Source-table classification, 2024
The embedded dataset is copied unchanged from ARPI_PK_Interactions_Teaching_Tool.html: 157 source rows across 17 classes. It is a historical source record, not a live Lexicomp assessment. Duplicate names and all original compact fields are retained.
ANo know interactionBSource label: “No action needed.”CSource label: “Monitor therapy.”DSource label: “Consider therapy modification.”XSource label: “Avoid combination.”
These labels describe the source classification; they are not current individualized treatment recommendations.
How filtering works
Search AND drug class AND the risk/no-data condition. Selected risks are combined with OR; a matching row retains all four ARPI values. “Include no-data rows” additionally includes rows with any missing risk, but only if at least one risk category is selected. Missing risk never becomes A. No-data cells remain visible in any retained row.
Data transparency
- Valproic acid and “Antiplatelet digoxin” have no risk values in the embedded source. The unusual latter row name is preserved and requires verification.
- Original mechanism, affected entity and
u / d / empty direction codes are retained separately from readable labels. ↑ / ↓ reproduce source direction, not an automatic parent-drug concentration claim. - “Source field requires verification” identifies mismatched drug labels, incomplete mechanisms, uncertain fields and non-PK or ambiguous entities. It does not overwrite the record.
- Abiraterone–spironolactone lists AR activity: the arrow must not be represented as proven lower abiraterone plasma concentration.
- Abiraterone–statin OATP explanations are hypotheses requiring evidence review; reported myopathy is a clinical-effect field, not a measured statin concentration field.
- Darolutamide–rosuvastatin remains D. Bolek’s narrative uses avoidance wording; this discrepancy is disclosed, not converted to X.
- Apalutamide remains fully represented in all 157 table rows. No apalutamide pair is in this intentionally limited six-case library; its cells show source details without a guessed animation.
Pathway-specific roles
Substrate: the drug processed or transported by the selected pathway.
Inhibitor: a drug that reduces the pathway’s activity.
Inducer: a drug that increases the pathway’s capacity/activity over time.
These are roles in one pathway, not permanent categories. An ARPI may cause an interaction in one pair and be the affected substrate in another. Increased parent-drug exposure may increase adverse-effect risk; decreased exposure may reduce efficacy. Neither consequence is inevitable. Active-metabolite formation and PD effects are distinct outputs.
Primary review / cases 1–5
Bolek H, et al. Androgen receptor pathway inhibitors and drug–drug interactions in prostate cancer. ESMO Open. 2024;9(11):103736.
doi:10.1016/j.esmoop.2024.103736
Table 2 and “Drug–drug interactions between ARPIs and concomitant medications,” pp. 6–12. Reviewed against the supplied local PDF. Table 2 includes actual and predicted interactions; not every pair or clinical consequence was directly measured.
Advanced PBPK example / case 6
Otsuka Y, et al. Physiologically-based pharmacokinetic modeling to predict drug-drug interaction of enzalutamide with combined P-gp and CYP3A substrates. J Pharmacokinet Pharmacodyn. 2023;50:365–376.
Full text: PMC10460728
Methods—Application to DDI simulation; Results—DDI simulation with apixaban and rivaroxaban; Discussion—P-gp model assumptions and limitations.
References open only when explicitly followed. The presentation itself uses no external assets or network requests. Conceptual illustrations are not PK predictions, concentrations, numerical curves, or dosing tools.
