Repositioning Candidate Details

Candidate ID: R0017
Source ID: DB00051
Source Type: approved; experimental
Compound Type: biotech
Compound Name: Adalimumab
Synonyms: Adalimumab; Adalimumab (genetical recombination); adalimumab-adaz; adalimumab-adbm; adalimumab-afzb; adalimumab-atto; adalimumab-bwwd; adalimumab-fkjp
Molecular Formula: --
SMILES: --
DrugBank Description: Adalimumab is a subcutaneously administered biological disease modifier for the treatment of rheumatoid arthritis and other chronic debilitating diseases mediated by tumor necrosis factor , . It was originally launched by Abbvie in the U.S. and approved in 2002 by the FDA . This drug is frequently known as _Humira_. It is produced by recombinant DNA technology using a mammalian cell expression system. This drug is available in a prefilled syringe form and convenient pen form for subcutaneous self-administered doses . A new biosimilar to adalimumab, named _adalimumab-adaz_, was approved by the FDA on October 31, 2018. This biosimilar is known as _Hyrimoz_, and is a trademark of Novartis AG .
CAS Number: 331731-18-1
Molecular Weight:
DrugBank Indication: The following are conditions for which adalimumab has been indicated , , , , , . Rheumatoid Arthritis (Moderate to Severe) Juvenile Idiopathic Arthritis (Moderately to Severely Active) Psoriatic Arthritis (Active) Ankylosing Spondylitis (Active) Crohn’s Disease (Moderately to Severely Active) Ulcerative Colitis (Moderately to Severely Active) Plaque Psoriasis (Moderate to Severe Chronic) Non-infectious Intermediate, Posterior and Panuveitis Hidradenitis Suppurativa (Moderate to Severe) Pyoderma Gangrenosum (off-label)
DrugBank Pharmacology: After treatment with adalimumab, a decrease in levels of acute phase reactant proteins of inflammation (C­ reactive protein and erythrocyte sedimentation rate ) and serum cytokines (IL-6) was measured compared to baseline in patients diagnosed with rheumatoid arthritis. A decrease in CRP levels was also observed in patients diagnosed with Crohn’s disease. Serum levels of matrix metalloproteinases (MMP-1 and MMP-3) that lead to the tissue remodeling responsible for cartilage destruction were also found to be decreased after administration of adalimumab , . A reduction in signs and symptoms of disease, the induction of a clinical response, an inhibition of structural damage, and improvements in physical function in adult and pediatric patients with various inflammatory conditions have been demonstrated , , .
DrugBank MoA: Adalimumab binds with specificity to tumor necrosis factor-alpha (TNF-alpha) , and inhibits its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface tumor necrosis factor expressing cells in vitro when in the presence of complement. Adalimumab does not bind or inactivate lymphotoxin (Tumor necrosis factor-beta). TNF is a naturally occurring cytokine that plays a role in normal inflammatory and immune responses . Increased levels of TNF are found in the joint synovial fluid of rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis patients, and play an imperative role in pathologic inflammation and the joint destruction that are major complications of these diseases. Increased levels of TNF are also measured in psoriasis plaques. In plaque psoriasis, treatment with adalimumab may decrease the epidermal thickness and inflammatory cell infiltration. The relationship between these pharmacodynamics and the mechanism(s) by which adalimumab achieves its clinical effects is not known. Additionally, adalimumab alters biological responses that are induced/regulated by TNF, including changes in the levels of adhesion molecules responsible for leukocyte migration during inflammation (ELAM-1, VCAM-1, and ICAM-1 with an IC50 of 1-2 X 10-10M) .
Targets: Tumor necrosis factor antibody
Inclusion Criteria: Therapeutic strategy associated