Briakinumab for Treatment of Crohnʼs Disease

Panaccione, Remo; Sandborn, William J.; Gordon, Glenn; Lee, Scott D.; Safdi, Alan; Sedghi, Shahriar; Feagan, Brian G.; Hanauer, Stephen B.; Reinisch, Walter; Valentine, John F.; Huang, Bidan; Carcereri, Roberto

doi:10.1097/mib.0000000000000366

Cited by 53 publications

(50 citation statements)

References 22 publications

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“…Ustekinumab significantly increased the rates of response and remission as maintenance therapy, and it may be particularly useful in patients who previously did not respond to anti-TNF therapy [266]. Briakinumab, however, in patients with moderate to severe CD was not effective for the induction or maintenance of remission ( [267].…”

Section: Inhibition Of Il-12 and Il-23mentioning

confidence: 99%

Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

Gyires¹,

Tóth²,

Zádori

2014

CPD

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Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory condition of the gastrointestinal tract. The two main forms of IBD are Crohn's disease and ulcerative colitis. According to the recent concept the disease is caused by a combination of factors, including genetics, immune dysregulation, barrier dysfunction and the change in microbial flora. Environmental factors, such as changes in diet, antibiotic use, smoking or improved domestic hygiene (e.g. eradication of intestinal helminths) probably contribute to the development and increased prevalence of IBD. Dysregulation of mucosal immunity in IBD causes an overproduction of inflammatory cytokines which resulted in uncontrolled intestinal inflammation. Based on extensive research over the last decade, besides the conventional therapy, there are several novel pathways and specific targets, on which focus new therapeutics. New therapeutics aim 1./ to correct genetic susceptibility by stimulating NOD2 expression, TLR3 signaling or inhibition of TLR4 pathway, 2./ to restore the immune dysregulation by inhibition of pro-inflammatory cytokines (TNF-, IL-6, IL-13, IL-17, IL-18, IL-21), Th1 polarisation (IL-2, IL-12, IL-23, IFN-), T-cell activation, leukocyte adhesion, as well as by immunostimulation (GM-CSF, G-CSF) and anti-inflammatory cytokines (IL-10, IL-11, IFN--1a), 3./ to restore mucosal barrier function and stimulate mucosal healing by different growth factors, such as GH, EGF, KGF, TGF-, VEGF, 4./ to restore the normal bacterial flora by antibiotics, probiotics. However, in spite of these numerous potential targets, the true value and clinical significance of most of the new biologics and molecules are not clear yet.

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Section: Inhibition Of Il-12 and Il-23mentioning

confidence: 99%

Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

Gyires¹,

Tóth²,

Zádori

2014

CPD

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“…However, it may become an alternative in patients not responding to anti-TNF therapy [42]. This is also supported by the fact that other antibodies against IL-23 such as briakinumab did not achieve significant differences to placebo in phase II trials in CD patient [43,44]. In contrast to the limited efficacy of anti-IL23 antibodies therapeutic antibodies directed against IL-17 have failed in clinical trials in CD.…”

Section: Antibodies Directed Against Cytokinesmentioning

confidence: 89%

Where are we heading to in pharmacological IBD therapy?

Rogler

2015

Pharmacological Research

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“…New inhibitors of interleukin 23 (IL-23; eg, risankizumab) and IL-12/IL-23 (eg, briakinumab) are currently under development. 240 However, one IL-12/IL-23 inhibitor, ustekinumab, which is used in the management of psoriasis and psoriatic arthritis, 241 was FDA approved for the treatment of Crohn's disease in September 2016. 242 Response and remission rates on ustekinumab were significantly superior to placebo in phase II and phase III studies, in patients who had not responded to anti-TNF agents and anti-TNF naive patients.…”

Section: Malignancy and Infectionmentioning

confidence: 99%

Update on anti-tumor necrosis factor agents and other new drugs for inflammatory bowel disease

Cohen

Sachar

2017

BMJ

115

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The treatment of inflammatory bowel disease (IBD)-ulcerative colitis (UC) and Crohn's disease (CD)-has evolved beyond surgery with the introduction of biologic agents, primarily antibodies against mediators of inflammation and cell attraction. Anti-tumor necrosis factor (TNF) agents have been the first line treatment for moderate to severe ulcerative colitis and Crohn's disease for more than 15 years. During that time much has been learnt about how best to use these agents. This review will assess the evidence on how to optimize the use of anti-TNF agents; when and how to start treatment; how to monitor treatment and when to de-escalate it; and the potential adverse effects of these drugs. New and emerging treatments such as anti-attractants, anti-interleukins, and Janus kinase (JAK) inhibitors will also be discussed.

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Briakinumab for Treatment of Crohnʼs Disease

Abstract: Article first published online 29 April 2015.

Cited by 53 publications

References 22 publications

Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

Where are we heading to in pharmacological IBD therapy?

Update on anti-tumor necrosis factor agents and other new drugs for inflammatory bowel disease

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