In vitro: Adalimumab blocks the interaction of TNF with the p55 and p75 cell surface TNF receptors, thereby neutralising the activity of this cytokine. Through its anti-TNF actions, adalimumab reduces concentrations of matrix metalloproteases (MMP-1 and -3) and other markers of cartilage and synovium turnover, reduces of matrix metalloproteases (MMP-1 and -3) and other markers of cartilage and synovium turnover, and reduces concentrations of acute phase reactants of inflammation (C-reactive protein [CRP] and erythrocyte sedimentation rate [ESR]) and serum cytokines (IL-1β mRNA, IL-1 receptor antagonist, IL-6).
In vivo: Adalimumab is safe and well tolerated. In healthy adults, the average absolute bioavailability of adalimumab 40 mg administered subcutaneously (s.c.) is 64%. Concentrations in the synovial fluid are 31-96% of those of the serum. Maximum plasma concentrations occur at 131 (± 56) h, and the mean half-life is ∼ 2 weeks (range, 10-20 days). Adalimumab treatment attenuates the Ovalbumin(OVA)-induced increase in serum IgE, TH2 and TH1 derived inflammatory cytokines (IL-4 and IFN-γ, respectively) in bronchoalveolar lavage (BAL) fluid, suppresses recruitment of inflammatory cells in BAL fluid and lung, and inhibits BAL fluid neutrophilia. It also ameliorates goblet cell metaplasia and bronchial fibrosis.
|Cell lines||Caco-2 BBE cells|
|Preparation method||T-84 and Caco-2 cells grown on transwell inserts were primed with IFN-γ (2.5 and 5 ng/ml, respectively) for 24 h followed by treatment with TNF-α (5 ng/ml), adalimumab (10 μg/ ml), or both.|
|Concentrations||10 μg/ ml|
|Incubation time||24 h|
|Animal models||CD1 mice|
|Dosages||1 ml/100 g b.wt|
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.
Rapid deterioration in a patient with primary aggressive cutaneous epidermotropic CD8+ cytotoxic T-cell ('Berti') lymphoma after administration of adalimumab.
Jacks SM, et al. J Am Acad Dermatol. 2014 Sep;71(3):e86-7. PMID: 25128139.
Adalimumab prevents barrier dysfunction and antagonizes distinct effects of TNF-α on tight junction proteins and signaling pathways in intestinal epithelial cells.
Fischer A, et al. Am J Physiol Gastrointest Liver Physiol. 2013 Jun 1;304(11):G970-9. PMID: 23538493.
|Related TNF-alpha Products|
Lenalidomide (Revlimid, CC-5013) is a TNF-α secretion inhibitor with IC50 of 13 nM.
Acetylcysteine(N-acetyl-l-cysteine) is a ROS(reactive oxygen species) inhibitor that antagonizes the activity of proteasome inhibitors. It is also a tumor necrosis factor production inhibitor.
Bioymifi, a small-molecule death receptor 5 (DR5) agonist, binds to the extracellular domain(ECD) of DR5 with a Kd of 1.2 μM but showed little binding affinity to the DR4 ECD. It induces DR5 clustering and aggregation, leading to apoptosis.
GSK481 is a highly potent and monoselective Receptor Interacting Protein 1 kinase inhibitor.
Necrostatin-1 is a specific RIP1 inhibitor and inhibits TNF-α-induced necroptosis with EC50 of 490 nM.
Products are for research use only. Not for human use. We do not sell to patients.
© Copyright 2010-2017 AbMole BioScience. All Rights Reserved.