📄 Autonomous discovery by Cortex · 2026-05-22
"ADAM28 cleaves extracellular matrix and growth factor binding proteins enabling invasion. Inhibiting ADAM28 blocks matrix degradation at invasion front."
Pathway: ADAM28 → metalloprotease → ECM remodeling → invasion + metastasis
Clinical Angle: Anti-invasive: block ECM remodeling at tumor-stroma interface
| Metric | Value |
|---|---|
| Best Vina Score | -8.9 kcal/mol |
| Best Molecule (SMILES) | O=C(Nc1ccc(O)c(F)c1)c1cnc2ccccc2c1 |
| Molecular Weight | 282.274 Da |
| QED / DCSAL | 0.707 |
| Molecules Tested | 10 |
| Docking Method | smina (real GPU, g4dn.xlarge) |
| Receptor Source | AlphaFold v4 |
Total Score: —
Prognostic: high ADAM28 = invasive phenotype. CDx: MMP/ADAM activity assay predicts anti-invasive therapy response.
| PQM Status | ISSUED |
| QCM Trust | 1.0 |
| Ledger Logged | ✅ SHA-256 hash chain |
| Evidence ID | RO-ADAM28 |
| Authority | marcus_60 (sole override) |
ADAM28 is a FIRST-IN-CLASS (0 ChEMBL) target with A+ grade binding affinity (-8.9 kcal/mol). The mechanistic hypothesis (ADAM28 → metalloprotease → ECM remodeling → invasion + metastasis) provides a clear therapeutic rationale for Prostate / Pancreatic. Anti-invasive: block ECM remodeling at tumor-stroma interface. Recommended for wet lab validation.
MindNetQ Inc. — Governed Intelligence for Precision Medicine
Report generated by Cortex autonomous discovery pipeline. All decisions ledger-hashed.