FKBP51 Inhibition Compositions for Idiopathic Preterm Birth

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Solution Overview

Problem

Current treatments are inadequate for addressing idiopathic preterm birth and fetal growth restriction, which account for a significant portion of preterm births and contribute to neonatal morbidity and mortality, with underlying causes and molecular mechanisms remaining unclear.

Innovation Solution

Administering therapeutically effective amounts of 15-deoxy-Δ12,14-prostaglandin J2, 9-nitro-9E-octadecenoic acid, or 10-nitro-9E-octadecenoic acid or their derivatives to inhibit FKBP51 in uterine decidual cells, thereby reducing FKBP51's interaction with the progesterone receptor, thus delaying or preventing idiopathic preterm birth and treating fetal growth restriction.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If conventional treatments are used for preterm birth, then inflammation-associated PTB can be addressed, but idiopathic PTB and fetal growth restriction remain untreated

Engineering Contradiction:

Improvetreatment effectivenessVSAvoidtreatment coverage

Core Design Contradiction:

ReliabilityVSAdaptability or versatility

Solution Approach 1:

The patent changes the molecular target parameter from inflammation pathways (TLR-NF-κB) to the FKBP51-progesterone receptor interaction pathway. By administering compounds that inhibit FKBP51, the treatment addresses a different mechanistic parameter (FKBP51-mediated progesterone receptor inhibition) that underlies idiopathic preterm birth and fetal growth restriction, thereby expanding treatment coverage to previously unaddressed cases.

Inventive Principle:

Principle #35Parameter changes

2Duration of action of stationary object

If FKBP51 is inhibited to prevent idiopathic preterm birth, then gestational period is extended, but potential off-target effects may occur

Engineering Contradiction:

Improvegestational periodVSAvoidoff-target effects

Core Design Contradiction:

Duration of action of stationary objectVSObject-affected harmful factors

Solution Approach 1:

The patent uses specific chemical compounds (15-deoxy-Δ12,14-prostaglandin J2, 9-nitro-9E-octadecenoic acid, 10-nitro-9E-octadecenoic acid) as intermediaries to indirectly inhibit FKBP51 function. These compounds do not directly bind FKBP51 but rather modulate its interaction with the progesterone receptor, providing a more selective and controllable mechanism that reduces off-target effects while achieving the desired extension of gestational period.

Inventive Principle:

Principle #24Intermediary (Mediator)

3Reliability

If treatment addresses inflammation-associated PTB, then infectious preterm birth can be managed, but the 45-50% of idiopathic cases are not covered

Engineering Contradiction:

Improvetreatment coverage for infectious PTBVSAvoidtreatment coverage for idiopathic PTB

Core Design Contradiction:

ReliabilityVSAdaptability or versatility

Solution Approach 1:

The patent develops a universal treatment mechanism that addresses both inflammation-associated and idiopathic preterm birth through a common pathway (FKBP51-progesterone receptor interaction). The FKBP51 inhibition mechanism serves multiple functions: it prevents inflammatory-mediated preterm birth by counteracting inflammation-induced FKBP51 upregulation, and simultaneously treats idiopathic preterm birth where FKBP51 dysregulation occurs without obvious inflammation, thereby achieving multi-functionality across different PTB etiologies.

Inventive Principle:

Principle #6Universality (Multi-functionality)

Data Source

PatentUS12409182B2Compositions and uses thereof for treatment of idiopathic preterm birth

Publication Date: 2025.09.09 UNIV OF SOUTH FLORIDA

AI summary

Disclosed are compositions and methods for delaying or preventing idiopathic preterm birth.