Fimasartan
| Evidence Level: L5 | Predicted Indications: 10 |
Table of Contents
Fimasartan: From Hypertension to Pulmonary Hypertension
The first-ranked prediction (pulmonary hypertension) rests on model score alone, with no trials or literature behind it. This report therefore also reviews the better-supported candidate, cerebrovascular disorder, in the evidence sections below.
One-Sentence Summary
Fimasartan is an angiotensin II receptor blocker (ARB) originally used to treat hypertension. The TxGNN model predicts it may be effective for pulmonary hypertension with unclear multifactorial mechanism, but there are currently 0 clinical trials and 0 publications supporting this specific prediction. The best-supported alternative is cerebrovascular disorder, with 1 clinical trial and 7 publications, mostly preclinical or surrogate-endpoint studies.
Quick Overview
| Item | Content |
|---|---|
| Original Indication | Hypertension (the Singapore licence records contain no approved indication text) |
| Predicted New Indication | Pulmonary hypertension with unclear multifactorial mechanism |
| TxGNN Prediction Score | 99.20% |
| Evidence Level | L5 |
| Singapore Market Status | ✓ Marketed |
| Number of Registrations | 2 |
| Recommended Decision | Hold |
Why is This Prediction Reasonable?
Detailed mechanism of action data is not available for this report. Based on known information, fimasartan is an angiotensin II type 1 (AT1) receptor blocker. Its efficacy in hypertension has been established, and mechanistically it may be applicable to vascular conditions driven by the renin-angiotensin system.
For pulmonary hypertension, the link is speculative. AT1 blockade could plausibly affect vascular remodelling, but this has not been tested for fimasartan in this disease. The prediction is based only on a high model score.
Other predictions are closer to the original indication:
- Malignant hypertensive renal disease and malignant renovascular hypertension (score 99.16%): renin-angiotensin blockade is biologically plausible, but no trials or literature exist. In renovascular disease, ARBs can harm kidney function in bilateral renal artery stenosis, so safety is a concern.
- Cerebrovascular disorder (score 91.80%): preclinical work shows reduced NLRP3 inflammasome-mediated neuroinflammation, less neointimal formation after carotid injury, and benefit in rat focal ischaemia. Clinical studies in ischaemic stroke report haemodynamic and plaque-inflammation endpoints rather than hard outcomes. Blood pressure lowering itself confounds attribution to a stroke-specific mechanism.
- Intracerebral haemorrhage (score 87.21%): two preclinical papers report anti-inflammatory effects, which is indirect evidence only.
- Braddock syndrome, chronic pulmonary heart disease, obsolete susceptibility to ischaemic stroke, and brain stem infarction: prediction only, with no supporting studies.
Clinical Trial Evidence
No clinical trials are registered for the top-ranked prediction (pulmonary hypertension). The only registered trial is for the cerebrovascular disorder prediction:
| Trial Number | Phase | Status | Enrollment | Key Findings |
|---|---|---|---|---|
| NCT02403349 | Phase 4 | Unknown | 105 | Fimasartan vs valsartan vs atenolol: central blood pressure and peripheral/cerebral arterial flow in hypertensive patients with acute ischaemic stroke (surrogate haemodynamic endpoints) |
Literature Evidence
Literature for the top-ranked prediction (pulmonary hypertension with unclear mechanism) is absent. The table below covers the best-supported prediction, cerebrovascular disorder, and the related intracerebral haemorrhage prediction.
| PMID | Year | Type | Journal | Key Findings |
|---|---|---|---|---|
| 31772615 | 2019 | RCT (double-blind) | Cardiovasc Ther | Fimasartan vs valsartan on blood pressure variability in 80 acute ischaemic stroke patients over 8 weeks |
| 29367614 | 2018 | RCT (double-blind, FAVOR) | Sci Rep | Central and cerebral haemodynamics with atenolol, valsartan or fimasartan in 105 hypertensive ischaemic stroke patients over 12 weeks |
| 30537083 | 2019 | Clinical comparative study | Clin Cardiol | Fimasartan vs amlodipine on carotid atherosclerotic plaque inflammation |
| 37365730 | 2023 | Cohort | J Korean Med Sci | Fimasartan vs other ARBs in heart failure after acute myocardial infarction |
| 30171865 | 2018 | Preclinical | Exp Neurol | Low-dose fimasartan pretreatment reduced NLRP3 inflammasome-mediated neuroinflammation and brain injury after intracerebral haemorrhage |
| 26448932 | 2015 | Preclinical | Biomed Res Int | Long-term low-dose fimasartan in rat transient focal brain ischaemia |
| 31307370 | 2019 | Preclinical | Mol Med | Fimasartan reduced neointimal formation and inflammation after carotid injury in ApoE knockout mice |
| 26608500 | 2016 | In vitro | Inflamm Res | Anti-inflammatory effects via Akt, ERK and NFκB pathways in hemolysate-stimulated astrocytes |
| 23642815 | 2013 | Preclinical | Int J Cardiol | Cardioprotective effect in myocardial ischaemia/reperfusion injury (does not address pulmonary hypertension; linked to the hypoxia-related lung disease prediction) |
Singapore Market Information
| Authorization Number | Product Name | Dosage Form | Approved Indication |
|---|---|---|---|
| SIN15221P | KANARB TABLET 60MG | Tablet | Not stated in the available records |
| SIN15222P | KANARB TABLET 120MG | Tablet | Not stated in the available records |
Both licences are valid single-ingredient products from Boryung Corporation, and there are no cancelled registrations.
Safety Considerations
Please refer to the package insert for safety information.
One point from the prediction analysis: ARBs can harm kidney function in bilateral renal artery stenosis, which matters for any renovascular hypertension use. No drug interaction records were found.
Conclusion and Next Steps
Decision: Hold
Rationale: The top-ranked pulmonary hypertension prediction has a high model score (99.20%) but no trials or literature, and the mechanistic link is speculative (Evidence Level L5). The most promising direction is cerebrovascular disorder (L3), but its evidence is mostly preclinical or based on surrogate endpoints, so it remains a research question rather than a candidate for action.
To proceed, the following is needed:
- Package insert warnings and contraindications (a blocking gap for safety screening)
- Mechanism of action data
- For pulmonary hypertension: preclinical or early clinical data showing an effect in pulmonary vascular disease
- For cerebrovascular disorder: outcome-based clinical trials (not just haemodynamic surrogates) that separate stroke-specific benefit from blood pressure lowering
- Renal safety assessment for renovascular hypertension indications
Disclaimer
This content is for research purposes only and does not constitute medical advice. Clinical validation is required before any clinical application.