About Clavis
"The platform couples Clavis (Latin for key), an exploratory knowledge graph traversing preclinical hypotheses and chemical space, with Kiu (welcome rain after drought), a canonical graph restricted strictly to peer-reviewed consensus, regulatory approvals, and clinical trial evidence."
Our Mission
Clavis addresses an epistemic vulnerability in automated biomedical information systems: the conflation of early-stage exploratory hypotheses with peer-reviewed clinical validation. Generative models frequently blend speculative mechanistic correlations with established standards of care.
Our platform resolves this through structural graph partitioning rather than prompt-based guardrails, maintaining clear separation between preclinical discovery pipelines and validated clinical evidence.
Provenance-Anchored Evidence
Every biomolecular relationship is anchored to primary peer-reviewed literature, registered clinical trials (ClinicalTrials.gov), or curated molecular databases (dbSNP, ClinVar, ChEMBL). The architecture verifies existential proof alongside supportive textual alignment, establishing auditable evidence chains.
Dual-Graph Partitioning
The architecture enforces hard graph partitioning between distinct evidentiary domains. Preclinical screening and patent landscapes are mapped within the exploratory Shadow Graph, while patient-facing contexts and clinical guideline evaluation are restricted exclusively to the validated Canonical Graph.
Deterministic Guideline Logic
Clinical decision support systems risk patient safety when generative models attempt to infer prescriptive therapy. We encode guideline contraindications and escalations as deterministic relational data tuples, ensuring the system surfaces objective evidence context rather than probabilistic treatment recommendations.
Sample Query Document: "STK11 Mutation"
STK11 (LKB1) is a tumor suppressor gene. Co-mutation of STK11 and KRAS in Non-Small Cell Lung Cancer (NSCLC) is robustly associated with primary resistance to immune checkpoint inhibitors (PD-1/PD-L1 blockade) and characterized by a "cold" tumor microenvironment.
- WARNING: STK11 mutations are a known negative predictor for Pembrolizumab monotherapy efficacy [Source: KEYNOTE-042 Retrospective].
- Standard of care typically pivots to chemoimmunotherapy combinations or clinical trials targeting the LKB1/AMPK/mTOR axis.
Pre-clinical models suggest that inhibiting FAK or targeting the glutamine metabolism pathway may re-sensitize STK11-mutant tumors.
Provenance: PubMed:34526781 | Confidence: 0.62 | Status: PENDING_CLINICAL