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Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

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Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
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Inflammatory Bowel Disease IV: Pharmacological Management01:29

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Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...
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Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

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Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
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Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids01:21

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Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2...
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NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Related Experiment Video

Updated: Sep 17, 2025

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
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Selective CBP/EP300 Bromodomain Inhibitors: Novel Epigenetic Tools to Counter TNF-α-Driven Inflammation.

Katherine A Gosselé1,2, Irene Latino3, Eleen Laul1

  • 1Department of Chemistry, University of Zurich, Zurich CH-8057, Switzerland.

JACS Au
|June 27, 2025
PubMed
Summary

New inhibitors targeting CBP/EP300 bromodomains reduce inflammation by blocking key signaling pathways. These findings offer a promising therapeutic strategy for autoimmune diseases like rheumatoid arthritis driven by tumor necrosis factor α.

Keywords:
CBP/EP300NFκBTNF-αbromodomain inhibitorsepigeneticsinflammation

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Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • Tumor necrosis factor α (TNF-α) drives inflammation in autoimmune diseases.
  • CBP/EP300 bromodomains (BRDs) role in immune response is not fully understood.
  • Targeting epigenetic regulators for cytokine expression is a therapeutic strategy.

Purpose of the Study:

  • To investigate the role of CBP/EP300-BRDs in immune responses.
  • To develop selective CBP/EP300-BRD inhibitors.
  • To evaluate the therapeutic potential of these inhibitors in TNF-α-mediated inflammation.

Main Methods:

  • High-throughput fragment docking to identify inhibitors.
  • In vitro assays to assess cytokine expression and NFκB signaling.
  • In vivo murine model to evaluate anti-inflammatory effects.

Main Results:

  • Selective CBP/EP300-BRD inhibitors were identified.
  • Inhibitors reduced TNF-α-driven cytokine expression by blocking NFκB signaling.
  • In vivo studies showed decreased cytokine secretion and immune cell migration.

Conclusions:

  • CBP/EP300-BRDs are promising therapeutic targets for autoimmune diseases.
  • Developed inhibitors demonstrate anti-inflammatory effects.
  • These inhibitors may complement therapies for TNF-α-mediated conditions like rheumatoid arthritis.