Infliximab

Explore a selection of our essential drug information below, or:

Unlock enhanced features & extensive drug insights, including detailed interaction data & regulatory status. Create a free account.

SUBSCRIBERECOMMENDED FOR PHARMA

Explore the full scope of our drug knowledge tailored for pharmaceutical research needs in our data library. Learn more.

Identification

Summary

Infliximab is a monoclonal anti tumor necrosis factor alpha antibody used in the treatment of a wide variety of inflammatory conditions such as rheumatoid arthritis, Crohn's disease, and ankylosing spondylitis.

Brand Names

Avsola, Flixabi, Inflectra, Remicade, Renflexis, Zymfentra

Generic Name

Infliximab

DrugBank Accession Number

DB00065

Background

Infliximab is a tumor necrosis factor (TNF-alpha or TNF-α) blocker and a chimeric monoclonal IgG1 antibody composed of human constant (75%) and murine variable (25%) regions ³. Infliximab is produced by a recombinant cell line cultured by continuous perfusion. Tumor necrosis factor-alpha (TNF-α) is a key proinflammatory cytokine involved in chronic inflammatory diseases ³. Its hyperactivity and enhanced signalling pathways can be observed in inflammatory diseases where it activates further pro-inflammatory cascades. By binding to both the soluble subunit and the membrane-bound precursor of TNF-α ¹, infliximab disrupts the interaction of TNF-α with its receptors and may also cause lysis of cells that produce TNF-α ¹.

Infliximab was first approved by the FDA in 1998 under the market name Remicade as an intravenous injection. It is indicated for the treatment of various inflammatory disorders such as adult or pediatric Chron's disease, adult or pediatric ulcerative colitis, rheumatoid arthritis in combination with methotrexate, ankylosing spondyliti, psoriatic arthritis, and plaque psoriasis ^Label. In clinical trials, multiple infusions of infliximab displayed in a reduction of signs and symptoms of inflammatory diseases and induction of remission in patients who have had an inadequate response to alternative first-line therapies for that disorder ^Label.

There are currently two biosilimars of infliximab available in the US market that demonstrate a high degree of similarity to the reference product, Remicade. They are approved for all eligible indications of the reference product. Inflectra, a first biosimilar drug product, was approved in 2016. In December 2017, Ixifi, a second biosimilar that was developed by Pfizer, was granted approval by the FDA.

Type

Biotech

Groups

Approved

Biologic Classification

Protein Based Therapies
Monoclonal antibody (mAb)

Protein Structure

Protein Chemical Formula: C₆₄₂₈H₉₉₁₂N₁₆₉₄O₁₉₈₇S₄₆
Protein Average Weight: 144190.3 Da

Sequences

Not Available

Synonyms

Infliximab
Infliximab (genetical recombination)
Infliximab-abda
Infliximab-axxq
Infliximab-dyyb
Infliximab-qbtx

External IDs

ABP 710
ABP-710
BOW-015
BOW015
CT-P-13
CT-P13
GP 1111
GP-1111
PF-06438179
TA-650

Unlock the secrets to drugging the undruggable

Discover how groundbreaking research is turning "undruggable" targets into therapeutic opportunities.

Download eBook

Unlock the secrets to drugging the undruggable

Download eBook

Pharmacology

Indication

Indicated for reducing signs and symptoms and inducing and maintaining clinical remission in adult or pediatric (≥ 6 years of age) patients with moderately to severely active Crohn’s disease who have had an inadequate response to conventional therapy
Indicated for reducing the number of draining enterocutaneous and rectovaginal fistulas and maintaining fistula closure in adult patients with fistulizing Crohn’s disease.
Indicated for reducing signs and symptoms, inducing and maintaining clinical remission and mucosal healing, and eliminating corticosteroid use in adult or pediatric (≥ 6 years of age) patients with moderately to severely active ulcerative colitis who have had an inadequate response to conventional therapy.
Indicated for, in combination with methotrexate, reducing signs and symptoms, inhibiting the progression of structural damage, and improving physical function in patients with moderately to severely active rheumatoid arthritis.
Indicated for reducing signs and symptoms in patients with active ankylosing spondylitis.
Indicated for reducing signs and symptoms of active arthritis, inhibiting the progression of structural damage, and improving physical function in patients with psoriatic arthritis.
Indicated for the treatment of adult patients with chronic severe (i.e., extensive and/or disabling) plaque psoriasis who are candidates for systemic therapy and when other systemic therapies are medically less appropriate.

Reduce drug development failure rates

Build, train, & validate machine-learning models
with evidence-based and structured datasets.

See how

Build, train, & validate predictive machine-learning models with structured datasets.

See how

Associated Conditions

Indication Type	Indication	Combined Product Details	Approval Level	Age Group	Patient Characteristics	Dose Form
Management of	Ankylosing spondylitis (as)		••••••••••••	•••••		•••••••••
Management of	Chronic plaque psoriasis		••••••••••••	•••••	•••••••• •• •••••• ••••••• •••••• ••••••••• ••• ••• •••••••••• ••• •••••••• ••••••• •• ••••••••••••• ••• •••• ••••• •••••••• ••••••••• ••• ••••••••• •••• •••••••••••	•••••••••
Management of	Fistulizing crohn's disease		••••••••••••	•••••		•••••••••
Management of	Moderately to severely active crohn's disease		••••••••••••	•••••	•••••••••• •••••••• •• •••••••••••• •••••••	•••••••••
Used in combination to manage	Moderately to severely active rheumatoid arthritis	Regimen in combination with: Methotrexate (DB00563)	••••••••••••	•••••		•••••••••

Contraindications & Blackbox Warnings

Prevent Adverse Drug Events Today

Tap into our Clinical API for life-saving information on contraindications & blackbox warnings, population restrictions, harmful risks, & more.

Learn more

Avoid life-threatening adverse drug events with our Clinical API

Learn more

Pharmacodynamics

Infliximab disrupts the activation of pro-inflammaory cascade signalling. Infliximab has shown to reduce infiltration of inflammatory cells into sites of inflammation. It also attenautes the expression of molecules mediating cellular adhesion {including E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)}, chemoattraction {[IL-8 and monocyte chemotactic protein (MCP-1)} and tissue degradation {matrix metalloproteinase (MMP) 1 and 3} ^Label.

Mechanism of action

Infliximab is a IgG1κ monoclonal antibody that binds to soluble and transmembrane forms of TNF-α with high affinity to disrupt the pro-inflammatory cascade signalling. Binding of the antibody to TNF-α prevents TNF-α from interacting with its receptors. Infliximab does not neutralize TNF-β (lymphotoxin-α), a related cytokine that utilizes the same receptors as TNF-α ^Label. Blocked actions of TNF-α further leads to downregulation of local and systemic pro-inflammatory cytokines (i.e. IL-1, IL-6), reduction of lymphocyte and leukocyte migration to sites of inflammation, induction of apoptosis of TNF-producing cells (i.e. activated monocytes and T lymphocytes), increased levels of nuclear factor-κB inhibitor, and reduction of reduction of endothelial adhesion molecules and acute phase proteins ³. Its inhibitory actions on TNF-α was demonstrated in human fibroblasts, endothelial cells, neutrophils, B and Tlymphocytes and epithelial cells ^Label. Infliximab also atteunates the production of tissue degrading enzymes synthesized by synoviocytes and/or chondrocytes. According to a transgenic mice study that developed polyarthritis due to consitutive levels of human TNF-α, infliximab decreased synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal ^Label.

Target	Actions	Organism
ATumor necrosis factor	inhibitor	Humans

Absorption

Following a single intravenous infusion, infliximab absorption displays a linear relationship between the dose administered and the maximum serum concentration ^Label.

In patients with Crohn's disease, the maximum plasma concentration (Cmax) of infliximab following single doses of 5 mg/kg and 10 mg/kg was 75 µg/mL and 181 µg/mL, respectively. In a maintenance therapy study, multiple infusions of infliximab (at week 0, 2 and 6) at the same dose of 5 mg/kg and 10 mg/kg resulted in Cmax of 120 µg/mL and 189 µg/mL , respectively ³.

In patients with rheumatoid arthritis, the Cmax of infliximab following a single dose infusion of 5 mg/kg, 10 mg/kg and 20 mg/kg were 192±51 µg/mL, 427±106 µg/mL, and 907±183 µg/mL, respectively ³.

Volume of distribution

Based on a pharmacokinetic study of adult patients, the distribution at steady state was independent of dose and indicated that infliximab was distributed primarily within the vascular compartment ^Label.

In patients with Crohn's disease, the apparent volume of distribution at steady state (Vss) of infliximab following single doses of 5 mg/kg and 10 mg/kg was 80 mL/kg and 65 mL/kg, respectively. In a maintenance therapy study, multiple infusions of infliximab (at week 0, 2 and 6) at the same dose of 5 mg/kg and 10 mg/kg resulted in Vss of 70 mL/kg and 81 mL/kg , respectively ³.

In patients with rheumatoid arthritis, the Vss of infliximab following a single dose infusion of 5 mg/kg, 10 mg/kg and 20 mg/kg were 4.3±2.5 L, 3.2±0.7 L, and 3.1±0.6 L, respectively ³.

Protein binding

Not Available

Metabolism

Not Available

Route of elimination

Therapeutic monoclonal antibodies including infliximab are predicted to be nonspecifically metabolized to peptides and amino acids that can be re-used in the body for de novo synthesis of proteins or arc excreted by the kidney ⁴. The reticuloendothelial system (RES) are phagocytic cells of the immune system such as macrophages and monocytes that play a role in the elimination of endogenous IgG antibodies. Although administered infliximab accounts for a small fraction of total endogenous IgG and this route is not likely saturated by therapeutic mAbs, infliximab may be removed by opsonization via RES following binding of the Fc part of the antibody to Fcy-receptors expressed on the RES ⁴.

Half-life

The median terminal half-life of infliximab is 7.7 to 9.5 days. The data is based on a pharmacokinetic study in patients with Crohn's disease, plaque psoriasis and rheumatoid arthritis receiving a single dose of infliximab ^Label.

Clearance

In patients with Crohn's disease, the total body clearance (CL) of infliximab following single doses of 5 mg/kg and 10 mg/kg was 18.4 mL/h and 14.3 mL/h, respectively. In a maintenance therapy study, multiple infusions of infliximab (at week 0, 2 and 6) at the same dose of 5 mg/kg and 10 mg/kg resulted in CL of 15.2 mL/h and 15.2 mL/h, respectively ³.

In patients with rheumatoid arthritis, the CL of infliximab following a single dose infusion of 5 mg/kg, 10 mg/kg and 20 mg/kg were 11±7.5 mL/h, 11.4±5 mL/h, and 11±8.9 mL/h, respectively ³.

Development of antibodies to infliximab increased infliximab clearance ^Label.

Adverse Effects

Improve decision support & research outcomes

With structured adverse effects data, including: blackbox warnings, adverse reactions, warning & precautions, & incidence rates. View sample adverse effects data in our new Data Library!

See the data

Improve decision support & research outcomes with our structured adverse effects data.

See a data sample

Toxicity

In an acute toxicity animal study, the NOAEL of intravenous infliximab in rats was 50 mg/kg. In a repeated dose animal study, the NOAEL values of intravenous infliximab was 50 mg/kg in rats at 2 weeks following 3 doses and 40 mg/kg/day in mice at 6 months ^MSDS.

The toxicological potential of infliximab in humans has not yet been fully established. According to an analogous antibody study, infliximab is not predicted to induce tumorigenic, clastogenic or mutagenic effects. No impairment of fertility was observed in a fertility and general reproduction toxicity study with the analogous mouse antibody used in the 6-month chronic toxicity study ^Label.

Pathways

Not Available

Pharmacogenomic Effects/ADRs

Interacting Gene/Enzyme	Allele name	Genotype(s)	Defining Change(s)	Type(s)	Description	Details
Low affinity immunoglobulin gamma Fc region receptor III-A	---	(C;C)	CC Allele (homozygous)	Effect Directly Studied	Patients with this genotype have increased ACR20 response when using infliximab to treat rheumatoid arthritis.	Details

Interactions

Drug Interactions

This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.

Drug	Interaction
Integrate drug-drug interactions in your software
Abatacept	The risk or severity of infection can be increased when Infliximab is combined with Abatacept.
Abciximab	The risk or severity of adverse effects can be increased when Abciximab is combined with Infliximab.
Abemaciclib	The metabolism of Abemaciclib can be increased when combined with Infliximab.
Abrocitinib	The metabolism of Abrocitinib can be increased when combined with Infliximab.
Acalabrutinib	The metabolism of Acalabrutinib can be increased when combined with Infliximab.

Food Interactions

No interactions found.

Products

Drug product information from 10+ global regions

Our datasets provide approved product information including:
dosage, form, labeller, route of administration, and marketing period.

Access now

Access drug product information from over 10 global regions.

Access now

International/Other Brands

Avsola (Amgen)

Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End
Avsola	Powder, for solution	100 mg / vial	Intravenous	Amgen Europe B.V.	2020-06-01	Not applicable
Avsola	Injection, powder, lyophilized, for solution	100 mg/10mL	Intravenous	Amgen Europe B.V.	2019-12-12	Not applicable
Flixabi	Injection, powder, for solution	100 mg	Intravenous	Samsung Bioepis Nl B.V.	2016-09-08	Not applicable
Flixabi	Injection, powder, for solution	100 mg	Intravenous	Samsung Bioepis Nl B.V.	2016-09-08	Not applicable
Flixabi	Injection, powder, for solution	100 mg	Intravenous	Samsung Bioepis Nl B.V.	2016-09-08	Not applicable

Chemical Identifiers

UNII: B72HH48FLU
CAS number: 170277-31-3

References

General References

Present DH, Rutgeerts P, Targan S, Hanauer SB, Mayer L, van Hogezand RA, Podolsky DK, Sands BE, Braakman T, DeWoody KL, Schaible TF, van Deventer SJ: Infliximab for the treatment of fistulas in patients with Crohn's disease. N Engl J Med. 1999 May 6;340(18):1398-405. [Article]
Sands BE, Anderson FH, Bernstein CN, Chey WY, Feagan BG, Fedorak RN, Kamm MA, Korzenik JR, Lashner BA, Onken JE, Rachmilewitz D, Rutgeerts P, Wild G, Wolf DC, Marsters PA, Travers SB, Blank MA, van Deventer SJ: Infliximab maintenance therapy for fistulizing Crohn's disease. N Engl J Med. 2004 Feb 26;350(9):876-85. [Article]
Klotz U, Teml A, Schwab M: Clinical pharmacokinetics and use of infliximab. Clin Pharmacokinet. 2007;46(8):645-60. doi: 10.2165/00003088-200746080-00002. [Article]
Keizer RJ, Huitema AD, Schellens JH, Beijnen JH: Clinical pharmacokinetics of therapeutic monoclonal antibodies. Clin Pharmacokinet. 2010 Aug;49(8):493-507. doi: 10.2165/11531280-000000000-00000. [Article]
Link [Link]
Link [Link]
FDA Label: INFLECTRA (infliximab-dyyb) for Injection, for Intravenous Use [Link]
FDA Label: IXIFI (infliximab-qbtx) for injection, for Intravenous Use [Link]
FDA Approved Drug Products: REMICADE (infliximab) injection [Link]

External Links

UniProt: P01857
Genbank: J00228
PubChem Substance: 46505602
RxNav: 1790539
ChEMBL: CHEMBL1201581
Therapeutic Targets Database: DAP000107
PharmGKB: PA452639
RxList: RxList Drug Page
Drugs.com: Drugs.com Drug Page
Wikipedia: Infliximab

FDA label

Download (1.21 MB)

MSDS

Download (39.6 KB)

Clinical Trials

Clinical Trials Clinical Trial & Rare Diseases Add-on Data Package Explore 4,000+ rare diseases, orphan drugs & condition pairs, clinical trial why stopped data, & more. Preview package

Phase	Status	Purpose	Conditions	Count	Start Date	Why Stopped	100+ additional columns
Unlock 175K+ rows when you subscribe.View sample data
Not Available	Active Not Recruiting	Not Available	Crohn's Disease (CD)	1	somestatus	stop reason	just information to hide
Not Available	Active Not Recruiting	Not Available	Crohn's Disease (CD) / Indeterminate Colitis / Inflammatory Bowel Diseases (IBD) / Ulcerative Colitis	1	somestatus	stop reason	just information to hide
Not Available	Active Not Recruiting	Not Available	Inflammatory Bowel Diseases (IBD)	1	somestatus	stop reason	just information to hide
Not Available	Active Not Recruiting	Not Available	Rheumatoid Arthritis	1	somestatus	stop reason	just information to hide
Not Available	Active Not Recruiting	Not Available	Ulcerative Colitis	1	somestatus	stop reason	just information to hide

Pharmacoeconomics

Manufacturers

J&J and Mitsubisi Tanabe

Packagers

Centocor Ortho Biotech Inc.
Hospira Inc.

Dosage Forms

Form	Route	Strength
Powder	Parenteral	100 MG
Injection, powder, for solution	Intravenous; Parenteral	100 MG
Injection, powder, lyophilized, for solution	Intravenous	100 mg/10mL
Injection, powder, lyophilized, for solution	Intravenous	100 mg
Powder		100 mg/1vial
Powder	Intravenous; Parenteral	100 MG
Powder, for solution	Intravenous	100 mg / vial
Injection, powder, for solution	Intravenous	100 mg
Injection, solution	Parenteral; Subcutaneous	120 MG
Injection, solution	Subcutaneous	120 mg
Injection, solution, concentrate	Intravenous	100 mg/1vial
Solution	Intravenous	100.000 mg
Injection	Intravenous	100 mg
Solution		120 mg
Solution	Subcutaneous	120 mg
Solution	Subcutaneous	12000000 mg
Kit; solution	Subcutaneous	120 mg / mL
Solution	Subcutaneous	120.00 mg
Injection, solution	Subcutaneous	120 mg/ml
Injection, powder, lyophilized, for suspension	Intravenous	100 mg
Injection, powder, lyophilized, for solution	Intravenous	100 mg/1
Injection, powder, for solution		100 mg
Injection	Subcutaneous	120 mg/1mL

Prices

Unit description	Cost	Unit
Remicade 100 mg Solution Vial	821.02USD	vial
Remicade 100 mg vial	789.44USD	vial

DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)	Region
CA2106299	No	2001-02-06	2012-03-18

Properties

State

Liquid

Experimental Properties

Property	Value	Source
melting point (°C)	61 °C (FAB fragment), 71 °C (whole mAb)	Vermeer, A.W.P. & Norde, W., Biophys. J. 78:394-404 (2000)
hydrophobicity	-0.441	Not Available
isoelectric point	8.25	Not Available

Targets

Build, predict & validate machine-learning models

Use our structured and evidence-based datasets to unlock new
insights and accelerate drug research.

Learn more

Use our structured and evidence-based datasets to unlock new insights and accelerate drug research.

Learn more

Details1. Tumor necrosis factor

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Inhibitor

General Function: Cytokine that binds to TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. It is mainly secreted by macrophages and can induce cell death of certain tumor cell lines. It is potent pyrogen causing fever by direct action or by stimulation of interleukin-1 secretion and is implicated in the induction of cachexia, Under certain conditions it can stimulate cell proliferation and induce cell differentiation. Impairs regulatory T-cells (Treg) function in individuals with rheumatoid arthritis via FOXP3 dephosphorylation. Up-regulates the expression of protein phosphatase 1 (PP1), which dephosphorylates the key 'Ser-418' residue of FOXP3, thereby inactivating FOXP3 and rendering Treg cells functionally defective (PubMed:23396208). Key mediator of cell death in the anticancer action of BCG-stimulated neutrophils in combination with DIABLO/SMAC mimetic in the RT4v6 bladder cancer cell line (PubMed:16829952, PubMed:22517918, PubMed:23396208). Induces insulin resistance in adipocytes via inhibition of insulin-induced IRS1 tyrosine phosphorylation and insulin-induced glucose uptake. Induces GKAP42 protein degradation in adipocytes which is partially responsible for TNF-induced insulin resistance (By similarity). Plays a role in angiogenesis by inducing VEGF production synergistically with IL1B and IL6 (PubMed:12794819). Promotes osteoclastogenesis and therefore mediates bone resorption (By similarity)
Specific Function: cytokine activity
Gene Name: TNF
Uniprot ID: P01375
Uniprot Name: Tumor necrosis factor
Molecular Weight: 25644.15 Da

References

Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [Article]
Mimura T: [Selection of one of the TNF blockers; infliximab and etanercept]. Nihon Rinsho. 2007 Jul;65(7):1282-6. [Article]
Braun J, Baraliakos X, Listing J, Sieper J: Decreased incidence of anterior uveitis in patients with ankylosing spondylitis treated with the anti-tumor necrosis factor agents infliximab and etanercept. Arthritis Rheum. 2005 Aug;52(8):2447-51. [Article]
Danese S, Sans M, Scaldaferri F, Sgambato A, Rutella S, Cittadini A, Pique JM, Panes J, Katz JA, Gasbarrini A, Fiocchi C: TNF-alpha blockade down-regulates the CD40/CD40L pathway in the mucosal microcirculation: a novel anti-inflammatory mechanism of infliximab in Crohn's disease. J Immunol. 2006 Feb 15;176(4):2617-24. [Article]
Magro F, Pereira P, Carneiro F, Veloso FT: Reactive hepatitis in a patient with Crohn's disease successfully treated with infliximab: does tumor necrosis factor alpha play a role in reactive hepatitis? Inflamm Bowel Dis. 2005 Jan;11(1):88-90. [Article]
Mori S, Imamura F, Kiyofuji C, Ito K, Koga Y, Honda I, Sugimoto M: Pneumocystis jiroveci pneumonia in a patient with rheumatoid arthritis as a complication of treatment with infliximab, anti-tumor necrosis factor alpha neutralizing antibody. Mod Rheumatol. 2006;16(1):58-62. [Article]
Maini RN, Feldmann M: How does infliximab work in rheumatoid arthritis? Arthritis Res. 2002;4 Suppl 2:S22-8. Epub 2002 Mar 27. [Article]
Sapienza MS, Cohen S, Dimarino AJ: Treatment of pyoderma gangrenosum with infliximab in Crohn's disease. Dig Dis Sci. 2004 Sep;49(9):1454-7. [Article]
Tobin AM, Kirby B: TNF alpha inhibitors in the treatment of psoriasis and psoriatic arthritis. BioDrugs. 2005;19(1):47-57. [Article]
Shen C, Assche GV, Colpaert S, Maerten P, Geboes K, Rutgeerts P, Ceuppens JL: Adalimumab induces apoptosis of human monocytes: a comparative study with infliximab and etanercept. Aliment Pharmacol Ther. 2005 Feb 1;21(3):251-8. [Article]
Popa C, Netea MG, Barrera P, Radstake TR, van Riel PL, Kullberg BJ, Van der Meer JW: Cytokine production of stimulated whole blood cultures in rheumatoid arthritis patients receiving short-term infliximab therapy. Cytokine. 2005 Apr 21;30(2):72-7. [Article]

Drug created at June 13, 2005 13:24 / Updated at August 02, 2024 07:21

Infliximab

Identification

Pharmacology

Interactions

Products

Categories

Chemical Identifiers

References

Clinical Trials

Clinical Trial & Rare Diseases Add-on Data Package

Pharmacoeconomics

Properties

Targets

References