02.02 / Scientific foundations
After individual analysis and profile structuring, CCRM connects compounds, molecular targets and pathways while preserving what each connection demonstrates.
Nodes can represent compounds, proteins, reactions and pathways. Each edge needs a defined relationship—binding, activation, inhibition or association—and a source. Store species, tissue, assay and experimental conditions alongside the edge. Reactome provides curated pathway knowledge; it does not establish clinical efficacy for a compound. [1]
Binding affinity does not by itself establish cellular target engagement. Free concentration, permeability, metabolism and competing interactions can change exposure. A downstream expression change may be indirect and should not automatically become a causal edge.
Pathway over-representation compares an observed gene list with an appropriate background set. Results depend on identifier mapping, pathway overlap and multiple-testing correction. Enrichment supports hypothesis generation; it is not proof that a pathway causes an individual outcome. [1]
Assess pharmacokinetic mechanisms such as CYP enzyme or transporter effects separately from pharmacodynamic mechanisms such as convergent signaling. Two compounds sharing a pathway does not prove synergy; synergy requires a defined reference model and combination experiments. NCI documents clinically relevant supplement–drug interaction concerns. [2]
Select a relationship. Solid lines show the selected hypothetical relation; the dashed downstream link remains an untested hypothesis.
The diagram uses generic nodes and hypothetical edges. It is not a map of a named compound, an actual patient or the proprietary CCRM.
References support the methods described, not the validation or performance of Curetanics. Source titles are shown in their original language.