Detailed description page of THPdb

Details of Th1054 which contains 4 entries.

Entry 1
(1) Primary information
ID 1368
ThPP ID Th1054
Therapeutic Peptide/Protein Name Infliximab
Sequence N.A. view full sequnce in fasta
Functional Classification IIa
Molecular Weight 144190.3
Chemical Formula C6428H9912N1694O1987S46
Isoelectric Point 8.25
Hydrophobicity -0.441
Melting Point (℃) 61 (FAB f
Half Life 9.5 days
Description Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion.
Indication/Disease To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis.
Pharmacodynamics Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal.
Mechanism of Action Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation.
Toxicity N.A.
Metabolism Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production
Absorption N.A.
Volume of Distribution N.A.
Clearance N.A.
Categories Antirheumatic Agents, Anti-Inflammatory Agents, Non-Steroidal, Dermatologic Agents, Gastrointestinal Agents and Immunosuppressive Agents
Patents Number CA2106299
Date of Issue 07/02/05
Date of Expiry 19/03/16
Drug Interaction Golimumab avoid combination with infliximab due to the potential increased immunosuppression of infliximab
Target Tumor necrosis factor
Information of corresponding available drug in the market
Brand Name REMICADE
Company Centocor Inc
Brand Discription Infliximab, the active ingredient in REMICADE, is a chimeric IgG1Îº monoclonal antibody (composed of human constant and murine variable regions) specific for human tumor necrosis factor-alpha (TNFÎ±). It has a molecular weight of approximately 149.1 kilodaltons. Infliximab is produced by a recombinant cell line cultured by continuous perfusion and is purified by a series of steps that includes measures to inactivate and remove viruses.
Prescribed for used in crohn disease, Ankylosing pondylitis, Psoriatic Arthritis, Plaque Psoriasis and ulcerative colitis
Chemical Name N.A.
Formulation Each single-use vial contains 100 mg infliximab, 500 mg sucrose, 0.5 mg polysorbate 80, 2.2 mg monobasic sodium phosphate, monohydrate, and 6.1 mg dibasic sodium phosphate, dihydrate. No preservatives are present.
Physcial Appearance REMICADE is supplied as a Sterile, white, lyophilized powder, Following reconstitution with 10 mL of Sterile Water for Injection, USP, the resulting pH is approximately 7.2.
Route of Administration Intravenous infusion
Recommended Dosage for crohn disease, Ankylosing pondylitis, Psoriatic Arthritis, Plaque Psoriasis and ulcerative colitis : The recommended dose of REMICADE is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks for rhematoid arthritis: The recommended dose of REMICADE is 3 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks
Contraindication REMICADE at doses > 5 mg/kg should not be administered to patients with moderate to severe heart failure.; REMICADE should not be re-administered to patients who have experienced a severe hypersensitivity reaction to REMICADE
Side Effects Hepatotoxicity, Immunogenicity, Nausea, Diarrhea, Dysepsia, Sinusitis, Bronchitis, Phrayngitis, Rash, Fatigue, Fever, urinary tract infections.
Useful Link 1. American Thoracic Society, Centers for Disease Control and Prevention. Targeted tuberculin testing and treatment of latent tuberculosis infection. Am J Respir Crit Care Med 2000;161:S221-S247. 2. http://www.rxlist.com/remicade-drug.htm
PubMed ID 14985485, 10228190, 25641691, 25629655, 25586216, 23620660
3-D Structure N.A.

Entry 2
(2) Primary information
ID 1369
ThPP ID Th1054
Therapeutic Peptide/Protein Name Infliximab
Sequence N.A. view full sequnce in fasta
Functional Classification IIa
Molecular Weight 144190.3
Chemical Formula C6428H9912N1694O1987S46
Isoelectric Point 8.25
Hydrophobicity -0.441
Melting Point (℃) 62 (FAB f
Half Life 9.5 days
Description Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion.
Indication/Disease To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis.
Pharmacodynamics Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal.
Mechanism of Action Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation.
Toxicity N.A.
Metabolism Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production
Absorption N.A.
Volume of Distribution N.A.
Clearance N.A.
Categories Antirheumatic Agents, Anti-Inflammatory Agents, Non-Steroidal, Dermatologic Agents, Gastrointestinal Agents and Immunosuppressive Agents
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 14985485, 10228190, 25641691, 25629655, 25586216, 23620660
3-D Structure N.A.

Entry 3
(3) Primary information
ID 1370
ThPP ID Th1054
Therapeutic Peptide/Protein Name Infliximab
Sequence N.A. view full sequnce in fasta
Functional Classification IIa
Molecular Weight 144190.3
Chemical Formula C6428H9912N1694O1987S46
Isoelectric Point 8.25
Hydrophobicity -0.441
Melting Point (℃) 63 (FAB f
Half Life 9.5 days
Description Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion.
Indication/Disease To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis.
Pharmacodynamics Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal.
Mechanism of Action Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation.
Toxicity N.A.
Metabolism Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production
Absorption N.A.
Volume of Distribution N.A.
Clearance N.A.
Categories Antirheumatic Agents, Anti-Inflammatory Agents, Non-Steroidal, Dermatologic Agents, Gastrointestinal Agents and Immunosuppressive Agents
Patents Number N.A.
Date of Issue N.A.
Date of Expiry N.A.
Drug Interaction Tofacitinib avoid combination with infliximab and other anti-TNF drugs due to the potential enhancement of 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 14985485, 10228190, 25641691, 25629655, 25586216, 23620660
3-D Structure N.A.

Entry 4
(4) Primary information
ID 1371
ThPP ID Th1054
Therapeutic Peptide/Protein Name Infliximab
Sequence N.A. view full sequnce in fasta
Functional Classification IIa
Molecular Weight 144190.3
Chemical Formula C6428H9912N1694O1987S46
Isoelectric Point 8.25
Hydrophobicity -0.441
Melting Point (℃) 64 (FAB f
Half Life 9.5 days
Description Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion.
Indication/Disease To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis.
Pharmacodynamics Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal.
Mechanism of Action Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation.
Toxicity N.A.
Metabolism Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production
Absorption N.A.
Volume of Distribution N.A.
Clearance N.A.
Categories Antirheumatic Agents, Anti-Inflammatory Agents, Non-Steroidal, Dermatologic Agents, Gastrointestinal Agents and Immunosuppressive Agents
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 N.A.
PubMed ID 14985485, 10228190, 25641691, 25629655, 25586216, 23620660
3-D Structure N.A.

OSDDlinux

Raghava's Group

IMTECH

CSIR

CRDD
CPPSITE 2.0

(1) Primary information
Entry 1
ID	1368
ThPP ID	Th1054
Therapeutic Peptide/Protein Name	Infliximab
Sequence	N.A. view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	144190.3
Chemical Formula	C6428H9912N1694O1987S46
Isoelectric Point	8.25
Hydrophobicity	-0.441
Melting Point (℃)	61 (FAB f
Half Life	9.5 days
Description	Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion.
Indication/Disease	To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis.
Pharmacodynamics	Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal.
Mechanism of Action	Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation.
Toxicity	N.A.
Metabolism	Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production
Absorption	N.A.
Volume of Distribution	N.A.
Clearance	N.A.
Categories	Antirheumatic Agents, Anti-Inflammatory Agents, Non-Steroidal, Dermatologic Agents, Gastrointestinal Agents and Immunosuppressive Agents
Patents Number	CA2106299
Date of Issue	07/02/05
Date of Expiry	19/03/16
Drug Interaction	Golimumab avoid combination with infliximab due to the potential increased immunosuppression of infliximab
Target	Tumor necrosis factor
Information of corresponding available drug in the market
Brand Name	REMICADE
Company	Centocor Inc
Brand Discription	Infliximab, the active ingredient in REMICADE, is a chimeric IgG1Îº monoclonal antibody (composed of human constant and murine variable regions) specific for human tumor necrosis factor-alpha (TNFÎ±). It has a molecular weight of approximately 149.1 kilodaltons. Infliximab is produced by a recombinant cell line cultured by continuous perfusion and is purified by a series of steps that includes measures to inactivate and remove viruses.
Prescribed for	used in crohn disease, Ankylosing pondylitis, Psoriatic Arthritis, Plaque Psoriasis and ulcerative colitis
Chemical Name	N.A.
Formulation	Each single-use vial contains 100 mg infliximab, 500 mg sucrose, 0.5 mg polysorbate 80, 2.2 mg monobasic sodium phosphate, monohydrate, and 6.1 mg dibasic sodium phosphate, dihydrate. No preservatives are present.
Physcial Appearance	REMICADE is supplied as a Sterile, white, lyophilized powder, Following reconstitution with 10 mL of Sterile Water for Injection, USP, the resulting pH is approximately 7.2.
Route of Administration	Intravenous infusion
Recommended Dosage	for crohn disease, Ankylosing pondylitis, Psoriatic Arthritis, Plaque Psoriasis and ulcerative colitis : The recommended dose of REMICADE is 5 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks for rhematoid arthritis: The recommended dose of REMICADE is 3 mg/kg given as an intravenous induction regimen at 0, 2 and 6 weeks
Contraindication	REMICADE at doses > 5 mg/kg should not be administered to patients with moderate to severe heart failure.; REMICADE should not be re-administered to patients who have experienced a severe hypersensitivity reaction to REMICADE
Side Effects	Hepatotoxicity, Immunogenicity, Nausea, Diarrhea, Dysepsia, Sinusitis, Bronchitis, Phrayngitis, Rash, Fatigue, Fever, urinary tract infections.
Useful Link	1. American Thoracic Society, Centers for Disease Control and Prevention. Targeted tuberculin testing and treatment of latent tuberculosis infection. Am J Respir Crit Care Med 2000;161:S221-S247. 2. http://www.rxlist.com/remicade-drug.htm
PubMed ID	14985485, 10228190, 25641691, 25629655, 25586216, 23620660
3-D Structure	N.A.

(2) Primary information
Entry 2
ID	1369
ThPP ID	Th1054
Therapeutic Peptide/Protein Name	Infliximab
Sequence	N.A. view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	144190.3
Chemical Formula	C6428H9912N1694O1987S46
Isoelectric Point	8.25
Hydrophobicity	-0.441
Melting Point (℃)	62 (FAB f
Half Life	9.5 days
Description	Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion.
Indication/Disease	To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis.
Pharmacodynamics	Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal.
Mechanism of Action	Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation.
Toxicity	N.A.
Metabolism	Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production
Absorption	N.A.
Volume of Distribution	N.A.
Clearance	N.A.
Categories	Antirheumatic Agents, Anti-Inflammatory Agents, Non-Steroidal, Dermatologic Agents, Gastrointestinal Agents and Immunosuppressive Agents
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	14985485, 10228190, 25641691, 25629655, 25586216, 23620660
3-D Structure	N.A.

(3) Primary information
Entry 3
ID	1370
ThPP ID	Th1054
Therapeutic Peptide/Protein Name	Infliximab
Sequence	N.A. view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	144190.3
Chemical Formula	C6428H9912N1694O1987S46
Isoelectric Point	8.25
Hydrophobicity	-0.441
Melting Point (℃)	63 (FAB f
Half Life	9.5 days
Description	Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion.
Indication/Disease	To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis.
Pharmacodynamics	Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal.
Mechanism of Action	Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation.
Toxicity	N.A.
Metabolism	Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production
Absorption	N.A.
Volume of Distribution	N.A.
Clearance	N.A.
Categories	Antirheumatic Agents, Anti-Inflammatory Agents, Non-Steroidal, Dermatologic Agents, Gastrointestinal Agents and Immunosuppressive Agents
Patents Number	N.A.
Date of Issue	N.A.
Date of Expiry	N.A.
Drug Interaction	Tofacitinib avoid combination with infliximab and other anti-TNF drugs due to the potential enhancement of 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	14985485, 10228190, 25641691, 25629655, 25586216, 23620660
3-D Structure	N.A.

(4) Primary information
Entry 4
ID	1371
ThPP ID	Th1054
Therapeutic Peptide/Protein Name	Infliximab
Sequence	N.A. view full sequnce in fasta
Functional Classification	IIa
Molecular Weight	144190.3
Chemical Formula	C6428H9912N1694O1987S46
Isoelectric Point	8.25
Hydrophobicity	-0.441
Melting Point (℃)	64 (FAB f
Half Life	9.5 days
Description	Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion.
Indication/Disease	To manage the signs and symptoms, as well as to induce and maintain clinical remission in adults with moderate to severe active Crohn's disease or ulcerative colitis. Also used to manage signs and symptoms of rheumatoid arthritis (in conjunction with methotrexate), ankylosing spondylitis, psoriatic arthritis, and juvenile arthritis.
Pharmacodynamics	Infliximab is a chimeric human-murine anti-human tumor necrosis factor (TNF) monoclonal antibody. It binds to tumor necrosis factor alpha (TNFa) and inhibits binding of TNFa with its receptors. This reduces production of pro-inflammatory cytokines such as interleukins (IL) 1 and 6. This also limits leukocyte migration and expression of adhesion molecules by endothelial cells and leukocytes. Infliximab also limits the activation of neutrophil and eosinophil functional activity, reduces production of tissue degrading enzymes produced by synoviocytes and/or chondrocytes. Infliximab decreases synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal.
Mechanism of Action	Infliximab neutralizes the biological activity of TNFa by binding with high affinity to the soluble and transmembrane forms of TNFa and inhibits binding of TNFa with its receptors. Infliximab does not neutralize TNFb (lymphotoxin a), a related cytokine that utilizes the same receptors as TNFa. Neutralization of the biological activity of TNFa leads to an overall reduction in inflammation.
Toxicity	N.A.
Metabolism	Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production
Absorption	N.A.
Volume of Distribution	N.A.
Clearance	N.A.
Categories	Antirheumatic Agents, Anti-Inflammatory Agents, Non-Steroidal, Dermatologic Agents, Gastrointestinal Agents and Immunosuppressive Agents
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	N.A.
PubMed ID	14985485, 10228190, 25641691, 25629655, 25586216, 23620660
3-D Structure	N.A.