Detailed description page of ThPDB2
| This page displays user query in tabular form. |
Th1431 details |
| Primary information | |
|---|---|
| ID | 13754 |
| Therapeutic ID | Th1431 |
| Protein Name | Ligelizumab |
| Sequence | >Th1431_Ligelizumab QVQLVQSGAEVMKPGSSVKVSCKASGYTFSWYWLEWVRQAPGHGLEWMGEIDPGTFTTNYNEKFKARVTFTADTSTSTAYMELSSLRSEDTAVYYCARFSHFSGSNYDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK |
| Molecular Weight | NA |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | NA |
| Description | Ligelizumab is a humanized IgG1k monoclonal antibody targeted against immunoglobulin E (IgE). Similar in mechanism to [omalizumab], another IgE-directed monoclonal antibody, ligelizumab has a distinct binding epitope as compared to its peer (with a small degree of overlap) which appears to confer a greater affinity for free serum IgE and an altered sensitivity to IgE conformation.[A242292] Ligelizumab is currently under investigation for the treatment of chronic spontaneous urticaria (CSU), an autoimmune-driven inflammatory condition. While the precise pathogenesis of CSU is not entirely clear, autoantibodies against IgE receptors, and sometimes against IgE itself, are thought to exist in 30-40% of patients,[A242362,A242367] and the efficacy anti-IgE antibody therapy in the treatment of CSU has been previously established with omalizumab. Initial trials of ligelizumab suggest a greater efficacy over its predecessor for the treatment of CSU.[A242367] |
| Indication/Disease | NA |
| Pharmacodynamics | NA |
| Mechanism of Action | Immunoglobulin E (IgE) is a key driver of hypersensitivity reactions, and has thus become an attractive target in the treatment of immune-mediated hypersensitivity disorders. Immediate hypersensitivity reactions are due to IgE binding with FceRI, which activates allergic effector cells that undergo degranulation to release vasoactive and pro-inflammatory mediators.[A242292] IgE also binds to CD23/FceRII, which appears responsible for antigen presentation, antigen transport across airway/epithelial barriers, and the regulation of IgE synthesis.[A242292] Ligelizumab is a monoclonal antibody directed at IgE, binding specifically to an epitope in the IgE Ce3 domain.[A242292] It neutralizes serum IgE and also appears to inhibit the production of IgE via inhibition of IgE-FceRI binding activity and, to a lesser extent, IgE binding to CD23. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| NA | |
| Clearance | NA |
| Categories | Amino Acids, Peptides, and Proteins |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Immunoglobulin heavy constant epsilon |
| 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 | 13755 |
| Therapeutic ID | Th1431 |
| Protein Name | Ligelizumab |
| Sequence | >Th1431_Ligelizumab QVQLVQSGAEVMKPGSSVKVSCKASGYTFSWYWLEWVRQAPGHGLEWMGEIDPGTFTTNYNEKFKARVTFTADTSTSTAYMELSSLRSEDTAVYYCARFSHFSGSNYDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK |
| Molecular Weight | NA |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | NA |
| Description | Ligelizumab is a humanized IgG1k monoclonal antibody targeted against immunoglobulin E (IgE). Similar in mechanism to [omalizumab], another IgE-directed monoclonal antibody, ligelizumab has a distinct binding epitope as compared to its peer (with a small degree of overlap) which appears to confer a greater affinity for free serum IgE and an altered sensitivity to IgE conformation.[A242292] Ligelizumab is currently under investigation for the treatment of chronic spontaneous urticaria (CSU), an autoimmune-driven inflammatory condition. While the precise pathogenesis of CSU is not entirely clear, autoantibodies against IgE receptors, and sometimes against IgE itself, are thought to exist in 30-40% of patients,[A242362,A242367] and the efficacy anti-IgE antibody therapy in the treatment of CSU has been previously established with omalizumab. Initial trials of ligelizumab suggest a greater efficacy over its predecessor for the treatment of CSU.[A242367] |
| Indication/Disease | NA |
| Pharmacodynamics | NA |
| Mechanism of Action | Immunoglobulin E (IgE) is a key driver of hypersensitivity reactions, and has thus become an attractive target in the treatment of immune-mediated hypersensitivity disorders. Immediate hypersensitivity reactions are due to IgE binding with FceRI, which activates allergic effector cells that undergo degranulation to release vasoactive and pro-inflammatory mediators.[A242292] IgE also binds to CD23/FceRII, which appears responsible for antigen presentation, antigen transport across airway/epithelial barriers, and the regulation of IgE synthesis.[A242292] Ligelizumab is a monoclonal antibody directed at IgE, binding specifically to an epitope in the IgE Ce3 domain.[A242292] It neutralizes serum IgE and also appears to inhibit the production of IgE via inhibition of IgE-FceRI binding activity and, to a lesser extent, IgE binding to CD23. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| NA | |
| Clearance | NA |
| Categories | Antibodies |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Immunoglobulin heavy constant epsilon |
| 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 | 13756 |
| Therapeutic ID | Th1431 |
| Protein Name | Ligelizumab |
| Sequence | >Th1431_Ligelizumab QVQLVQSGAEVMKPGSSVKVSCKASGYTFSWYWLEWVRQAPGHGLEWMGEIDPGTFTTNYNEKFKARVTFTADTSTSTAYMELSSLRSEDTAVYYCARFSHFSGSNYDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK |
| Molecular Weight | NA |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | NA |
| Description | Ligelizumab is a humanized IgG1k monoclonal antibody targeted against immunoglobulin E (IgE). Similar in mechanism to [omalizumab], another IgE-directed monoclonal antibody, ligelizumab has a distinct binding epitope as compared to its peer (with a small degree of overlap) which appears to confer a greater affinity for free serum IgE and an altered sensitivity to IgE conformation.[A242292] Ligelizumab is currently under investigation for the treatment of chronic spontaneous urticaria (CSU), an autoimmune-driven inflammatory condition. While the precise pathogenesis of CSU is not entirely clear, autoantibodies against IgE receptors, and sometimes against IgE itself, are thought to exist in 30-40% of patients,[A242362,A242367] and the efficacy anti-IgE antibody therapy in the treatment of CSU has been previously established with omalizumab. Initial trials of ligelizumab suggest a greater efficacy over its predecessor for the treatment of CSU.[A242367] |
| Indication/Disease | NA |
| Pharmacodynamics | NA |
| Mechanism of Action | Immunoglobulin E (IgE) is a key driver of hypersensitivity reactions, and has thus become an attractive target in the treatment of immune-mediated hypersensitivity disorders. Immediate hypersensitivity reactions are due to IgE binding with FceRI, which activates allergic effector cells that undergo degranulation to release vasoactive and pro-inflammatory mediators.[A242292] IgE also binds to CD23/FceRII, which appears responsible for antigen presentation, antigen transport across airway/epithelial barriers, and the regulation of IgE synthesis.[A242292] Ligelizumab is a monoclonal antibody directed at IgE, binding specifically to an epitope in the IgE Ce3 domain.[A242292] It neutralizes serum IgE and also appears to inhibit the production of IgE via inhibition of IgE-FceRI binding activity and, to a lesser extent, IgE binding to CD23. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| NA | |
| Clearance | NA |
| Categories | Antibodies, Monoclonal |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Immunoglobulin heavy constant epsilon |
| 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 | 13757 |
| Therapeutic ID | Th1431 |
| Protein Name | Ligelizumab |
| Sequence | >Th1431_Ligelizumab QVQLVQSGAEVMKPGSSVKVSCKASGYTFSWYWLEWVRQAPGHGLEWMGEIDPGTFTTNYNEKFKARVTFTADTSTSTAYMELSSLRSEDTAVYYCARFSHFSGSNYDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK |
| Molecular Weight | NA |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | NA |
| Description | Ligelizumab is a humanized IgG1k monoclonal antibody targeted against immunoglobulin E (IgE). Similar in mechanism to [omalizumab], another IgE-directed monoclonal antibody, ligelizumab has a distinct binding epitope as compared to its peer (with a small degree of overlap) which appears to confer a greater affinity for free serum IgE and an altered sensitivity to IgE conformation.[A242292] Ligelizumab is currently under investigation for the treatment of chronic spontaneous urticaria (CSU), an autoimmune-driven inflammatory condition. While the precise pathogenesis of CSU is not entirely clear, autoantibodies against IgE receptors, and sometimes against IgE itself, are thought to exist in 30-40% of patients,[A242362,A242367] and the efficacy anti-IgE antibody therapy in the treatment of CSU has been previously established with omalizumab. Initial trials of ligelizumab suggest a greater efficacy over its predecessor for the treatment of CSU.[A242367] |
| Indication/Disease | NA |
| Pharmacodynamics | NA |
| Mechanism of Action | Immunoglobulin E (IgE) is a key driver of hypersensitivity reactions, and has thus become an attractive target in the treatment of immune-mediated hypersensitivity disorders. Immediate hypersensitivity reactions are due to IgE binding with FceRI, which activates allergic effector cells that undergo degranulation to release vasoactive and pro-inflammatory mediators.[A242292] IgE also binds to CD23/FceRII, which appears responsible for antigen presentation, antigen transport across airway/epithelial barriers, and the regulation of IgE synthesis.[A242292] Ligelizumab is a monoclonal antibody directed at IgE, binding specifically to an epitope in the IgE Ce3 domain.[A242292] It neutralizes serum IgE and also appears to inhibit the production of IgE via inhibition of IgE-FceRI binding activity and, to a lesser extent, IgE binding to CD23. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| NA | |
| Clearance | NA |
| Categories | Antibodies, Monoclonal, Humanized |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Immunoglobulin heavy constant epsilon |
| 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 | 13758 |
| Therapeutic ID | Th1431 |
| Protein Name | Ligelizumab |
| Sequence | >Th1431_Ligelizumab QVQLVQSGAEVMKPGSSVKVSCKASGYTFSWYWLEWVRQAPGHGLEWMGEIDPGTFTTNYNEKFKARVTFTADTSTSTAYMELSSLRSEDTAVYYCARFSHFSGSNYDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK |
| Molecular Weight | NA |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | NA |
| Description | Ligelizumab is a humanized IgG1k monoclonal antibody targeted against immunoglobulin E (IgE). Similar in mechanism to [omalizumab], another IgE-directed monoclonal antibody, ligelizumab has a distinct binding epitope as compared to its peer (with a small degree of overlap) which appears to confer a greater affinity for free serum IgE and an altered sensitivity to IgE conformation.[A242292] Ligelizumab is currently under investigation for the treatment of chronic spontaneous urticaria (CSU), an autoimmune-driven inflammatory condition. While the precise pathogenesis of CSU is not entirely clear, autoantibodies against IgE receptors, and sometimes against IgE itself, are thought to exist in 30-40% of patients,[A242362,A242367] and the efficacy anti-IgE antibody therapy in the treatment of CSU has been previously established with omalizumab. Initial trials of ligelizumab suggest a greater efficacy over its predecessor for the treatment of CSU.[A242367] |
| Indication/Disease | NA |
| Pharmacodynamics | NA |
| Mechanism of Action | Immunoglobulin E (IgE) is a key driver of hypersensitivity reactions, and has thus become an attractive target in the treatment of immune-mediated hypersensitivity disorders. Immediate hypersensitivity reactions are due to IgE binding with FceRI, which activates allergic effector cells that undergo degranulation to release vasoactive and pro-inflammatory mediators.[A242292] IgE also binds to CD23/FceRII, which appears responsible for antigen presentation, antigen transport across airway/epithelial barriers, and the regulation of IgE synthesis.[A242292] Ligelizumab is a monoclonal antibody directed at IgE, binding specifically to an epitope in the IgE Ce3 domain.[A242292] It neutralizes serum IgE and also appears to inhibit the production of IgE via inhibition of IgE-FceRI binding activity and, to a lesser extent, IgE binding to CD23. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| NA | |
| Clearance | NA |
| Categories | Blood Proteins |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Immunoglobulin heavy constant epsilon |
| 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 | 13759 |
| Therapeutic ID | Th1431 |
| Protein Name | Ligelizumab |
| Sequence | >Th1431_Ligelizumab QVQLVQSGAEVMKPGSSVKVSCKASGYTFSWYWLEWVRQAPGHGLEWMGEIDPGTFTTNYNEKFKARVTFTADTSTSTAYMELSSLRSEDTAVYYCARFSHFSGSNYDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK |
| Molecular Weight | NA |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | NA |
| Description | Ligelizumab is a humanized IgG1k monoclonal antibody targeted against immunoglobulin E (IgE). Similar in mechanism to [omalizumab], another IgE-directed monoclonal antibody, ligelizumab has a distinct binding epitope as compared to its peer (with a small degree of overlap) which appears to confer a greater affinity for free serum IgE and an altered sensitivity to IgE conformation.[A242292] Ligelizumab is currently under investigation for the treatment of chronic spontaneous urticaria (CSU), an autoimmune-driven inflammatory condition. While the precise pathogenesis of CSU is not entirely clear, autoantibodies against IgE receptors, and sometimes against IgE itself, are thought to exist in 30-40% of patients,[A242362,A242367] and the efficacy anti-IgE antibody therapy in the treatment of CSU has been previously established with omalizumab. Initial trials of ligelizumab suggest a greater efficacy over its predecessor for the treatment of CSU.[A242367] |
| Indication/Disease | NA |
| Pharmacodynamics | NA |
| Mechanism of Action | Immunoglobulin E (IgE) is a key driver of hypersensitivity reactions, and has thus become an attractive target in the treatment of immune-mediated hypersensitivity disorders. Immediate hypersensitivity reactions are due to IgE binding with FceRI, which activates allergic effector cells that undergo degranulation to release vasoactive and pro-inflammatory mediators.[A242292] IgE also binds to CD23/FceRII, which appears responsible for antigen presentation, antigen transport across airway/epithelial barriers, and the regulation of IgE synthesis.[A242292] Ligelizumab is a monoclonal antibody directed at IgE, binding specifically to an epitope in the IgE Ce3 domain.[A242292] It neutralizes serum IgE and also appears to inhibit the production of IgE via inhibition of IgE-FceRI binding activity and, to a lesser extent, IgE binding to CD23. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| NA | |
| Clearance | NA |
| Categories | Immunoglobulins |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Immunoglobulin heavy constant epsilon |
| 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 | 13760 |
| Therapeutic ID | Th1431 |
| Protein Name | Ligelizumab |
| Sequence | >Th1431_Ligelizumab QVQLVQSGAEVMKPGSSVKVSCKASGYTFSWYWLEWVRQAPGHGLEWMGEIDPGTFTTNYNEKFKARVTFTADTSTSTAYMELSSLRSEDTAVYYCARFSHFSGSNYDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK |
| Molecular Weight | NA |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | NA |
| Description | Ligelizumab is a humanized IgG1k monoclonal antibody targeted against immunoglobulin E (IgE). Similar in mechanism to [omalizumab], another IgE-directed monoclonal antibody, ligelizumab has a distinct binding epitope as compared to its peer (with a small degree of overlap) which appears to confer a greater affinity for free serum IgE and an altered sensitivity to IgE conformation.[A242292] Ligelizumab is currently under investigation for the treatment of chronic spontaneous urticaria (CSU), an autoimmune-driven inflammatory condition. While the precise pathogenesis of CSU is not entirely clear, autoantibodies against IgE receptors, and sometimes against IgE itself, are thought to exist in 30-40% of patients,[A242362,A242367] and the efficacy anti-IgE antibody therapy in the treatment of CSU has been previously established with omalizumab. Initial trials of ligelizumab suggest a greater efficacy over its predecessor for the treatment of CSU.[A242367] |
| Indication/Disease | NA |
| Pharmacodynamics | NA |
| Mechanism of Action | Immunoglobulin E (IgE) is a key driver of hypersensitivity reactions, and has thus become an attractive target in the treatment of immune-mediated hypersensitivity disorders. Immediate hypersensitivity reactions are due to IgE binding with FceRI, which activates allergic effector cells that undergo degranulation to release vasoactive and pro-inflammatory mediators.[A242292] IgE also binds to CD23/FceRII, which appears responsible for antigen presentation, antigen transport across airway/epithelial barriers, and the regulation of IgE synthesis.[A242292] Ligelizumab is a monoclonal antibody directed at IgE, binding specifically to an epitope in the IgE Ce3 domain.[A242292] It neutralizes serum IgE and also appears to inhibit the production of IgE via inhibition of IgE-FceRI binding activity and, to a lesser extent, IgE binding to CD23. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| NA | |
| Clearance | NA |
| Categories | Immunoproteins |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Immunoglobulin heavy constant epsilon |
| 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 | 13761 |
| Therapeutic ID | Th1431 |
| Protein Name | Ligelizumab |
| Sequence | >Th1431_Ligelizumab QVQLVQSGAEVMKPGSSVKVSCKASGYTFSWYWLEWVRQAPGHGLEWMGEIDPGTFTTNYNEKFKARVTFTADTSTSTAYMELSSLRSEDTAVYYCARFSHFSGSNYDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK |
| Molecular Weight | NA |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | NA |
| Description | Ligelizumab is a humanized IgG1k monoclonal antibody targeted against immunoglobulin E (IgE). Similar in mechanism to [omalizumab], another IgE-directed monoclonal antibody, ligelizumab has a distinct binding epitope as compared to its peer (with a small degree of overlap) which appears to confer a greater affinity for free serum IgE and an altered sensitivity to IgE conformation.[A242292] Ligelizumab is currently under investigation for the treatment of chronic spontaneous urticaria (CSU), an autoimmune-driven inflammatory condition. While the precise pathogenesis of CSU is not entirely clear, autoantibodies against IgE receptors, and sometimes against IgE itself, are thought to exist in 30-40% of patients,[A242362,A242367] and the efficacy anti-IgE antibody therapy in the treatment of CSU has been previously established with omalizumab. Initial trials of ligelizumab suggest a greater efficacy over its predecessor for the treatment of CSU.[A242367] |
| Indication/Disease | NA |
| Pharmacodynamics | NA |
| Mechanism of Action | Immunoglobulin E (IgE) is a key driver of hypersensitivity reactions, and has thus become an attractive target in the treatment of immune-mediated hypersensitivity disorders. Immediate hypersensitivity reactions are due to IgE binding with FceRI, which activates allergic effector cells that undergo degranulation to release vasoactive and pro-inflammatory mediators.[A242292] IgE also binds to CD23/FceRII, which appears responsible for antigen presentation, antigen transport across airway/epithelial barriers, and the regulation of IgE synthesis.[A242292] Ligelizumab is a monoclonal antibody directed at IgE, binding specifically to an epitope in the IgE Ce3 domain.[A242292] It neutralizes serum IgE and also appears to inhibit the production of IgE via inhibition of IgE-FceRI binding activity and, to a lesser extent, IgE binding to CD23. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| NA | |
| Clearance | NA |
| Categories | Proteins |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Immunoglobulin heavy constant epsilon |
| 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 | 13762 |
| Therapeutic ID | Th1431 |
| Protein Name | Ligelizumab |
| Sequence | >Th1431_Ligelizumab QVQLVQSGAEVMKPGSSVKVSCKASGYTFSWYWLEWVRQAPGHGLEWMGEIDPGTFTTNYNEKFKARVTFTADTSTSTAYMELSSLRSEDTAVYYCARFSHFSGSNYDYFDYWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK |
| Molecular Weight | NA |
| Chemical Formula | NA |
| Isoelectric Point | NA |
| Hydrophobicity | NA |
| Melting point | NA |
| Half-life | NA |
| Description | Ligelizumab is a humanized IgG1k monoclonal antibody targeted against immunoglobulin E (IgE). Similar in mechanism to [omalizumab], another IgE-directed monoclonal antibody, ligelizumab has a distinct binding epitope as compared to its peer (with a small degree of overlap) which appears to confer a greater affinity for free serum IgE and an altered sensitivity to IgE conformation.[A242292] Ligelizumab is currently under investigation for the treatment of chronic spontaneous urticaria (CSU), an autoimmune-driven inflammatory condition. While the precise pathogenesis of CSU is not entirely clear, autoantibodies against IgE receptors, and sometimes against IgE itself, are thought to exist in 30-40% of patients,[A242362,A242367] and the efficacy anti-IgE antibody therapy in the treatment of CSU has been previously established with omalizumab. Initial trials of ligelizumab suggest a greater efficacy over its predecessor for the treatment of CSU.[A242367] |
| Indication/Disease | NA |
| Pharmacodynamics | NA |
| Mechanism of Action | Immunoglobulin E (IgE) is a key driver of hypersensitivity reactions, and has thus become an attractive target in the treatment of immune-mediated hypersensitivity disorders. Immediate hypersensitivity reactions are due to IgE binding with FceRI, which activates allergic effector cells that undergo degranulation to release vasoactive and pro-inflammatory mediators.[A242292] IgE also binds to CD23/FceRII, which appears responsible for antigen presentation, antigen transport across airway/epithelial barriers, and the regulation of IgE synthesis.[A242292] Ligelizumab is a monoclonal antibody directed at IgE, binding specifically to an epitope in the IgE Ce3 domain.[A242292] It neutralizes serum IgE and also appears to inhibit the production of IgE via inhibition of IgE-FceRI binding activity and, to a lesser extent, IgE binding to CD23. |
| Toxicity | NA |
| Metabolism | NA |
| Absorption | NA |
| NA | |
| Clearance | NA |
| Categories | Serum Globulins |
| Patents Number | NA |
| Date of Issue | NA |
| Date of Expiry | NA |
| Drug Interaction | NA |
| Target | Immunoglobulin heavy constant epsilon |
| 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 |