INVESTIGATIONAL Preclinical‑stage. Not approved by FDA.
INVESTIGATIONAL Under development. Not cleared by FDA.

A NEW MODALITY · SEQUENCE ABLATION THERAPEUTICS (SAT)

Every disease has a sequence
Our therapeutic technology ablates it at the source.

Viruses and tumors depend on genetic sequences they cannot afford to lose. Sequence Ablation Therapeutics (SAT) finds and ablates those sequences — directly, precisely, at their source — reducing disease burden and giving the immune system what it needs to clear what remains. We’ve demonstrated 57% survival against a pathogen that kills nearly every animal it infects.

Watch SAT in action
Explore the platform

Introducing Sequence Ablation Therapeutics (SAT)

THE PROBLEM

Disease exploits genetic sequences to survive, replicate, and evade treatment.

Every virus, bacterium, and tumor carries genetic sequences it cannot afford to lose. These sequences are its instruction set — the code that tells it how to copy itself, evade your immune system, and resist treatment. Current therapeutics either inhibit a single protein, edit the host genome, or suppress the immune system. Very few directly target the disease’s code itself.

THE SOLUTION

SAT finds those sequences and ablates them — directly, precisely, at their genetic source.

Sequence Ablation Therapeutics (SAT) is a CRISPR‑based modality that locates and ablates multiple conserved disease sequences simultaneously. When a sequence is ablated, the disease loses its ability to replicate. Ablation reduces viral and tumor load, giving the immune system what it needs to clear what remains. No host‑genome editing. No immune suppression. Targeted to what the disease cannot afford to lose.

In our ASFV swine challenge — a pathogen with no approved treatment anywhere — 57% of SAT‑treated animals survived. Untreated controls: 0%.

See Sequence Ablation Therapeutics in action

DISEASE SEQUENCE
Patient torso
Antibody levels
Protective Immunity
Days
1

SAT accesses diseased cell

SAT reaches cells where the disease is multiplying. Once inside, it releases the instructions needed to activate sequence ablation.

2

CRISPR ablators are formed

Once inside, SAT’s instructions are read by the cell. This creates CRISPR ablators, which assemble and move into position to destroy the disease sequence.

3

SAT ablates the disease code

Each CRISPR ablator is guided to an escape-resistant disease sequence. The disease instructions are destroyed while the host cell’s DNA is left untouched.

4

SAT lowers disease burden

SAT targets infected cells throughout the body. By destroying the instructions needed for replication, SAT lowers overall disease burden.

5

The immune system clears what remains

SAT breaks apart the disease, creating fragments the immune system can recognize to clear the remaining infection.

Our path to therapy

An integrated architecture:
From AI discovery to SAT therapeutics — powered by PTAP™

BioSeeker™ The AI‑powered discovery engine
PTAP™ The programmable platform
SAT The therapeutic product

See the programs our AI‑powered platform enables.

Click to explore our pipeline
BioSeeker™ The AI‑powered discovery engine

Finds escape-resistant targets

BioSeeker™ is our AI‑powered discovery engine for identifying the DNA or RNA sequences that disease depends on most.

Features

Genome-wide analysis

Scans complete pathogen genomes and human cancer sequences to identify conserved, essential targets.

Multi-target identification

Finds 3–8 independent essential sites per pathogen to prevent single-point escape.

Safety screen

Cross‑references candidate guides against more than 170,000 reference genomes to minimize host and off‑target effects.

Advantages

Speed

Compresses months of discovery iteration into hours of compute.

Broad coverage

Enables a single SAT to pan-target multiple strains, variants, or related pathogens.

Future-proofing

Multi-site targeting makes simultaneous resistance mutations statistically improbable.

Platform programmability

BioSeeker™’s systematic approach enables guide re-design for newly emergent or engineered strains and mutational variants.

PTAP™ The Programmable Platform

Converts targets into SAT

PTAP™ translates BioSeeker™ targets into SAT therapeutic constructs through standardized, modular design principles.

Features

Plug-and-play construct

Packs BioSeeker™ targets into a pre‑programmed therapeutic template, enabling new disease‑specific constructs through a simple target‑swap architecture.

Delivery toolkit

Uses a configurable family of non-viral delivery vehicles that can be selected or swapped based on disease and tissue context.

Advantages

Platform scalability

New programs can be launched by swapping disease-specific target sequences while preserving the same foundational construct architecture across DNA viruses, RNA viruses, and oncogenes.

Manufacturing efficiency

Standardized building blocks enable a single production line to serve multiple therapeutic programs.

SAT The Therapeutic Product

Disables disease at the genetic source

SAT directly cuts essential DNA and RNA sequences that diseases cannot survive without, enabling immune‑mediated clearance and recovery.

Features

Targeted ablation

Cuts 3–8 essential sequences per pathogen or oncogene simultaneously using CRISPR ablators.

Targeted delivery

Reaches target tissues through optimized non-viral formulations and routes.

Immune partnership

Disabled pathogens and tumor cells become targets for natural immune clearance mechanisms.

Advantages

Post-exposure treatment

Intervenes after infection or tumor development, unlike prophylactic approaches.

Escape-resistant

Multi-site targeting makes simultaneous resistance mutations statistically improbable.

BioSeeker™ decodes. PTAP™ builds. SAT resolves.

Scroll to see how BioSeeker and PTAP program our therapeutics

A different kind of therapeutic
A new benchmark across modalities

How Sequence Ablation Therapeutics compares across the dimensions that matter

Dimension Small-molecule antivirals Monoclonal antibodies mRNA vaccines In vivo gene editing SAT
Mechanism Blocks one protein / enzyme Neutralizes a surface protein Primes immune system pre-exposure Edits or disrupts the host genome CRISPR ablators directly cut multiple escape-resistant disease-driving sequences
Resistance risk High. Single-point mutations Moderate. Epitope drift High. Antigenic drift and shift N/A. Acts on host, not pathogen Low. Multiplexed targeting of conserved, escape-resistant sequences
Multi-strain coverage Low. Strain-specific protein targets Low. Epitope-specific; misses variants Moderate. Multivalent possible but drift escapes N/A. Acts on host, not pathogen High. Multiplexed guides hit escape-resistant regions across strains
Immune assisted clearance No. Direct pharmacologic action only Yes. ADCC, CDC, and phagocytosis effector functions Yes. Induces immune response. Boosters often required Not a primary mechanism Yes. Disabled targets enable immune clearance
Host genome Not edited Not edited Not edited Permanently edited Not edited
Development speed for new targets Slow. New chemistry per target Slow. New antibody discovery per target Moderate. New antigen design per target Moderate. New payload per target Fast. Same construct, swap guide cassette
Platform reuse Low. Target-specific chemistry Low. Target-specific biologic Moderate. Reusable mRNA backbone, new antigen High. Platform reusable High. Modular design across indications
Therapy cost Moderate branded therapy cost High biologic cost profile Low only at massive scale Highest specialty therapy cost Platform economics: one manufacturing line, multiple indications

One Programmable Platform:
Common machinery, Distinct targets, Multiple diseases

Our platform is versatile by design. The architecture stays constant: BioSeeker™ guide design, programmable ablators, and a standardized development path. What we ablate changes: the genetic sequences we target and the delivery formulation we choose. This is how SAT can move fast across indications. Reprogrammed CRISPR means faster target ID to IND, while BioSeeker™ enables systematic target identification instead of one‑off discovery. Scalable development means each new program builds on the last.

Universal

What stays the same

  • Platform mechanism. Cut the disease code, let the body finish. Same biological logic across every disease.
  • CRISPR machinery. Same DNA or RNA targeting CRISPR ablators in each program.
  • Multi-guide architecture. Multiple guides cut simultaneously, by design.
  • Manufacturing path. One manufacturing process. Add a new program without retooling the line.
  • Regulatory strategy. Established precedent for CRISPR therapeutics; platform learnings transfer across programs.

Per program

What changes

  • BioSeeker-designed guides. New guide sequences target the escape-resistant regions of each disease. Disease-specificity lives here.
  • Route and formulation optimization. The same non-viral delivery family is tailored to the target tissue and indication, whether intranasal, IV, IM, or subcutaneous. Disease intervention lives here.

The pipeline

One platform. Many programs.

Tap Click for more on any program to see the disease context, why SAT fits, and where the program stands today.

Proof & Horizon

The validation and the future

ASFV demonstrated that SAT can clear a lethal pathogen in vivo. Oncology is where we believe SAT goes next.

Proof Point

African Swine Fever (ASFV) · swine

A veterinary-only program that proved SAT can clear a lethal pathogen in vivo.

ASFV has ~100% fatality in domestic swine and no approved vaccine or treatment anywhere. In our SAT swine challenge study, 57% of treated animals survived vs. untreated controls. To our knowledge, this is the first peer‑reviewed report demonstrating survival benefit from a CRISPR‑based therapeutic in an ASFV swine challenge model. Additional studies evaluating safety, reproducibility, durability, and potential translatability are being scoped. Published in Viruses (MDPI), November 2025.

ASFV is a veterinary-only program. It is not a human clinical track — it is the platform proof point that everything else builds on.

~100%
Fatality (untreated)
57%
Survival (SAT-treated)
Peer‑reviewed
Viruses (MDPI), 2025
First
of its kind in the world
Early‑Stage Research

Oncology

Forward horizon · Exploratory

Cancer is a sequence problem too: oncogenic drivers, fusions, and viral integrations are often conserved in ways the disease cannot easily escape without losing function. SAT’s ability to cut multiple targets directly and simultaneously addresses the limitations of many single‑target oncology treatments. This is a long‑horizon program — we are establishing the scientific basis before committing resources to a clinical track.

Exploratory. Not a near‑term clinical program.

Drivers
Oncogenic targets
Fusions
Conserved breakpoints
Integrations
Viral oncogenesis
Multiplex
Parallel cuts

Partner with us

Three ways to put programmable therapeutics to work. Tell us the disease area, the program, and the partnership shape — we’ll match an option to it.

Co-development

Joint programs against priority pathogens. Shared IP, shared risk, shared upside. Best fit for partners with a target they already care about and a need for platform leverage.

Start a conversation →

Licensing

Target-specific or family-specific PTAP™ licenses. Use the platform to design SAT constructs against pathogens already on a partner’s roadmap. We bring the chassis; you bring the program.

Discuss a license →

Government & global health

Active across U.S. federal innovation networks: BARDA RRPV, MTEC, MCDC. International collaborations in Australia and Vietnam. Open to global health organizations, sovereign health agencies, and international biodefense and pandemic preparedness programs.

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