Platform design

What your asset needs beside it.

We search targets, partners, payloads, sequences and settings against what your asset actually does, and hand back the few worth building. The model runs in seconds, so the search is wide enough to find the pairings nobody would think to try.

60B+possible combinations and sequences in a single cancer, narrowed to the handful worth the lab
The problem

What decides an asset is usually what sits beside it.

Biology runs on redundancy and feedback, so blocking one route very often means the cell reroutes through another. Which partner closes that route, in which setting, in which order, is where the outcome is actually decided. It is also the part no screen was built to answer.

01

The obvious indication is chosen for familiarity. Where a mechanism separates depends on the biology of the setting, and the setting closest to the last paper is rarely it.

02

Screens throw away the best partners. Sensitisers, immune primers and resistance-breakers carry weak signals on their own, so a pipeline tuned for single-agent efficacy discards them.

03

Resistance arrives on schedule. Durability erodes unless the escape routes are designed around from the start, which means knowing them before the disease finds them.

A full pairwise screen of 100 drugs at 100 doses runs to roughly 50 million experiments, and a dish still cannot see the immune compartment clearing a clone, the stroma walling a drug out, or what changes when you reverse the order of two agents. So we do it in a model that can, fast enough to search the whole space rather than a corner of it.

Built for  Founders & CSOs · Discovery · Lifecycle Management · Franchise & TA leads · Portfolio Strategy

What the model weighs

Every candidate regimen is walked through the same questions.

These are the factors that decide a real outcome and that a screen or a frequency-trained model leaves out. The distilled model carries all of them, which is what makes a search this wide worth running.

  • Target stateIs the state the drug engages actually present and active in these patients, or has the backbone already switched it off?
  • CouplingDoes what the first agent does create the state the second one needs, or do the two simply co-occur?
  • Resistance routesWhich escape routes are open, which does the regimen close, and which opens next once it does.
  • FeedbackWhere a blocked pathway reactivates through a loop, and how long that takes.
  • Population structureThe fraction cycling, dormant, immune-evasive or already resistant, and how each moves under the regimen.
  • AccessHow much of a dose reaches each disease site, including the ones a primary response leaves behind.
One engine, four questions

Search across the whole landscape, or only inside your own portfolio.

Combinatorial target ID

Discovery · Target ID

Rank pairs and triples of targets rather than single ones, scored on whether the combination closes the routes a tumour would otherwise take. In our first months we found that despite enormous genomic variability, resistance strategies recur across cancers in a similar order, which is what makes a search this size tractable.

Indication and context

Founders & CSOs · Portfolio Strategy

The setting where your mechanism separates first, the patient context that defines it, and the partner that widens the margin. Ranked by where the biology actually wins, with the experiments that de-risk the choice before you commit the programme.

Payload and vector

ADC · LNP · viral vectors · cell therapy

A delivery platform can carry almost anything almost anywhere, which is the hard part. We search payload against target against indication using what your platform genuinely does well, and hand back a lead with a resistance map showing where a second cargo will be needed later.

Lifecycle and franchise

Lifecycle Management · TA leads

The combination, sequence and setting that keep a marketed asset first-line while the backbone moves under it. Each candidate comes with a predicted survival benefit and the escape route it was designed to close.

Worked example

Same two drugs, largely similar disease biology, opposite result.

Venetoclax blocks the survival protein BCL-2. Azacitidine pushes blasts into depending on it. In acute myeloid leukaemia that pair became a standard of care. In myelodysplastic syndrome, a blood cancer with largely similar biology, it deepened remissions and then missed on survival. Any argument from resemblance calls both the same way.

VIALE-A

Azacitidine + venetoclax · AML

Standard of care

Tumour populations over time

0 12 24 36 100 50 0 MONTHS
Cycling blasts Primed, BCL-2 dependent Resistant

Overall survival

0 50 100 0 12 24 36 MONTHS % ALIVE 9.614.7 mo
Combination Azacitidine alone

Priming converts. The blasts that azacitidine pushes into BCL-2 dependence are killed, the burden stays down, and the curves separate. Median OS 14.7 months against 9.6.

VERONA

Azacitidine + venetoclax · higher-risk MDS

Survival not met

Tumour populations over time

0 12 24 36 100 50 0 MONTHS
Cycling blasts Primed, BCL-2 dependent Resistant

Overall survival

0 50 100 0 12 24 36 MONTHS % ALIVE NO SEPARATION
Combination Azacitidine alone

Priming happens and does not convert. Remissions deepen, the resistant fraction keeps growing underneath, and the curves close again. The overall-survival co-primary was not met.

The one variable

Is the marrow primed and dependent on BCL-2, so that killing the primed fraction removes what drives the disease? In AML it is. In MDS the priming happens, and the cells that carry the disease forward are not the ones it kills.

Population plots are model output. Survival plots are drawn to the published read-outs: VIALE-A reported a median OS of 14.7 months against 9.6 (NEJM 2020;383:617); VERONA (NCT04401748) deepened remissions with the overall-survival co-primary not met, and is drawn to that shape rather than to published medians.

Getting started

With just a target and a disease context, we can tell you what we expect to happen.

Send us a mechanism, an asset you want to defend, or a platform looking for its first indication. Because the model runs in seconds we can usually turn an initial review around within hours, and often for free, to show what can be done and to suggest a pathway to the optimal approach.

More than once a partner has come back somewhere between impressed and unsettled, because what we sent matched what they had spent a year working out in the lab, and included things they had not found yet. Those are the conversations we like having.