Adalimumab is a subcutaneously administered organic ailment modifier for the remedy of rheumatoid arthritis and different continual debilitating diseases mediated by means of tumor necrosis thing [A39984], [A39999]. It turned into at the start launched by means of Abbvie within the U.S. and approved in 2002 by the FDA [A39983]. This drug is regularly known as _Humira_. it is produced through recombinant DNA generation the use of a mammalian cell expression machine. This drug is to be had in a prefilled syringe shape and convenient pen shape for subcutaneous self-administered doses [A39983]. a new biosimilar to adalimumab, named _adalimumab-adaz_, became authorized by the FDA on October 31, 2018. This biosimilar is known as _Hyrimoz_, and is a trademark of Novartis AG [L4799].
After treatment with adalimumab, a decrease in levels of acute phase reactant proteins of inflammation (CÂ reactive protein [CRP] and erythrocyte sedimentation rate [ESR]) 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 Crohnâ€™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 [F2118], [FDA label]. 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 [A39983], [A39999], [FDA label].
The following are conditions for which adalimumab has been indicated [F2118], [FDA label], [L4805], [A40001], [A40002], [L4806]. Rheumatoid Arthritis (Moderate to Severe) Juvenile Idiopathic Arthritis (Moderately to Severely Active) Psoriatic Arthritis (Active) Ankylosing Spondylitis (Active) Crohnâ€™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)
Adalimumab binds with specificity to tumor necrosis factor-alpha (TNF-alpha) [A39984], [A39999] 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 [A39999]. 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) [F2118].