Using AI-MIDD for Mechanistic Model of Aspirin Linking COX-1 Acetylation, TXB₂ Turnover, and Resolvin Pathways.
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2025
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| _version_ | 1866901183719800832 |
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| author | Goryanin, Igor |
| author_facet | Goryanin, Igor |
| contents | <p>Aspirin (acetylsalicylic acid, ASA) remains a cornerstone antiplatelet therapy, yet mechanistic models describing its irreversible acetylation of cyclooxygenases (COX-1/2) and downstream effects on thromboxane B₂ (TXB₂) and pro-resolving mediators remain scarce in interoperable formats. We present an open, Systems Biology Markup Language (SBML) model linking ASA pharmacokinetics (PK) to COX-1 acetylation kinetics and TXB₂ pharmacodynamics (PD), validated against human clinical data from enteric-coated aspirin formulations (80 and 160 mg daily). The model reproduces day-1 and steady-state TXB₂ inhibition (R² > 0.95) and extends to simulate aspirin-triggered resolvin D1 biosynthesis. This standardized, reusable quantitative systems pharmacology (QSP) module enables mechanistic simulations of platelet inhibition, inflammation resolution, and aspirin combination therapy design, advancing open, reproducible modeling in pharmacology. The model with supplementary materials were created using IQANOVA patented AI-MIDD technology and checked by human.</p> |
| format | Recurso digital |
| id | zenodo_https___doi_org_10_5281_zenodo_17672989 |
| institution | Zenodo |
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| publishDate | 2025 |
| publisher | Zenodo |
| record_format | zenodo |
| spellingShingle | Using AI-MIDD for Mechanistic Model of Aspirin Linking COX-1 Acetylation, TXB₂ Turnover, and Resolvin Pathways. Goryanin, Igor Aspirin, COX-1 acetylation, Thromboxane B₂, Pharmacokinetic–Pharmacodynamic modeling, SBML, Quantitative systems pharmacology, Resolvin D1 <p>Aspirin (acetylsalicylic acid, ASA) remains a cornerstone antiplatelet therapy, yet mechanistic models describing its irreversible acetylation of cyclooxygenases (COX-1/2) and downstream effects on thromboxane B₂ (TXB₂) and pro-resolving mediators remain scarce in interoperable formats. We present an open, Systems Biology Markup Language (SBML) model linking ASA pharmacokinetics (PK) to COX-1 acetylation kinetics and TXB₂ pharmacodynamics (PD), validated against human clinical data from enteric-coated aspirin formulations (80 and 160 mg daily). The model reproduces day-1 and steady-state TXB₂ inhibition (R² > 0.95) and extends to simulate aspirin-triggered resolvin D1 biosynthesis. This standardized, reusable quantitative systems pharmacology (QSP) module enables mechanistic simulations of platelet inhibition, inflammation resolution, and aspirin combination therapy design, advancing open, reproducible modeling in pharmacology. The model with supplementary materials were created using IQANOVA patented AI-MIDD technology and checked by human.</p> |
| title | Using AI-MIDD for Mechanistic Model of Aspirin Linking COX-1 Acetylation, TXB₂ Turnover, and Resolvin Pathways. |
| topic | Aspirin, COX-1 acetylation, Thromboxane B₂, Pharmacokinetic–Pharmacodynamic modeling, SBML, Quantitative systems pharmacology, Resolvin D1 |
| url | https://doi.org/10.5281/zenodo.17672989 |