Canakinumab for the treatment of active systemic juvenile idiopathic arthritis

Orrock, Janet E.; Ilowite, Norman T.

doi:10.1080/17512433.2016.1204910

Cited by 22 publications

(10 citation statements)

References 23 publications

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“…This drug, with anti-inflammatory and immunosuppressive functions, also has important collateral effects, especially in pediatric age since it blocks growth, delays bone development, and causes weight gain and mood instability. Therefore, the identification of cytokines as therapeutic targets has great relevance: examples of this are canakinumab and anakinra, inhibitors of soluble IL-1β and its receptor, respectively; infliximab and certolizumab, which bind TNF-α; tocilizumab, which blocks IL-6 ( Table 1 ) [ 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 , 99 , 100 , 101 , 102 , 103 , 104 , 105 , 106 , 107 , 108 , 109 , 110 , 111 , 112 , 113 , 114 , 115 , 116 , 117 , …”

Section: Autoinflammatory Disease: Since the Beginning Of ’90s A New Branch Of Medicinementioning

confidence: 99%

Autoinflammatory Diseases and Cytokine Storms—Imbalances of Innate and Adaptative Immunity

Marcuzzi

Melloni

Zauli

et al. 2021

IJMS

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Innate and adaptive immune responses have a well-known link and represent the distinctive origins of several diseases, many of which may be the consequence of the loss of balance between these two responses. Indeed, autoinflammation and autoimmunity represent the two extremes of a continuous spectrum of pathologic conditions with numerous overlaps in different pathologies. A common characteristic of these dysregulations is represented by hyperinflammation, which is an exaggerated response of the immune system, especially involving white blood cells, macrophages, and inflammasome activation with the hyperproduction of cytokines in response to various triggering stimuli. Moreover, hyperinflammation is of great interest, as it is one of the main manifestations of COVID-19 infection, and the cytokine storm and its most important components are the targets of the pharmacological treatments used to combat COVID-19 damage. In this context, the purpose of our review is to provide a focus on the pathogenesis of autoinflammation and, in particular, of hyperinflammation in order to generate insights for the identification of new therapeutic targets and strategies.

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Section: Autoinflammatory Disease: Since the Beginning Of ’90s A New Branch Of Medicinementioning

confidence: 99%

Autoinflammatory Diseases and Cytokine Storms—Imbalances of Innate and Adaptative Immunity

Marcuzzi

Melloni

Zauli

et al. 2021

IJMS

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“…Canakinumab is a human monoclonal antibody against IL-1β that was first approved by the FDA in 2009 for the treatment of cryopyrin-associated periodic syndromes (CAPS), and, subsequently, it was approved for the treatment of SJIA and JIA in 2013 [148,149]. Canakinumab inhibits IL-1β by directly binding and neutralizing IL-1β signaling.…”

Section: Canakinumabmentioning

confidence: 99%

Biological Therapies that Target Inflammatory Cytokines to Treat Uveitis

Reddy¹,

Muhammad²,

Lee³

2019

Advances in the Diagnosis and Management of Uveitis

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Uveitis is a leading cause of blindness that presents a considerable challenge given that our understanding of the mechanisms of disease is still evolving. Both innate and adaptive immunity play a role in disease and mediators of these responses can serve as therapeutic targets. TNF-α and IL-1β inflammatory cytokines are central mediators of immunity and are involved in the dysregulated inflammatory response during uveitis. Because toxicity limits the use of steroids and other steroid-sparing agents, biologics that target a specific cell type or pathway are being explored for the treatment of autoimmune uveitis. This chapter begins with a broad overview of the aberrant immune response resulting in uveitis, and highlights key mediators such as TNF-α, IL-1β, IL-6, and IL-17 and their potential use as therapeutic targets. Most biological agents discussed in this review have not been FDAapproved for uveitis. However, favorable outcomes in early trials and FDA approval of these drugs for the treatment of other autoimmune diseases associated with uveitis support the potential for these biological agents in the management of uveitis. This review aims to provide an updated report on the efficacy of biologics that target TNF-α, IL-1β, IL-6, and IL-17 for the treatment of autoimmune uveitis.

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“…The IL‐1 family represents another potential therapeutic target, and there are a number of IL‐1 inhibitors currently on the market or in development. A couple of these (rilonacept and canakinumab) are used for a group of rare, inherited auto‐inflammatory diseases in which IL‐1β is overproduced . Anakinra, however, is a recombinant IL‐1 receptor antagonist that competitively inhibits IL‐1, specifically IL‐1α and IL‐1β, and is used for the treatment of rheumatoid arthritis (RA) in patients who have failed one or more disease modifying antirheumatic drugs (DMARDs) …”

Section: Current Drug Targetsmentioning

confidence: 99%

“…A couple of these (rilonacept and canakinumab) are used for a group of rare, inherited auto-inflammatory diseases in which IL-1b is overproduced. [33,34] Anakinra, however, is a recombinant IL-1 receptor antagonist that competitively inhibits IL-1, specifically IL-1a and IL-1b, and is used for the treatment of rheumatoid arthritis (RA) in patients who have failed one or more disease modifying antirheumatic drugs (DMARDs). [35] In addition to IL-1 and TNF-a, IL-6 which is released by T cells and macrophages in response to infection and trauma often contributes to the pathophysiology of inflammatory diseases such as RA.…”

Section: Non-tnf Cytokine Targetsmentioning

confidence: 99%

Current and novel anti-inflammatory drug targets for inhibition of cytokines and leucocyte recruitment in rheumatic diseases

Szollosi

Manzoor

Aquilato

et al. 2018

Journal of Pharmacy and Pharmacology

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Objectives Many studies of disease state mechanisms reveal that unbridled inflammation is to blame for many of the symptoms associated with autoimmune diseases such as Crohn’s and Rheumatoid Arthritis (RA). While therapies aimed at decreasing levels of pro‐inflammatory cytokines exist, some have failed clinically or have extensive adverse effects. The aim of this review is to discuss common drug targets for anti‐inflammatory therapies as well as explore potential mechanisms of action for new therapies. Various studies done on novel mechanisms targeting pro‐inflammatory cytokine release as well as leukocyte chemotaxis have been researched for discussion here. Both of these contribute to tissue injury and patient symptoms in inflammatory and autoimmune disease states. Key findings While many current drug targets suppress inflammation via the receptor, research aimed at identifying new compounds and signaling mechanisms is ongoing to identify new targets within pro‐inflammatory signaling pathways, or specific immune cell types. Conclusions While glucocorticoids and monoclonal antibodies have shown to be efficacious, some patients have encountered mixed results. Biologic therapies also come with a high price tag Thus, novel compounds with new immune drug targets are ideal for patients whose therapies have not been successful.

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Canakinumab for the treatment of active systemic juvenile idiopathic arthritis

Cited by 22 publications

References 23 publications

Autoinflammatory Diseases and Cytokine Storms—Imbalances of Innate and Adaptative Immunity

Autoinflammatory Diseases and Cytokine Storms—Imbalances of Innate and Adaptative Immunity

Biological Therapies that Target Inflammatory Cytokines to Treat Uveitis

Current and novel anti-inflammatory drug targets for inhibition of cytokines and leucocyte recruitment in rheumatic diseases

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