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Th1023 details

Primary information
ID 1180
ThPP ID Th1023
Therapeutic Peptide/Protein Name Anakinra
Sequence MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification IIa
Molecular Weight 17257.6
Chemical Formula C759H1186N208O232S10
Isoelectric Point 5.46
Hydrophobicity -0.412
Melting Point (℃) N.A.
Half Life Healthy subjects = 4 - 6 hours
Description Anakinra 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/Disease To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics Anakinra 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 Action Anakinra 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.
Toxicity Most 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
Metabolism N.A.
Absorption When 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 Distribution N.A.
Clearance Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories Antirheumatic Agents
Patents Number CA2141953
Date of Issue 08/04/08
Date of Expiry 17/09/13
Drug Interaction Canakinumab results in increased immunosuppressive effects; increases the risk of infection.
Target Interleukin-1 receptor type 1
Information of corresponding available drug in the market
Brand Name Kineret
Company Amgen Inc
Brand Discription Kineret 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 for To treat the symptoms of moderate to severe rheumatoid arthritis in adults. Anakinra may also help slow the progress of the disease.
Chemical Name N.A.
Formulation The 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 Appearance Sterile, clear, colorless-to-white, preservative free solution
Route of Administration Subcutaneous (Subcutaneous) administration
Recommended Dosage 100 mg/day administered daily
Contraindication Contraindicated in patients with known hypersensitivity to E coli-derived proteins, Kineret, or any components of the product
Side Effects Nausea, 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 Link http://www.rxlist.com/kineret-drug.htm
PubMed ID 17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure Th1023 (View) or (Download)

Primary information
ID 1181
ThPP ID Th1023
Therapeutic Peptide/Protein Name Anakinra
Sequence MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification IIa
Molecular Weight 17257.6
Chemical Formula C759H1186N208O232S10
Isoelectric Point 5.46
Hydrophobicity -0.412
Melting Point (℃) N.A.
Half Life NOMID patients = 5.7 hours (range of 3.1 - 28.2 hours)
Description Anakinra 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/Disease To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics Anakinra 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 Action Anakinra 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.
Toxicity Most 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
Metabolism N.A.
Absorption When 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 Distribution N.A.
Clearance Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories Immunosuppressive Agents
Patents Number CA1341322
Date of Issue 27/11/01
Date of Expiry 27/11/18
Drug Interaction Certolizumab pegol Co-administration with other TNF-blocking agents may increase the risk of serious infections. Concomitant therapy is not recommended.
Target N.A.
Information of corresponding available drug in the market
Brand Name N.A.
Company N.A.
Brand Discription N.A.
Prescribed for N.A.
Chemical Name N.A.
Formulation N.A.
Physcial Appearance N.A.
Route of Administration N.A.
Recommended Dosage N.A.
Contraindication N.A.
Side Effects N.A.
Useful Link http://www.drugs.com/kineret.html
PubMed ID 17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure Th1023 (View) or (Download)

Primary information
ID 1182
ThPP ID Th1023
Therapeutic Peptide/Protein Name Anakinra
Sequence MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification IIa
Molecular Weight 17257.6
Chemical Formula C759H1186N208O232S10
Isoelectric Point 5.46
Hydrophobicity -0.412
Melting Point (℃) N.A.
Half Life N.A.
Description Anakinra 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/Disease To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics Anakinra 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 Action Anakinra 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.
Toxicity Most 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
Metabolism N.A.
Absorption When 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 Distribution N.A.
Clearance Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories N.A.
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events.
Target N.A.
Information of corresponding available drug in the market
Brand Name N.A.
Company N.A.
Brand Discription N.A.
Prescribed for N.A.
Chemical Name N.A.
Formulation N.A.
Physcial Appearance N.A.
Route of Administration N.A.
Recommended Dosage N.A.
Contraindication N.A.
Side Effects N.A.
Useful Link http://www.kineretrx.com/
PubMed ID 17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure Th1023 (View) or (Download)

Primary information
ID 1183
ThPP ID Th1023
Therapeutic Peptide/Protein Name Anakinra
Sequence MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification IIa
Molecular Weight 17257.6
Chemical Formula C759H1186N208O232S10
Isoelectric Point 5.46
Hydrophobicity -0.412
Melting Point (℃) N.A.
Half Life N.A.
Description Anakinra 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/Disease To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics Anakinra 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 Action Anakinra 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.
Toxicity Most 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
Metabolism N.A.
Absorption When 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 Distribution N.A.
Clearance Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories N.A.
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction Golimumab. Avoid combination with anakinra due to the increased chance of serious infection.
Target N.A.
Information of corresponding available drug in the market
Brand Name N.A.
Company N.A.
Brand Discription N.A.
Prescribed for N.A.
Chemical Name N.A.
Formulation N.A.
Physcial Appearance N.A.
Route of Administration N.A.
Recommended Dosage N.A.
Contraindication N.A.
Side Effects N.A.
Useful Link N.A.
PubMed ID 17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure Th1023 (View) or (Download)

Primary information
ID 1184
ThPP ID Th1023
Therapeutic Peptide/Protein Name Anakinra
Sequence MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification IIa
Molecular Weight 17257.6
Chemical Formula C759H1186N208O232S10
Isoelectric Point 5.46
Hydrophobicity -0.412
Melting Point (℃) N.A.
Half Life N.A.
Description Anakinra 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/Disease To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics Anakinra 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 Action Anakinra 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.
Toxicity Most 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
Metabolism N.A.
Absorption When 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 Distribution N.A.
Clearance Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories N.A.
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction Rilonacept results in increased immunosuppressive effects; increases the risk of infection.
Target N.A.
Information of corresponding available drug in the market
Brand Name N.A.
Company N.A.
Brand Discription N.A.
Prescribed for N.A.
Chemical Name N.A.
Formulation N.A.
Physcial Appearance N.A.
Route of Administration N.A.
Recommended Dosage N.A.
Contraindication N.A.
Side Effects N.A.
Useful Link N.A.
PubMed ID 17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure Th1023 (View) or (Download)

Primary information
ID 1185
ThPP ID Th1023
Therapeutic Peptide/Protein Name Anakinra
Sequence MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification IIa
Molecular Weight 17257.6
Chemical Formula C759H1186N208O232S10
Isoelectric Point 5.46
Hydrophobicity -0.412
Melting Point (℃) N.A.
Half Life N.A.
Description Anakinra 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/Disease To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics Anakinra 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 Action Anakinra 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.
Toxicity Most 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
Metabolism N.A.
Absorption When 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 Distribution N.A.
Clearance Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories N.A.
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction Tofacitinib. Avoid combination due to the potential increase in tofacitinib related adverse effects.
Target N.A.
Information of corresponding available drug in the market
Brand Name N.A.
Company N.A.
Brand Discription N.A.
Prescribed for N.A.
Chemical Name N.A.
Formulation N.A.
Physcial Appearance N.A.
Route of Administration N.A.
Recommended Dosage N.A.
Contraindication N.A.
Side Effects N.A.
Useful Link N.A.
PubMed ID 17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure Th1023 (View) or (Download)

Primary information
ID 1186
ThPP ID Th1023
Therapeutic Peptide/Protein Name Anakinra
Sequence MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification IIa
Molecular Weight 17257.6
Chemical Formula C759H1186N208O232S10
Isoelectric Point 5.46
Hydrophobicity -0.412
Melting Point (℃) N.A.
Half Life N.A.
Description Anakinra 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/Disease To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics Anakinra 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 Action Anakinra 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.
Toxicity Most 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
Metabolism N.A.
Absorption When 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 Distribution N.A.
Clearance Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories N.A.
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction Thalidomide may increase the adverse effects of Anakinra. Increased risk of serious infection. Concomitant therapy should be avoided.
Target N.A.
Information of corresponding available drug in the market
Brand Name N.A.
Company N.A.
Brand Discription N.A.
Prescribed for N.A.
Chemical Name N.A.
Formulation N.A.
Physcial Appearance N.A.
Route of Administration N.A.
Recommended Dosage N.A.
Contraindication N.A.
Side Effects N.A.
Useful Link N.A.
PubMed ID 17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure Th1023 (View) or (Download)

OSDDlinux

Raghava's Group

IMTECH

CSIR

CRDD
CPPSITE 2.0

Primary information
ID	1180
ThPP ID	Th1023
Therapeutic Peptide/Protein Name	Anakinra
Sequence	MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	17257.6
Chemical Formula	C759H1186N208O232S10
Isoelectric Point	5.46
Hydrophobicity	-0.412
Melting Point (℃)	N.A.
Half Life	Healthy subjects = 4 - 6 hours
Description	Anakinra 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/Disease	To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics	Anakinra 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 Action	Anakinra 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.
Toxicity	Most 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
Metabolism	N.A.
Absorption	When 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 Distribution	N.A.
Clearance	Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories	Antirheumatic Agents
Patents Number	CA2141953
Date of Issue	08/04/08
Date of Expiry	17/09/13
Drug Interaction	Canakinumab results in increased immunosuppressive effects; increases the risk of infection.
Target	Interleukin-1 receptor type 1
Information of corresponding available drug in the market
Brand Name	Kineret
Company	Amgen Inc
Brand Discription	Kineret 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 for	To treat the symptoms of moderate to severe rheumatoid arthritis in adults. Anakinra may also help slow the progress of the disease.
Chemical Name	N.A.
Formulation	The 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 Appearance	Sterile, clear, colorless-to-white, preservative free solution
Route of Administration	Subcutaneous (Subcutaneous) administration
Recommended Dosage	100 mg/day administered daily
Contraindication	Contraindicated in patients with known hypersensitivity to E coli-derived proteins, Kineret, or any components of the product
Side Effects	Nausea, 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 Link	http://www.rxlist.com/kineret-drug.htm
PubMed ID	17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure	Th1023 (View) or (Download)

Primary information
ID	1181
ThPP ID	Th1023
Therapeutic Peptide/Protein Name	Anakinra
Sequence	MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	17257.6
Chemical Formula	C759H1186N208O232S10
Isoelectric Point	5.46
Hydrophobicity	-0.412
Melting Point (℃)	N.A.
Half Life	NOMID patients = 5.7 hours (range of 3.1 - 28.2 hours)
Description	Anakinra 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/Disease	To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics	Anakinra 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 Action	Anakinra 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.
Toxicity	Most 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
Metabolism	N.A.
Absorption	When 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 Distribution	N.A.
Clearance	Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories	Immunosuppressive Agents
Patents Number	CA1341322
Date of Issue	27/11/01
Date of Expiry	27/11/18
Drug Interaction	Certolizumab pegol Co-administration with other TNF-blocking agents may increase the risk of serious infections. Concomitant therapy is not recommended.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	N.A.
Company	N.A.
Brand Discription	N.A.
Prescribed for	N.A.
Chemical Name	N.A.
Formulation	N.A.
Physcial Appearance	N.A.
Route of Administration	N.A.
Recommended Dosage	N.A.
Contraindication	N.A.
Side Effects	N.A.
Useful Link	http://www.drugs.com/kineret.html
PubMed ID	17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure	Th1023 (View) or (Download)

Primary information
ID	1182
ThPP ID	Th1023
Therapeutic Peptide/Protein Name	Anakinra
Sequence	MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	17257.6
Chemical Formula	C759H1186N208O232S10
Isoelectric Point	5.46
Hydrophobicity	-0.412
Melting Point (℃)	N.A.
Half Life	N.A.
Description	Anakinra 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/Disease	To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics	Anakinra 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 Action	Anakinra 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.
Toxicity	Most 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
Metabolism	N.A.
Absorption	When 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 Distribution	N.A.
Clearance	Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories	N.A.
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	N.A.
Company	N.A.
Brand Discription	N.A.
Prescribed for	N.A.
Chemical Name	N.A.
Formulation	N.A.
Physcial Appearance	N.A.
Route of Administration	N.A.
Recommended Dosage	N.A.
Contraindication	N.A.
Side Effects	N.A.
Useful Link	http://www.kineretrx.com/
PubMed ID	17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure	Th1023 (View) or (Download)

Primary information
ID	1183
ThPP ID	Th1023
Therapeutic Peptide/Protein Name	Anakinra
Sequence	MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	17257.6
Chemical Formula	C759H1186N208O232S10
Isoelectric Point	5.46
Hydrophobicity	-0.412
Melting Point (℃)	N.A.
Half Life	N.A.
Description	Anakinra 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/Disease	To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics	Anakinra 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 Action	Anakinra 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.
Toxicity	Most 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
Metabolism	N.A.
Absorption	When 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 Distribution	N.A.
Clearance	Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories	N.A.
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	Golimumab. Avoid combination with anakinra due to the increased chance of serious infection.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	N.A.
Company	N.A.
Brand Discription	N.A.
Prescribed for	N.A.
Chemical Name	N.A.
Formulation	N.A.
Physcial Appearance	N.A.
Route of Administration	N.A.
Recommended Dosage	N.A.
Contraindication	N.A.
Side Effects	N.A.
Useful Link	N.A.
PubMed ID	17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure	Th1023 (View) or (Download)

Primary information
ID	1184
ThPP ID	Th1023
Therapeutic Peptide/Protein Name	Anakinra
Sequence	MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	17257.6
Chemical Formula	C759H1186N208O232S10
Isoelectric Point	5.46
Hydrophobicity	-0.412
Melting Point (℃)	N.A.
Half Life	N.A.
Description	Anakinra 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/Disease	To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics	Anakinra 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 Action	Anakinra 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.
Toxicity	Most 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
Metabolism	N.A.
Absorption	When 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 Distribution	N.A.
Clearance	Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories	N.A.
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	Rilonacept results in increased immunosuppressive effects; increases the risk of infection.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	N.A.
Company	N.A.
Brand Discription	N.A.
Prescribed for	N.A.
Chemical Name	N.A.
Formulation	N.A.
Physcial Appearance	N.A.
Route of Administration	N.A.
Recommended Dosage	N.A.
Contraindication	N.A.
Side Effects	N.A.
Useful Link	N.A.
PubMed ID	17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure	Th1023 (View) or (Download)

Primary information
ID	1185
ThPP ID	Th1023
Therapeutic Peptide/Protein Name	Anakinra
Sequence	MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	17257.6
Chemical Formula	C759H1186N208O232S10
Isoelectric Point	5.46
Hydrophobicity	-0.412
Melting Point (℃)	N.A.
Half Life	N.A.
Description	Anakinra 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/Disease	To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics	Anakinra 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 Action	Anakinra 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.
Toxicity	Most 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
Metabolism	N.A.
Absorption	When 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 Distribution	N.A.
Clearance	Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories	N.A.
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	Tofacitinib. Avoid combination due to the potential increase in tofacitinib related adverse effects.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	N.A.
Company	N.A.
Brand Discription	N.A.
Prescribed for	N.A.
Chemical Name	N.A.
Formulation	N.A.
Physcial Appearance	N.A.
Route of Administration	N.A.
Recommended Dosage	N.A.
Contraindication	N.A.
Side Effects	N.A.
Useful Link	N.A.
PubMed ID	17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure	Th1023 (View) or (Download)

Primary information
ID	1186
ThPP ID	Th1023
Therapeutic Peptide/Protein Name	Anakinra
Sequence	MRPSGRKSSKMQAFRIWDVNQKTFYLRNNQLVAGYLQGPNVNLEEKIDVV view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	17257.6
Chemical Formula	C759H1186N208O232S10
Isoelectric Point	5.46
Hydrophobicity	-0.412
Melting Point (℃)	N.A.
Half Life	N.A.
Description	Anakinra 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/Disease	To treat adult rheumatoid arthritis and Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
Pharmacodynamics	Anakinra 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 Action	Anakinra 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.
Toxicity	Most 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
Metabolism	N.A.
Absorption	When 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 Distribution	N.A.
Clearance	Clearance is variable and increases with increasing creatinine clearance and body weight.
Categories	N.A.
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	Thalidomide may increase the adverse effects of Anakinra. Increased risk of serious infection. Concomitant therapy should be avoided.
Target	N.A.
Information of corresponding available drug in the market
Brand Name	N.A.
Company	N.A.
Brand Discription	N.A.
Prescribed for	N.A.
Chemical Name	N.A.
Formulation	N.A.
Physcial Appearance	N.A.
Route of Administration	N.A.
Recommended Dosage	N.A.
Contraindication	N.A.
Side Effects	N.A.
Useful Link	N.A.
PubMed ID	17947302, 18251718, 23553601, 23319019, 19169963
3-D Structure	Th1023 (View) or (Download)

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