Detailed description page of ThPDB2

This page displays user query in tabular form.

Th1086 details
Primary information
ID10472
Therapeutic IDTh1086
Protein NameInterferon alfa-2b
Sequence>Th1086_Interferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMNEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE
Molecular Weight19271
Chemical FormulaC860H1353N229O255S9
Isoelectric Point5.99
Hydrophobicity-0.339
Melting point61
Half-lifeThe elimination half-life following both intramuscular and subcutaneous injections was approximately 2 to 3 hours
DescriptionRecombinant type-I Interferon alpha 2b (human leukocyte clone hif-sn 206 protein moiety reduced), composed of 165 amino acid residues with R at position 23. It resembles leukocyte secreted interferon. Widely used as an antiviral or antineoplastic agent.
Indication/DiseaseFor the treatment of hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma.
PharmacodynamicsUpregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R.
Mechanism of ActionInterferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta.
ToxicityThere is limited experience with overdosage. Postmarketing surveillance includes reports of patients receiving a single dose as great as 10 times the recommended dose. In general, the primary effects of an overdose are consistent with the effects seen with therapeutic doses of interferon alfa-2b. Hepatic enzyme abnormalities, renal failure, hemorrhage, and myocardial infarction have been reported with single administration overdoses and/or with longer durations of treatment than prescribed. Toxic effects after ingestion of interferon alfa-2b are not expected because interferons are poorly absorbed orally.
MetabolismNA
AbsorptionAbsorption is high (greater than 80%) when administered intramuscularly or subcutaneously.
NA
ClearanceNA
CategoriesImmunosuppressive Agents
Patents NumberCA1341567
Date of Issue19-Feb-2008
Date of Expiry19-Feb-2025
Drug InteractionNA
TargetInterferon alpha/beta receptor 2,Interferon alpha/beta receptor 1
Brand NameINTRON A
CompanyMerck
Brand DescriptionMerck
Prescribed ForHairy Cell Leukemia, Malignant Melanoma, Follicular Lymphoma, Condylomata Acuminata, AIDS-Related Kaposi's Sarcoma, Chronic Hepatitis C, Chronic Hepatitis B,
Chemical NameNA
FormulationINTRON A Powder for Injection, 10 million IU per vial and Diluent for INTRON A (Sterile Water for Injection USP) 1 mL per vial, INTRON A Solution for Injection, 18 million IU multidose vial (22.8 million IU per 3.8 mL per vial); boxes containing 1 vial of INTRON A Solution for Injection
Physical Appearance Powder or solution
Route of AdministrationIntramuSubcutaneousular, Subcutaneous, Intralesion
Recommended DosageNot all dosage forms and strengths are appropriate for some indications. To enhance the tolerability of INTRON A, injections should be administered in the evening when possible; To reduce the incidence of certain adverse reactions, acetaminophen may be administered at the time of injection;The solution should be allowed to come to room temperature before using.
ContraindicationAlpha interferons, including INTRON A, cause or aggravate fatal or life-threatening neuropsychiatric, autoimmune, ischemic, and infectious disorders. Patients should be monitored closely with periodic clinical and laboratory evaluations. Patients with persistently severe or worsening signs or symptoms of these conditions should be withdrawn from therapy. In many but not all cases these disorders resolve after stopping INTRON A therapy.
Side Effectsmost frequently reported adverse reactions were “flu-like” symptoms, particularly fever, headache, chills, myalgia, and fatigue. More severe toxicities are observed generally at higher doses and may be difficult for patients to tolerate.
Useful Link 1Link
Useful Link 2NA
RemarksNA


Primary information
ID10473
Therapeutic IDTh1086
Protein NameInterferon alfa-2b
Sequence>Th1086_Interferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMNEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE
Molecular Weight19271
Chemical FormulaC860H1353N229O255S10
Isoelectric Point5.99
Hydrophobicity-0.339
Melting point61
Half-lifeThe elimination half-life following both intramuscular and subcutaneous injections was approximately 2 to 3 hours
DescriptionRecombinant type-I Interferon alpha 2b (human leukocyte clone hif-sn 206 protein moiety reduced), composed of 165 amino acid residues with R at position 23. It resembles leukocyte secreted interferon. Widely used as an antiviral or antineoplastic agent.
Indication/DiseaseFor the treatment of hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma.
PharmacodynamicsUpregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R.
Mechanism of ActionInterferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta.
ToxicityThere is limited experience with overdosage. Postmarketing surveillance includes reports of patients receiving a single dose as great as 10 times the recommended dose. In general, the primary effects of an overdose are consistent with the effects seen with therapeutic doses of interferon alfa-2b. Hepatic enzyme abnormalities, renal failure, hemorrhage, and myocardial infarction have been reported with single administration overdoses and/or with longer durations of treatment than prescribed. Toxic effects after ingestion of interferon alfa-2b are not expected because interferons are poorly absorbed orally.
MetabolismNA
AbsorptionAbsorption is high (greater than 80%) when administered intramuscularly or subcutaneously.
NA
ClearanceNA
CategoriesImmunosuppressive Agents
Patents NumberCA2201749
Date of Issue15-Jun-1999
Date of Expiry10-Oct-2015
Drug InteractionNA
TargetInterferon alpha/beta receptor 2,Interferon alpha/beta receptor 1
Brand NameNA
CompanyNA
Brand DescriptionNA
Prescribed ForNA
Chemical NameNA
FormulationNA
Physical Appearance NA
Route of AdministrationNA
Recommended DosageNA
ContraindicationNA
Side EffectsNA
Useful Link 1NA
Useful Link 2NA
RemarksNA


Primary information
ID10474
Therapeutic IDTh1086
Protein NameInterferon alfa-2b
Sequence>Th1086_Interferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMNEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE
Molecular Weight19271
Chemical FormulaC860H1353N229O255S11
Isoelectric Point5.99
Hydrophobicity-0.339
Melting point61
Half-lifeThe elimination half-life following both intramuscular and subcutaneous injections was approximately 2 to 3 hours
DescriptionRecombinant type-I Interferon alpha 2b (human leukocyte clone hif-sn 206 protein moiety reduced), composed of 165 amino acid residues with R at position 23. It resembles leukocyte secreted interferon. Widely used as an antiviral or antineoplastic agent.
Indication/DiseaseFor the treatment of hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma.
PharmacodynamicsUpregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R.
Mechanism of ActionInterferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta.
ToxicityThere is limited experience with overdosage. Postmarketing surveillance includes reports of patients receiving a single dose as great as 10 times the recommended dose. In general, the primary effects of an overdose are consistent with the effects seen with therapeutic doses of interferon alfa-2b. Hepatic enzyme abnormalities, renal failure, hemorrhage, and myocardial infarction have been reported with single administration overdoses and/or with longer durations of treatment than prescribed. Toxic effects after ingestion of interferon alfa-2b are not expected because interferons are poorly absorbed orally.
MetabolismNA
AbsorptionAbsorption is high (greater than 80%) when administered intramuscularly or subcutaneously.
NA
ClearanceNA
CategoriesImmunosuppressive Agents
Patents NumberNA
Date of IssueNA
Date of ExpiryNA
Drug InteractionNA
TargetInterferon alpha/beta receptor 2,Interferon alpha/beta receptor 1
Brand NameNA
CompanyNA
Brand DescriptionNA
Prescribed ForNA
Chemical NameNA
FormulationNA
Physical Appearance NA
Route of AdministrationNA
Recommended DosageNA
ContraindicationNA
Side EffectsNA
Useful Link 1NA
Useful Link 2NA
RemarksNA


Primary information
ID10475
Therapeutic IDTh1086
Protein NameInterferon alfa-2b
Sequence>Th1086_Interferon_alfa-2b CDLPQTHSLGSRRTLMLLAQMRRISLFSCLKDRHDFGFPQEEFGNQFQKAETIPVLHEMIQQIFNLFSTKDSSAAWDETLLDKFYTELYQQLNDLEACVIQGVGVTETPLMNEDSILAVRKYFQRITLYLKEKKYSPCAWEVVRAEIMRSFSLSTNLQESLRSKE
Molecular Weight19271
Chemical FormulaC860H1353N229O255S12
Isoelectric Point5.99
Hydrophobicity-0.339
Melting point61
Half-lifeThe elimination half-life following both intramuscular and subcutaneous injections was approximately 2 to 3 hours
DescriptionRecombinant type-I Interferon alpha 2b (human leukocyte clone hif-sn 206 protein moiety reduced), composed of 165 amino acid residues with R at position 23. It resembles leukocyte secreted interferon. Widely used as an antiviral or antineoplastic agent.
Indication/DiseaseFor the treatment of hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma.
PharmacodynamicsUpregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R.
Mechanism of ActionInterferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta.
ToxicityThere is limited experience with overdosage. Postmarketing surveillance includes reports of patients receiving a single dose as great as 10 times the recommended dose. In general, the primary effects of an overdose are consistent with the effects seen with therapeutic doses of interferon alfa-2b. Hepatic enzyme abnormalities, renal failure, hemorrhage, and myocardial infarction have been reported with single administration overdoses and/or with longer durations of treatment than prescribed. Toxic effects after ingestion of interferon alfa-2b are not expected because interferons are poorly absorbed orally.
MetabolismNA
AbsorptionAbsorption is high (greater than 80%) when administered intramuscularly or subcutaneously.
NA
ClearanceNA
CategoriesImmunosuppressive Agents
Patents NumberNA
Date of IssueNA
Date of ExpiryNA
Drug InteractionNA
TargetInterferon alpha/beta receptor 2,Interferon alpha/beta receptor 1
Brand NameNA
CompanyNA
Brand DescriptionNA
Prescribed ForNA
Chemical NameNA
FormulationNA
Physical Appearance NA
Route of AdministrationNA
Recommended DosageNA
ContraindicationNA
Side EffectsNA
Useful Link 1NA
Useful Link 2NA
RemarksNA