Move every translational program forward, defensibly.
Inflexa runs the analyses that drive a translational decision: responder stratification, biomarker discovery, mechanism of action, and target prioritization. Every conclusion arrives with PubMed-cited literature and a complete audit trail.
Analytics
An analysis agent reads the literature for your biology, picks methods that fit your cohort, and runs every step end-to-end with full provenance.
Learn more ›Reporting
Build interactive reports and dossiers from your analysis output, in one conversation. Share with translational, clinical, and external collaborators.
Learn more ›Provenance
Every claim traced to source: PubMed-cited literature, immutable audit logs, and end-to-end data lineage. Defensible by design.
Learn more ›Method choices that fit your cohort.
An analysis agent reads the existing literature for your biology, evaluates the shape of your dataset, and designs a multi-step plan with method choices you can inspect and override. The agent does not run a single canned pipeline. It reasons about which pipeline applies to your biology and your cohort structure.
When multiple methods are applicable, the agent runs all of them and surfaces only the findings that hold up across approaches. Multi-method consensus separates signal from statistical artifacts, especially in underpowered translational cohorts where analytical choice can change the conclusion.
Coverage spans bulk and single-cell transcriptomics, proteomics, metabolomics, and multi-omics integration. Every step is traceable: method, parameters, intermediate results, and the agent’s reasoning are all captured in the provenance record.
Click a step to see details
Reports your translational team can actually use.
Tell Inflexa what story you need to tell: responder stratification, biomarker association, survival by signature, pathway breakdown. The platform assembles a navigable, interactive report in the same conversation as the analysis, with no exporting and no reformatting.
Reports are designed for iteration. Ask for a different visualization, pull in additional context, or tighten the interpretation. Every version is preserved with its provenance intact. Share directly with translational leadership, clinical collaborators, or external partners.
Each section of the report is linked back to the analysis steps and source data that produced it. When a reviewer asks why a finding appears, the answer is one click away.
Generated by Inflexa on February 20, 2026 at 9:00 PM
Survival & Prognosis
Total ancestry effect on survival is null
After adjusting for subtype, age, and stage, African ancestry does not confer a survival advantage or disadvantage (OS endpoint, n=957, 137 events). Breast cancer survival disparities are largely explained by clinical factors, not ancestry-specific molecular features.
SHAP Feature Importance: Ancestry-Specific Survival Models
Top 20 features by mean |SHAP| value for each ancestry-specific CoxPH model. Colors indicate feature group.
EA Model (C-index = 0.652)
Mean |SHAP|
AA Model (C-index = 0.408)
Mean |SHAP|
AA model is dominated by PI3K–Akt–mTOR (SHAP=0.510), while EA spreads importance across TF and checkpoint features. NT5E (CD73) is the top EA feature, consistent with adenosine-driven immunosuppression.
Causal Mediation: Ancestry → Survival
Indirect effect of ancestry on OS through each mediator (n=957, 137 events).
Prognostic Signature Divergence
Of 165 unique prognostic genes, only 2 (1.2%) are shared between EA and AA, the most extreme divergence at any molecular layer.
Top Prognostic Genes by Ancestry
CoxPH coefficient and hazard ratio. Direction indicates risk-up vs risk-down.
EA Signature
n=726, 101 events, C=0.652
Showing 3 of 82 genes
AA Signature
n=106, 13 events, C=0.408
Showing 3 of 85 genes
Defensible by design.
Every conclusion in an Inflexa dossier rests on three foundations a reviewer can audit without talking to you: PubMed-grounded literature, an immutable record of every step, and a walkable map from raw input to final figure.
Targeted PubMed queries against each programme's hub genes, transcription factors, and pathways. Every claim links to its supporting PMID, tiered from basic biology to preclinical to clinical.
Every action (input, method, parameters, output) is logged the moment it occurs and sha256-verified. Entries are immutable, and reproducibility is built in.
Click any conclusion and walk back through transformation steps to the source data. Every intermediate artefact is versioned and content-hashed.
- Basic biologyPMID 19620293
CXCL13 is expressed by T follicular helper cells and drives B-cell recruitment in inflamed tissue.
- PreclinicalPMID 28842433
CXCL13 blockade reduces B-cell infiltration and attenuates colitis severity in murine UC models.
- ClinicalPMID 36792466
Elevated CXCL13 associates with treatment non-response in pediatric UC cohorts.
- final_recommendation.mdT4S2/output4/19/26, 9:02 PM1eae4274
- molecule_grid_top_candidates.pngT4S2/figures4/19/26, 9:02 PM28331cb7
- scaffold_ranking.csvT4S2/output4/19/26, 9:02 PM492baa68
- comparison_table.csvT4S2/output4/19/26, 9:02 PM47498e57
Built for teams doing the hardest translational work.
Inflexa is not a general-purpose bioinformatics tool. It is purpose-built for translational medicine, where the biology is uncertain, the cohorts are small, and the bar for defensibility is high.
Translational medicine teams
Bring Phase 1/2 cohorts, trial-adjacent datasets, or retrospective multi-omics. Inflexa runs the analysis, builds the dossier, and produces evidence chains ready for an IND or an internal translational review.
Learn more ›Exploratory biomarker scientists
Identify responder signatures, biomarker candidates, and confounders across omics layers, without writing a single pipeline. Get to testable hypotheses faster, with the literature context already embedded.
Learn more ›Translational safety and clinical pharmacology
Assess mechanism-of-action hypotheses, cross-species signal translation, and emerging safety signals from expression data. Every finding is literature-grounded, scored for evidence strength, and audit-ready.
Learn more ›From Confounded Cohort to Druggable Hypotheses
A translational deep-dive into pediatric UC non-response: 206 patients, three actionable programmes, one major disqualification, and a novel anti-CXCL13 target.
After PK/safety/readiness penalties, rosiglitazone falls despite top biology; sodium butyrate rises to #1.
Bring us a Phase 1/2 cohort.
Tell us about a translational dataset you care about. We’ll scope a paid discovery collaboration in 2–3 weeks and run a full analysis.