First time available for research use

TNF-α-antibody

Infliximab antibody from Remicade®

Therapeutic TNF-α-antibody from the original Remicade® commercial drug targeting the TNF-α-antigen, also referred to as Remicade® or infliximab antibody. Research-relevant quantities are available as licence-free consumable in aliquoted or diluted variant. Therapeutic monoclonal antibodies can be used from researchers in in vitro and in vivo experiments, biosimilar developers can order different batches at the same time.

Choose your antibody
tnf-α-antibody-infliximab
Easy Access

Easy Access

Easy to order as license-free research consumable
Multiple batches

Multiple batches

Up to 10 batches of original drugs for examining batch-to-batch variations
Reduce costs

Reduce costs

Up to 80% less compared to the original pharmaceutical price
Prompt delivery

Prompt delivery

Shipment within days worldwide according to GDP-standards
Documented origin

Documented origin

Information on batch, registration number, expiry date, GDP-compliant pedigree

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Infliximab / Remicade

Product Reference

Drug nameRemicade®
INNInfliximab
API typeInfliximab is a chimeric human-murine IgG1 monoclonal antibody produced in murine hybridoma cells by recombinant DNA technology. After reconstitution each ml contains 10 mg of infliximab.
Pharmacotherapeutic group
tumour necrosis factor alpha (TNFα) inhibitors
ATC code
L04AB02
Target of antibody
TNF-α; Synonyms: DIF, TNF-alpha, TNFA, TNFSF2, RATTNF, Tnfa, tnf, TNF-a, TNFalpha, Tnfsf1a, TNFa, cTNF, Tnf-alpha, tnfa-like, TNF-ALPHA, dif, tnfa, xtnf, tnfsf2, tnf-alpha, Cachectin
General function
Short description
Pharmacodynamic properties
(Mechanism of action; Source EMA document)
Infliximab is a chimeric human-murine monoclonal antibody that binds with high affinity to both soluble and transmembrane forms of TNFα but not to lymphotoxin α (TNFß).
Pharmacodynamic properties (Pharmacodynamic effects; Source EMA document)Infliximab inhibits the functional activity of TNFα in a wide variety of in vitro bioassays. Infliximab prevented disease in transgenic mice that develop polyarthritis as a result of constitutive expression of human TNFα and when administered after disease onset, it allowed eroded joints to heal. In vivo, infliximab rapidly forms stable complexes with human TNFα, a process that parallels the loss of TNFα bioactivity.
Elevated concentrations of TNFα have been found in the joints of rheumatoid arthritis patients and correlate with elevated disease activity. In rheumatoid arthritis, treatment with infliximab reduced infiltration of inflammatory cells into inflamed areas of the joint as well as expression of molecules mediating cellular adhesion, chemoattraction and tissue degradation. After infliximab treatment, patients exhibited decreased levels of serum interleukin 6 (IL-6) and C-reactive protein (CRP), and increased haemoglobin levels in rheumatoid arthritis patients with reduced haemoglobin levels, compared with baseline. Peripheral blood lymphocytes further showed no significant decrease in number or in proliferative responses to in vitro mitogenic stimulation when compared with untreated patients’ cells. In psoriasis patients, treatment with infliximab resulted in decreases in epidermal inflammation and normalization of keratinocyte differentiation in psoriatic plaques. In psoriatic arthritis, short term treatment with Remicade reduced the number of T-cells and blood vessels in the synovium and psoriatic skin.
Histological evaluation of colonic biopsies, obtained before and 4 weeks after administration of infliximab, revealed a substantial reduction in detectable TNFα. Infliximab treatment of Crohn’s disease patients was also associated with a substantial reduction of the commonly elevated serum inflammatory marker, CRP. Total peripheral white blood cell counts were minimally affected in infliximab-treated patients, although changes in lymphocytes, monocytes and neutrophils reflected shifts towards normal ranges. Peripheral blood mononuclear cells (PBMC) from infliximab-treated patients showed undiminished proliferative responsiveness to stimuli compared with untreated patients, and no substantial changes in cytokine production by stimulated PBMC were observed following treatment with infliximab. Analysis of lamina propria mononuclear cells obtained by biopsy of the intestinal mucosa showed that infliximab treatment caused a reduction in the number of cells capable of expressing TNFα and interferonγ. Additional histological studies provided evidence that treatment with infliximab reduces the infiltration of inflammatory cells into affected areas of the intestine and the presence of inflammation markers at these sites. Endoscopic studies of intestinal mucosa have shown evidence of mucosal healing in infliximab-treated patients.
Original license holder
Marketing authorisation numbers
EU/1/99/116/001 - 005
Marketing authorisation holder
Janssen Biologics B.V.
Einsteinweg 101
2333 CB Leiden
The Netherlands
Name of the manufacturer of the biological active substance
Janssen Biologics B.V.
Einsteinweg 101
2333 CB Leiden
The Netherlands

Janssen Biotech Inc.
200 Great Valley Parkway Malvern
Pennsylvania 19355-1307, United States of America
Name and address of the manufacturer(s) responsible for batch releaseJanssen Biologics B.V.
Einsteinweg 101
2333 CB Leiden
The Netherlands
Max shelf life
36 months
Storage conditions
2°C – 8°C
List of excipients
Sucrose
Polysorbate
80
Monobasic sodium phosphate
Dibasic sodium phosphate