TPB-L-E3B Proteolysis Compound for eRF3a, SRD5A1, and SRD5A3

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Solution Overview

Problem

Current treatments for human tumors, particularly prostate cancer, ovarian cancer, and other cancers, lack effective mechanisms to target and degrade eRF3a and inhibit SRD5A1 and SRD5A3, leading to drug resistance and progression to castration-resistant prostate cancer, with existing therapies failing to address abnormal expression of these proteins effectively.

Innovation Solution

Development of a proteolysis-targeting compound, TPB-L-E3B, which includes a target protein-binding moiety (TPB) and an E3 ligase-binding moiety (E3B) linked by a specific linker (L), designed to degrade eRF3a and inhibit SRD5A1 and SRD5A3, thereby reducing their expression and impacting key proteins like AR and AR-V7 in tumor cells.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If conventional therapies are used to treat human tumors, then treatment is provided for common cancers, but they fail to effectively target and degrade eRF3a and inhibit SRD5A1 and SRD5A3, leading to drug resistance

Engineering Contradiction:
Improveeffectiveness of tumor treatmentVSAvoidability to target multiple proteins (eRF3a, SRD5A1, SRD5A3)
Core Design Contradiction:
ReliabilityVSAdaptability or versatility

Solution Approach 1:

The compound is divided into three functional segments: a target protein-binding moiety (TPB) that binds to eRF3a, a linker (L) that connects the moieties, and an E3 ligase-binding moiety (E3B) that recruits the ubiquitin-proteasome system. This segmentation allows the single compound to simultaneously achieve protein degradation of eRF3a and inhibition of SRD5A1/SRD5A3, overcoming the limitations of conventional single-target therapies

Inventive Principle:
Principle #1Segmentation

Solution Approach 2:

The compound acts as an intermediary molecule that mediates the interaction between the target protein eRF3a and the E3 ligase system. By binding to both eRF3a and the E3 ligase, the compound facilitates the ubiquitination and degradation of eRF3a, while simultaneously inhibiting SRD5A1 and SRD5A3, thereby providing multi-target therapeutic effects

Inventive Principle:
Principle #24Intermediary (Mediator)

2Duration of action of stationary object

If existing therapies are used, then some tumor treatment is achieved, but they cannot prevent progression to castration-resistant prostate cancer due to inability to inhibit SRD5A1 and SRD5A3

Engineering Contradiction:
Improveduration of therapeutic effectVSAvoidprevention of drug resistance
Core Design Contradiction:
Duration of action of stationary objectVSReliability

Solution Approach 1:

The compound performs multiple functions simultaneously: it degrades eRF3a through the ubiquitin-proteasome system and inhibits SRD5A1 and SRD5A3 enzymes. This multi-functionality addresses multiple pathological mechanisms involved in tumor progression and castration-resistant prostate cancer development, thereby extending therapeutic duration and preventing drug resistance

Inventive Principle:
Principle #6Universality (Multi-functionality)

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 compound effectively degrades eRF3a and inhibits SRD5A1 and SRD5A3, demonstrating potential in treating various human tumors, including prostate cancer, ovarian cancer, and others, by downregulating critical proteins that influence tumor survival and proliferation, thus offering a novel therapeutic approach.

Implementation Method 1

Proteolysis-targeting chimeras (PROTACs) are bifunctional molecules that use the cell's own ubiquitin-proteasome system to label a target protein and facilitate the degradation of same

Methodology Applied
Scientific EffectProteolysis-targeting mechanism:

Implementation Method 2

Molecular glues (MGs) are a class of small molecules that can induce the interaction between E3 ligase and the target protein, thereby helping degrade the target protein through the ubiquitin-proteasome system of the cells

Methodology Applied
Scientific EffectMolecular glue mechanism:

Implementation Method 3

SRD5A1 and SRD5A2 primarily serve to reduce specific steroid substrates, such as testosterone to dihydrotestosterone

Methodology Applied
Scientific EffectEnzyme inhibition: Enzyme

Data Source

PatentEP4596535A1Drug for treating human tumor by erf3a targeted protein degradation mechanism
Publication Date: 2025.08.06 SUZHOU DEGEN BIO-MEDICAL CO LTD
  • EP4596535A1 patent drawingFigure 1~2
  • EP4596535A1 patent drawingFigure 3~4
  • EP4596535A1 patent drawingFigure 5~7

AI summary

The present disclosure provides a proteolysis-targeting compound TPB-L-E3B, a method for synthesizing the same, and use thereof. The compound can treat human tumor diseases through the eRF3a-targeting proteolysis mechanism, and exhibits great potential in treating such diseases in in-vitro studies, particularly, in treating diseases such as prostate cancer, ovarian cancer, liver cancer, cervical cancer, leukemia, breast cancer, and the like.