Intercept IQ™
The molecular substrate behind every Kihealth programme — cell-free DNA, beta-cell methylation signatures and AI-driven tissue-of-origin inference.
Kihealth Europe is pioneering a new category of molecular diagnostics focused on identifying the biological changes that precede Type 1 Diabetes, Type 2 Diabetes, and metabolic disease — helping move healthcare from disease management to disease prevention.

Performance figures reference Kihealth research studies on the InterceptIQ™ platform. BetaIntercept™ assays are intended to support research and are not yet authorised for routine clinical diagnosis in the European Union.
Beta-cell mass typically lost before Type 1 Diabetes is diagnosed.
Children presenting in diabetic ketoacidosis at first diagnosis.
Often required to reach conventional clinical endpoints.
Beta cells are responsible for producing insulin and maintaining glucose control. Their dysfunction and loss are central events in the development of both Type 1 and Type 2 Diabetes.

Diabetes is fundamentally a disease of beta-cell dysfunction and loss. Measure the cell, and you measure the disease — before it declares itself.
From insulin-producing engine to apoptotic body — the seven phases that shape the biology of diabetes, and the points at which Kihealth seeks to generate insight.

A mature beta cell sits inside a pancreatic islet, packed with insulin granules and tightly tuned to ambient glucose.
Healthy beta-cell mass is the foundation of glucose homeostasis. Even small reductions compromise long-term metabolic resilience.
A reservoir — silent, sufficient, in balance with demand.
Baseline cfDNA signal is quiet. Establishes a personal reference state.
Glucose enters the cell, ATP rises, channels close, calcium triggers exocytosis. Insulin granules release in pulses matched to need.
This is the engine of metabolic control. Pulsatile insulin secretion is what keeps post-meal glucose excursions narrow.
Reserve is intact; the cell responds without strain.
Methylation patterns reflect a healthy, actively secreting beta-cell population.
Chronic glucose load, lipid exposure or autoimmune signals overwhelm the endoplasmic reticulum. The cell begins making misfolded proinsulin.
Stress is the first reversible step. Catching it here defines the window for prevention rather than management.
Function is preserved on the surface; molecular distress is already accumulating.
Early shifts in tissue-specific cfDNA suggest beta-cell turnover is rising.
Immune cells infiltrate the islet. Cytokines amplify ER stress, oxidative damage rises, and signalling pathways tip toward injury.
Inflammation is the bridge between stress and irreversible loss. It is also a measurable, biologically distinct phase.
The local environment turns hostile; some cells begin to dedifferentiate.
Inflammation-associated methylation marks emerge in circulating cfDNA.
Insulin secretion becomes erratic. Mitochondria struggle, granule pools shrink, glucose sensing drifts out of calibration.
Glucose may still appear normal because surviving cells compensate. The biology has moved long before HbA1c reflects it.
Functional reserve is silently depleted; symptoms still absent.
Beta-cell-derived cfDNA fragments rise — the platform's central biological signal.
Damage exceeds repair. Caspases activate, chromatin condenses, the cell fragments into apoptotic bodies and releases its DNA.
Apoptosis is the molecular event that ends a beta cell — and the one most directly visible to liquid-biopsy diagnostics.
Total beta-cell mass declines toward clinical thresholds.
Unmethylated INS promoter cfDNA spikes — a fingerprint of dying beta cells.
Sufficient beta-cell mass is lost. Insulin reserve collapses, glucose rises, and diabetes meets diagnostic criteria.
By this stage, the underlying biology has been in motion for years. The diagnosis closes a long, previously invisible chapter.
Standard diagnosis. Management begins; biology continues.
Longitudinal cfDNA monitoring tracks residual beta-cell mass and therapeutic response.

Between the first molecular signs of beta-cell injury and the appearance of clinical symptoms lies a silent biological window — measurable, potentially actionable, and previously invisible to routine diagnostics.
A shared molecular substrate — cell-free DNA, epigenetics, and machine learning — engineered to scale across disease areas where active cellular injury leaves a signal in the bloodstream.
See the platform architectureLow-input library chemistry designed to preserve fragmentomic and methylation detail from picogram-level cell-free DNA.
Whole-genome bisulfite sequencing tuned for cfDNA fragment biology, with quality-audited basecalling.
Reproducible pipelines decoding methylation, fragmentomic and end-motif signal at single-molecule resolution.
Multi-task models being investigated to jointly resolve tissue-of-origin and disease state, with calibrated probability outputs.
Physician-facing reports being developed under accredited laboratory standards and delivered through standards-based interfaces.
The molecular substrate behind every Kihealth programme — cell-free DNA, beta-cell methylation signatures and AI-driven tissue-of-origin inference.
Beta-cell unmethylated INS cfDNA designed to evaluate active immune-mediated beta-cell destruction across Stage 1–3 Type 1 Diabetes.
Multi-tissue metabolic methylation panel surfacing beta-cell stress and dysfunction long before traditional markers move.
Forward-looking research extending Intercept IQ™ into adjacent metabolic indications where beta-cell biology offers a measurable signal.
Traditional diabetes monitoring relies on glucose, HbA1c, insulin and C-peptide — markers that typically reflect metabolic dysfunction after substantial biological change has already occurred.
BetaIntercept™ is designed to evaluate biological signals associated with pancreatic beta-cell health, providing insight into processes being investigated that may precede traditional markers of progression.


Our network spans pharmaceutical leaders, leading universities, academic medical centres and reference laboratories — the institutions shaping precision medicine across Europe.
Explore partnership opportunitiesRepresentative categories of European collaborators. Specific organisations are referenced for illustrative purposes and do not imply endorsement.
Measuring biology before symptoms — when intervention may be most effective.
Designed to surface the active biology driving disease, not only its downstream markers.
Supporting research into disease while it may remain reversible, and monitoring response over time.