TECHNOLOGY

INDUCE-seq® Platform

Why measuring breaks changes everything

Genome editing holds enormous therapeutic promise, but unintended DNA damage remains a critical barrier to safe development. Off-target effects are difficult to predict and often challenging to detect using traditional approaches.

As regulatory expectations for genome-wide assessment continue to evolve, empirical measurement of off-target activity is becoming essential.

Existing methods measure the final genetic outcome after DNA repair, limiting the ability to understand how and why off-target events occur.

±õ±·¶Ù±«°ä·¡-²õ±ð±ç® directly labels and captures DNA breaks in cells, enabling genome-wide detection of editing events as they happen.

By measuring break formation rather than downstream repair outcomes, the platform provides deeper insight into: nuclease behaviour, guide RNA performance, editing kinetics, cell-specific DNA repair pathways.

This enables earlier, more informed decisions and accelerates the development of safer gene-editing therapies.

Current industry challenges with off-target analysis

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Technical

Indirect measurement of editing outcomes, not break events

Noisy and inconsistent signals

PCR amplification introduces bias

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Operational & scalability

Growing demand for empirical, genome-wide data

Late-stage surprises increase program risk

Low confidence drives repeated testing

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Regulatory & decision risk

Fragmented workflows across multiple assays

Limited scalability in discovery

Expensive, inflexible outsourcing

A single workflow combines wet lab, sequencing and integrated bioinformatics

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Cell editing &
immobilization

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DNA break labeling
& library prep

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Sequencing

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Data analysis

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Reporting

±õ±·¶Ù±«°ä·¡-²õ±ð±ç® is a scalable platform technology for mapping and characterizing DNA breaks, leveraging a novel PCR-free in situ break labelling approach coupled with next-generation sequencing. It enables unbiased, genome-wide detection of DNA damage induced by any nuclease-based genome editing system.

What makes this technology different:

• PCR-free workflow eliminating amplification bias
• Cell-based, in situ break capture
• Compatible with any cell type
• Applicable to any nuclease-based editor

What this enables

Confident actionable data

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Scalable across the drug discovery pipeline

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In house control over critical safety data

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Simultaneous on- and off-target detection in one simple workflow

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±õ±·¶Ù±«°ä·¡-²õ±ð±ç® supports confident decision making from discovery to IND-enabling

A flowchart depicts a process involving applicant screening, characterization and optimization, lead selection, and IND-enabling phases. It includes segments labeled BreakMapâ„¢, BreakMapâ„¢ IND-enabling, and BreakMapâ„¢ High-Throughput, with various steps such as guide and nucleases screening, early on/off signal, compare editing conditions, mechanism & kinetics, ROU to GMP validation, rank specificity & performance, and regulatory grade assessment.
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Gene editing applications

INDUCE-seq® pairs its unbiased wet lab assay with an integrated bioinformatics platform designed to convert complex sequencing outputs into clear, ranked, and actionable insights facilitating:

• Off-target assessment
• Guide selection and ranking
• Editing optimization and strategy design
• On-target editing mechanism and kinetics
• Nuclease and editor characterization

All cell types: Tested examples

  • • Bone Marrow​

    • Glioblastoma​

    • Neurons

    • Motor Neurons​
    ​
    • Lung Carcinoma​

    • T Cells&²Ô²ú²õ±è;​

    • Dermal Fibroblasts​

    • Human Hepatocytes

  • • Embryonic stem cells
    &²Ô²ú²õ±è;​
    • Hematopoietic stem and progenitor cells&²Ô²ú²õ±è;​

    • Induced pluripotent stem cells

    • Neural progenitors 

  • • T309 (Brain)

    • T393 (Brain)

    • TK6 (Blood, lymphoblast)

    • CH12F3 (Blood)

    • HeLa (Uterus, epithelial)

    • Jurkat (T lymphocyte)

    • HEK293 (Embryonic Kidney)

    • KBM7 (Bone marrow)

    • MCF10A (Breast)

    • MCF7 (Breast)

    • RPE1 (Retina)

    • SH-SY5Y (Neuroblastoma)

    • RPE1 (Retina)

    • A549 (Lung)

    • U2OS (Bone)

    • HepG2 (Liver)

    • CX18 (Neuronal, Brain)

    • GM24385 (B-Lymphocyte)