==== Reference: Usmani SS, Bedi G, Samuel JS, Singh S, Kalra S, Kumar P, et al. (2017) THPdb: Database of FDA-approved peptide and protein therapeutics. PLoS ONE 12(7) e0181748.====

Detailed description page of THPdb


Details of Th1054 which contains 4 entries.


Entry 1
(1) Primary information
ID1368
ThPP IDTh1054
Therapeutic Peptide/Protein NameInfliximab
SequenceN.A. view full sequnce in fasta
Functional ClassificationIIa
Molecular Weight144190.3
Chemical FormulaC6428H9912N1694O1987S46
Isoelectric Point8.25
Hydrophobicity-0.441
Melting Point (℃)61 (FAB f
Half Life9.5 days
DescriptionTumor 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/DiseaseTo 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.
PharmacodynamicsInfliximab 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 ActionInfliximab 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.
ToxicityN.A.
MetabolismMost likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production
AbsorptionN.A.
Volume of DistributionN.A.
ClearanceN.A.
CategoriesAntirheumatic Agents, Anti-Inflammatory Agents, Non-Steroidal, Dermatologic Agents, Gastrointestinal Agents and Immunosuppressive Agents
Patents NumberCA2106299
Date of Issue07/02/05
Date of Expiry19/03/16
Drug InteractionGolimumab avoid combination with infliximab due to the potential increased immunosuppression of infliximab
TargetTumor necrosis factor
Information of corresponding available drug in the market
Brand NameREMICADE
CompanyCentocor Inc
Brand DiscriptionInfliximab, the active ingredient in REMICADE, is a chimeric IgG1κ monoclonal antibody (composed of human constant and murine variable regions) specific for human tumor necrosis factor-alpha (TNFα). 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 forused in crohn disease, Ankylosing pondylitis, Psoriatic Arthritis, Plaque Psoriasis and ulcerative colitis
Chemical NameN.A.
FormulationEach 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 AppearanceREMICADE 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 AdministrationIntravenous infusion
Recommended Dosagefor 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
ContraindicationREMICADE 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 EffectsHepatotoxicity, Immunogenicity, Nausea, Diarrhea, Dysepsia, Sinusitis, Bronchitis, Phrayngitis, Rash, Fatigue, Fever, urinary tract infections.
Useful Link1. 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 ID14985485, 10228190, 25641691, 25629655, 25586216, 23620660
3-D StructureN.A.


Entry 2
(2) Primary information
ID1369
ThPP IDTh1054
Therapeutic Peptide/Protein NameInfliximab
SequenceN.A. view full sequnce in fasta
Functional ClassificationIIa
Molecular Weight144190.3
Chemical FormulaC6428H9912N1694O1987S46
Isoelectric Point8.25
Hydrophobicity-0.441
Melting Point (℃)62 (FAB f
Half Life9.5 days
DescriptionTumor 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/DiseaseTo 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.
PharmacodynamicsInfliximab 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 ActionInfliximab 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.
ToxicityN.A.
MetabolismMost likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production
AbsorptionN.A.
Volume of DistributionN.A.
ClearanceN.A.
CategoriesAntirheumatic Agents, Anti-Inflammatory Agents, Non-Steroidal, Dermatologic Agents, Gastrointestinal Agents and Immunosuppressive Agents
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 ID14985485, 10228190, 25641691, 25629655, 25586216, 23620660
3-D StructureN.A.


Entry 3
(3) Primary information
ID1370
ThPP IDTh1054
Therapeutic Peptide/Protein NameInfliximab
SequenceN.A. view full sequnce in fasta
Functional ClassificationIIa
Molecular Weight144190.3
Chemical FormulaC6428H9912N1694O1987S46
Isoelectric Point8.25
Hydrophobicity-0.441
Melting Point (℃)63 (FAB f
Half Life9.5 days
DescriptionTumor 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/DiseaseTo 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.
PharmacodynamicsInfliximab 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 ActionInfliximab 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.
ToxicityN.A.
MetabolismMost likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production
AbsorptionN.A.
Volume of DistributionN.A.
ClearanceN.A.
CategoriesAntirheumatic Agents, Anti-Inflammatory Agents, Non-Steroidal, Dermatologic Agents, Gastrointestinal Agents and Immunosuppressive Agents
Patents NumberN.A.
Date of IssueN.A.
Date of ExpiryN.A.
Drug InteractionTofacitinib avoid combination with infliximab and other anti-TNF drugs due to the potential enhancement of 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 ID14985485, 10228190, 25641691, 25629655, 25586216, 23620660
3-D StructureN.A.


Entry 4
(4) Primary information
ID1371
ThPP IDTh1054
Therapeutic Peptide/Protein NameInfliximab
SequenceN.A. view full sequnce in fasta
Functional ClassificationIIa
Molecular Weight144190.3
Chemical FormulaC6428H9912N1694O1987S46
Isoelectric Point8.25
Hydrophobicity-0.441
Melting Point (℃)64 (FAB f
Half Life9.5 days
DescriptionTumor 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/DiseaseTo 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.
PharmacodynamicsInfliximab 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 ActionInfliximab 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.
ToxicityN.A.
MetabolismMost likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production
AbsorptionN.A.
Volume of DistributionN.A.
ClearanceN.A.
CategoriesAntirheumatic Agents, Anti-Inflammatory Agents, Non-Steroidal, Dermatologic Agents, Gastrointestinal Agents and Immunosuppressive Agents
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 LinkN.A.
PubMed ID14985485, 10228190, 25641691, 25629655, 25586216, 23620660
3-D StructureN.A.