);
}
// Panels reused by the standalone Prediction + Lazarus sections below.
function TaxonomyPanel(){
return (
{TAXONOMY_LAYERS.map(l=>(
{l.num}Tier {l.num}
{l.count}
{l.sub}
{l.title}
{l.body}
{l.chips.map(c=>{c})}
))}
);
}
function ScoringPanel(){
const principles = [
{ k:"Multi-omic", d:"Each prediction integrates orthogonal layers — human genetics, transcriptomics, functional genomics, and known pharmacology — never a single signal." },
{ k:"Directionally aware", d:"We check a drug pushes the pathway the right way — inhibit vs. activate — matched to what the subtype actually needs, from established pharmacology." },
{ k:"Mechanism-grounded & auditable", d:"Every prediction traces to a named, inspectable rule against the subtype's causal biology. No black-box score to take on faith." },
{ k:"Safety-gated", d:"Contraindication and adverse-event signals act as a final gate, so unsafe pairings can't surface near the top." },
];
return (
{principles.map((p,i)=>(
0{i+1}
{p.k}
{p.d}
))}
Calibrated against FDA-validated repurposing successes. The underlying feature set and weights are proprietary.
);
}
// Causal-genetics content as a ticker panel (three evidence axes + convergence
// stats + the "honest by design" note). IP-clean: no internal names/weights.
function CausalGeneticsPanel(){
const AXES = [
{ tag:"Population genetics", sub:"GWAS × QTL",
body:"Colocalization + Mendelian randomization: disease signal and gene expression trace to the same causal variant, replicated across ancestries.",
chips:["PCSK9 → coronary disease","IL23R → IBD","HMGCR → lipids"] },
{ tag:"Functional dependency", sub:"CRISPR screens",
body:"Genome-wide screens confirm cells truly depend on the gene — pan-essential housekeeping genes are filtered out.",
chips:["selective dependency","not pan-essential"] },
{ tag:"Clinical genetics", sub:"ClinVar · ClinGen · Orphanet",
body:"Pathogenic variants and curated gene–disease validity add rare-Mendelian proof that GWAS alone can't see.",
chips:["pathogenic variants","curated validity","rare Mendelian"] },
];
const CONV = [
{ n:"~130K", l:"causal gene–disease links" },
{ n:"3", l:"independent evidence axes" },
{ n:"17 / 19", l:"orthogonal substrates confirm (p < 0.05)" },
];
return (
{AXES.map((a,i)=>(
0{i+1}
{a.tag}
{a.sub}
{a.body}
{a.chips.map(c=>{c})}
))}
{CONV.map(c=>(
{c.n}{c.l}
))}
Honest by design
Genetics tells us which gene drives a disease — not which way to push it. Direction comes from established pharmacology.
);
}
// Auto-cycling "ticker" that slides through the platform internals so the page
// stays short. Pauses on hover/focus; respects reduced motion.
function PlatformTabs(){
const tabs = [
{ key:"taxonomy", label:"Taxonomy",
eyebrow:"Mechanism-based classification",
title:"Three layers of mechanistic organization.",
lede:"BioAtlas replaces traditional organ-based disease classification with a three-tier mechanism hierarchy. Every disease is placed within its molecular context, from broad signaling families down to atomic endotype definitions.",
Panel: TaxonomyPanel },
{ key:"genetics", label:"Causal genetics",
eyebrow:"Causal genetics",
title:"Association isn't causation. We require proof of cause.",
lede:"Every endotype is anchored to a causal gene — confirmed across three independent classes of human evidence — before we predict a single drug for it.",
Panel: CausalGeneticsPanel },
{ key:"scoring", label:"How prediction works",
eyebrow:"Multi-omic prediction",
title:"How every drug–subtype match is predicted.",
lede:"Each prediction integrates multiple orthogonal layers of evidence and is directionally aware — it checks a drug pushes the pathway the right way, not just that it hits the target. A bounded AI reviewer can promote a well-reasoned candidate but never override the safety gate. Every prediction is auditable.",
Panel: ScoringPanel },
{ key:"lazarus", label:"Lazarus revival",
eyebrow:"Lazarus revival engine",
title:"Revive the failed trial.",
lede:"Phase 2 and Phase 3 failures aren't always biological dead ends. Lazarus re-examines a failed compound against BioAtlas endotypes — separating responders from non-responders — to find the rescue population a shelved asset still helps, plus adjacent diseases that share the same mechanism.",
Panel: LazarusPanel },
];
const FADE_MS = 240;
const CYCLE_MS = 7000;
const [active, setActive] = React.useState(0);
const [shown, setShown] = React.useState(0);
const [fading, setFading] = React.useState(false);
const [cycleId, setCycleId] = React.useState(0);
const pausedRef = React.useRef(false);
const intervalRef = React.useRef(null);
const reducedRef = React.useRef(false);
const sectionRef = React.useRef(null);
const startInterval = React.useCallback(() => {
clearInterval(intervalRef.current);
if (reducedRef.current) return;
intervalRef.current = setInterval(() => {
if (pausedRef.current) return;
setActive(prev => (prev + 1) % tabs.length);
setCycleId(c => c + 1);
}, CYCLE_MS);
}, [tabs.length]);
React.useEffect(() => {
reducedRef.current = window.matchMedia?.("(prefers-reduced-motion: reduce)").matches || false;
if (reducedRef.current) { setShown(active); return; }
startInterval();
return () => clearInterval(intervalRef.current);
}, [startInterval]);
React.useEffect(() => {
if (active === shown) return;
if (reducedRef.current) { setShown(active); return; }
setFading(true);
const t = setTimeout(() => { setShown(active); setFading(false); }, FADE_MS);
return () => clearTimeout(t);
}, [active, shown]);
const onTabClick = (i) => {
setActive(i);
setCycleId(c => c + 1);
startInterval();
};
// Let an in-page CTA (e.g. the hero's "See the scoring engine") jump here.
React.useEffect(() => {
const handler = (e) => {
const idx = tabs.findIndex(t => t.key === e.detail);
if (idx < 0) return;
setActive(idx);
setCycleId(c => c + 1);
startInterval();
const el = sectionRef.current;
if (el) {
const reduced = window.matchMedia?.("(prefers-reduced-motion: reduce)").matches;
el.scrollIntoView({ behavior: reduced ? "auto" : "smooth", block: "start" });
}
};
window.addEventListener("vm:show-platform-tab", handler);
return () => window.removeEventListener("vm:show-platform-tab", handler);
}, [startInterval, tabs.length]);
const tab = tabs[shown];
return (
{ pausedRef.current = true; }}
onPointerLeave={()=>{ pausedRef.current = false; }}
onFocusCapture={()=>{ pausedRef.current = true; }}
onBlurCapture={()=>{ pausedRef.current = false; }}
>
Inside the platform
Four systems, one operating model.
A mechanism taxonomy, causal-genetics proof, a multi-omic prediction engine, and a revival pathway for trial failures — each working off the same endotype layer.
{tabs.map((t, i) => (
))}
{tab.eyebrow}
{tab.title}
{tab.lede}
);
}
function CTAStrip(){
return (
Ready to stratify your pipeline?
Run your candidate compounds against 79,000+ molecular endotypes. Identify the responsive subpopulation. Generate the biomarker. Design the trial.