Enalaprilat
| 證據等級: L5 | 預測適應症: 1 個 |
目錄
Enalaprilat: From ACE Inhibition (Antihypertensive) to Primary Hereditary Glaucoma
One-Sentence Summary
Enalaprilat is the active metabolite of enalapril, an ACE inhibitor that suppresses the renin-angiotensin system (RAS) to lower blood pressure; no confirmed original indication or approved labeling data is currently on file for this compound. The TxGNN model predicts it may be effective for Primary Hereditary Glaucoma, but this prediction is currently supported by 0 clinical trials and 0 publications. This is a pure model-generated hypothesis with no corroborating clinical or mechanistic evidence to date.
Quick Overview
| Item | Content |
|---|---|
| Original Indication | Not available — no approved indication or license record found; drug is pharmacologically classified as an ACE inhibitor (antihypertensive) |
| Predicted New Indication | Primary Hereditary Glaucoma |
| TxGNN Prediction Score | 99.09% |
| Evidence Level | L5 |
| US Market Status | Not Marketed |
| Number of NDAs | 0 |
| Recommended Decision | Hold |
Why is This Prediction Reasonable?
Detailed mechanism of action data is not available in the current record for enalaprilat. Based on known pharmacological classification, enalaprilat is the active diacid metabolite of enalapril and acts as an ACE (angiotensin-converting enzyme) inhibitor, suppressing the renin-angiotensin system (RAS) to reduce systemic blood pressure. No original indication data is on file, so the drug’s approved clinical use cannot be confirmed from this evidence pack.
Primary hereditary glaucoma is a congenital condition driven by anterior chamber angle developmental abnormalities and associated gene mutations (e.g., CYP1B1, MYOC), which elevate intraocular pressure through a structural/genetic mechanism rather than systemic RAS activity. While isolated exploratory reports have examined topical ACE inhibition for intraocular pressure control, there is no established mechanistic pathway connecting systemic RAS inhibition to the angle-development defects underlying hereditary glaucoma.
The TxGNN score of 0.99 reflects knowledge-graph embedding similarity only and should not be interpreted as mechanistic or clinical evidence. Given the absence of MOA confirmation, original indication data, and any supporting trials or literature, the mechanistic plausibility of this prediction is currently low and unverified.
Clinical Trial Evidence
Currently no related clinical trials registered
Literature Evidence
Currently no related literature available
Safety Considerations
Please refer to the package insert for safety information.
Conclusion and Next Steps
Decision: Hold
Rationale: This candidate is supported only by a TxGNN embedding score (L5, no clinical trials, no literature, no confirmed MOA), and the proposed mechanism (systemic RAS inhibition) has no established link to the genetic/structural pathology of primary hereditary glaucoma. The drug is also not currently marketed, with zero license records.
To proceed, the following is needed:
- TFDA/product labeling — warnings, contraindications (currently blocking data gap DG001)
- Confirmed mechanism of action from DrugBank or primary literature (data gap DG002)
- Original approved indication(s) for enalaprilat
- Preclinical or mechanistic studies linking ACE inhibition to intraocular pressure or angle-development pathways
- Any emerging clinical or case-level evidence in glaucoma populations before advancing beyond S0
Disclaimer
This content is for research purposes only and does not constitute medical advice. Clinical validation is required before any clinical application.