Nicorandil
| 證據等級: L5 | 預測適應症: 10 個 |
目錄
Nicorandil: From Angina Pectoris to Benign Prostatic Hyperplasia
One-Sentence Summary
Nicorandil is an antianginal agent with a dual mechanism — a K_ATP channel opener and a nitric oxide (NO) donor — traditionally used in the treatment of stable angina pectoris. The TxGNN model predicts it may be effective for Benign Prostatic Hyperplasia (BPH), with 0 clinical trials and 3 publications currently supporting this direction.
Quick Overview
| Item | Content |
|---|---|
| Original Indication | Angina pectoris (based on established pharmacology; no India regulatory record available) |
| Predicted New Indication | Benign Prostatic Hyperplasia (BPH) |
| TxGNN Prediction Score | 99.71% |
| Evidence Level | L4 |
| India Market Status | ✗ Not Marketed |
| Number of Registrations | 0 |
| Recommended Decision | Research Question |
Why is This Prediction Reasonable?
Nicorandil has a dual mechanism of action: it opens ATP-sensitive potassium (K_ATP) channels to relax vascular smooth muscle, and simultaneously acts as a nitric oxide (NO) donor to promote vasodilation through a second independent pathway. This makes it a distinctively effective agent for improving microcirculation in tissues where ischemia plays a pathological role.
The link to BPH is grounded in vascular biology. A growing body of evidence suggests that impaired blood supply to the lower urinary tract — prostatic ischemia — is a key contributor to BPH development and its associated lower urinary tract symptoms (LUTS). Conditions such as hypertension and atherosclerosis compromise the prostate’s microvasculature, and this chronic ischemia is thought to drive tissue remodeling and hyperplasia. Nicorandil’s capacity to improve microcirculation and reduce oxidative stress (as reflected by malondialdehyde levels in animal studies) positions it as a mechanistically relevant candidate.
Animal model evidence directly supports this hypothesis: treatment of spontaneously hypertensive rats (SHRs) with nicorandil improved prostatic blood flow and attenuated ventral prostatic hyperplasia (PMID 24448152). A separate Japanese clinical pilot study went one step further and directly examined nicorandil as a vasodilator intervention for LUTS (PMID 26165338). While evidence remains at the preclinical and pilot stage, the biological plausibility is clear — and distinguishes this prediction from the model’s lower-ranked outputs, which involve genetic or autoimmune mechanisms entirely unrelated to nicorandil’s pharmacology.
Clinical Trial Evidence
Currently no related clinical trials registered.
Literature Evidence
| PMID | Year | Type | Journal | Key Findings |
|---|---|---|---|---|
| 26165338 | 2015 | Clinical Pilot / Review | Nihon yakurigaku zasshi (Folia Pharmacologica Japonica) | Directly investigates nicorandil as a vasodilator for LUTS; provides the strongest direct support for this repurposing direction (abstract not retrieved, but study type confirms clinical focus) |
| 24448152 | 2014 | Animal Study (SHR model) | Scientific Reports | Six weeks of nicorandil treatment in hypertensive rats improved prostatic blood flow and reduced malondialdehyde levels; prostatic ischemia demonstrated to induce BPH; findings suggest improved microcirculation may reverse hyperplastic changes |
| 31735753 | 2019 | Review | Nihon yakurigaku zasshi (Folia Pharmacologica Japonica) | Summarizes evidence linking impaired prostatic blood supply to BPH/BPE pathogenesis; association with atherosclerotic disease (hypertension) contextualized; provides the epidemiological rationale for a vascular-targeted approach |
India Market Information
Nicorandil currently has no registered products in India. No authorization records are available in the regulatory database.
Safety Considerations
Please refer to the package insert for safety information.
Conclusion and Next Steps
Decision: Research Question
Rationale: The mechanistic basis for nicorandil in BPH is biologically coherent — K_ATP channel opening and NO-mediated vasodilation directly address prostatic ischemia, a recognized contributor to BPH — but existing evidence is limited to one animal study and a Japanese-language pilot/review (L4). No registered clinical trials exist, and India currently has no regulatory pathway to build on, making this a hypothesis that requires prospective clinical investigation before any development decision can be reached.
To proceed, the following is needed:
- Full mechanism of action (MOA) documentation from DrugBank to strengthen mechanistic justification
- Safety profile (key warnings, contraindications, DDI data) — requires retrieving and parsing the package insert PDF
- At least one prospective Phase 2 clinical study in BPH/LUTS patients to generate human efficacy and safety data
- Pharmacokinetic assessment for BPH-relevant dosing: oral bioavailability, tissue distribution to prostate, effective concentration range
- Regulatory pathway scoping for India (CDSCO) — including whether bridging data from Japan or other approved markets could support a local filing
- Evaluation of whether topical or sustained-release formulations could improve prostatic tissue exposure relative to the approved oral antianginal dose
Disclaimer
This content is for research purposes only and does not constitute medical advice. Clinical validation is required before any clinical application.