Nimotop: Targeted Cerebral Vasospasm Management Post-SAH
| Product dosage: 30mg | |||
|---|---|---|---|
| Package (num) | Per cap | Price | Buy |
| 30 | $1.34 | $40.30 (0%) | 🛒 Add to cart |
| 60 | $1.13 | $80.60 $67.50 (16%) | 🛒 Add to cart |
| 90 | $1.05 | $120.90 $94.71 (22%) | 🛒 Add to cart |
| 120 | $1.02 | $161.20 $121.91 (24%) | 🛒 Add to cart |
| 180 | $0.98 | $241.80 $176.31 (27%) | 🛒 Add to cart |
| 270 | $0.96 | $362.70 $257.92 (29%) | 🛒 Add to cart |
| 360 | $0.95
Best per cap | $483.60 $340.54 (30%) | 🛒 Add to cart |
Synonyms
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Nimotop (nimodipine) is a calcium channel blocker specifically formulated for the improvement of neurological outcomes by reducing the incidence and severity of ischemic deficits in patients with subarachnoid hemorrhage (SAH) from ruptured congenital intracranial aneurysms. Its unique cerebroselective action targets cerebral arteries without significantly affecting systemic blood pressure at recommended doses, making it a cornerstone in neurosurgical and neurocritical care protocols. Administered orally, it is indicated for use within 96 hours of the hemorrhage event.
Features
- Active pharmaceutical ingredient: Nimodipine 30 mg
- Pharmaceutical form: Soft gelatin capsule for oral administration
- Mechanism: Calcium channel blocker with high cerebroselectivity
- Bioavailability: Approximately 13% following oral administration due to first-pass metabolism
- Half-life: Terminal elimination half-life is 8-9 hours
- Metabolism: Primarily hepatic via cytochrome P450 3A4 (CYP3A4)
- Excretion: Approximately 50% in urine as metabolites, 32% in feces
Benefits
- Reduces the incidence of cerebral infarction and secondary ischemia by approximately one-third in patients with SAH
- Improves overall neurological outcomes by mitigating delayed cerebral ischemia
- Demonstrates preferential activity on cerebral arteries over peripheral vasculature
- Supported by robust clinical evidence from randomized controlled trials
- Facilitates standardized treatment protocols in neurointensive care settings
- Available in convenient unit-dose packaging for accurate administration
Common use
Nimotop is exclusively indicated for the improvement of neurological outcome by reducing the incidence and severity of ischemic deficits in patients with subarachnoid hemorrhage from ruptured congenital intracranial aneurysms who are in good neurological condition post-ictus (e.g., Hunt and Hess Grades I-III). Treatment should be initiated within 96 hours of the SAH event and continued for 21 consecutive days.
Dosage and direction
The recommended dosage is 60 mg (two 30 mg capsules) every 4 hours for 21 consecutive days. For patients with hepatic impairment or those experiencing significant hypotension, the dose should be reduced to 30 mg every 4 hours. Capsules should be swallowed whole with a glass of water, and may be taken with or without food, though consistent administration relative to meals is recommended. If the patient is unable to swallow, the capsule may be pierced and the contents emptied into a nasogastric tube using appropriate flushing protocols.
Precautions
Blood pressure should be monitored regularly during therapy, particularly in patients with pre-existing hypotension or those receiving concomitant antihypertensive medications. Liver function tests should be performed periodically in patients with hepatic impairment. Use with caution in elderly patients who may be more susceptible to hypotensive effects. Patients should be advised against grapefruit juice consumption during therapy due to potential interaction with CYP3A4 metabolism. Special caution is required when administering to patients with increased intracranial pressure.
Contraindications
Hypersensitivity to nimodipine, other calcium channel blockers, or any component of the formulation. Concomitant use with strong CYP3A4 inhibitors (e.g., ketoconazole, clarithromycin, ritonavir) in the plasma concentration range known to inhibit CYP3A4. Patients with cardiogenic shock or significantly impaired liver function. History of severe hypotension or unstable angina. Concomitant administration with rifampicin or other potent CYP3A4 inducers.
Possible side effects
Most common adverse reactions (≥10%) include hypotension (4-15%) and headache (2-11%). Less frequent reactions (1-10%) include nausea, bradycardia, rash, diarrhea, and edema. Rare but serious adverse effects (<1%) include hepatitis, thrombocytopenia, and neurological deterioration. Isolated cases of ileus and gastrointestinal hemorrhage have been reported. The incidence of side effects is generally dose-dependent and more prevalent in patients with hepatic impairment.
Drug interaction
Strong CYP3A4 inhibitors (ketoconazole, itraconazole, clarithromycin) significantly increase nimodipine plasma concentrations - coadministration is contraindicated. CYP3A4 inducers (rifampicin, carbamazepine, phenytoin) may decrease nimodipine levels. Concomitant use with antihypertensive agents, beta-blockers, or other calcium channel blockers may potentiate hypotensive effects. Nimodipine may increase concentrations of CYP3A4 substrates with narrow therapeutic indices. Grapefruit juice should be avoided due to inhibition of CYP3A4 metabolism.
Missed dose
If a dose is missed, it should be taken as soon as remembered unless it is nearly time for the next scheduled dose. Do not double the dose to make up for a missed administration. Maintain the regular dosing schedule of every 4 hours. If multiple doses are missed, consult the treating physician for guidance on resumption of therapy.
Overdose
Symptoms may include severe hypotension, bradycardia, palpitations, flushing, nausea, and neurological depression. Management includes cardiovascular monitoring and supportive measures. Gastric lavage may be considered if ingestion was recent. Hypotension should be treated with vasopressors such as dopamine or norepinephrine. Calcium gluconate administration may be beneficial. Hemodialysis is not effective due to high protein binding.
Storage
Store at controlled room temperature 20-25°C (68-77°F). Excursions permitted to 15-30°C (59-86°F). Protect from light and moisture. Keep in original packaging until time of use. Do not freeze. Keep out of reach of children and pets. Do not use after expiration date printed on packaging.
Disclaimer
This information is provided for educational purposes only and does not constitute medical advice. Treatment decisions should be made by qualified healthcare professionals based on individual patient circumstances. Always follow the prescribing information approved in your country. Patients should not alter dosage or discontinue medication without consulting their physician.
Reviews
Clinical trials demonstrate consistent efficacy in reducing cerebral infarction rates from approximately 33% to 22% in SAH patients. Meta-analyses confirm significant improvement in neurological outcomes with number needed to treat of 9-11 to prevent one poor outcome. Real-world evidence supports the benefit particularly in good-grade SAH patients treated within the therapeutic window. Some studies suggest potential neuroprotective effects beyond vasodilation mechanisms. The 21-day treatment duration is well-established in clinical guidelines worldwide.