Nimotop

Nimotop (Nimodipine) is used to improve symptoms caused by spasms as a result of a brain hemorrhage (ruptured blood vessels).

Product dosage: 30mg
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30	1.56 $	46.80 $ (0%)	🛒 Add to cart
60	1.31 $	93.60 $ 78.39 $ (16%)	🛒 Add to cart
90	1.22 $	140.40 $ 109.98 $ (22%)	🛒 Add to cart
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180	1.14 $	280.80 $ 204.75 $ (27%)	🛒 Add to cart
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360	1.10 $ Best per cap	561.60 $ 395.46 $ (30%)	🛒 Add to cart
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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 cerebroselective action helps mitigate cerebral vasospasm, a common and serious complication following SAH. Administered orally, it represents a critical component in the neurocritical care protocol to support patient recovery and functional prognosis.

Features

• Active ingredient: Nimodipine 30 mg
• Pharmaceutical form: Soft gelatin capsules
• Mechanism: Calcium channel blocker with high cerebroselectivity
• Bioavailability: Approximately 13% following oral administration
• Half-life: 8–9 hours
• Metabolism: Hepatic via cytochrome P450 3A4
• Excretion: Primarily renal (approximately 50%) and fecal (32%)

Benefits

• Reduces the incidence of cerebral vasospasm following aneurysmal subarachnoid hemorrhage
• Lowers the risk of severe neurological deficits and secondary ischemia
• Improves overall neurological outcomes and functional recovery
• Supports cerebral perfusion through selective vasodilation of cerebral arteries
• Convenient oral administration facilitates use in both hospital and post-discharge settings
• Well-established efficacy supported by extensive clinical evidence and guidelines

Common use

Nimotop is primarily indicated for the improvement of neurological outcome after subarachnoid hemorrhage resulting from ruptured congenital intracranial aneurysms, regardless of the patient’s post-ictus neurological condition (e.g., Hunt and Hess Grades I-V). It is typically initiated within 96 hours of the hemorrhage and continued for 21 consecutive days as part of a comprehensive management strategy that may include surgical intervention or endovascular coiling.

Dosage and direction

The recommended dosage is 60 mg (two 30 mg capsules) every 4 hours for 21 consecutive days. Administration should begin within 96 hours of the subarachnoid hemorrhage. Capsules should be swallowed whole with a glass of water, preferably at consistent intervals throughout the 24-hour period. For patients who are unable to swallow, the capsules may be pierced and the contents emptied into a nasogastric tube followed by flushing with 30 mL of normal saline. Dosage adjustment is required in patients with hepatic impairment.

Precautions

Hepatic function should be monitored during treatment, particularly in patients with pre-existing liver disease. Blood pressure should be regularly monitored as nimodipine can cause hypotension. Use with caution in patients with heart failure or significantly impaired cardiac function. Grapefruit juice should be avoided during treatment as it may increase plasma concentrations of nimodipine. The capsules contain sorbitol; caution is advised in patients with hereditary fructose intolerance.

Contraindications

Hypersensitivity to nimodipine, other calcium channel blockers, or any component of the formulation. Concurrent administration with strong CYP3A4 inhibitors such as ketoconazole, itraconazole, clarithromycin, or HIV protease inhibitors. Patients with cardiogenic shock, significant hypotension (systolic pressure <90 mmHg), or decompensated heart failure. History of severe hepatic impairment (Child-Pugh class C).

Possible side effects

• Hypotension (most common, occurring in approximately 4-9% of patients)
• Headache (2-5%)
• Nausea (1-3%)
• Bradycardia (1-2%)
• Gastrointestinal discomfort
• Peripheral edema
• Rash or skin reactions
• Dizziness or lightheadedness
• Flushing
• Rare cases of hepatitis and elevated liver enzymes

Drug interaction

Strong CYP3A4 inhibitors (ketoconazole, itraconazole, clarithromycin, ritonavir) significantly increase nimodipine plasma concentrations. CYP3A4 inducers (rifampin, carbamazepine, phenytoin) may decrease nimodipine levels. Concurrent use with other antihypertensive agents may potentiate hypotensive effects. Beta-blockers may increase the risk of bradycardia and heart failure. Nimodipine may increase concentrations of drugs metabolized by CYP3A4. Grapefruit juice should be avoided due to inhibition of CYP3A4.

Missed dose

If a dose is missed, it should be taken as soon as possible. However, if it is almost time for the next dose, skip the missed dose and continue with the regular dosing schedule. Do not double the dose to make up for a missed administration. Maintain the every-4-hour dosing schedule consistently throughout the 21-day treatment period.

Overdose

Symptoms may include severe hypotension, bradycardia, and cardiovascular collapse. Gastric lavage may be considered if ingestion was recent. Activated charcoal may be administered. Cardiovascular monitoring is essential. Treatment is supportive and symptomatic: elevate legs, administer intravenous fluids, and consider vasopressors (such as dopamine or norepinephrine) for hypotension. Atropine may be used for bradycardia. Calcium gluconate administration (1 g IV) may be considered to counteract calcium channel blockade effects.

Storage

Store at controlled room temperature (20-25°C or 68-77°F). Excursions permitted to 15-30°C (59-86°F). Protect from light and moisture. Keep in original container with lid tightly closed. Do not freeze. Keep out of reach of children and pets. Do not use after the expiration date printed on the packaging.

Disclaimer

This information is for educational purposes only and does not constitute medical advice. Always consult with a qualified healthcare professional for diagnosis and treatment recommendations. The prescribing physician should be familiar with the complete prescribing information and current treatment guidelines for subarachnoid hemorrhage management. Individual patient response may vary, and treatment decisions should be based on professional clinical judgment.

Reviews

Clinical studies demonstrate that nimodipine reduces poor outcomes (death or severe disability) by approximately 40% compared to placebo in patients with subarachnoid hemorrhage. Meta-analyses of randomized controlled trials consistently show significant benefit in neurological outcomes, with number needed to treat of 11-13 to prevent one poor outcome. The 2023 American Heart Association/American Stroke Association guidelines give a Class I recommendation for nimodipine administration in all patients with aneurysmal subarachnoid hemorrhage. Long-term follow-up studies indicate sustained functional benefits at 3-month and 12-month assessments.