
At a glance
- Models
- 1,500+ characterized
- Pretreated
- 65% of models
- Late stage
- 80% of models
- Since 2007
- 400+ biopharma partners

Champions Oncology data platform
Matched multi-omic, clinical and drug-response data from 1,500+ patient-derived tumor models, delivered as licensed data or as the answer to the question your program is asking.
Overview
Public datasets such as TCGA, DepMap and CPTAC were built for different questions. They profile primary, mostly untreated tumors or immortalized cell lines, and few carry drug response measured on the same sample. When the response and the molecular profile come from different tumors, every attribution between them rests on an assumption you cannot test.
We profile and dose the same patient-derived models. Exome and RNA sequencing, whole-cell and cell-surface proteomics, IHC, clinical history and in vivo response are matched by donor, so a candidate marker and the response it explains come from one tumor. Because the models are renewable, you can return to that tumor and test the next hypothesis in it.
Most models come from late-stage, pretreated patients, so the bank carries the resistance biology that public data largely misses. You can license the data into your own environment, or have our scientists run the analysis and deliver the result as a defined package, starting with target discovery.

What you can ask
Is the target present, localized at the surface and accessible in tumors that have already seen therapy? Matched surface and whole-cell proteomics answer it directly.
Ranked surface candidates
What separates responders from non-responders? Baseline profiles are matched to response on the same models, so the marker and the response it explains share a tumor.
Candidate response markers
Why does a response stop? Profiling through treatment and into acquired resistance shows the mechanism as it develops, and points to combinations worth testing.
Combination hypotheses
How does your compound compare to the standard of care? We run it against a concurrent reference arm on the models you select, not against historical controls.
Head-to-head response data
Ways to work

New
Name the indication you care about. We return a target report for it, with each candidate's prevalence, RNA, protein and membrane expression, a normal-tissue safety screen, validation scores, the competitive landscape and the models available to validate it.
Every surface call is labeled as measured by direct membrane proteomics or inferred from other data, and every report is checked by a named scientific reviewer before it is issued.
Best suited to

Analysis service
We design the study around your question, select the models, run your compound in vivo where needed and analyze the result against the matched molecular data already held on those models.
You receive a report with the figures, tables and methods behind each conclusion. The data underneath is available on request, so any finding can be traced back and checked.
Best suited to

Data licensing
Curated cohorts are licensed by indication or data layer and delivered into your own systems, ready to enrich internal and public datasets with deeply characterized, donor-matched tumors.
Licenses are scoped by cohort and term. Layers can be generated on demand for models you select that have not yet been profiled, so the cohort fits your question.
Best suited to
You will be able to analyze our data alongside your own in a governed workspace without either dataset leaving it. Tell us if this is how your team would prefer to work.
How it grows
Exit criterion — models chosen against existing molecular and clinical data.
Exit criterion — response measured beside a same-model reference arm.
Exit criterion — response linked to baseline data on each model.
Exit criterion — new layers generated on models already validated.
Exit criterion — hypothesis tested in the tumor it came from.
Clinical relevance
Our models come from patients with recorded treatment and response histories: 80% late stage, 65% pretreated and 55% metastatic. That matters because resistance biology is shaped by prior therapy, and models built from untreated primary tumors cannot show it.
In matched patient cases, the models predicted clinical outcome with a positive predictive value of 85% and a negative predictive value of 91% (Izumchenko et al., Annals of Oncology, 2017). Ask us for the paper, cohort and endpoints behind those figures.

Get Started
Discover how surface expression correlates with treatment response.
Explore new target opportunities validated in real human tumors.
Assess the quality and interpretability of our data for your own programs.
FAQ
Related pages
The dataset
Every data layer, its coverage by tumor type and the clinical annotation each model carries.
Cell-surface proteomics
How surface abundance is measured, validated and used to rank conjugate targets.
KRAS-Mutant Atlas
A response and resistance reference built on daraxonrasib for KRAS-directed programs.
Mouse clinical trials
Run your compound across a cohort of models the way a trial enrolls patients.

Start here
A data scientist replies to every request personally
Model and layer availability included in the reply
CDA handled before any program detail is shared