The CNS small-molecule translational evidence pack, with mechanism-by-mechanism receipts.
DiscoveryLab sits beside a phenotypic / systems-pharmacology screening process — it does not generate molecules and does not replace screening. It routes mechanism hypotheses, CNS developability, receptor occupancy, and partner-readiness, with every claim bounded by evidence.
Public-literature hypothesis (mixed evidence): dopamine D3-receptor antagonism is investigated for levodopa-induced dyskinesia. Not an established clinical mechanism — needs circuit and endpoint evidence.
Public-literature hypothesis (mixed evidence): 5-HT7 and α2-adrenergic modulation of prefrontal signaling, studied for balance/falls and cognition. Therapeutic-window dependent; rank-only.
Public-literature hypothesis: combined D1/D2 agonism for motor-symptom relief, with duration-of-action and dyskinesia tradeoffs. Preclinical-stage hypothesis, not an established outcome.
Public-literature hypothesis: cortico-striatal signaling underlies apathy/motivation, but the molecular target is undefined here. No mechanism claim until target, circuit, and endpoint evidence are attached.
Load a public or supplied compound profile with explicit source labels — public, supplied, generated, imported, or calibrated.
Lay out receptor → circuit → endpoint links as hypotheses with evidence tiers and competing explanations. Never rendered as fact.
Route imported descriptors through rank-only triage. Missing P-gp / hERG / CYP data shows as missing — never imputed.
Occupancy = C / (C + Kd), computed only from supplied affinity and free-brain concentration. No number without data.
A diligence brief separating known facts, this layer's interpretation, evidence gaps, and the next de-risking experiment.
Occupancy is computed only from supplied affinity and free-brain concentration. Missing exposure, P-gp, hERG, or CYP data is shown as missing — the pack never infers it.