Therapeutic TNF-α-antibody from the original Humira® commercial drug targeting the TNF-α-antigen, also referred to as Humira® or adalimumab 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.
What our clients say
”Evidentic can supply different batches of reference products for precilinical research.The quick access to the on-stock batches allows for adhoc ordering, keeps costs down and makes a headstart possible!”
“Evidentic is a new source of cost-efficient therapeutic mAbs for our immonassays. And easy to order!”
“We develop innovative and biosimilar mAbs for a global market. Evidentic’s aRMPs are a great source of cost-efficient reference products for our research and development program.”
“Evidentic gives rapid access to originator biologics and different batches. For biosimilar developers and regulators, it will shorten the time to gauge the analytical acceptance range for multiple CQAs of biotherapeutics.”
Adalimumab / Humira
|API type||Adalimumab is a recombinant human monoclonal antibody expressed in Chinese Hamster Ovary cells.|
|Pharmacotherapeutic group||Immunosuppressants, Tumour Necrosis Factor alpha (TNF-α) inhibitors.
|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||Adalimumab binds specifically to TNF and neutralizes the biological function of TNF by blocking its
interaction with the p55 and p75 cell surface TNF receptors.
Adalimumab also modulates biological responses that are induced or regulated by TNF, including
changes in the levels of adhesion molecules responsible for leukocyte migration (ELAM-1, VCAM-1,
and ICAM-1 with an IC50 of0.1-0.2 nM).
(Mechanism of action; Source EMA document)
|Adalimumab binds specifically to TNF and neutralizes the biological function of TNF by blocking its interaction with the p55 and p75 cell surface TNF receptors.
Adalimumab also modulates biological responses that are induced or regulated by TNF, including changes in the levels of adhesion molecules responsible for leukocyte migration (ELAM-1, VCAM-1, and ICAM-1 with an IC50 of0.1-0.2 nM).
|Pharmacodynamic properties (Pharmacodynamic effects; Source EMA document)||After treatment with Humira, a rapid decrease in levels of acute phase reactants of inflammation (C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR)) and serum cytokines (IL-6) was observed, compared to baseline in patients with rheumatoid arthritis. Serum levels of matrix metalloproteinases (MMP-1 and MMP-3) that produce tissue remodelling responsible for cartilage destruction were also decreased after Humira administration. Patients treated with Humira usually experienced improvement in haematological signs of chronic inflammation.
A rapid decrease in CRP levels was also observed in patients with polyarticular juvenile idiopathic arthritis, Crohn's disease, ulcerative colitis and hidradenitis suppurativa after treatment with Humira. In patients with Crohn’s disease, a reduction of the number of cells expressing inflammatory markers in the colon including a significant reduction of expression of TNFα was seen. Endoscopic studies in intestinal mucosa have shown evidence of mucosal healing in adalimumab treated patients.
|Original license holder|
|Marketing authorisation numbers||EU/1/03/256/001 - 015
|Marketing authorisation holder||AbbVie Ltd
|Name of the manufacturer of the biological active substance|
|Name and address of the manufacturer(s) responsible for batch release|
|Max shelf life||24 months
|Storage conditions||2°C – 8°C
|List of excipients||Mannitol
Citric acid monohydrate
Sodium dihydrogen phosphate dihydrate
Disodium phosphate dihydrate
Water for injections