AI algorithms are now included in the NCCN (National Comprehensive Cancer Network) clinical guidelines for patient stratification.

Recursion's FAP drug achieved its median polyp reduction after three months of treatment, whereas other experimental drugs have taken 12 months to achieve approximately half that effect.

The reduction in polyp burden from Recursion's FAP drug was sustained for at least three months after patients stopped taking the medication.

Recursion's integration with Exscientia expanded its capabilities from novel biology discovery to AI-driven small molecule design.

Recursion's strategy is to be an end-to-end platform covering biology, chemistry, and clinical development, differentiating it from competitors who focus on point solutions.

Familial adenomatous polyposis (FAP) affects over 50,000 patients in the United States and European Union.

There are currently no approved pharmacotherapies for familial adenomatous polyposis (FAP), with surgery being the only standard of care.

There are currently no approved disease-modifying drugs for Parkinson's disease.

Recursion synthesizes an average of 330 compounds to identify a final drug candidate, compared to an industry average of 5,000.

Recursion plans to begin conversations with the FDA this year to design a Phase 3 registrational study for its familial adenomatous polyposis (FAP) drug.

Recursion has generated a dataset of one trillion iPSC-derived neuronal cells in which every gene in the human genome has been knocked out.

Patients with familial adenomatous polyposis (FAP) have a 100% risk of developing colorectal cancer if the condition is left untreated.

Recursion positions itself as the first end-to-end, AI-native platform company for drug discovery and development.

In clinical trials, Recursion's drug for familial adenomatous polyposis (FAP) demonstrated a 43% median reduction in polyp burden.

Recursion's drug design process takes an average of 17 months, compared to an industry average of 42 months.

Recursion's platform identified that an allosteric MEK1/2 inhibitor can reverse the cellular phenotype of APC gene loss-of-function, a novel biological insight.