Optimized PBGD Gene Therapy via AAV Vector

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Solution Overview

Problem

Current treatments for acute intermittent porphyria (AIP), such as liver transplantation, have limitations due to donor availability and morbidity, and existing gene therapy approaches show only transient efficacy, necessitating improved vectors and protocols for delivering functional porphobilinogen deaminase (PBGD) to address the enzyme deficiency.

Innovation Solution

Development of a parvoviral virion comprising a nucleic acid construct with a nucleotide sequence coding for human porphobilinogen deaminase, combined with an AAT promoter and mouse albumin gene enhancer, and AAV serotype 5 capsid proteins, to create an efficient AAV vector for targeted gene therapy.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If liver transplantation is used to treat AIP, then the enzyme deficiency is corrected, but donor availability is limited and morbidity is high

Engineering Contradiction:
Improveenzyme deficiency correctionVSAvoidtransplantation procedure
Core Design Contradiction:
ReliabilityVSDevice complexity

Solution Approach 1:

The patent extracts the essential therapeutic function (PBGD enzyme replacement) from the complex liver transplantation procedure, delivering only the necessary gene therapy component via AAV vectors to correct the enzyme deficiency without requiring organ transplantation

Inventive Principle:
Principle #2Taking out (Extraction)

Solution Approach 2:

The patent introduces AAV vectors as an intermediary delivery system to transport the PBGD gene into hepatic cells, serving as a bridge between the therapeutic goal and the cellular target, thereby avoiding the complexity of direct liver transplantation

Inventive Principle:
Principle #24Intermediary (Mediator)

2Reliability

If existing gene therapy approaches are used, then PBGD delivery is attempted, but efficacy is only transient

Engineering Contradiction:
ImprovePBGD deliveryVSAvoidtherapeutic efficacy
Core Design Contradiction:
ReliabilityVSDuration of action of moving object

Solution Approach 1:

The patent changes critical parameters of the gene delivery system by selecting AAV serotype 5 capsid proteins with enhanced stability and liver tropism, and optimizing the promoter-enhancer configuration (AAT promoter with mouse albumin gene enhancer) to achieve sustained long-term expression of PBGD enzyme

Inventive Principle:
Principle #35Parameter changes

Solution Approach 2:

The patent creates a composite gene therapy vector combining multiple functional elements: AAV serotype 5 capsid proteins for targeted delivery, AAT promoter for tissue-specific expression, mouse albumin gene enhancer for enhanced expression levels, and the human PBGD coding sequence, achieving synergistic sustained therapeutic efficacy

Inventive Principle:
Principle #40Composite materials

Data Source

PatentEP2352823B1Porphobilinogen deaminase gene therapy
Publication Date: 2014.08.06 UNIQURE IP BV
  • EP2352823B1 patent drawingFigure 1~2
  • EP2352823B1 patent drawingFigure 3~4
  • EP2352823B1 patent drawingFigure 5~6

AI summary

The present invention relates to nucleotide sequences coding for human porphobilinogen deaminase that are optimised for higher expression in mammalian cells. The invention further relates to DNA constructs comprising such optimised synthetic coding sequences for use in gene therapy of conditions caused by a deficiency in porphobilinogen deaminase, such as acute intermittent porphyria. Accordingly, the present invention relates to anucleic acid or a nucleic acid construct comprising a nucleotide sequence coding for a human porphobilinogen deaminase, wherein at least 320 of the codons coding for the human porphobilinogen deaminase are identical to the codons in SEQ ID NO: 1 or wherein at least 305 of the codons coding for the human porphobilinogen deaminase are identical to the codons in SEQ ID NO: 3.