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Th1023 details
Primary information
ID1180
ThPP IDTh1023
Therapeutic Peptide/Protein NameAnakinra
SequenceMRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional ClassificationIIa
Molecular Weight17257.6
Chemical FormulaC759H1186N208O232S10
Isoelectric Point5.46
Hydrophobicity-0.412
Melting Point (℃)N.A.
Half LifeHealthy subjects = 4 - 6 hours
DescriptionAnakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001.
Indication/DiseaseTo treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
PharmacodynamicsAnakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1.
Mechanism of ActionAnakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption.
ToxicityMost common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used
MetabolismN.A.
AbsorptionWhen a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail
Volume of DistributionN.A.
ClearanceClearance is variable and increases with increasing creatinine clearance and body weight.
CategoriesAntirheumatic Agents
Patents NumberCA2141953
Date of Issue08/04/08
Date of Expiry17/09/13
Drug InteractionCanakinumab results in increased immunosuppressive effects; increases the risk of infection.
TargetInterleukin-1 receptor type 1
Information of corresponding available drug in the market
Brand NameKineret
CompanyAmgen Inc
Brand DiscriptionKineret is a recombinant, nonglycosylated form of the human interleukin-1 receptor antagonist (IL-1Ra). Kineret differs from native human IL-1Ra in that it has the addition of a single methionine residue at its amino terminus. Kineret consists of 153 amin
Prescribed forTo treat the symptoms of moderate to severe rheumatoid arthritis in adults. Anakinra may also help slow the progress of the disease.
Chemical NameN.A.
FormulationThe solution may contain trace amounts of small, translucent-to-white amorphous proteinaceous particles. Each prefilled glass syringe contains: 0.67 mL (100 mg) of anakinra in a solution (pH 6.5) containing disodium EDTA (0.12 mg), sodium chloride (5.48 m
Physcial AppearanceSterile, clear, colorless-to-white, preservative free solution
Route of AdministrationSubcutaneous (Subcutaneous) administration
Recommended Dosage100 mg/day administered daily
ContraindicationContraindicated in patients with known hypersensitivity to E coli-derived proteins, Kineret, or any components of the product
Side EffectsNausea, diarrhea, stomach pain; headache; cold symptoms such as stuffy nose, sneezing, sore throat; or redness, bruising, pain, or swelling where the injection was given.
Useful Linkhttp://www.rxlist.com/kineret-drug.htm
PubMed ID17947302, 18251718, 23553601, 23319019, 19169963
3-D StructureTh1023 (View) or (Download)
Primary information
ID1181
ThPP IDTh1023
Therapeutic Peptide/Protein NameAnakinra
SequenceMRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional ClassificationIIa
Molecular Weight17257.6
Chemical FormulaC759H1186N208O232S10
Isoelectric Point5.46
Hydrophobicity-0.412
Melting Point (℃)N.A.
Half LifeNOMID patients = 5.7 hours (range of 3.1 - 28.2 hours)
DescriptionAnakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001.
Indication/DiseaseTo treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
PharmacodynamicsAnakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1.
Mechanism of ActionAnakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption.
ToxicityMost common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used
MetabolismN.A.
AbsorptionWhen a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail
Volume of DistributionN.A.
ClearanceClearance is variable and increases with increasing creatinine clearance and body weight.
CategoriesImmunosuppressive Agents
Patents NumberCA1341322
Date of Issue27/11/01
Date of Expiry27/11/18
Drug InteractionCertolizumab pegol Co-administration with other TNF-blocking agents may increase the risk of serious infections. Concomitant therapy is not recommended.
TargetN.A.
Information of corresponding available drug in the market
Brand NameN.A.
CompanyN.A.
Brand DiscriptionN.A.
Prescribed forN.A.
Chemical NameN.A.
FormulationN.A.
Physcial AppearanceN.A.
Route of AdministrationN.A.
Recommended DosageN.A.
ContraindicationN.A.
Side EffectsN.A.
Useful Linkhttp://www.drugs.com/kineret.html
PubMed ID17947302, 18251718, 23553601, 23319019, 19169963
3-D StructureTh1023 (View) or (Download)
Primary information
ID1182
ThPP IDTh1023
Therapeutic Peptide/Protein NameAnakinra
SequenceMRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional ClassificationIIa
Molecular Weight17257.6
Chemical FormulaC759H1186N208O232S10
Isoelectric Point5.46
Hydrophobicity-0.412
Melting Point (℃)N.A.
Half LifeN.A.
DescriptionAnakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001.
Indication/DiseaseTo treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
PharmacodynamicsAnakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1.
Mechanism of ActionAnakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption.
ToxicityMost common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used
MetabolismN.A.
AbsorptionWhen a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail
Volume of DistributionN.A.
ClearanceClearance is variable and increases with increasing creatinine clearance and body weight.
CategoriesN.A.
Patents NumberN.A.
Date of IssueN.A.
Date of ExpiryN.A.
Drug InteractionTrastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events.
TargetN.A.
Information of corresponding available drug in the market
Brand NameN.A.
CompanyN.A.
Brand DiscriptionN.A.
Prescribed forN.A.
Chemical NameN.A.
FormulationN.A.
Physcial AppearanceN.A.
Route of AdministrationN.A.
Recommended DosageN.A.
ContraindicationN.A.
Side EffectsN.A.
Useful Linkhttp://www.kineretrx.com/
PubMed ID17947302, 18251718, 23553601, 23319019, 19169963
3-D StructureTh1023 (View) or (Download)
Primary information
ID1183
ThPP IDTh1023
Therapeutic Peptide/Protein NameAnakinra
SequenceMRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional ClassificationIIa
Molecular Weight17257.6
Chemical FormulaC759H1186N208O232S10
Isoelectric Point5.46
Hydrophobicity-0.412
Melting Point (℃)N.A.
Half LifeN.A.
DescriptionAnakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001.
Indication/DiseaseTo treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
PharmacodynamicsAnakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1.
Mechanism of ActionAnakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption.
ToxicityMost common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used
MetabolismN.A.
AbsorptionWhen a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail
Volume of DistributionN.A.
ClearanceClearance is variable and increases with increasing creatinine clearance and body weight.
CategoriesN.A.
Patents NumberN.A.
Date of IssueN.A.
Date of ExpiryN.A.
Drug InteractionGolimumab. Avoid combination with anakinra due to the increased chance of serious infection.
TargetN.A.
Information of corresponding available drug in the market
Brand NameN.A.
CompanyN.A.
Brand DiscriptionN.A.
Prescribed forN.A.
Chemical NameN.A.
FormulationN.A.
Physcial AppearanceN.A.
Route of AdministrationN.A.
Recommended DosageN.A.
ContraindicationN.A.
Side EffectsN.A.
Useful LinkN.A.
PubMed ID17947302, 18251718, 23553601, 23319019, 19169963
3-D StructureTh1023 (View) or (Download)
Primary information
ID1184
ThPP IDTh1023
Therapeutic Peptide/Protein NameAnakinra
SequenceMRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional ClassificationIIa
Molecular Weight17257.6
Chemical FormulaC759H1186N208O232S10
Isoelectric Point5.46
Hydrophobicity-0.412
Melting Point (℃)N.A.
Half LifeN.A.
DescriptionAnakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001.
Indication/DiseaseTo treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
PharmacodynamicsAnakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1.
Mechanism of ActionAnakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption.
ToxicityMost common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used
MetabolismN.A.
AbsorptionWhen a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail
Volume of DistributionN.A.
ClearanceClearance is variable and increases with increasing creatinine clearance and body weight.
CategoriesN.A.
Patents NumberN.A.
Date of IssueN.A.
Date of ExpiryN.A.
Drug InteractionRilonacept results in increased immunosuppressive effects; increases the risk of infection.
TargetN.A.
Information of corresponding available drug in the market
Brand NameN.A.
CompanyN.A.
Brand DiscriptionN.A.
Prescribed forN.A.
Chemical NameN.A.
FormulationN.A.
Physcial AppearanceN.A.
Route of AdministrationN.A.
Recommended DosageN.A.
ContraindicationN.A.
Side EffectsN.A.
Useful LinkN.A.
PubMed ID17947302, 18251718, 23553601, 23319019, 19169963
3-D StructureTh1023 (View) or (Download)
Primary information
ID1185
ThPP IDTh1023
Therapeutic Peptide/Protein NameAnakinra
SequenceMRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional ClassificationIIa
Molecular Weight17257.6
Chemical FormulaC759H1186N208O232S10
Isoelectric Point5.46
Hydrophobicity-0.412
Melting Point (℃)N.A.
Half LifeN.A.
DescriptionAnakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001.
Indication/DiseaseTo treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
PharmacodynamicsAnakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1.
Mechanism of ActionAnakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption.
ToxicityMost common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used
MetabolismN.A.
AbsorptionWhen a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail
Volume of DistributionN.A.
ClearanceClearance is variable and increases with increasing creatinine clearance and body weight.
CategoriesN.A.
Patents NumberN.A.
Date of IssueN.A.
Date of ExpiryN.A.
Drug InteractionTofacitinib. Avoid combination due to the potential increase in tofacitinib related adverse effects.
TargetN.A.
Information of corresponding available drug in the market
Brand NameN.A.
CompanyN.A.
Brand DiscriptionN.A.
Prescribed forN.A.
Chemical NameN.A.
FormulationN.A.
Physcial AppearanceN.A.
Route of AdministrationN.A.
Recommended DosageN.A.
ContraindicationN.A.
Side EffectsN.A.
Useful LinkN.A.
PubMed ID17947302, 18251718, 23553601, 23319019, 19169963
3-D StructureTh1023 (View) or (Download)
Primary information
ID1186
ThPP IDTh1023
Therapeutic Peptide/Protein NameAnakinra
SequenceMRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional ClassificationIIa
Molecular Weight17257.6
Chemical FormulaC759H1186N208O232S10
Isoelectric Point5.46
Hydrophobicity-0.412
Melting Point (℃)N.A.
Half LifeN.A.
DescriptionAnakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001.
Indication/DiseaseTo treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
PharmacodynamicsAnakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1.
Mechanism of ActionAnakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption.
ToxicityMost common adverse reactions (incidence 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu like-symptoms, and abdominal pain when anakinra is used
MetabolismN.A.
AbsorptionWhen a 70 mg subcutaneous bolus injection is given to healthy subjects, the absolute bioavailability is 95%. Accumulation does not occur following daily subcutaneous doses. Tmax, SubQ, 1-2 mg/kg, healthy subjects = 3-7 hours; Cmax, SubQ, 3 mg/kg once dail
Volume of DistributionN.A.
ClearanceClearance is variable and increases with increasing creatinine clearance and body weight.
CategoriesN.A.
Patents NumberN.A.
Date of IssueN.A.
Date of ExpiryN.A.
Drug InteractionThalidomide may increase the adverse effects of Anakinra. Increased risk of serious infection. Concomitant therapy should be avoided.
TargetN.A.
Information of corresponding available drug in the market
Brand NameN.A.
CompanyN.A.
Brand DiscriptionN.A.
Prescribed forN.A.
Chemical NameN.A.
FormulationN.A.
Physcial AppearanceN.A.
Route of AdministrationN.A.
Recommended DosageN.A.
ContraindicationN.A.
Side EffectsN.A.
Useful LinkN.A.
PubMed ID17947302, 18251718, 23553601, 23319019, 19169963
3-D StructureTh1023 (View) or (Download)