The ground truth for drug discovery

We measure real interactions between real molecules, on the hardest targets and the most complex modalities.

Who we help

For the targets and molecules that stall discovery

We work with discovery teams with hard targets, AI drug discovery companies, and teams developing complex modalities such as molecular glues, degraders and PPI inhibitors.

  • Hard targetsScreening and characterisation from micrograms of protein, for targets that are scarce, unstable or hard to make.
  • AI-designed moleculesBinding measured directly for each design: which bind, how strongly and how selectively, with data to feed back into the models.
  • Complex modalitiesComplexes formed by glues and degraders, or disrupted by PPI inhibitors: observed directly and without labels.
  • Co-developmentJoint programmes that pair partners’ biology with our chemistry and platform.

Discovery engine

Make. Identify. Optimise.

From primary screen to lead optimisation.

  1. Make. Your compounds or AI-designed molecules, screened one at a time or thousands at once.
  2. Identify. What binds, detected directly by its exact mass, from micrograms of protein: free of labels, immobilisation and custom assays.
  3. Optimise. What binds shapes the next library, round after round, through to the characterisation of analogue series.

Proof points

Proven on hard targets

Case 01 / 04

PROTAC-induced ternary complex

One measurement resolves every species in the mixture: KRAS G12C, free and covalently bound to the PROTAC LC-2; the VHL E3 ligase complex and its subunits; and the 68.3 kDa ternary complex, which forms only with the PROTAC.

With PROTAC (LC-2) Without PROTAC 68.3ternary complex KRAS + LC-223.5 VHL complex44.7 KRAS 22.4 20 40 60 kDa

Case 02 / 04

Kir4.2 ion channel

A screen of 2,000 natural products, multiplexed in pools of 100, identified a new Kir4.2 binder: ginsenoside Rg1. A control protein showed no binding to the same compounds. The channel’s known agonist, polymyxin B, added to one pool as a control, was also identified.

Gu et al., ACS Chem. Biol. 2024 · doi:10.1021/acschembio.3c00781

Kir4.2 + library pool 839.5 ginsenoside Rg1 823.5 Control protein + same pool No ions detected 820 830 840 850 m/z

Case 03 / 04

Highly multiplexed screening

Macrocycle pools from 20 to more than 160,000 compounds were screened against the E3 ligase KEAP1. The binders found match the amino acid sequences recognised by KEAP1 in vivo, including ETGE and ESGE, plus further variants. Without the ligase, nothing was found.

KEAP1 + 8,000 macrocycles ESGE ETGE + 13 more motif variants Same pool, no KEAP1 No binders detected 700 750 800 m/z

Case 04 / 04

TRPM2 ion channel

A screen of 2,000 natural products, multiplexed in pools of 100, identified a new TRPM2 binder by its exact mass: ginsenoside F3. The known inhibitor clotrimazole was also identified. A control off-target protein showed no binding to the same compounds.

Gu et al., ChemBioChem 2024 · doi:10.1002/cbic.202300790

TRPM2 + 100-compound pool 809.4 ginsenoside F3 771.5 793.5 Control protein + same pool No ions detected 770 790 810 m/z

Our pipeline

Our own programmes in endometriosis

One in ten women of reproductive age live with it, yet there is no cure. We apply our platform to our own discovery pipeline, and we’re open to partners.

  • Target-led discoveryFirst-in-class programmes on prioritised endometriosis targets, progressing hits towards lead compounds.
  • Patient-biology-led discoveryStarting from patient tissue, to uncover new disease-driving targets and the patients most likely to benefit.

Contact

Bring us your hardest target

Whether you have a target to screen, hits to confirm, or a question your assays can’t answer, a short call is usually enough to say whether we can help, and how fast.

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