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Th1369 details

Primary information
ID	12923
Therapeutic ID	Th1369
Protein Name	Teplizumab
Sequence	>Th1369_Teplizumab QVQLVQSGGGVVQPGRSLRLSCKASGYTFTRYTMHWVRQAPGKGLEWIGYINPSRGYTNYNQKVKDRFTISRDNSKNTAFLQMDSLRPEDTGVYFCARYYDDHYCLDYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
Molecular Weight	NA
Chemical Formula	NA
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	NA
Description	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin.[A241490] Targeting T cells can be achieved through antibodies against the T cell receptor (TCR) component CD3 e. However, if Fc binding is left intact, severe adverse effects related to cytokine release syndrome (CRS) are observed, and therefore Fc-nonbinding antibodies are the preferred method of choice.[A241480] Anti-CD3 therapy has traditionally been used to prevent graft-versus-host-disease in organ transplantation but more recently has been explored to prolong the onset of (T1D) in high-risk patients.[A241480, A241500] Teplizumab is a humanized IgG1 Fc-nonbinding anti-CD3 monoclonal antibody currently under development for use in T1D.[A241480, A241045, A241475]
Indication/Disease	Investigated for use/treatment in diabetes mellitus type 1.
Pharmacodynamics	NA
Mechanism of Action	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin. T1D is a progressive disease with three recognizable stages and in which only Stage 3 is associated with clinically apparent symptoms.[A241490] The earliest indication of T1D risk is the presence of at least two autoantibodies against relevant antigens, confirming an important role for B cells in what has traditionally been considered a T cell-dominated condition.[A241490, A241495] Combined with other observations from animal and human studies, it is clear that the T-B axis plays a role in T1D; treatment has focussed on targeting B and T cells independently, as well as their interactions.[A241495] The T cell receptor (TCR) comprises TCR a and ß chains together with six CD3 molecules, including two CD3 e chains. It is responsible for recognizing antigens displayed on the MHC complex of other cells to elicit a response.[A241480] Teplizumab, a humanized IgG1 Fc-nonbinding version of an existing mouse OKT3 antibody (also designated huOKT3ala-ala), is specific for CD3 e and inhibits T cell activation through steric inhibition of antigen recognition.[A241480, A241045, A241475] Recently, teplizumab has shown efficacy in delaying the time to diagnosis in patients at high risk of developing T1D.[A241500] However, the exact mechanism underlying this effect remains clear. One hypothesis is that teplizumab acts as a partial agonist at the TCR, increasing the number of exhausted T cells positive for KLRG1, TIGIT, and CD8. These exhausted T cells persist but cannot perform effector functions and, therefore, would be unlikely to contribute to further ß cell destruction.[A241490, A241505] Other studies have noted changes in the T cell populations of clinical responders, including an increase in circulating CD8⁺ central memory (CD8CM) T cells.[A241510] It is clear, however, that treatment is most effective in patients who have very recently or not yet progressed to Stage 3 and who have an active immune response.[A241490]
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	T-cell surface glycoprotein CD3 epsilon chain
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	12924
Therapeutic ID	Th1369
Protein Name	Teplizumab
Sequence	>Th1369_Teplizumab QVQLVQSGGGVVQPGRSLRLSCKASGYTFTRYTMHWVRQAPGKGLEWIGYINPSRGYTNYNQKVKDRFTISRDNSKNTAFLQMDSLRPEDTGVYFCARYYDDHYCLDYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
Molecular Weight	NA
Chemical Formula	NA
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	NA
Description	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin.[A241490] Targeting T cells can be achieved through antibodies against the T cell receptor (TCR) component CD3 e. However, if Fc binding is left intact, severe adverse effects related to cytokine release syndrome (CRS) are observed, and therefore Fc-nonbinding antibodies are the preferred method of choice.[A241480] Anti-CD3 therapy has traditionally been used to prevent graft-versus-host-disease in organ transplantation but more recently has been explored to prolong the onset of (T1D) in high-risk patients.[A241480, A241500] Teplizumab is a humanized IgG1 Fc-nonbinding anti-CD3 monoclonal antibody currently under development for use in T1D.[A241480, A241045, A241475]
Indication/Disease	Investigated for use/treatment in diabetes mellitus type 1.
Pharmacodynamics	NA
Mechanism of Action	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin. T1D is a progressive disease with three recognizable stages and in which only Stage 3 is associated with clinically apparent symptoms.[A241490] The earliest indication of T1D risk is the presence of at least two autoantibodies against relevant antigens, confirming an important role for B cells in what has traditionally been considered a T cell-dominated condition.[A241490, A241495] Combined with other observations from animal and human studies, it is clear that the T-B axis plays a role in T1D; treatment has focussed on targeting B and T cells independently, as well as their interactions.[A241495] The T cell receptor (TCR) comprises TCR a and ß chains together with six CD3 molecules, including two CD3 e chains. It is responsible for recognizing antigens displayed on the MHC complex of other cells to elicit a response.[A241480] Teplizumab, a humanized IgG1 Fc-nonbinding version of an existing mouse OKT3 antibody (also designated huOKT3ala-ala), is specific for CD3 e and inhibits T cell activation through steric inhibition of antigen recognition.[A241480, A241045, A241475] Recently, teplizumab has shown efficacy in delaying the time to diagnosis in patients at high risk of developing T1D.[A241500] However, the exact mechanism underlying this effect remains clear. One hypothesis is that teplizumab acts as a partial agonist at the TCR, increasing the number of exhausted T cells positive for KLRG1, TIGIT, and CD8. These exhausted T cells persist but cannot perform effector functions and, therefore, would be unlikely to contribute to further ß cell destruction.[A241490, A241505] Other studies have noted changes in the T cell populations of clinical responders, including an increase in circulating CD8⁺ central memory (CD8CM) T cells.[A241510] It is clear, however, that treatment is most effective in patients who have very recently or not yet progressed to Stage 3 and who have an active immune response.[A241490]
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	T-cell surface glycoprotein CD3 epsilon chain
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	12925
Therapeutic ID	Th1369
Protein Name	Teplizumab
Sequence	>Th1369_Teplizumab QVQLVQSGGGVVQPGRSLRLSCKASGYTFTRYTMHWVRQAPGKGLEWIGYINPSRGYTNYNQKVKDRFTISRDNSKNTAFLQMDSLRPEDTGVYFCARYYDDHYCLDYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
Molecular Weight	NA
Chemical Formula	NA
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	NA
Description	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin.[A241490] Targeting T cells can be achieved through antibodies against the T cell receptor (TCR) component CD3 e. However, if Fc binding is left intact, severe adverse effects related to cytokine release syndrome (CRS) are observed, and therefore Fc-nonbinding antibodies are the preferred method of choice.[A241480] Anti-CD3 therapy has traditionally been used to prevent graft-versus-host-disease in organ transplantation but more recently has been explored to prolong the onset of (T1D) in high-risk patients.[A241480, A241500] Teplizumab is a humanized IgG1 Fc-nonbinding anti-CD3 monoclonal antibody currently under development for use in T1D.[A241480, A241045, A241475]
Indication/Disease	Investigated for use/treatment in diabetes mellitus type 1.
Pharmacodynamics	NA
Mechanism of Action	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin. T1D is a progressive disease with three recognizable stages and in which only Stage 3 is associated with clinically apparent symptoms.[A241490] The earliest indication of T1D risk is the presence of at least two autoantibodies against relevant antigens, confirming an important role for B cells in what has traditionally been considered a T cell-dominated condition.[A241490, A241495] Combined with other observations from animal and human studies, it is clear that the T-B axis plays a role in T1D; treatment has focussed on targeting B and T cells independently, as well as their interactions.[A241495] The T cell receptor (TCR) comprises TCR a and ß chains together with six CD3 molecules, including two CD3 e chains. It is responsible for recognizing antigens displayed on the MHC complex of other cells to elicit a response.[A241480] Teplizumab, a humanized IgG1 Fc-nonbinding version of an existing mouse OKT3 antibody (also designated huOKT3ala-ala), is specific for CD3 e and inhibits T cell activation through steric inhibition of antigen recognition.[A241480, A241045, A241475] Recently, teplizumab has shown efficacy in delaying the time to diagnosis in patients at high risk of developing T1D.[A241500] However, the exact mechanism underlying this effect remains clear. One hypothesis is that teplizumab acts as a partial agonist at the TCR, increasing the number of exhausted T cells positive for KLRG1, TIGIT, and CD8. These exhausted T cells persist but cannot perform effector functions and, therefore, would be unlikely to contribute to further ß cell destruction.[A241490, A241505] Other studies have noted changes in the T cell populations of clinical responders, including an increase in circulating CD8⁺ central memory (CD8CM) T cells.[A241510] It is clear, however, that treatment is most effective in patients who have very recently or not yet progressed to Stage 3 and who have an active immune response.[A241490]
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	T-cell surface glycoprotein CD3 epsilon chain
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	12926
Therapeutic ID	Th1369
Protein Name	Teplizumab
Sequence	>Th1369_Teplizumab QVQLVQSGGGVVQPGRSLRLSCKASGYTFTRYTMHWVRQAPGKGLEWIGYINPSRGYTNYNQKVKDRFTISRDNSKNTAFLQMDSLRPEDTGVYFCARYYDDHYCLDYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
Molecular Weight	NA
Chemical Formula	NA
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	NA
Description	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin.[A241490] Targeting T cells can be achieved through antibodies against the T cell receptor (TCR) component CD3 e. However, if Fc binding is left intact, severe adverse effects related to cytokine release syndrome (CRS) are observed, and therefore Fc-nonbinding antibodies are the preferred method of choice.[A241480] Anti-CD3 therapy has traditionally been used to prevent graft-versus-host-disease in organ transplantation but more recently has been explored to prolong the onset of (T1D) in high-risk patients.[A241480, A241500] Teplizumab is a humanized IgG1 Fc-nonbinding anti-CD3 monoclonal antibody currently under development for use in T1D.[A241480, A241045, A241475]
Indication/Disease	Investigated for use/treatment in diabetes mellitus type 1.
Pharmacodynamics	NA
Mechanism of Action	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin. T1D is a progressive disease with three recognizable stages and in which only Stage 3 is associated with clinically apparent symptoms.[A241490] The earliest indication of T1D risk is the presence of at least two autoantibodies against relevant antigens, confirming an important role for B cells in what has traditionally been considered a T cell-dominated condition.[A241490, A241495] Combined with other observations from animal and human studies, it is clear that the T-B axis plays a role in T1D; treatment has focussed on targeting B and T cells independently, as well as their interactions.[A241495] The T cell receptor (TCR) comprises TCR a and ß chains together with six CD3 molecules, including two CD3 e chains. It is responsible for recognizing antigens displayed on the MHC complex of other cells to elicit a response.[A241480] Teplizumab, a humanized IgG1 Fc-nonbinding version of an existing mouse OKT3 antibody (also designated huOKT3ala-ala), is specific for CD3 e and inhibits T cell activation through steric inhibition of antigen recognition.[A241480, A241045, A241475] Recently, teplizumab has shown efficacy in delaying the time to diagnosis in patients at high risk of developing T1D.[A241500] However, the exact mechanism underlying this effect remains clear. One hypothesis is that teplizumab acts as a partial agonist at the TCR, increasing the number of exhausted T cells positive for KLRG1, TIGIT, and CD8. These exhausted T cells persist but cannot perform effector functions and, therefore, would be unlikely to contribute to further ß cell destruction.[A241490, A241505] Other studies have noted changes in the T cell populations of clinical responders, including an increase in circulating CD8⁺ central memory (CD8CM) T cells.[A241510] It is clear, however, that treatment is most effective in patients who have very recently or not yet progressed to Stage 3 and who have an active immune response.[A241490]
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	T-cell surface glycoprotein CD3 epsilon chain
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	12927
Therapeutic ID	Th1369
Protein Name	Teplizumab
Sequence	>Th1369_Teplizumab QVQLVQSGGGVVQPGRSLRLSCKASGYTFTRYTMHWVRQAPGKGLEWIGYINPSRGYTNYNQKVKDRFTISRDNSKNTAFLQMDSLRPEDTGVYFCARYYDDHYCLDYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
Molecular Weight	NA
Chemical Formula	NA
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	NA
Description	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin.[A241490] Targeting T cells can be achieved through antibodies against the T cell receptor (TCR) component CD3 e. However, if Fc binding is left intact, severe adverse effects related to cytokine release syndrome (CRS) are observed, and therefore Fc-nonbinding antibodies are the preferred method of choice.[A241480] Anti-CD3 therapy has traditionally been used to prevent graft-versus-host-disease in organ transplantation but more recently has been explored to prolong the onset of (T1D) in high-risk patients.[A241480, A241500] Teplizumab is a humanized IgG1 Fc-nonbinding anti-CD3 monoclonal antibody currently under development for use in T1D.[A241480, A241045, A241475]
Indication/Disease	Investigated for use/treatment in diabetes mellitus type 1.
Pharmacodynamics	NA
Mechanism of Action	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin. T1D is a progressive disease with three recognizable stages and in which only Stage 3 is associated with clinically apparent symptoms.[A241490] The earliest indication of T1D risk is the presence of at least two autoantibodies against relevant antigens, confirming an important role for B cells in what has traditionally been considered a T cell-dominated condition.[A241490, A241495] Combined with other observations from animal and human studies, it is clear that the T-B axis plays a role in T1D; treatment has focussed on targeting B and T cells independently, as well as their interactions.[A241495] The T cell receptor (TCR) comprises TCR a and ß chains together with six CD3 molecules, including two CD3 e chains. It is responsible for recognizing antigens displayed on the MHC complex of other cells to elicit a response.[A241480] Teplizumab, a humanized IgG1 Fc-nonbinding version of an existing mouse OKT3 antibody (also designated huOKT3ala-ala), is specific for CD3 e and inhibits T cell activation through steric inhibition of antigen recognition.[A241480, A241045, A241475] Recently, teplizumab has shown efficacy in delaying the time to diagnosis in patients at high risk of developing T1D.[A241500] However, the exact mechanism underlying this effect remains clear. One hypothesis is that teplizumab acts as a partial agonist at the TCR, increasing the number of exhausted T cells positive for KLRG1, TIGIT, and CD8. These exhausted T cells persist but cannot perform effector functions and, therefore, would be unlikely to contribute to further ß cell destruction.[A241490, A241505] Other studies have noted changes in the T cell populations of clinical responders, including an increase in circulating CD8⁺ central memory (CD8CM) T cells.[A241510] It is clear, however, that treatment is most effective in patients who have very recently or not yet progressed to Stage 3 and who have an active immune response.[A241490]
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	T-cell surface glycoprotein CD3 epsilon chain
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	12928
Therapeutic ID	Th1369
Protein Name	Teplizumab
Sequence	>Th1369_Teplizumab QVQLVQSGGGVVQPGRSLRLSCKASGYTFTRYTMHWVRQAPGKGLEWIGYINPSRGYTNYNQKVKDRFTISRDNSKNTAFLQMDSLRPEDTGVYFCARYYDDHYCLDYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
Molecular Weight	NA
Chemical Formula	NA
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	NA
Description	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin.[A241490] Targeting T cells can be achieved through antibodies against the T cell receptor (TCR) component CD3 e. However, if Fc binding is left intact, severe adverse effects related to cytokine release syndrome (CRS) are observed, and therefore Fc-nonbinding antibodies are the preferred method of choice.[A241480] Anti-CD3 therapy has traditionally been used to prevent graft-versus-host-disease in organ transplantation but more recently has been explored to prolong the onset of (T1D) in high-risk patients.[A241480, A241500] Teplizumab is a humanized IgG1 Fc-nonbinding anti-CD3 monoclonal antibody currently under development for use in T1D.[A241480, A241045, A241475]
Indication/Disease	Investigated for use/treatment in diabetes mellitus type 1.
Pharmacodynamics	NA
Mechanism of Action	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin. T1D is a progressive disease with three recognizable stages and in which only Stage 3 is associated with clinically apparent symptoms.[A241490] The earliest indication of T1D risk is the presence of at least two autoantibodies against relevant antigens, confirming an important role for B cells in what has traditionally been considered a T cell-dominated condition.[A241490, A241495] Combined with other observations from animal and human studies, it is clear that the T-B axis plays a role in T1D; treatment has focussed on targeting B and T cells independently, as well as their interactions.[A241495] The T cell receptor (TCR) comprises TCR a and ß chains together with six CD3 molecules, including two CD3 e chains. It is responsible for recognizing antigens displayed on the MHC complex of other cells to elicit a response.[A241480] Teplizumab, a humanized IgG1 Fc-nonbinding version of an existing mouse OKT3 antibody (also designated huOKT3ala-ala), is specific for CD3 e and inhibits T cell activation through steric inhibition of antigen recognition.[A241480, A241045, A241475] Recently, teplizumab has shown efficacy in delaying the time to diagnosis in patients at high risk of developing T1D.[A241500] However, the exact mechanism underlying this effect remains clear. One hypothesis is that teplizumab acts as a partial agonist at the TCR, increasing the number of exhausted T cells positive for KLRG1, TIGIT, and CD8. These exhausted T cells persist but cannot perform effector functions and, therefore, would be unlikely to contribute to further ß cell destruction.[A241490, A241505] Other studies have noted changes in the T cell populations of clinical responders, including an increase in circulating CD8⁺ central memory (CD8CM) T cells.[A241510] It is clear, however, that treatment is most effective in patients who have very recently or not yet progressed to Stage 3 and who have an active immune response.[A241490]
Toxicity	NA
Metabolism	NA
Absorption	NA
	NA
Clearance	NA
Categories	Globulins
Patents Number	NA
Date of Issue	NA
Date of Expiry	NA
Drug Interaction	NA
Target	T-cell surface glycoprotein CD3 epsilon chain
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	12929
Therapeutic ID	Th1369
Protein Name	Teplizumab
Sequence	>Th1369_Teplizumab QVQLVQSGGGVVQPGRSLRLSCKASGYTFTRYTMHWVRQAPGKGLEWIGYINPSRGYTNYNQKVKDRFTISRDNSKNTAFLQMDSLRPEDTGVYFCARYYDDHYCLDYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
Molecular Weight	NA
Chemical Formula	NA
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	NA
Description	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin.[A241490] Targeting T cells can be achieved through antibodies against the T cell receptor (TCR) component CD3 e. However, if Fc binding is left intact, severe adverse effects related to cytokine release syndrome (CRS) are observed, and therefore Fc-nonbinding antibodies are the preferred method of choice.[A241480] Anti-CD3 therapy has traditionally been used to prevent graft-versus-host-disease in organ transplantation but more recently has been explored to prolong the onset of (T1D) in high-risk patients.[A241480, A241500] Teplizumab is a humanized IgG1 Fc-nonbinding anti-CD3 monoclonal antibody currently under development for use in T1D.[A241480, A241045, A241475]
Indication/Disease	Investigated for use/treatment in diabetes mellitus type 1.
Pharmacodynamics	NA
Mechanism of Action	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin. T1D is a progressive disease with three recognizable stages and in which only Stage 3 is associated with clinically apparent symptoms.[A241490] The earliest indication of T1D risk is the presence of at least two autoantibodies against relevant antigens, confirming an important role for B cells in what has traditionally been considered a T cell-dominated condition.[A241490, A241495] Combined with other observations from animal and human studies, it is clear that the T-B axis plays a role in T1D; treatment has focussed on targeting B and T cells independently, as well as their interactions.[A241495] The T cell receptor (TCR) comprises TCR a and ß chains together with six CD3 molecules, including two CD3 e chains. It is responsible for recognizing antigens displayed on the MHC complex of other cells to elicit a response.[A241480] Teplizumab, a humanized IgG1 Fc-nonbinding version of an existing mouse OKT3 antibody (also designated huOKT3ala-ala), is specific for CD3 e and inhibits T cell activation through steric inhibition of antigen recognition.[A241480, A241045, A241475] Recently, teplizumab has shown efficacy in delaying the time to diagnosis in patients at high risk of developing T1D.[A241500] However, the exact mechanism underlying this effect remains clear. One hypothesis is that teplizumab acts as a partial agonist at the TCR, increasing the number of exhausted T cells positive for KLRG1, TIGIT, and CD8. These exhausted T cells persist but cannot perform effector functions and, therefore, would be unlikely to contribute to further ß cell destruction.[A241490, A241505] Other studies have noted changes in the T cell populations of clinical responders, including an increase in circulating CD8⁺ central memory (CD8CM) T cells.[A241510] It is clear, however, that treatment is most effective in patients who have very recently or not yet progressed to Stage 3 and who have an active immune response.[A241490]
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	T-cell surface glycoprotein CD3 epsilon chain
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	12930
Therapeutic ID	Th1369
Protein Name	Teplizumab
Sequence	>Th1369_Teplizumab QVQLVQSGGGVVQPGRSLRLSCKASGYTFTRYTMHWVRQAPGKGLEWIGYINPSRGYTNYNQKVKDRFTISRDNSKNTAFLQMDSLRPEDTGVYFCARYYDDHYCLDYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
Molecular Weight	NA
Chemical Formula	NA
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	NA
Description	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin.[A241490] Targeting T cells can be achieved through antibodies against the T cell receptor (TCR) component CD3 e. However, if Fc binding is left intact, severe adverse effects related to cytokine release syndrome (CRS) are observed, and therefore Fc-nonbinding antibodies are the preferred method of choice.[A241480] Anti-CD3 therapy has traditionally been used to prevent graft-versus-host-disease in organ transplantation but more recently has been explored to prolong the onset of (T1D) in high-risk patients.[A241480, A241500] Teplizumab is a humanized IgG1 Fc-nonbinding anti-CD3 monoclonal antibody currently under development for use in T1D.[A241480, A241045, A241475]
Indication/Disease	Investigated for use/treatment in diabetes mellitus type 1.
Pharmacodynamics	NA
Mechanism of Action	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin. T1D is a progressive disease with three recognizable stages and in which only Stage 3 is associated with clinically apparent symptoms.[A241490] The earliest indication of T1D risk is the presence of at least two autoantibodies against relevant antigens, confirming an important role for B cells in what has traditionally been considered a T cell-dominated condition.[A241490, A241495] Combined with other observations from animal and human studies, it is clear that the T-B axis plays a role in T1D; treatment has focussed on targeting B and T cells independently, as well as their interactions.[A241495] The T cell receptor (TCR) comprises TCR a and ß chains together with six CD3 molecules, including two CD3 e chains. It is responsible for recognizing antigens displayed on the MHC complex of other cells to elicit a response.[A241480] Teplizumab, a humanized IgG1 Fc-nonbinding version of an existing mouse OKT3 antibody (also designated huOKT3ala-ala), is specific for CD3 e and inhibits T cell activation through steric inhibition of antigen recognition.[A241480, A241045, A241475] Recently, teplizumab has shown efficacy in delaying the time to diagnosis in patients at high risk of developing T1D.[A241500] However, the exact mechanism underlying this effect remains clear. One hypothesis is that teplizumab acts as a partial agonist at the TCR, increasing the number of exhausted T cells positive for KLRG1, TIGIT, and CD8. These exhausted T cells persist but cannot perform effector functions and, therefore, would be unlikely to contribute to further ß cell destruction.[A241490, A241505] Other studies have noted changes in the T cell populations of clinical responders, including an increase in circulating CD8⁺ central memory (CD8CM) T cells.[A241510] It is clear, however, that treatment is most effective in patients who have very recently or not yet progressed to Stage 3 and who have an active immune response.[A241490]
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	T-cell surface glycoprotein CD3 epsilon chain
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	12931
Therapeutic ID	Th1369
Protein Name	Teplizumab
Sequence	>Th1369_Teplizumab QVQLVQSGGGVVQPGRSLRLSCKASGYTFTRYTMHWVRQAPGKGLEWIGYINPSRGYTNYNQKVKDRFTISRDNSKNTAFLQMDSLRPEDTGVYFCARYYDDHYCLDYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
Molecular Weight	NA
Chemical Formula	NA
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	NA
Description	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin.[A241490] Targeting T cells can be achieved through antibodies against the T cell receptor (TCR) component CD3 e. However, if Fc binding is left intact, severe adverse effects related to cytokine release syndrome (CRS) are observed, and therefore Fc-nonbinding antibodies are the preferred method of choice.[A241480] Anti-CD3 therapy has traditionally been used to prevent graft-versus-host-disease in organ transplantation but more recently has been explored to prolong the onset of (T1D) in high-risk patients.[A241480, A241500] Teplizumab is a humanized IgG1 Fc-nonbinding anti-CD3 monoclonal antibody currently under development for use in T1D.[A241480, A241045, A241475]
Indication/Disease	Investigated for use/treatment in diabetes mellitus type 1.
Pharmacodynamics	NA
Mechanism of Action	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin. T1D is a progressive disease with three recognizable stages and in which only Stage 3 is associated with clinically apparent symptoms.[A241490] The earliest indication of T1D risk is the presence of at least two autoantibodies against relevant antigens, confirming an important role for B cells in what has traditionally been considered a T cell-dominated condition.[A241490, A241495] Combined with other observations from animal and human studies, it is clear that the T-B axis plays a role in T1D; treatment has focussed on targeting B and T cells independently, as well as their interactions.[A241495] The T cell receptor (TCR) comprises TCR a and ß chains together with six CD3 molecules, including two CD3 e chains. It is responsible for recognizing antigens displayed on the MHC complex of other cells to elicit a response.[A241480] Teplizumab, a humanized IgG1 Fc-nonbinding version of an existing mouse OKT3 antibody (also designated huOKT3ala-ala), is specific for CD3 e and inhibits T cell activation through steric inhibition of antigen recognition.[A241480, A241045, A241475] Recently, teplizumab has shown efficacy in delaying the time to diagnosis in patients at high risk of developing T1D.[A241500] However, the exact mechanism underlying this effect remains clear. One hypothesis is that teplizumab acts as a partial agonist at the TCR, increasing the number of exhausted T cells positive for KLRG1, TIGIT, and CD8. These exhausted T cells persist but cannot perform effector functions and, therefore, would be unlikely to contribute to further ß cell destruction.[A241490, A241505] Other studies have noted changes in the T cell populations of clinical responders, including an increase in circulating CD8⁺ central memory (CD8CM) T cells.[A241510] It is clear, however, that treatment is most effective in patients who have very recently or not yet progressed to Stage 3 and who have an active immune response.[A241490]
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	T-cell surface glycoprotein CD3 epsilon chain
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	12932
Therapeutic ID	Th1369
Protein Name	Teplizumab
Sequence	>Th1369_Teplizumab QVQLVQSGGGVVQPGRSLRLSCKASGYTFTRYTMHWVRQAPGKGLEWIGYINPSRGYTNYNQKVKDRFTISRDNSKNTAFLQMDSLRPEDTGVYFCARYYDDHYCLDYWGQGTPVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPEAAGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK
Molecular Weight	NA
Chemical Formula	NA
Isoelectric Point	NA
Hydrophobicity	NA
Melting point	NA
Half-life	NA
Description	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin.[A241490] Targeting T cells can be achieved through antibodies against the T cell receptor (TCR) component CD3 e. However, if Fc binding is left intact, severe adverse effects related to cytokine release syndrome (CRS) are observed, and therefore Fc-nonbinding antibodies are the preferred method of choice.[A241480] Anti-CD3 therapy has traditionally been used to prevent graft-versus-host-disease in organ transplantation but more recently has been explored to prolong the onset of (T1D) in high-risk patients.[A241480, A241500] Teplizumab is a humanized IgG1 Fc-nonbinding anti-CD3 monoclonal antibody currently under development for use in T1D.[A241480, A241045, A241475]
Indication/Disease	Investigated for use/treatment in diabetes mellitus type 1.
Pharmacodynamics	NA
Mechanism of Action	Type 1 diabetes (T1D) is an autoimmune condition in which T cell-mediated destruction of pancreatic ß cells leads to loss of insulin production, impaired glycemic control, and reliance on exogenous insulin. T1D is a progressive disease with three recognizable stages and in which only Stage 3 is associated with clinically apparent symptoms.[A241490] The earliest indication of T1D risk is the presence of at least two autoantibodies against relevant antigens, confirming an important role for B cells in what has traditionally been considered a T cell-dominated condition.[A241490, A241495] Combined with other observations from animal and human studies, it is clear that the T-B axis plays a role in T1D; treatment has focussed on targeting B and T cells independently, as well as their interactions.[A241495] The T cell receptor (TCR) comprises TCR a and ß chains together with six CD3 molecules, including two CD3 e chains. It is responsible for recognizing antigens displayed on the MHC complex of other cells to elicit a response.[A241480] Teplizumab, a humanized IgG1 Fc-nonbinding version of an existing mouse OKT3 antibody (also designated huOKT3ala-ala), is specific for CD3 e and inhibits T cell activation through steric inhibition of antigen recognition.[A241480, A241045, A241475] Recently, teplizumab has shown efficacy in delaying the time to diagnosis in patients at high risk of developing T1D.[A241500] However, the exact mechanism underlying this effect remains clear. One hypothesis is that teplizumab acts as a partial agonist at the TCR, increasing the number of exhausted T cells positive for KLRG1, TIGIT, and CD8. These exhausted T cells persist but cannot perform effector functions and, therefore, would be unlikely to contribute to further ß cell destruction.[A241490, A241505] Other studies have noted changes in the T cell populations of clinical responders, including an increase in circulating CD8⁺ central memory (CD8CM) T cells.[A241510] It is clear, however, that treatment is most effective in patients who have very recently or not yet progressed to Stage 3 and who have an active immune response.[A241490]
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	T-cell surface glycoprotein CD3 epsilon chain
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