KORVIONIX SYNLETH DDR PLATFORM

Synthetic lethality, designed into the asset.

Korvionix builds small-molecule DDR programs around biomarker-defined cancer dependencies and resistance states. SynLeth co-designs the molecule, tumor-selection logic, and experimental proof needed to create a differentiated oncology asset.

01Vulnerability-first biology
02Molecule + biomarker co-design
03Experiment-defined assets
Our differentiation

SYNLETH

A DDR platform built around conditional cancer vulnerabilities—not target lists.

SynLeth asks where a tumor becomes dependent on a DNA-repair pathway, why that dependency should be druggable, and what experiment could disprove the thesis. That context stays attached from target selection through molecular nomination.

01

Start with the vulnerability

SynLeth begins with a tumor-state dependency—HRD, replication stress, a repair defect, or therapy resistance—not with a target in isolation.

02

Co-design the asset

Chemistry, selectivity, biomarker logic, resistance strategy, and indication fit are designed as one product thesis rather than sequential workstreams.

03

Design the disproof

Every program carries the assays, counter-screens, failure thresholds, and stop rules needed to challenge the thesis before capital-intensive development.

01

Vulnerability

Define the tumor state and the dependency that creates selective pressure.

02

Mechanism

Connect target engagement to lethality, resistance, and pharmacodynamic logic.

03

Chemistry

Design differentiated, synthesizable series for the relevant target states.

04

Falsification

Challenge selectivity, exposure, safety, biomarker, and IP assumptions.

05

Asset

Nominate a molecule series with a responder thesis and decisive experiments.

Programs

A focused portfolio across DDR vulnerabilities.

Korvionix is building across PAR turnover, replication-stress control, and alternative DNA repair. Each program pairs a differentiated small-molecule thesis with a biomarker-defined tumor context and the experiments needed to test it.

Flagship

PARG

Poly(ADP-ribose) glycohydrolase

Lead program · Computational discovery

Building differentiated PARG inhibitor hypotheses for PARP-inhibitor-resistant and replication-stressed tumor contexts, pairing binding-site design with biomarker and proof-of-mechanism strategy.

  • Multi-state pocket design
  • PARPi-resistance biology
  • HRD & replication stress
Expansion

PKMYT1

Replication-stress checkpoint kinase

Active expansion program · Computational design

Developing a second-generation design strategy for replication-stressed tumor contexts, with early emphasis on chemical differentiation, kinase selectivity, and resistance-aware tumor selection.

  • Replication-stress biology
  • Kinase selectivity
  • Biomarker-linked design
Expansion

POLQ

DNA polymerase theta

Active expansion program · Target and chemistry design

Building a distinct small-molecule program for homologous-recombination-deficient tumor contexts, integrating structural tractability, selectivity, and resistance strategy.

  • HRD synthetic lethality
  • Structure-led design
  • Resistance strategy
Research-stage disclosure

These are computational discovery programs. Molecule-level hypotheses require synthesis, analytical confirmation, and reproducible experimental validation before they can be described as confirmed hits or drug candidates.

What drives SynLeth

Four questions drive every program.

A molecule does not advance because a model scores it highly. It advances only when selective tumor biology, defensible chemistry, and a decisive validation path form one coherent asset thesis.

01

Who should respond?

Define the genotype, functional state, prior treatment, or resistance mechanism that creates a target dependency—and the biomarker strategy that can identify it.

02

Why should inhibition be selectively lethal?

Connect genetic dependency, pathway state, target engagement, pharmacodynamic response, and escape routes before a molecule is treated as an asset.

03

What makes the chemistry defensible?

Integrate receptor states, conserved waters, measured SAR, scaffold white space, selectivity, synthesis, developability, safety, and composition-of-matter opportunity.

04

What evidence could prove us wrong?

Specify orthogonal assays, counter-screens, liability tests, responder comparisons, and stop criteria so weak theses fail early and visibly.

Platform output

Not a score. An experiment-ready asset package.

SynLeth is designed to hand a scientific or CRO partner a testable program: who the therapy is for, why the chemistry is differentiated, which experiments matter, and what would stop the program.

01 · Therapeutic thesis

A defined responder

A target, tumor context, biomarker hypothesis, pharmacodynamic logic, and resistance or combination strategy that belong together.

02 · Chemistry package

A defensible series

Ranked, synthesizable designs with binding rationale, scaffold differentiation, selectivity intent, developability risks, and explicit IP questions.

03 · Validation blueprint

A decisive experiment

Biochemical and cellular confirmation, target engagement, biomarker comparisons, counter-screens, early DMPK, and predeclared go/no-go thresholds.

Company

Focused on DDR assets—not a general-purpose AI platform.

Korvionix is a founder-led computational oncology company in Rockville, Maryland. Its thesis is simple: DDR drugs should be designed together with the tumor context that makes them selectively lethal.

SynLeth directs that work internally; specialized partners execute synthesis, biochemical and cellular assays, DMPK, safety, and translational validation. The result is a lean path from a focused vulnerability thesis to experimental proof.

Model
Asset-centric computational biotechnology
Focus
Small-molecule DDR oncology
Location
Rockville, Maryland
Legal entity
Virovance Inc. · Delaware C corporation

Connect

Advance a focused DDR program with us.

Korvionix welcomes accelerator, scientific, infrastructure, CRO, and strategic partnering conversations.

Contact Korvionix