Dashboard
Open sortable data table →Interactive views over the 1,948-molecule catalog. Charts are hoverable; the step chart is clickable. Each panel has a “How to read this” toggle with what it shows, how to read it, and the takeaway.
Reading the confidence & step buckets. 417 of 1,948 molecules (21%) carry a low pathway-step confidence — treat their placement as tentative. The “systemic / off-pathway” step (432 molecules) is a deliberate catch-all for circulating markers of MI risk or injury that do not sit at a specific point in the atherothrombotic cascade (e.g. systemic metabolic markers); it is not one of the eight ordered cascade steps.
Molecules per cascade step
Click a bar to jump to that step. Lighter overlay = druggable targets.
Evidence coverage by step
Count of molecules with each evidence type, per cascade step.
Molecule types
1,948 molecules by biochemical class.
Pathway-step assignment confidence
Confidence of each molecule's pathway-step assignment (evidence-tagged inference).
Discrimination & diagnostic analytics
Deeper views over the Type-I-vs-non-Type-I scoring, assay logistics, and evidence coverage. The signature map and leaderboard are clickable; every chart is hoverable.
Linked cross-filter explorer
Click any bar to filter every panel at once — e.g. pick a pathway step, then see the class / type / evidence breakdown for just those molecules, with the matching set listed below. Stack filters; each chip removes one.
1,948of 1,948 molecules match
By pathway step
By discrimination class
By molecule type
By evidence source
Matching molecules (1,948) — click to open · top 60 by T1DI
ⓘ Scoring glossary — what R, C, D, T1DI and the classes mean
R — Rupture / Type-I responsiveness (0–100). How strongly a marker tracks the plaque-rupture / atherothrombotic process that defines a Type 1 MI. Higher = more responsive to rupture biology.
C — Non-Type-I responsiveness (0–100). How strongly the same marker also rises in the other ways myocardium infarcts: supply–demand mismatch (tachycardia, anemia, sepsis — Type 2), periprocedural injury after PCI (4a) or CABG (5), stent thrombosis (4b), in-stent restenosis (4c) and sudden cardiac death (Type 3). Twelve axes in all. Higher = less specific to Type 1.
D — Direct evidence. Whether a marker has been tested in a study that directly compares Type 1 patients against a non-Type-I comparator group (as opposed to inferred from mechanism). Only a handful of markers have this.
T1DI — Type-I Discrimination Index (0–100). A composite that rewards high R, penalizes high C, and up-weights markers with direct evidence. It is the single ranking score for “how cleanly does this separate Type 1 from every non-Type-I cause of infarction?”
Tiers. Tier 1 (deep-scored) markers were individually reviewed with full R/C/D scoring; the rest carry lighter, mechanism-derived estimates. Filter to Tier 1 when you want the most defensible numbers.
Discrimination classes. Type-I-specific = high R, low C (currently empty — no molecule reaches it under this comparator) · Shared = rises in both (e.g. troponin) · Non-Type-I-associated = tracks non-atherothrombotic drivers · the greyed classes flag proxy-only or insufficient evidence.
Type-I vs non-Type-I signature map (R vs C)
Each point is a scored biomarker: x = rupture/Type-I responsiveness (R), y = non-Type-I responsiveness (C) across the 12-axis UDMI-4 panel. Bottom-right = rises with plaque rupture but NOT with non-atherothrombotic drivers (ideal Type-I-specific). Top-right = rises with both (e.g. troponin). Color = discrimination class. Click a point to open the molecule.
Harvested per-axis evidence. R and C are independent here (r = 0.03).
Discrimination class by pathway step
How each cascade step's molecules distribute across T1-vs-non-T1 classes. Hover for counts.
Scoring coverage by evidence axis
How many of the 1,948 catalogued molecules carry each kind of scored evidence. The steep drop to direct T1-vs-non-T1 studies (D) is the core data gap.
Evidence sources by pathway step
Molecules with each evidence type at each step (literature, trials, omics, genetic, druggable).
Assay method families
How the whole catalog would be measured — dominated by immunoassay, with mass-spec/NMR for metabolites & lipids.
Specimen collection tubes
Primary blood-collection tube per marker (color-coded phlebotomy standard). K2-EDTA whole-blood entries are the gene-locus/genotyping records.
Assay validation status
Whether each marker's assay profile is a specific validated clinical assay, a specialized reference method, or a class-level default inferred from analyte type.
Evidence-source co-occurrence (UpSet)
How evidence types stack up per marker. Each row is a combination of sources; the bar is how many molecules have exactly that set. Dots below mark which sources are in each combination.
933
653
99
87
55
51
18
18
15
10
3
3
Literature (1,793)
Trials (89)
Omics (19)
Genetic (280)
Druggable (890)
Mechanism vocabulary frequency
How often each mechanistic concept appears across all 1,948 curated mechanism descriptions — the biology the catalog is built on.
Top discriminators by T1DI (deep-scored)
Highest Type-I Discrimination Index among Tier-1 markers. Click a row to open the molecule. Color = class.
166
262
361
447
541
640
737
837
935
1035
1133
1233
1332
1432
1532
1631
1731
1831
1931
2030