CRISPR Base Editing PCSK9 Loss-of-Function Variants

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Solution Overview

Problem

Current methods for generating PCSK9 protective variants and loss-of-function mutants in vivo are ineffective due to the need to modify a large number of cells to modulate cholesterol levels, and are associated with off-target effects and genome instability.

Innovation Solution

The use of CRISPR/Cas9-based base-editing technology to precisely target and modify the PCSK9, LDLR, IDOL, or APOC3 genes, resulting in loss-of-function variants that reduce LDL and overall cholesterol levels while minimizing off-target effects and genomic instability.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If engineered nucleases are used to create random indels in the PCSK9 genomic locus, then PCSK9 loss-of-function variants can be generated, but off-target effects and genome instability occur

Engineering Contradiction:
Improvegeneration of PCSK9 loss-of-function variantsVSAvoidoff-target effects and genome instability
Core Design Contradiction:
ReliabilityVSObject-affected harmful factors

Solution Approach 1:

The patent replaces the mechanical cutting mechanism of engineered nucleases (ZFNs, TALENs, CRISPR-Cas9) with a chemical editing mechanism using base editors. Instead of creating double-strand breaks that require cellular repair machinery (prone to errors and off-target effects), the base editor uses a modified deaminase enzyme to directly convert cytosine to uracil at the target site, which is then processed by cellular repair mechanisms to generate precise C-to-T transitions without requiring DNA cleavage.

Inventive Principle:
Principle #28Mechanics substitution (Replace mechanical system)

Solution Approach 2:

The patent changes the fundamental parameter of genome editing from creating random insertions/deletions (indels) through non-homologous end joining to generating precise point mutations through base substitution. This parameter change from random to precise editing eliminates the need for homology-directed repair and significantly reduces off-target effects while maintaining the ability to generate loss-of-function variants.

Inventive Principle:
Principle #35Parameter changes

2Reliability

If a large number of cells are modified to modulate cholesterol levels, then cholesterol modulation can be achieved, but the complexity and scale of the procedure increases

Engineering Contradiction:
Improvecholesterol level modulationVSAvoidnumber of cells to be modified
Core Design Contradiction:
ReliabilityVSDevice complexity

Solution Approach 1:

The base editing technology enables more efficient gene modification that requires fewer cells to achieve the desired therapeutic effect. The precise C-to-T transitions created by base editors are more likely to produce functional loss-of-function variants compared to random indels, reducing the number of cells that need to be modified and treated to achieve sufficient cholesterol level modulation.

Inventive Principle:
Principle #28Mechanics substitution (Replace mechanical system)

3Object-affected harmful factors

If precise targeting methods are used to modify PCSK9, then loss-of-function variants can be generated with low off-target effects, but the technology complexity increases

Engineering Contradiction:
Improveoff-target effectsVSAvoidbase-editing technology
Core Design Contradiction:
Object-affected harmful factorsVSDevice complexity

Solution Approach 1:

The base editor system replaces complex nuclease-based editing with a simpler deamination chemistry approach. The fusion protein combines a programmable DNA-binding domain (dCas9 or dCpf1) with a cytosine deaminase, creating a more straightforward mechanism that relies on enzymatic conversion rather than DNA cleavage and repair, thereby reducing technology complexity while improving precision.

Inventive Principle:
Principle #28Mechanics substitution (Replace mechanical system)

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 approach generates loss-of-function variants with cardioprotective functions, effectively lowering LDL and overall cholesterol levels while maintaining genomic stability and reducing the risk of oncogenic modifications.

Implementation Method 1

contacting results in deamination of the target C base by the fusion protein, resulting in a cytosine (C) to thymine (T) change in the PCSK9-encoding polynucleotide

Methodology Applied
Scientific EffectDeamination:

Data Source

PatentEP3559223A1Gene editing of PCSK9
Publication Date: 2019.10.30 PRESIDENT & FELLOWS OF HARVARD COLLEGE

AI summary

Provided herein are systems, compositions, and methods of introducing loss-of- function mutations in to protein factors involved in the LDL-R-mediated cholesterol clearance pathway, e.g., PCSK9, APOC3, LDL-R, or IDOL. Loss-of-function mutations may be introduced using a CRISPR/Cas9-based nucleobase editor described in. Further provided herein are compositions and methods of treating conditions related to high circulating cholesterol levels.