Simulate Therapy Outcomes. Compare With Confidence.

DNAI converts multi-omics and pathology data into physics-constrained digital twins — enabling oncologists and biopharma to compare treatment scenarios with quantified uncertainty.

Trained on 9,400+ patients (TCGA)
33 cancer types
Structured abstention when uncertain
Research use only. Not for clinical decision-making or diagnostic procedures.8 U.S. Provisional Patents
DNAI Patient Simulation
ILLUSTRATIVE EXAMPLE
Patient SummaryBRCA — Stage IIA
Key Mutation
PIK3CA H1047R
Subtype
ER+ / HER2−
Ki-67
32% (high)
Treatment Comparison
A
Paclitaxel + Alpelisib
PIK3CA-targeted combination
78%
2yr survival [72–83%]
B
AC → Paclitaxel
Standard of care
64%
2yr survival [57–70%]
PROJECTED TUMOR VOLUME
0 mo12 mo24 mo
Option A (with 95% CI)
Option B — SoC
KEY DRIVERS
PIK3CA driverHigh proliferationER+ sensitivity
All parameters within biological bounds — physics compliant

Validated Architecture. Biologically Bounded.

Evaluated across multiple independent cohorts. Every simulation is constrained by biological law — performance reported per cancer type and modality.

9,400+
Training patients
33 cancer types (TCGA)
5
External cohorts evaluated
6,000+ patients; varies by type
0%
Physics violations
Biologically valid by design
5 ms
Core inference
Real-time trajectory emulation

Biologically Constrained

Tumor growth rates, drug sensitivity, and immune parameters are bounded to biologically plausible ranges. Outputs that violate physical constraints are rejected.

Interpretable by Design

Every simulation traces to specific genes, pathways, and physics parameters. Driver gene rankings, pathway-level attributions, and uncertainty intervals — not a black-box score.

Audit-Compatible

21 CFR Part 11 audit trail, calibrated probabilities, and signed execution tokens. Designed for regulatory compatibility.

Structured Abstention

When patient data is insufficient or out-of-distribution, the system flags uncertainty and explains what is missing — rather than forcing a prediction.

How It Works

Three steps from patient data to actionable simulation.

1. Patient Data In

RNA-seq, DNA mutations, CNV, methylation, histopathology — the platform ingests what you already have. Probabilistic fusion handles missing modalities; best results with matched pathology (WSI).

2. Digital Twin Simulates

A patient-specific tumor model simulates growth, drug response, resistance timing, and immune dynamics — all constrained by biological physics.

3. Decision-Ready Output

Ranked treatment options with survival projections, confidence intervals, and the specific genes and pathways driving each simulation.

Unlike black-box AI, DNAI simulations are constrained by biological physics.

Growth rates, drug sensitivity, and immune parameters are bounded to biologically plausible ranges. If data is insufficient, the system abstains and explains what is missing — rather than guessing.

A New Category

Why DNAI?

Most oncology AI predicts static risk. DNAI simulates treatment scenarios, quantifies reliability, and abstains when evidence is insufficient — backed by mechanistic constraints and external validation.

Reliability-gated, counterfactual digital twins that simulate tumor dynamics per patient

Counterfactual Treatment Simulation

Don't just predict risk — simulate the remedy. We model 6 distinct treatment scenarios for every patient to rank options by potential benefit under uncertainty.

6treatment futures simulated per patient
Significant stratification of responders vs. non-responders (p < 10⁻⁹) · Retrospective
How decisioning works

Structured Reliability Gating

Engineered to abstain when data is insufficient. Every patient receives a High / Medium / Low reliability score based on information sufficiency — not a forced prediction.

0.744C-index on high-confidence tier (n=229/1,031, CPTAC)
Pre-specified gating rule · ~20% qualify as high-confidence · Precision over coverage
See reliability policy

Physics-Constrained Dynamics

Not just pattern-matching — tumor dynamics. We use differential equations with bounded biological parameters: proliferation, drug sensitivity, and immune killing. Predictions are plausible by design.

100%biological constraint compliance across all patients
Parameters bounded to physiological ranges · Non-negative volume · Doubling time limits
Explore the architecture

Evaluated on External Cohorts

Tested where it matters — outside the training data. Multi-site external cohorts with per-patient reliability checks, not just internal cross-validation. Performance varies by cancer type and modality.

5,000+external patients across independent cohorts
CPTAC (10 sites, 9 cancer types) · CGGA (glioma) · Performance reported per cohort
See validation data

How DNAI compares

Core Logic
Standard AI: Statistical correlation — finds patterns in outcomes
DNAI: Mechanistic simulation — models tumor growth dynamics
Output
Standard AI: Static risk score for every patient
DNAI: Treatment scenario ranking with reliability gating
Safety
Standard AI: Always predicts — silent failures on edge cases
DNAI: Structured abstention — flags insufficient evidence
Validation
Standard AI: Internal cross-validation
DNAI: External multi-site evaluation with per-patient reliability scores
Category comparison — not referencing specific companiesRead full comparison
For Drug Development

PDX-to-Human Translation

Our patented Domain Separation Network bridges preclinical mouse models to human biology — removing species-specific stroma while preserving tumor signal. Translate PDX efficacy signals toward human endpoints for research prioritization.

2 U.S. Provisional Applications573 PDX Models AnalyzedAllometric Scaling
0.704
Internal C-index (Path A)
0.009
Calibration error (ICI)
R² 0.997
Emulator vs. full ODE
6
U.S. provisional applications

Research use only. Not cleared or approved for clinical decision-making. Survival estimates based on observational counterfactual modeling.

For Clinicians

Simulation-informed treatment planning

Virtual Tumor Board

Visualize likely outcomes for Standard of Care vs. experimental agents before making treatment decisions.

Resistance Forecasting

"Alert: Subpopulation 3 projected to drive resistance to Therapy A by Day 180." Plan adaptive strategies proactively.

Dose Optimization

Explore dosing schedules that balance efficacy and safety constraints — optimized through the differentiable tumor model.

For Biopharma

In silico trials and mechanism discovery

Hybrid Control Arms

Generate physics-constrained synthetic patient trajectories for control arms. Modeled potential to reduce control-arm enrollment by 30–50% — enabling more patients to receive experimental treatments.

Mechanism Discovery

Use the Driver module to understand why a drug works in Subgroup A but fails in Subgroup B. Identify predictive biomarkers.

Rescue Failed Assets

Identify the specific dosing schedule or patient subpopulation required to make a failed compound effective.

Virtual Trial — MDM2i + CDK4/6i in DDLPS
In silico simulation from SARC clinical repository cohort
Simulated results — not clinical outcomes
Simulated HR: 0.58 | Median PFS: 8.5 vs 4.2 months (model estimate)
See It In Action

The Platform at Work

From patient dashboard to tumor evolution simulations — explore the DNAI interface.

Ready to simulate?

See how DNAI can transform your oncology workflows.