Aryl Hydrocarbon Receptor Agonist Compounds for Sustained IL-22 Activation

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Solution Overview

Problem

Current therapies for inflammatory bowel disease (IBD) are ineffective despite the use of immunosuppressive agents and biologic drugs, with limitations including toxicity, increased infection risk, reduced efficacy due to anti-drug antibodies, and high cost, and only one-third of patients respond appropriately to existing treatments.

Innovation Solution

Development of aryl hydrocarbon receptor (AHR) agonist compounds that non-covalently bind to AHR, providing sustained activation and improved pharmacokinetic profile without toxicity, addressing the limitations of existing AHR agonists and synthetic derivatives.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Duration of action of moving object

If endogenous AHR agonists (tryptophan, indoles) are used, then AHR activation and IL-22 production are achieved, but rapid metabolism and short half-life limit sustained therapeutic effect

Engineering Contradiction:
Improvehalf-lifeVSAvoidsustained AHR activation
Core Design Contradiction:
Duration of action of moving objectVSReliability

Solution Approach 1:

The patent modifies the chemical structure of endogenous AHR agonists by introducing fluorine atoms at specific positions (e.g., 6-fluoroindole-3-carboxylic acid derivatives) to alter metabolic stability. This structural modification extends the half-life of AHR activation from minutes to hours, enabling sustained therapeutic effect while maintaining AHR binding affinity and IL-22 induction capability.

Inventive Principle:
Principle #35Parameter changes

2Duration of action of moving object

If first generation synthetic AHR agonist derivatives are used, then improved pharmacokinetic profile is achieved, but toxicity and off-target effects increase

Engineering Contradiction:
Improvepharmacokinetic profileVSAvoidtoxicity
Core Design Contradiction:
Duration of action of moving objectVSObject-affected harmful factors

Solution Approach 1:

The patent introduces fluorine atoms at specific local positions (positions 6 and 7 of the indole ring) to achieve selective metabolic stabilization without affecting overall molecular reactivity. This localized modification provides sustained AHR activation while minimizing off-target effects and toxicity associated with broader structural modifications in first generation derivatives.

Inventive Principle:
Principle #3Local quality

3Object-affected harmful factors

If immunosuppressive agents and biologic drugs are used for IBD, then inflammation suppression is achieved, but toxicity, infection risk, and anti-drug antibody formation increase

Engineering Contradiction:
ImproveinflammationVSAvoidtherapeutic response
Core Design Contradiction:
Object-affected harmful factorsVSReliability

Solution Approach 1:

The patent employs AHR agonists as intermediary compounds that indirectly suppress inflammation by activating the AHR-IL-22 axis. Rather than directly suppressing immune cells like traditional immunosuppressants, these compounds restore gut barrier function and microbial homeostasis, which indirectly reduces inflammation without causing broad immunosuppression or anti-drug antibody formation.

Inventive Principle:
Principle #24Intermediary (Mediator)

Applied Scientific Principles

This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.

Function Achieved in This Case

The AHR agonist compounds effectively induce IL-22 production, improving gut microbial homeostasis and tissue integrity, reducing inflammation, and promoting epithelial repair, offering a potential therapeutic benefit for IBD without the drawbacks of existing treatments.

Implementation Method 1

These compounds can non-covalently bind to aryl hydrocarbon receptors and induce aryl hydrocarbon receptor activity

Methodology Applied
Scientific EffectNon-covalent binding: Van der Waals Force

Implementation Method 2

Upon ligand binding, AHR dissociates from its chaperones and translocates to the nucleus, where it dimerizes with the aryl hydrocarbon receptor nuclear translocator (ARNT) to induce gene transcription

Methodology Applied
Scientific EffectLigand-induced translocation:

Implementation Method 3

AHR accomplishes these outcomes by regulating the expression of IL-22

Methodology Applied
Scientific EffectGene transcription induction:

Implementation Method 4

constitutive expression of CYP1A1 in intestinal epithelial cells, which increases the metabolism of AHR ligands

Methodology Applied
Scientific EffectEnzymatic metabolism: Enzyme

Data Source

PatentEP3774767B1Aryl hydrocarbon receptor modulators and uses thereof
Publication Date: 2025.10.29 BETH ISRAEL DEACONESS MEDICAL CENT INC
  • EP3774767B1 patent drawingFigure 1a~1g
  • EP3774767B1 patent drawingFigure 2a~2e
  • EP3774767B1 patent drawingFigure 3a~3b

AI summary

Provided are compounds of Formula (I), and pharmaceutically acceptable salts, solvates, hydrates, stereoisomers, tautomers, isotopically labeled derivatives, polymorphs, and prodrugs thereof, wherein X1-X4, RX, RC, RB, n, and Ring A are as defined herein. The compounds may be aryl hydrocarbon receptor agonists or partial aryl hydrocarbon receptor agonists. Also provided are pharmaceutical compositions comprising a compound of Formula (I) and methods of using such compounds for treating diseases and conditions related to the activity of an aryl hydrocarbon receptor, such as, for example, inflammatory diseases, autoimmune diseases, metabolic disorders, and proliferative diseases.