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.
Six 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.
| Target / Asset | Therapeutic area | Discovery stage | Partnering status |
|---|---|---|---|
| GPR75 Lead asset | Obesity / Metabolic | Virtual Screening | Lead asset, available for out-licensing |
| PCSK9 | Cardiovascular | Virtual Screening | Actively screening — available for discussion |
| CD73 / 5NTE | Oncology | Hit-to-Lead | Case study ready — available |
| IRAK4 | Inflammation | Hit Expansion | Available for discussion |
| IL17A | Inflammation | Hit Expansion | Available for discussion |
| Factor XI | Cardiovascular | Hit Expansion | Available for discussion |
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. Virtual screening underway.
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).
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.
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.
Applied physics-based docking and multi-parameter computational filtering to a virtual compound library before any synthesis was commissioned.
- 80B compounds screened — ~80 billion synthetically accessible compounds screened; 183 experimentally tested.
- 56 biochemical hits — including 54 <100 µM and 9 <10 µM IC₅₀.
- 14 cellularly active compounds — including a 570 nM lead.
- ~30% hit rate at <100 µM — substantially exceeding prior virtual-screening results.
- Chemically novel non-nucleotide scaffolds — with low similarity to known CD73 inhibitors (ECFP4 Tanimoto mean ~0.22–0.27).
- Hit-to-lead underway — using analogue-by-catalogue and cheminformatics-guided direct-to-biology strategies to accelerate DMTA cycles and lead optimization.
- 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
- 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.