Accession Number
DB00065 / B72HH48FLU

Infliximab is a tumor necrosis aspect (TNF-alpha or TNF-α) blocker and a chimeric monoclonal IgG1 antibody composed of human steady (seventy five%) and murine variable (25%) areas [A31469]. Infliximab is produced by using a recombinant cellular line cultured through continuous perfusion. Tumor necrosis component-alpha (TNF-α) is a key proinflammatory cytokine worried in persistent inflammatory illnesses [A31469]. Its hyperactivity and greater signalling pathways may be found in inflammatory sicknesses wherein it activates similarly seasoned-inflammatory cascades. via binding to both the soluble subunit and the membrane-sure precursor of TNF-α [A106], infliximab disrupts the interplay of TNF-α with its receptors and can additionally reason lysis of cells that produce TNF-α [A106]. Infliximab become first permitted by the FDA in 1998 below the market call Remicade as an intravenous injection. it's far indicated for the remedy of numerous inflammatory issues such as person or pediatric Chron's sickness, adult or pediatric ulcerative colitis, rheumatoid arthritis in aggregate with methotrexate, ankylosing spondyliti, psoriatic arthritis, and plaque psoriasis [FDA Label]. In medical trials, multiple infusions of infliximab displayed in a reduction of signs and signs of inflammatory illnesses and induction of remission in patients who've had an inadequate reaction to alternative first-line healing procedures for that disease [ FDA Label]. There are currently two biosilimars of infliximab to be had within the US marketplace that show a excessive diploma of similarity to the reference product, Remicade. they may be accepted for all eligible indicators of the reference product. Inflectra, a primary biosimilar drug product, become authorized in 2016. In December 2017, Ixifi, a 2d biosimilar that changed into developed by way of Pfizer, become granted approval via the FDA.



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} [FDA Label].


* 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.


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-α (lymphotoxin-α), a related cytokine that utilizes the same receptors as TNF-α [FDA 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 [A31469]. Its inhibitory actions on TNF-α was demonstrated in human fibroblasts, endothelial cells, neutrophils, B and Tlymphocytes and epithelial cells [FDA 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 [FDA Label].