Clinical Dementia Rating, and levels of p-tau in the cerebrospinal fluid.[A235715] |
| Toxicity | Patients experiencing dose-limiting toxicity may present with amyloid-related imaging abnormalities including edema or microhemorrhages of the brain.[A235730] Symptoms of dose limiting toxicity were generally transient,[A235730] however patients may need to be treated with symptomatic and supportive measures. |
| Metabolism | Aducanumab is expected to be broken down into smaller oligopeptides and amino acids.[A40006,L34393] |
| Absorption | A 10 mg/kg intravenous dose of aducanumab reached a Cmax of 182.7 µg/mL, with a Tmax of 3.0 hours, and an AUCinf of 31,400 h |
| The volume of distribution of aducanumab is 9.63 L.[L34393] | |
| Clearance | A 10 mg/kg intravenous dose of aducanumab has a clearance of 0.39 mL/h/kg.[A235730] |
| Categories | Amino Acids, Peptides, and Proteins |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Amyloid beta A4 protein |
| 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 | 14249 |
| Therapeutic ID | Th1480 |
| Protein Name | Aducanumab |
| Sequence | >Th1480_Aducanumab XVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG |
| Molecular Weight | 146000 |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | The terminal half life of aducanumab is 24.8 days.[L34393] |
| Description | Aducanumab, or BIIB037, is a monoclonal IgG1 antibody that targets extracellular amyloid-ß plaques in the brain; similar to [gantenerumab], [bapineuzumab] and [solanezumab].[A235668,A235730] Aducanumab is a recombinant antibody derived from patients with slow or absent cognitive decline, and phase 1b clinical trial data has shown patients treated with aducanumab show a reduction in amyloid-ß plaques.[A235668] Based on Mini-Mental State Examination and Clinical Dementia Rating (CDR), patients taking aducanumab showed signs of slowing progression, however these data are controversial.[A235668,A235720] Clinical trials showed a 23% relative difference between the experimental and placebo groups as determined by CDR, however this is equivalent to an absolute difference of 0.4/18.[A235720] Although aducanumab's approval represents the first drug treatment for Alzheimer's disease, the approval is conditional on further results.[L34420] Biogen enrolled patients in phase 3 clinical trials in 2015, but increased the size of the trials from 1350 patients to 1650 patients to maintain statistical power in the face of a high standard deviation.[A235720] Development of aducanumab was discontinued in March 2019 when two phase 3 clinical trials did not pass futility analysis, however Biogen sought FDA approval in October 2019 after reanalysis of the data.[A235720] Aducanumab was granted accelerated FDA approval on 7 June 2021.[L34393] Continued approval will be based on further trials confirming a clinical benefit over currently available therapy.[L34420] |
| Indication/Disease | Aducanumab is indicated in the treatment of Alzheimer's disease.[L34393] |
| Pharmacodynamics | Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß, reducing amyloid plaques in the brain.[L34393] It has a long duration of action as it is given once every 4 weeks.[L34393] Patients should be counselled regarding the risk of amyloid related imaging abnormalities, including microhemorrhages, and hypersensitivity reactions.[L34393] |
| Mechanism of Action | Alzheimer's disease is a neurodegenerative disease.[A235668] Part of the pathology of Alzheimer's disease is the presence of plaques forming extracellularly in the brain.[A235668] These plaques are mostly composed of amyloid-ß, a peptide of varying length formed by the cleavage of the amyloid precursor protein.[A235668] The "amyloid cascade hypothesis" suggests that the accumulation of amyloid-ß oligopeptides in the brain drives the pathogenesis of Alzheimer's disease.[A235730] Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß at amino acids 3-7.[A235668,L34393] The amyloid-ß residues Phe4, His6, Glu3, and Arg5 are responsible for the majority of the contact between amyloid-ß and aducanumab's Fab region.[A235668] Data from studies in mice and humans shows aducanumab treatment reduces amyloid-ß, however human trials show non-significant changes in amyloid-ß40 and amyloid-ß42 across a dose range of 0.3-30 mg/kg and an increase in amyloid-ß40 and amyloid-ß42 at 60 mg/kg.[A235730] Aducanumab treatment is associated with slowing the rate of progression of Alzheimer's disease, based on Mini-Mental State Examination, Clinical Dementia Rating, and levels of p-tau in the cerebrospinal fluid.[A235715] |
| Toxicity | Patients experiencing dose-limiting toxicity may present with amyloid-related imaging abnormalities including edema or microhemorrhages of the brain.[A235730] Symptoms of dose limiting toxicity were generally transient,[A235730] however patients may need to be treated with symptomatic and supportive measures. |
| Metabolism | Aducanumab is expected to be broken down into smaller oligopeptides and amino acids.[A40006,L34393] |
| Absorption | A 10 mg/kg intravenous dose of aducanumab reached a Cmax of 182.7 µg/mL, with a Tmax of 3.0 hours, and an AUCinf of 31,400 h |
| The volume of distribution of aducanumab is 9.63 L.[L34393] | |
| Clearance | A 10 mg/kg intravenous dose of aducanumab has a clearance of 0.39 mL/h/kg.[A235730] |
| Categories | Amyloid Beta-directed Antibody |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Amyloid beta A4 protein |
| 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 | 14250 |
| Therapeutic ID | Th1480 |
| Protein Name | Aducanumab |
| Sequence | >Th1480_Aducanumab XVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG |
| Molecular Weight | 146000 |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | The terminal half life of aducanumab is 24.8 days.[L34393] |
| Description | Aducanumab, or BIIB037, is a monoclonal IgG1 antibody that targets extracellular amyloid-ß plaques in the brain; similar to [gantenerumab], [bapineuzumab] and [solanezumab].[A235668,A235730] Aducanumab is a recombinant antibody derived from patients with slow or absent cognitive decline, and phase 1b clinical trial data has shown patients treated with aducanumab show a reduction in amyloid-ß plaques.[A235668] Based on Mini-Mental State Examination and Clinical Dementia Rating (CDR), patients taking aducanumab showed signs of slowing progression, however these data are controversial.[A235668,A235720] Clinical trials showed a 23% relative difference between the experimental and placebo groups as determined by CDR, however this is equivalent to an absolute difference of 0.4/18.[A235720] Although aducanumab's approval represents the first drug treatment for Alzheimer's disease, the approval is conditional on further results.[L34420] Biogen enrolled patients in phase 3 clinical trials in 2015, but increased the size of the trials from 1350 patients to 1650 patients to maintain statistical power in the face of a high standard deviation.[A235720] Development of aducanumab was discontinued in March 2019 when two phase 3 clinical trials did not pass futility analysis, however Biogen sought FDA approval in October 2019 after reanalysis of the data.[A235720] Aducanumab was granted accelerated FDA approval on 7 June 2021.[L34393] Continued approval will be based on further trials confirming a clinical benefit over currently available therapy.[L34420] |
| Indication/Disease | Aducanumab is indicated in the treatment of Alzheimer's disease.[L34393] |
| Pharmacodynamics | Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß, reducing amyloid plaques in the brain.[L34393] It has a long duration of action as it is given once every 4 weeks.[L34393] Patients should be counselled regarding the risk of amyloid related imaging abnormalities, including microhemorrhages, and hypersensitivity reactions.[L34393] |
| Mechanism of Action | Alzheimer's disease is a neurodegenerative disease.[A235668] Part of the pathology of Alzheimer's disease is the presence of plaques forming extracellularly in the brain.[A235668] These plaques are mostly composed of amyloid-ß, a peptide of varying length formed by the cleavage of the amyloid precursor protein.[A235668] The "amyloid cascade hypothesis" suggests that the accumulation of amyloid-ß oligopeptides in the brain drives the pathogenesis of Alzheimer's disease.[A235730] Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß at amino acids 3-7.[A235668,L34393] The amyloid-ß residues Phe4, His6, Glu3, and Arg5 are responsible for the majority of the contact between amyloid-ß and aducanumab's Fab region.[A235668] Data from studies in mice and humans shows aducanumab treatment reduces amyloid-ß, however human trials show non-significant changes in amyloid-ß40 and amyloid-ß42 across a dose range of 0.3-30 mg/kg and an increase in amyloid-ß40 and amyloid-ß42 at 60 mg/kg.[A235730] Aducanumab treatment is associated with slowing the rate of progression of Alzheimer's disease, based on Mini-Mental State Examination, Clinical Dementia Rating, and levels of p-tau in the cerebrospinal fluid.[A235715] |
| Toxicity | Patients experiencing dose-limiting toxicity may present with amyloid-related imaging abnormalities including edema or microhemorrhages of the brain.[A235730] Symptoms of dose limiting toxicity were generally transient,[A235730] however patients may need to be treated with symptomatic and supportive measures. |
| Metabolism | Aducanumab is expected to be broken down into smaller oligopeptides and amino acids.[A40006,L34393] |
| Absorption | A 10 mg/kg intravenous dose of aducanumab reached a Cmax of 182.7 µg/mL, with a Tmax of 3.0 hours, and an AUCinf of 31,400 h |
| The volume of distribution of aducanumab is 9.63 L.[L34393] | |
| Clearance | A 10 mg/kg intravenous dose of aducanumab has a clearance of 0.39 mL/h/kg.[A235730] |
| Categories | Antibodies |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Amyloid beta A4 protein |
| 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 | 14251 |
| Therapeutic ID | Th1480 |
| Protein Name | Aducanumab |
| Sequence | >Th1480_Aducanumab XVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG |
| Molecular Weight | 146000 |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | The terminal half life of aducanumab is 24.8 days.[L34393] |
| Description | Aducanumab, or BIIB037, is a monoclonal IgG1 antibody that targets extracellular amyloid-ß plaques in the brain; similar to [gantenerumab], [bapineuzumab] and [solanezumab].[A235668,A235730] Aducanumab is a recombinant antibody derived from patients with slow or absent cognitive decline, and phase 1b clinical trial data has shown patients treated with aducanumab show a reduction in amyloid-ß plaques.[A235668] Based on Mini-Mental State Examination and Clinical Dementia Rating (CDR), patients taking aducanumab showed signs of slowing progression, however these data are controversial.[A235668,A235720] Clinical trials showed a 23% relative difference between the experimental and placebo groups as determined by CDR, however this is equivalent to an absolute difference of 0.4/18.[A235720] Although aducanumab's approval represents the first drug treatment for Alzheimer's disease, the approval is conditional on further results.[L34420] Biogen enrolled patients in phase 3 clinical trials in 2015, but increased the size of the trials from 1350 patients to 1650 patients to maintain statistical power in the face of a high standard deviation.[A235720] Development of aducanumab was discontinued in March 2019 when two phase 3 clinical trials did not pass futility analysis, however Biogen sought FDA approval in October 2019 after reanalysis of the data.[A235720] Aducanumab was granted accelerated FDA approval on 7 June 2021.[L34393] Continued approval will be based on further trials confirming a clinical benefit over currently available therapy.[L34420] |
| Indication/Disease | Aducanumab is indicated in the treatment of Alzheimer's disease.[L34393] |
| Pharmacodynamics | Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß, reducing amyloid plaques in the brain.[L34393] It has a long duration of action as it is given once every 4 weeks.[L34393] Patients should be counselled regarding the risk of amyloid related imaging abnormalities, including microhemorrhages, and hypersensitivity reactions.[L34393] |
| Mechanism of Action | Alzheimer's disease is a neurodegenerative disease.[A235668] Part of the pathology of Alzheimer's disease is the presence of plaques forming extracellularly in the brain.[A235668] These plaques are mostly composed of amyloid-ß, a peptide of varying length formed by the cleavage of the amyloid precursor protein.[A235668] The "amyloid cascade hypothesis" suggests that the accumulation of amyloid-ß oligopeptides in the brain drives the pathogenesis of Alzheimer's disease.[A235730] Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß at amino acids 3-7.[A235668,L34393] The amyloid-ß residues Phe4, His6, Glu3, and Arg5 are responsible for the majority of the contact between amyloid-ß and aducanumab's Fab region.[A235668] Data from studies in mice and humans shows aducanumab treatment reduces amyloid-ß, however human trials show non-significant changes in amyloid-ß40 and amyloid-ß42 across a dose range of 0.3-30 mg/kg and an increase in amyloid-ß40 and amyloid-ß42 at 60 mg/kg.[A235730] Aducanumab treatment is associated with slowing the rate of progression of Alzheimer's disease, based on Mini-Mental State Examination, Clinical Dementia Rating, and levels of p-tau in the cerebrospinal fluid.[A235715] |
| Toxicity | Patients experiencing dose-limiting toxicity may present with amyloid-related imaging abnormalities including edema or microhemorrhages of the brain.[A235730] Symptoms of dose limiting toxicity were generally transient,[A235730] however patients may need to be treated with symptomatic and supportive measures. |
| Metabolism | Aducanumab is expected to be broken down into smaller oligopeptides and amino acids.[A40006,L34393] |
| Absorption | A 10 mg/kg intravenous dose of aducanumab reached a Cmax of 182.7 µg/mL, with a Tmax of 3.0 hours, and an AUCinf of 31,400 h |
| The volume of distribution of aducanumab is 9.63 L.[L34393] | |
| Clearance | A 10 mg/kg intravenous dose of aducanumab has a clearance of 0.39 mL/h/kg.[A235730] |
| Categories | Antibodies, Monoclonal |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Amyloid beta A4 protein |
| 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 | 14252 |
| Therapeutic ID | Th1480 |
| Protein Name | Aducanumab |
| Sequence | >Th1480_Aducanumab XVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG |
| Molecular Weight | 146000 |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | The terminal half life of aducanumab is 24.8 days.[L34393] |
| Description | Aducanumab, or BIIB037, is a monoclonal IgG1 antibody that targets extracellular amyloid-ß plaques in the brain; similar to [gantenerumab], [bapineuzumab] and [solanezumab].[A235668,A235730] Aducanumab is a recombinant antibody derived from patients with slow or absent cognitive decline, and phase 1b clinical trial data has shown patients treated with aducanumab show a reduction in amyloid-ß plaques.[A235668] Based on Mini-Mental State Examination and Clinical Dementia Rating (CDR), patients taking aducanumab showed signs of slowing progression, however these data are controversial.[A235668,A235720] Clinical trials showed a 23% relative difference between the experimental and placebo groups as determined by CDR, however this is equivalent to an absolute difference of 0.4/18.[A235720] Although aducanumab's approval represents the first drug treatment for Alzheimer's disease, the approval is conditional on further results.[L34420] Biogen enrolled patients in phase 3 clinical trials in 2015, but increased the size of the trials from 1350 patients to 1650 patients to maintain statistical power in the face of a high standard deviation.[A235720] Development of aducanumab was discontinued in March 2019 when two phase 3 clinical trials did not pass futility analysis, however Biogen sought FDA approval in October 2019 after reanalysis of the data.[A235720] Aducanumab was granted accelerated FDA approval on 7 June 2021.[L34393] Continued approval will be based on further trials confirming a clinical benefit over currently available therapy.[L34420] |
| Indication/Disease | Aducanumab is indicated in the treatment of Alzheimer's disease.[L34393] |
| Pharmacodynamics | Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß, reducing amyloid plaques in the brain.[L34393] It has a long duration of action as it is given once every 4 weeks.[L34393] Patients should be counselled regarding the risk of amyloid related imaging abnormalities, including microhemorrhages, and hypersensitivity reactions.[L34393] |
| Mechanism of Action | Alzheimer's disease is a neurodegenerative disease.[A235668] Part of the pathology of Alzheimer's disease is the presence of plaques forming extracellularly in the brain.[A235668] These plaques are mostly composed of amyloid-ß, a peptide of varying length formed by the cleavage of the amyloid precursor protein.[A235668] The "amyloid cascade hypothesis" suggests that the accumulation of amyloid-ß oligopeptides in the brain drives the pathogenesis of Alzheimer's disease.[A235730] Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß at amino acids 3-7.[A235668,L34393] The amyloid-ß residues Phe4, His6, Glu3, and Arg5 are responsible for the majority of the contact between amyloid-ß and aducanumab's Fab region.[A235668] Data from studies in mice and humans shows aducanumab treatment reduces amyloid-ß, however human trials show non-significant changes in amyloid-ß40 and amyloid-ß42 across a dose range of 0.3-30 mg/kg and an increase in amyloid-ß40 and amyloid-ß42 at 60 mg/kg.[A235730] Aducanumab treatment is associated with slowing the rate of progression of Alzheimer's disease, based on Mini-Mental State Examination, Clinical Dementia Rating, and levels of p-tau in the cerebrospinal fluid.[A235715] |
| Toxicity | Patients experiencing dose-limiting toxicity may present with amyloid-related imaging abnormalities including edema or microhemorrhages of the brain.[A235730] Symptoms of dose limiting toxicity were generally transient,[A235730] however patients may need to be treated with symptomatic and supportive measures. |
| Metabolism | Aducanumab is expected to be broken down into smaller oligopeptides and amino acids.[A40006,L34393] |
| Absorption | A 10 mg/kg intravenous dose of aducanumab reached a Cmax of 182.7 µg/mL, with a Tmax of 3.0 hours, and an AUCinf of 31,400 h |
| The volume of distribution of aducanumab is 9.63 L.[L34393] | |
| Clearance | A 10 mg/kg intravenous dose of aducanumab has a clearance of 0.39 mL/h/kg.[A235730] |
| Categories | Blood Proteins |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Amyloid beta A4 protein |
| 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 | 14253 |
| Therapeutic ID | Th1480 |
| Protein Name | Aducanumab |
| Sequence | >Th1480_Aducanumab XVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG |
| Molecular Weight | 146000 |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | The terminal half life of aducanumab is 24.8 days.[L34393] |
| Description | Aducanumab, or BIIB037, is a monoclonal IgG1 antibody that targets extracellular amyloid-ß plaques in the brain; similar to [gantenerumab], [bapineuzumab] and [solanezumab].[A235668,A235730] Aducanumab is a recombinant antibody derived from patients with slow or absent cognitive decline, and phase 1b clinical trial data has shown patients treated with aducanumab show a reduction in amyloid-ß plaques.[A235668] Based on Mini-Mental State Examination and Clinical Dementia Rating (CDR), patients taking aducanumab showed signs of slowing progression, however these data are controversial.[A235668,A235720] Clinical trials showed a 23% relative difference between the experimental and placebo groups as determined by CDR, however this is equivalent to an absolute difference of 0.4/18.[A235720] Although aducanumab's approval represents the first drug treatment for Alzheimer's disease, the approval is conditional on further results.[L34420] Biogen enrolled patients in phase 3 clinical trials in 2015, but increased the size of the trials from 1350 patients to 1650 patients to maintain statistical power in the face of a high standard deviation.[A235720] Development of aducanumab was discontinued in March 2019 when two phase 3 clinical trials did not pass futility analysis, however Biogen sought FDA approval in October 2019 after reanalysis of the data.[A235720] Aducanumab was granted accelerated FDA approval on 7 June 2021.[L34393] Continued approval will be based on further trials confirming a clinical benefit over currently available therapy.[L34420] |
| Indication/Disease | Aducanumab is indicated in the treatment of Alzheimer's disease.[L34393] |
| Pharmacodynamics | Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß, reducing amyloid plaques in the brain.[L34393] It has a long duration of action as it is given once every 4 weeks.[L34393] Patients should be counselled regarding the risk of amyloid related imaging abnormalities, including microhemorrhages, and hypersensitivity reactions.[L34393] |
| Mechanism of Action | Alzheimer's disease is a neurodegenerative disease.[A235668] Part of the pathology of Alzheimer's disease is the presence of plaques forming extracellularly in the brain.[A235668] These plaques are mostly composed of amyloid-ß, a peptide of varying length formed by the cleavage of the amyloid precursor protein.[A235668] The "amyloid cascade hypothesis" suggests that the accumulation of amyloid-ß oligopeptides in the brain drives the pathogenesis of Alzheimer's disease.[A235730] Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß at amino acids 3-7.[A235668,L34393] The amyloid-ß residues Phe4, His6, Glu3, and Arg5 are responsible for the majority of the contact between amyloid-ß and aducanumab's Fab region.[A235668] Data from studies in mice and humans shows aducanumab treatment reduces amyloid-ß, however human trials show non-significant changes in amyloid-ß40 and amyloid-ß42 across a dose range of 0.3-30 mg/kg and an increase in amyloid-ß40 and amyloid-ß42 at 60 mg/kg.[A235730] Aducanumab treatment is associated with slowing the rate of progression of Alzheimer's disease, based on Mini-Mental State Examination, Clinical Dementia Rating, and levels of p-tau in the cerebrospinal fluid.[A235715] |
| Toxicity | Patients experiencing dose-limiting toxicity may present with amyloid-related imaging abnormalities including edema or microhemorrhages of the brain.[A235730] Symptoms of dose limiting toxicity were generally transient,[A235730] however patients may need to be treated with symptomatic and supportive measures. |
| Metabolism | Aducanumab is expected to be broken down into smaller oligopeptides and amino acids.[A40006,L34393] |
| Absorption | A 10 mg/kg intravenous dose of aducanumab reached a Cmax of 182.7 µg/mL, with a Tmax of 3.0 hours, and an AUCinf of 31,400 h |
| The volume of distribution of aducanumab is 9.63 L.[L34393] | |
| Clearance | A 10 mg/kg intravenous dose of aducanumab has a clearance of 0.39 mL/h/kg.[A235730] |
| Categories | Globulins |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Amyloid beta A4 protein |
| 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 | 14254 |
| Therapeutic ID | Th1480 |
| Protein Name | Aducanumab |
| Sequence | >Th1480_Aducanumab XVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG |
| Molecular Weight | 146000 |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | The terminal half life of aducanumab is 24.8 days.[L34393] |
| Description | Aducanumab, or BIIB037, is a monoclonal IgG1 antibody that targets extracellular amyloid-ß plaques in the brain; similar to [gantenerumab], [bapineuzumab] and [solanezumab].[A235668,A235730] Aducanumab is a recombinant antibody derived from patients with slow or absent cognitive decline, and phase 1b clinical trial data has shown patients treated with aducanumab show a reduction in amyloid-ß plaques.[A235668] Based on Mini-Mental State Examination and Clinical Dementia Rating (CDR), patients taking aducanumab showed signs of slowing progression, however these data are controversial.[A235668,A235720] Clinical trials showed a 23% relative difference between the experimental and placebo groups as determined by CDR, however this is equivalent to an absolute difference of 0.4/18.[A235720] Although aducanumab's approval represents the first drug treatment for Alzheimer's disease, the approval is conditional on further results.[L34420] Biogen enrolled patients in phase 3 clinical trials in 2015, but increased the size of the trials from 1350 patients to 1650 patients to maintain statistical power in the face of a high standard deviation.[A235720] Development of aducanumab was discontinued in March 2019 when two phase 3 clinical trials did not pass futility analysis, however Biogen sought FDA approval in October 2019 after reanalysis of the data.[A235720] Aducanumab was granted accelerated FDA approval on 7 June 2021.[L34393] Continued approval will be based on further trials confirming a clinical benefit over currently available therapy.[L34420] |
| Indication/Disease | Aducanumab is indicated in the treatment of Alzheimer's disease.[L34393] |
| Pharmacodynamics | Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß, reducing amyloid plaques in the brain.[L34393] It has a long duration of action as it is given once every 4 weeks.[L34393] Patients should be counselled regarding the risk of amyloid related imaging abnormalities, including microhemorrhages, and hypersensitivity reactions.[L34393] |
| Mechanism of Action | Alzheimer's disease is a neurodegenerative disease.[A235668] Part of the pathology of Alzheimer's disease is the presence of plaques forming extracellularly in the brain.[A235668] These plaques are mostly composed of amyloid-ß, a peptide of varying length formed by the cleavage of the amyloid precursor protein.[A235668] The "amyloid cascade hypothesis" suggests that the accumulation of amyloid-ß oligopeptides in the brain drives the pathogenesis of Alzheimer's disease.[A235730] Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß at amino acids 3-7.[A235668,L34393] The amyloid-ß residues Phe4, His6, Glu3, and Arg5 are responsible for the majority of the contact between amyloid-ß and aducanumab's Fab region.[A235668] Data from studies in mice and humans shows aducanumab treatment reduces amyloid-ß, however human trials show non-significant changes in amyloid-ß40 and amyloid-ß42 across a dose range of 0.3-30 mg/kg and an increase in amyloid-ß40 and amyloid-ß42 at 60 mg/kg.[A235730] Aducanumab treatment is associated with slowing the rate of progression of Alzheimer's disease, based on Mini-Mental State Examination, Clinical Dementia Rating, and levels of p-tau in the cerebrospinal fluid.[A235715] |
| Toxicity | Patients experiencing dose-limiting toxicity may present with amyloid-related imaging abnormalities including edema or microhemorrhages of the brain.[A235730] Symptoms of dose limiting toxicity were generally transient,[A235730] however patients may need to be treated with symptomatic and supportive measures. |
| Metabolism | Aducanumab is expected to be broken down into smaller oligopeptides and amino acids.[A40006,L34393] |
| Absorption | A 10 mg/kg intravenous dose of aducanumab reached a Cmax of 182.7 µg/mL, with a Tmax of 3.0 hours, and an AUCinf of 31,400 h |
| The volume of distribution of aducanumab is 9.63 L.[L34393] | |
| Clearance | A 10 mg/kg intravenous dose of aducanumab has a clearance of 0.39 mL/h/kg.[A235730] |
| Categories | Immunoglobulins |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Amyloid beta A4 protein |
| 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 | 14255 |
| Therapeutic ID | Th1480 |
| Protein Name | Aducanumab |
| Sequence | >Th1480_Aducanumab XVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG |
| Molecular Weight | 146000 |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | The terminal half life of aducanumab is 24.8 days.[L34393] |
| Description | Aducanumab, or BIIB037, is a monoclonal IgG1 antibody that targets extracellular amyloid-ß plaques in the brain; similar to [gantenerumab], [bapineuzumab] and [solanezumab].[A235668,A235730] Aducanumab is a recombinant antibody derived from patients with slow or absent cognitive decline, and phase 1b clinical trial data has shown patients treated with aducanumab show a reduction in amyloid-ß plaques.[A235668] Based on Mini-Mental State Examination and Clinical Dementia Rating (CDR), patients taking aducanumab showed signs of slowing progression, however these data are controversial.[A235668,A235720] Clinical trials showed a 23% relative difference between the experimental and placebo groups as determined by CDR, however this is equivalent to an absolute difference of 0.4/18.[A235720] Although aducanumab's approval represents the first drug treatment for Alzheimer's disease, the approval is conditional on further results.[L34420] Biogen enrolled patients in phase 3 clinical trials in 2015, but increased the size of the trials from 1350 patients to 1650 patients to maintain statistical power in the face of a high standard deviation.[A235720] Development of aducanumab was discontinued in March 2019 when two phase 3 clinical trials did not pass futility analysis, however Biogen sought FDA approval in October 2019 after reanalysis of the data.[A235720] Aducanumab was granted accelerated FDA approval on 7 June 2021.[L34393] Continued approval will be based on further trials confirming a clinical benefit over currently available therapy.[L34420] |
| Indication/Disease | Aducanumab is indicated in the treatment of Alzheimer's disease.[L34393] |
| Pharmacodynamics | Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß, reducing amyloid plaques in the brain.[L34393] It has a long duration of action as it is given once every 4 weeks.[L34393] Patients should be counselled regarding the risk of amyloid related imaging abnormalities, including microhemorrhages, and hypersensitivity reactions.[L34393] |
| Mechanism of Action | Alzheimer's disease is a neurodegenerative disease.[A235668] Part of the pathology of Alzheimer's disease is the presence of plaques forming extracellularly in the brain.[A235668] These plaques are mostly composed of amyloid-ß, a peptide of varying length formed by the cleavage of the amyloid precursor protein.[A235668] The "amyloid cascade hypothesis" suggests that the accumulation of amyloid-ß oligopeptides in the brain drives the pathogenesis of Alzheimer's disease.[A235730] Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß at amino acids 3-7.[A235668,L34393] The amyloid-ß residues Phe4, His6, Glu3, and Arg5 are responsible for the majority of the contact between amyloid-ß and aducanumab's Fab region.[A235668] Data from studies in mice and humans shows aducanumab treatment reduces amyloid-ß, however human trials show non-significant changes in amyloid-ß40 and amyloid-ß42 across a dose range of 0.3-30 mg/kg and an increase in amyloid-ß40 and amyloid-ß42 at 60 mg/kg.[A235730] Aducanumab treatment is associated with slowing the rate of progression of Alzheimer's disease, based on Mini-Mental State Examination, Clinical Dementia Rating, and levels of p-tau in the cerebrospinal fluid.[A235715] |
| Toxicity | Patients experiencing dose-limiting toxicity may present with amyloid-related imaging abnormalities including edema or microhemorrhages of the brain.[A235730] Symptoms of dose limiting toxicity were generally transient,[A235730] however patients may need to be treated with symptomatic and supportive measures. |
| Metabolism | Aducanumab is expected to be broken down into smaller oligopeptides and amino acids.[A40006,L34393] |
| Absorption | A 10 mg/kg intravenous dose of aducanumab reached a Cmax of 182.7 µg/mL, with a Tmax of 3.0 hours, and an AUCinf of 31,400 h |
| The volume of distribution of aducanumab is 9.63 L.[L34393] | |
| Clearance | A 10 mg/kg intravenous dose of aducanumab has a clearance of 0.39 mL/h/kg.[A235730] |
| Categories | Immunoproteins |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Amyloid beta A4 protein |
| 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 | 14256 |
| Therapeutic ID | Th1480 |
| Protein Name | Aducanumab |
| Sequence | >Th1480_Aducanumab XVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG |
| Molecular Weight | 146000 |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | The terminal half life of aducanumab is 24.8 days.[L34393] |
| Description | Aducanumab, or BIIB037, is a monoclonal IgG1 antibody that targets extracellular amyloid-ß plaques in the brain; similar to [gantenerumab], [bapineuzumab] and [solanezumab].[A235668,A235730] Aducanumab is a recombinant antibody derived from patients with slow or absent cognitive decline, and phase 1b clinical trial data has shown patients treated with aducanumab show a reduction in amyloid-ß plaques.[A235668] Based on Mini-Mental State Examination and Clinical Dementia Rating (CDR), patients taking aducanumab showed signs of slowing progression, however these data are controversial.[A235668,A235720] Clinical trials showed a 23% relative difference between the experimental and placebo groups as determined by CDR, however this is equivalent to an absolute difference of 0.4/18.[A235720] Although aducanumab's approval represents the first drug treatment for Alzheimer's disease, the approval is conditional on further results.[L34420] Biogen enrolled patients in phase 3 clinical trials in 2015, but increased the size of the trials from 1350 patients to 1650 patients to maintain statistical power in the face of a high standard deviation.[A235720] Development of aducanumab was discontinued in March 2019 when two phase 3 clinical trials did not pass futility analysis, however Biogen sought FDA approval in October 2019 after reanalysis of the data.[A235720] Aducanumab was granted accelerated FDA approval on 7 June 2021.[L34393] Continued approval will be based on further trials confirming a clinical benefit over currently available therapy.[L34420] |
| Indication/Disease | Aducanumab is indicated in the treatment of Alzheimer's disease.[L34393] |
| Pharmacodynamics | Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß, reducing amyloid plaques in the brain.[L34393] It has a long duration of action as it is given once every 4 weeks.[L34393] Patients should be counselled regarding the risk of amyloid related imaging abnormalities, including microhemorrhages, and hypersensitivity reactions.[L34393] |
| Mechanism of Action | Alzheimer's disease is a neurodegenerative disease.[A235668] Part of the pathology of Alzheimer's disease is the presence of plaques forming extracellularly in the brain.[A235668] These plaques are mostly composed of amyloid-ß, a peptide of varying length formed by the cleavage of the amyloid precursor protein.[A235668] The "amyloid cascade hypothesis" suggests that the accumulation of amyloid-ß oligopeptides in the brain drives the pathogenesis of Alzheimer's disease.[A235730] Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß at amino acids 3-7.[A235668,L34393] The amyloid-ß residues Phe4, His6, Glu3, and Arg5 are responsible for the majority of the contact between amyloid-ß and aducanumab's Fab region.[A235668] Data from studies in mice and humans shows aducanumab treatment reduces amyloid-ß, however human trials show non-significant changes in amyloid-ß40 and amyloid-ß42 across a dose range of 0.3-30 mg/kg and an increase in amyloid-ß40 and amyloid-ß42 at 60 mg/kg.[A235730] Aducanumab treatment is associated with slowing the rate of progression of Alzheimer's disease, based on Mini-Mental State Examination, Clinical Dementia Rating, and levels of p-tau in the cerebrospinal fluid.[A235715] |
| Toxicity | Patients experiencing dose-limiting toxicity may present with amyloid-related imaging abnormalities including edema or microhemorrhages of the brain.[A235730] Symptoms of dose limiting toxicity were generally transient,[A235730] however patients may need to be treated with symptomatic and supportive measures. |
| Metabolism | Aducanumab is expected to be broken down into smaller oligopeptides and amino acids.[A40006,L34393] |
| Absorption | A 10 mg/kg intravenous dose of aducanumab reached a Cmax of 182.7 µg/mL, with a Tmax of 3.0 hours, and an AUCinf of 31,400 h |
| The volume of distribution of aducanumab is 9.63 L.[L34393] | |
| Clearance | A 10 mg/kg intravenous dose of aducanumab has a clearance of 0.39 mL/h/kg.[A235730] |
| Categories | Proteins |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Amyloid beta A4 protein |
| 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 | 14257 |
| Therapeutic ID | Th1480 |
| Protein Name | Aducanumab |
| Sequence | >Th1480_Aducanumab XVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG |
| Molecular Weight | 146000 |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | The terminal half life of aducanumab is 24.8 days.[L34393] |
| Description | Aducanumab, or BIIB037, is a monoclonal IgG1 antibody that targets extracellular amyloid-ß plaques in the brain; similar to [gantenerumab], [bapineuzumab] and [solanezumab].[A235668,A235730] Aducanumab is a recombinant antibody derived from patients with slow or absent cognitive decline, and phase 1b clinical trial data has shown patients treated with aducanumab show a reduction in amyloid-ß plaques.[A235668] Based on Mini-Mental State Examination and Clinical Dementia Rating (CDR), patients taking aducanumab showed signs of slowing progression, however these data are controversial.[A235668,A235720] Clinical trials showed a 23% relative difference between the experimental and placebo groups as determined by CDR, however this is equivalent to an absolute difference of 0.4/18.[A235720] Although aducanumab's approval represents the first drug treatment for Alzheimer's disease, the approval is conditional on further results.[L34420] Biogen enrolled patients in phase 3 clinical trials in 2015, but increased the size of the trials from 1350 patients to 1650 patients to maintain statistical power in the face of a high standard deviation.[A235720] Development of aducanumab was discontinued in March 2019 when two phase 3 clinical trials did not pass futility analysis, however Biogen sought FDA approval in October 2019 after reanalysis of the data.[A235720] Aducanumab was granted accelerated FDA approval on 7 June 2021.[L34393] Continued approval will be based on further trials confirming a clinical benefit over currently available therapy.[L34420] |
| Indication/Disease | Aducanumab is indicated in the treatment of Alzheimer's disease.[L34393] |
| Pharmacodynamics | Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß, reducing amyloid plaques in the brain.[L34393] It has a long duration of action as it is given once every 4 weeks.[L34393] Patients should be counselled regarding the risk of amyloid related imaging abnormalities, including microhemorrhages, and hypersensitivity reactions.[L34393] |
| Mechanism of Action | Alzheimer's disease is a neurodegenerative disease.[A235668] Part of the pathology of Alzheimer's disease is the presence of plaques forming extracellularly in the brain.[A235668] These plaques are mostly composed of amyloid-ß, a peptide of varying length formed by the cleavage of the amyloid precursor protein.[A235668] The "amyloid cascade hypothesis" suggests that the accumulation of amyloid-ß oligopeptides in the brain drives the pathogenesis of Alzheimer's disease.[A235730] Aducanumab is a monoclonal IgG1 antibody that binds to amyloid-ß at amino acids 3-7.[A235668,L34393] The amyloid-ß residues Phe4, His6, Glu3, and Arg5 are responsible for the majority of the contact between amyloid-ß and aducanumab's Fab region.[A235668] Data from studies in mice and humans shows aducanumab treatment reduces amyloid-ß, however human trials show non-significant changes in amyloid-ß40 and amyloid-ß42 across a dose range of 0.3-30 mg/kg and an increase in amyloid-ß40 and amyloid-ß42 at 60 mg/kg.[A235730] Aducanumab treatment is associated with slowing the rate of progression of Alzheimer's disease, based on Mini-Mental State Examination, Clinical Dementia Rating, and levels of p-tau in the cerebrospinal fluid.[A235715] |
| Toxicity | Patients experiencing dose-limiting toxicity may present with amyloid-related imaging abnormalities including edema or microhemorrhages of the brain.[A235730] Symptoms of dose limiting toxicity were generally transient,[A235730] however patients may need to be treated with symptomatic and supportive measures. |
| Metabolism | Aducanumab is expected to be broken down into smaller oligopeptides and amino acids.[A40006,L34393] |
| Absorption | A 10 mg/kg intravenous dose of aducanumab reached a Cmax of 182.7 µg/mL, with a Tmax of 3.0 hours, and an AUCinf of 31,400 h |
| The volume of distribution of aducanumab is 9.63 L.[L34393] | |
| Clearance | A 10 mg/kg intravenous dose of aducanumab has a clearance of 0.39 mL/h/kg.[A235730] |
| Categories | Serum Globulins |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Amyloid beta A4 protein |
| 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 |