Quinolinyl Modulators Targeting RORγt for Th17 Inhibition

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Solution Overview

Problem

Current treatments for immune-mediated inflammatory diseases, such as psoriasis and rheumatoid arthritis, often target broader pathways like IL-12 and IL-23, with limited specificity and efficacy in inhibiting the Th17 subset, highlighting the need for more targeted modulation of RORγt activity to effectively manage these conditions.

Innovation Solution

Development of substituted quinoline compounds that act as specific modulators of the nuclear receptor RORγt, designed to inhibit its activity and thereby reduce inflammation associated with Th17 cell-mediated disorders, offering a targeted approach to treat inflammatory syndromes and diseases.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If monoclonal antibodies targeting IL-12 and IL-23 are used, then broad pathway inhibition is achieved, but specificity for Th17 subset is reduced

Engineering Contradiction:
Improveefficacy in inhibiting Th17 subsetVSAvoidlack of specificity
Core Design Contradiction:
ReliabilityVSObject-generated harmful factors

Solution Approach 1:

The patent uses RORγt nuclear receptor as an intermediary target to achieve specific Th17 cell inhibition. Instead of directly targeting IL-12/IL-23 cytokines, the compounds modulate RORγt which is exclusively expressed in Th17 cells, providing pathway-specific inhibition without affecting other immune cell populations

Inventive Principle:
Principle #24Intermediary (Mediator)

Solution Approach 2:

The invention applies local quality by targeting a specific nuclear receptor (RORγt) that is uniquely expressed in Th17 cells. This allows selective modulation of Th17 cell differentiation and function without broadly suppressing the entire IL-12/IL-23 pathway or affecting other T cell subsets

Inventive Principle:
Principle #3Local quality

2Reliability

If RORγt activity is modulated, then Th17 cell differentiation is inhibited, but broader immune suppression may occur

Engineering Contradiction:
Improveinhibition of Th17 cell differentiationVSAvoidpotential immune suppression
Core Design Contradiction:
ReliabilityVSObject-affected harmful factors

Solution Approach 1:

RORγt nuclear receptor serves as a specific intermediary that controls Th17 cell differentiation. By modulating this intermediary rather than broadly suppressing cytokines, the invention achieves targeted inhibition of pathogenic Th17 cells while preserving other immune functions

Inventive Principle:
Principle #24Intermediary (Mediator)

Solution Approach 2:

The patent employs parameter changes by developing compounds with specific chemical structures (substituted quinolines, indoles, pyridines) that modulate RORγt activity with varying degrees of potency and selectivity, allowing optimization of therapeutic effect versus immune suppression risk

Inventive Principle:
Principle #35Parameter changes

Data Source

PatentEP2909189B8Heteroaryl linked quinolinyl modulators of ROR-gamma-t
Publication Date: 2017.04.19 JANSSEN PHARMA NV

AI summary

The present invention comprises compounds of Formula I. Wherein: R1, R2, R3, R4, R5, R6, R7, R8, and R9 are defined in the specification. The invention also comprises a method of treating or ameliorating a syndrome, disorder or disease, wherein said syndrome, disorder or disease is rheumatoid arthritis or psoriasis. The invention also comprises a method of modulating RORγt activity in a mammal by administration of a therapeutically effective amount of at least one compound of claim 1.