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Validated assets

We do not just run the models.
We run discovery programs.

These are not drugs we are developing in-house. They are vetted assets we have advanced through our discovery platform across oncology, cardiovascular, inflammation, and metabolic disease — available for out-licensing and co-development with partners ready to take them forward.

Available assets GPR75 spotlight CD73 case study
Available assets

Eleven assets across four therapeutic areas — available for partnership.

Each is a vetted target or hit series advanced through our discovery platform. Partners take them from here. Spotlights below carry the detailed content.

Engagement model

Out-licensing or co-development — not internal clinical development. We continue work on assets where partners want us to (or add new programs at partner request); the goal is dealable chemistry, not a drug-development pipeline of our own.

Target / Asset Therapeutic area Discovery stage Partnering status
GPR75 Lead asset Obesity / Metabolic Hit-to-Lead Lead asset, available for out-licensing
PCSK9 Cardiovascular Hit-to-Lead Available for discussion
CD73 / 5NTE Oncology Hit Discovery (30% hit rate) Case study + available
IRAK4 Inflammation Target Validation Available for discussion
IL17A Inflammation Target Validation Available for discussion
TYK2 Inflammation Target Validation Available for discussion
GLP1R Metabolic Disease Target Validation Available for discussion
AMPK Metabolic / Oncology Target Validation Available for discussion
MEN1 Oncology Target Validation Available for discussion
Factor XI Cardiovascular Target Validation Available for discussion
FcGRN Autoimmune / Rare Target Validation Available for discussion
Lead asset spotlight

GPR75 — an orphan GPCR with human genetic validation for obesity.

The target

GPR75 is an orphan GPCR validated by human genetics as a negative regulator of body weight. Loss-of-function variants associate with significantly lower BMI in large population studies, with no adverse effects in carriers — among the strongest human-genetic obesity signals published in the last decade.

No approved drugs. Open IP. Currently at Hit-to-Lead.

What this opens up

  • Human-genetic validation — population-scale loss-of-function evidence rather than animal or phenotypic surrogates.
  • Open IP landscape — no approved drugs at this target; first-in-class window without competing programs to navigate around.
  • A new mechanism beyond GLP-1 — complementary to or differentiated from incretin-based programs depending on combination strategy.
  • Tractable on a novel target — limited structural precedent for an orphan receptor would normally constrain foundation-model dockers; our platform retains predictivity at 0–20% Tanimoto similarity (see Why Deep Origin).
Request the GPR75 data package
Case study

CD73 — a 30× improvement over the industry hit-rate benchmark.

CD73 (5′-nucleotidase NT5E) — cell-surface enzyme converting AMP to adenosine; modulates immune suppression and tumor metabolism. Widely expressed in cancers.

Challenge

Industry screens against CD73 yield hit rates of 1% or less1,2 from hundreds to thousands of compounds synthesized. High-throughput screening is the standard approach — expensive, slow, and generates a lot of chemistry that goes nowhere.

What we did

Applied physics-based docking and multi-parameter computational filtering to a virtual compound library before any synthesis was commissioned.

Result
  • 48 of 159 compounds (30%) with binding affinity below 80 µM.
  • 9 compounds below 10 µM.
  • Dose-response — correlated single-dose inhibition with pIC₅₀ from full curves at both 10 and 100 µM.
  • Chemotype diversity — hits cluster at 0.2 Tanimoto similarity, well outside the training distribution.
  • Drug-like properties — SlogP, AMW, TPSA, and Lipinski HBA / HBD distributions all within drug-space.
30× improvement in hit rate vs. the industry benchmark — translating directly into synthesis cost savings, faster lead identification, and a smaller, better-characterized compound set entering lead optimization.
Tanimoto similarity — identified hits cluster at ≈0.2, outside the training distribution. Compounds advanced are chemically novel.
Ranking of foundational models across 22 TDC tasks — Deep Origin Togo leads on early-ADME tasks; CYP-mediated inhibition remains a tradeoff. Request access for more detailed information →
  1. The Atomwise AIMS Program. AI is a viable alternative to high throughput screening: a 318-target study. Sci Rep 14, 7526 (2024). doi:10.1038/s41598-024-54655-z
  2. Kumar M, Lowery R, Kumar V. High-Throughput Screening Assays for Cancer Immunotherapy Targets: Ectonucleotidases CD39 and CD73. SLAS Discov. 2020 Mar;25(3):320-326. doi:10.1177/2472555219893632.

Open to a deeper conversation?

Detailed data sets, IP positions, and partnership structures are shared under CDA on request. Initial calls are with our BD lead.

Request a CDA & data package Explore the science