The AI co-scientist for
drug development.
Structured programs that generate novel hypotheses and de novo candidates, and return reviewable, evidence-backed artifacts with every claim traced to its source.
Every answer stays connected to its sources.
Search and review the literature, and navigate a living knowledge graph of entities, claims and evidence: the surfaces the co-scientist reasons over, and traces every recommendation back to.
Literatureillustrativemechanism 4
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example sourceN Engl J Med
Risankizumab induction and maintenance therapy in Crohn's disease
Selective IL-23 p19 blockade produced significantly higher rates of clinical remission and endoscopic response than placebo across two induction trials, confirming the IL-23 axis as a driver of mucosal inflammation.
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example sourceNature
Structural basis of interleukin-23 recognition by its receptor
Cryo-EM of the IL-23–IL-23R complex reveals the p19 helix-D interface that governs receptor engagement and downstream JAK2 / TYK2 recruitment, defining a druggable binding epitope.
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example sourceImmunity
IL-23R signaling licenses pathogenic Th17 cells in the gut
Conditional deletion of IL-23R abrogated IL-17A / IL-22 production and protected mice against T-cell transfer colitis, establishing receptor signaling as necessary for the pathogenic Th17 program.
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example sourceGastroenterology
Residual TYK2–STAT3 signaling after IL-23 blockade in inflamed mucosa
Roughly one third of mucosal biopsies retained phospho-STAT3 despite complete IL-23 neutralization, implicating a parallel TYK2-dependent pathway that may limit monotherapy efficacy.
known binders 3
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example sourcemAbs
Engineering risankizumab, a high-affinity anti–IL-23 p19 antibody
Affinity maturation produced a Fab binding IL-23 p19 with sub-nanomolar KD and complete neutralization of receptor-mediated STAT3 activation in reporter assays.
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example sourceJ Immunol
Epitope mapping of guselkumab on the IL-23 p19 subunit
Hydrogen–deuterium exchange localizes the guselkumab epitope to a surface distinct from the receptor interface, supporting an allosteric mechanism of neutralization.
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example sourceNat Commun
A designed miniprotein antagonist of the IL-23 receptor
A computationally designed 74-residue mini-binder competes with IL-23 for IL-23R with low-nanomolar affinity and blocks Th17 differentiation in vitro.
disease association 3
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example sourceScience
A genome-wide association study identifies IL23R as an IBD susceptibility gene
The IL23R R381Q variant confers strong protection against Crohn's disease, providing human genetic validation of the IL-23 pathway as a therapeutic target.
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example sourceNat Genet
Fine-mapping of IBD loci implicates coding variation in IL23R and TYK2
Statistical fine-mapping resolves independent protective alleles across IL23R and TYK2, suggesting the two genes act in a shared pathway relevant to combination targeting.
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example sourceGut
Mucosal IL23R expression predicts response to anti-IL-23 therapy
Baseline IL23R transcript levels in colonic biopsies stratified endoscopic responders from non-responders, motivating a biomarker-enriched trial design.
safety 2
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example sourceLancet Gastroenterol Hepatol
Long-term safety of IL-23 inhibitors in inflammatory bowel disease
Pooled safety across three trials showed no increased serious-infection signal versus placebo through 52 weeks, supporting a favorable benefit–risk profile.
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example sourceClin Gastroenterol Hepatol
TYK2 inhibition and herpes zoster risk: a pharmacovigilance analysis
Selective TYK2 inhibitors carried a modest, dose-dependent zoster signal, informing the safety monitoring plan for a combination regimen.
Reviewer hint: Mechanistic support is strong (cryo-EM plus human genetics), but head-to-head human combination data remains limited to a single underpowered cohort. Flag that as the key evidence gap.
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