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Infliximab vs. Other Biologics: A Comparative Study in Autoimmune Treatment
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Journal of Inflammatory Bowel Diseases & Disorders

ISSN: 2476-1958

Open Access

Commentary - (2024) Volume 9, Issue 3

Infliximab vs. Other Biologics: A Comparative Study in Autoimmune Treatment

Feira Nishee*
*Correspondence: Feira Nishee, Department of Public Health, School of Health Sciences, University of Brasília, Brasília, Brazil, Email:
Department of Public Health, School of Health Sciences, University of Brasília, Brasília, Brazil

Received: 01-Aug-2024, Manuscript No. jibdd-24-153445; Editor assigned: 03-Aug-2024, Pre QC No. P-153445; Reviewed: 17-Aug-2024, QC No. Q-153445; Revised: 23-Aug-2024, Manuscript No. R-153445; Published: 30-Aug-2024 , DOI: 10.37421/2476-1958.2024.9.221
Citation: Nishee, Feira. “Infliximab vs. Other Biologics: A Comparative Study in Autoimmune Treatment.” J Inflamm Bowel Dis 9 (2024): 221.
Copyright: © 2024 Nishee F. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Introduction

Autoimmune diseases, such as Rheumatoid Arthritis (RA), Crohn’s disease, psoriatic arthritis, and Inflammatory Bowel Disease (IBD), represent a diverse group of disorders in which the immune system mistakenly attacks the body’s tissues, leading to chronic inflammation, tissue damage, and a reduction in quality of life. Over the past few decades, biologic therapies, which specifically target immune system components involved in inflammation, have revolutionized the management of autoimmune diseases. Among these biologics, Infliximab stands out as one of the first Tumor Necrosis Factor-Alpha (TNF-α) inhibitors developed to treat inflammatory conditions. Infliximab has been widely used in clinical practice for over two decades, demonstrating substantial efficacy in reducing disease activity and preventing tissue damage in conditions like rheumatoid arthritis, Crohn’s disease, and psoriasis. However, other biologic agents, such as adalimumab, etanercept, and newer therapies like IL-6 inhibitors (tocilizumab) and JAK inhibitors (tofacitinib), have since emerged, offering additional options for patients who either fail to respond to infliximab or experience adverse effects [1].

This article aims to compare Infliximab with other biologics in the treatment of autoimmune diseases, analyzing their mechanisms of action, clinical efficacy, safety profiles, and patient outcomes. By examining the strengths and limitations of these treatments, this study seeks to provide a comprehensive overview to guide clinicians in choosing the most appropriate biologic therapy for their patients.

Description

Infliximab is a chimeric monoclonal antibody that targets TNF-α, a pro-inflammatory cytokine involved in the pathogenesis of many autoimmune diseases. TNF-α plays a central role in promoting inflammation, immune cell activation, and tissue damage in diseases like rheumatoid arthritis and inflammatory bowel disease. By binding to TNF-α, infliximab neutralizes its activity and prevents it from interacting with its receptors (TNFR1 and TNFR2), thus reducing downstream inflammatory signaling. Clinically, infliximab has proven effective in treating a variety of autoimmune diseases, especially in patients with moderate to severe disease or those who have not responded adequately to conventional therapies. In rheumatoid arthritis, infliximab has been shown to reduce disease activity, prevent joint damage, and improve physical function. In Crohn’s disease and ulcerative colitis, infliximab is used to reduce inflammation in the gastrointestinal tract, induce remission, and promote mucosal healing. Psoriasis patients also experience significant improvements, with infliximab reducing the severity of skin lesions and inflammation [2].

Infliximab is typically administered intravenously, which requires a healthcare setting for infusion. The drug's infusion-based administration and relatively short half-life (requiring repeated infusions) may be seen as limitations for some patients. Adalimumab is another TNF-α inhibitor that is structurally similar to infliximab but is a fully human monoclonal antibody. Adalimumab also works by binding to TNF-α and preventing its interaction with its receptors. The major difference between infliximab and adalimumab lies in their administration routes—while infliximab is given via intravenous infusion, adalimumab is administered subcutaneously, typically by the patient themselves at home. This self-administration convenience makes adalimumab a more attractive option for some patients who prefer to avoid clinic visits for infusions. Both infliximab and adalimumab show similar efficacy in conditions such as rheumatoid arthritis, Crohn's disease, and psoriasis. However, studies have indicated that while the efficacy profiles of the two drugs are comparable, adalimumab might offer a slightly faster onset of action due to its higher bioavailability after subcutaneous injection [3].

Etanercept is another biologic therapy that targets TNF-α but differs from infliximab and adalimumab in its mechanism. Etanercept is a fusion protein composed of two soluble TNF Receptor (TNFR) molecules linked to the Fc portion of human IgG. It binds to TNF-α and prevents its interaction with the cell surface receptors. Unlike infliximab and adalimumab, which directly neutralize TNF-α, etanercept essentially acts as a decoy receptor for the cytokine. Etanercept has been effective in the treatment of rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. While it offers similar efficacy to infliximab in reducing symptoms of these diseases, its subcutaneous administration may be more convenient for patients. However, compared to infliximab, etanercept may be less effective for patients with Crohn’s disease or other IBD conditions, as it has shown lower efficacy in these disorders [4].

Tocilizumab is a biologic agent that targets interleukin-6 (IL-6), another pro-inflammatory cytokine involved in autoimmune diseases. IL-6 is involved in the acute-phase response and has been implicated in conditions such as rheumatoid arthritis, juvenile idiopathic arthritis, and giant cell arteritis [2]. Unlike TNF-α inhibitors, tocilizumab blocks the IL-6 receptor and inhibits IL-6 signaling, thus reducing inflammation and immune cell activation. Tocilizumab has demonstrated significant efficacy in treating rheumatoid arthritis, with several studies showing it to be comparable or even superior to TNF-α inhibitors in terms of disease control and symptom improvement, especially in patients with high disease activity. It is also given as an intravenous infusion or subcutaneously, depending on the formulation. While it is effective for many autoimmune conditions, the side effect profile of tocilizumab differs from that of TNF-α inhibitors, with higher risks for elevated liver enzymes, lipid abnormalities, and serious infections.

Janus Kinase (JAK) inhibitors are an emerging class of drugs that target intracellular signaling pathways involved in the immune response. JAK inhibitors, such as tofacitinib, work by blocking the activity of JAK enzymes, which are involved in the signaling of several cytokines, including IL-6, IL-2, and TNF-α. By inhibiting JAK, these drugs disrupt the signaling of multiple pro-inflammatory pathways and have been shown to be effective in treating rheumatoid arthritis, psoriatic arthritis, and ulcerative colitis. JAK inhibitors are orally administered, which is a significant advantage over infusion-based therapies like infliximab and tocilizumab [5]. However, they come with a risk of hematologic toxicities, increased risk of infections, and cardiovascular events, necessitating careful monitoring. Their newer status means they have a different safety profile compared to the more established biologics, and further studies are needed to fully understand their long-term effects.

Conclusion

The development of biologic therapies has fundamentally changed the treatment of autoimmune diseases, offering patients improved disease control, reduced symptoms, and prevention of tissue damage. Infliximab, as a TNF-α inhibitor, has been a cornerstone in the treatment of conditions such as rheumatoid arthritis, Crohn’s disease, and psoriasis. However, other biologics, including adalimumab, etanercept, tocilizumab, and JAK inhibitors, offer competitive alternatives, each with unique mechanisms of action, administration routes, and side effect profiles.

Infliximab remains a highly effective treatment, particularly for patients with more severe or refractory disease, but its intravenous administration and potential for infusion reactions may limit patient preference compared to the self-administered adalimumab or the oral administration of JAK inhibitors. On the other hand, tocilizumab and JAK inhibitors provide promising options for patients who either fail or do not respond to TNF-α inhibitors, expanding the therapeutic choices available. Ultimately, the decision to choose infliximab or another biologic depends on various factors, including the disease being treated, the patient's medical history, the drug's administration route, side effect profiles, and cost considerations. Personalized treatment plans that incorporate patient preferences and comorbidities are essential for optimizing outcomes in autoimmune disease management. As more data emerges from clinical trials and real-world experiences, it will become clearer which biologic therapies offer the most benefit for specific patient populations.

Acknowledgment

None.

Conflict of Interest

None.

References

  1. Davatchi, Fereydoun, Cheyda Chams-Davatchi, Hormoz Shams and Farhad Shahram, et al. "Behcet’s disease: Epidemiology, clinical manifestations and diagnosis.” Expert Rev Clin Immunol 13 (2017): 57-65.
  2. Google Scholar, Crossref, Indexed at

  3. Ozyazgan, Yilmaz, Didar Ucar, Gulen Hatemi and Yusuf Yazici. "Ocular involvement of Behçet’s syndrome: A comprehensive review." Clin Rev Allergy Immunol 49 (2015): 298-306.
  4. Google Scholar, Crossref, Indexed at

  5. Rotsos, Tryfon G. and Marilita M. Moschos. "Cystoid macular edema." Clin Ophthalmol 2 (2008): 919-930.
  6. Google Scholar, Crossref, Indexed at

  7. Caspi, Rachel R. "A look at autoimmunity and inflammation in the eye." J Clin Investig 120 (2010): 3073-3083.
  8. Google Scholar, Crossref, Indexed at

  9. Alibaz-Oner, Fatma and Haner Direskeneli. "Advances in the treatment of Behcet’s disease." Curr. Rheumatol. Rep 23 (2021): 47.
  10. Google Scholar, Crossref, Indexed at

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