{"id":60970,"date":"2024-02-28T07:18:18","date_gmt":"2024-02-28T07:18:18","guid":{"rendered":"https:\/\/medsname.com\/selgin\/"},"modified":"2026-05-01T10:49:16","modified_gmt":"2026-05-01T10:49:16","slug":"selgin","status":"publish","type":"product","link":"https:\/\/medsbase.com\/sv\/product\/selgin\/","title":{"rendered":"Selgin"},"content":{"rendered":"

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\u26a1 Snabbt svar<\/h3>\n

Selgin<\/strong> \u00e4r en oral selegiline<\/strong> (5 mg) tablet \u2014 a selective monoamine oxidase type B (MAO-B) inhibitor<\/strong> anv\u00e4nds f\u00f6r att behandla Parkinsons sjukdom<\/strong>. By blocking MAO-B in the brain, it slows the breakdown of dopamine and helps lengthen the time levodopa keeps working between doses (reduces “off” time). Selegiline is metabolised to L-amphetamine and L-methamphetamine<\/strong>, which can contribute to insomnia — take morning doses only. Common side effects: insomnia, headache, dyskinesia, dry mouth, postural hypotension. Viktigt:<\/strong> avoid combination with most antidepressants (SSRIs, SNRIs, TCAs), opioids such as pethidine and tramadol, and dextromethorphan — risk of serotoninsyndrom<\/em>.<\/p>\n<\/div>\n

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What Is Selgin?<\/h2>\n

Selgin is an oral tablet containing selegiline 5 mg<\/strong>. selegiline is a selective monoamine oxidase type B (MAO-B) inhibitor<\/strong> originally introduced as Eldepryl \/ Jumex<\/strong>. Selgin is manufactured by a WHO-GMP certified facility and is bioequivalent to the originator brand at the same strength.<\/p>\n

Selegiline was the first MAO-B inhibitor used in Parkinson disease, in clinical use since the 1980s. It can be used as monotherapy<\/em> in early Parkinson disease (modest symptomatic benefit, may delay the need for levodopa by months) or as adjunct<\/em> to levodopa to reduce “wearing-off” between doses. Its distinctive feature among MAO-B inhibitors is that it is metabolised to amphetamine derivatives, which contribute to a mild stimulant effect — useful for fatigue but a frequent cause of insomnia.<\/p>\n

How Does Selgin (selegiline) Work?<\/h2>\n

In the brain, dopamine is degraded mainly by monoamine oxidase type B (MAO-B). Selegiline irreversibly inactivates MAO-B at standard doses (5–10 mg\/day), so dopamine released from surviving neurones lingers longer in the synapse. The result: smoother symptom control and a longer benefit from each levodopa dose. Selegiline is also metabolised to L-amphetamine and L-methamphetamine, which independently contribute mild stimulant and dopaminergic effects. Above 10 mg\/day, selectivity for MAO-B is lost and MAO-A inhibition becomes clinically meaningful — tyramine restriction then becomes important.<\/p>\n

Comparing the MAO-B Inhibitors<\/h2>\n

The three MAO-B inhibitors used in Parkinson disease — selegiline, rasagiline and safinamide — share a common mechanism but differ meaningfully in metabolites, dosing and clinical positioning:<\/p>\n\n\n\n\n\n\n\n\n\n
Funktion<\/th>\nSelegiline<\/th>\nRasagiline<\/th>\nSafinamide<\/th>\n<\/tr>\n<\/thead>\n
Typical dose<\/td>\n5–10 mg\/day<\/td>\n0.5–1 mg\/day<\/td>\n50–100 mg\/day<\/td>\n<\/tr>\n
Active metabolites<\/td>\nAmphetamine + methamphetamine<\/td>\nAminoindan (non-amphetamine)<\/td>\nNo active stimulant metabolite<\/td>\n<\/tr>\n
Glutamate effect<\/td>\nNej<\/td>\nNej<\/td>\nJa<\/strong> — sodium-channel\/glutamate-release modulation<\/td>\n<\/tr>\n
Indikation<\/td>\nMonotherapy or adjunct<\/td>\nMonotherapy or adjunct<\/td>\nAdjunct only<\/strong> — for fluctuating PD on levodopa<\/td>\n<\/tr>\n
Insomnia risk<\/td>\nHigher (amphetamine metabolites)<\/td>\nL\u00e5g<\/td>\nL\u00e5g<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Who Is Selgin For?<\/h2>\n

Selgin is appropriate for adults with Parkinson disease — either as initial monotherapy in early disease (when symptoms are mild and the patient is reluctant to start levodopa) or as adjunct to levodopa in patients with end-of-dose “wearing-off”. Older patients prone to insomnia may tolerate rasagiline or safinamide better. Not appropriate during current SSRI\/SNRI\/TCA therapy or for patients planning to take pethidine, tramadol or other contraindicated medications.<\/p>\n

Dosering och administration<\/h2>\n

Den vanliga dosen f\u00f6r vuxna \u00e4r 5 mg once daily with breakfast<\/strong>, increased to 5 mg twice daily (breakfast and lunch) after 1–2 weeks<\/strong> if needed for symptom control. Avoid evening doses<\/em> — the amphetamine metabolites cause insomnia. Maximum 10 mg\/day at standard MAO-B selectivity. Doses up to 20–30 mg\/day have been used historically but cross into non-selective MAO inhibition with full tyramine-diet implications.<\/p>\n\n\n\n\n\n\n\n
Fas<\/th>\nDos<\/th>\nTidpunkt<\/th>\n<\/tr>\n<\/thead>\n
Week 1–2 (initiation)<\/td>\n5 mg en g\u00e5ng dagligen<\/td>\nWith breakfast<\/td>\n<\/tr>\n
Underh\u00e5ll<\/td>\n5 mg tv\u00e5 g\u00e5nger dagligen<\/td>\nBreakfast and lunch — never evening<\/td>\n<\/tr>\n
Maximum at MAO-B selectivity<\/td>\n10 mg\/day<\/td>\nBeyond this, tyramine restriction needed<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n
⚠ Tyramine and the “cheese effect”<\/strong> At standard MAO-B-selective doses, dietary tyramine restriction is generally inte<\/em> required. However, MAO-B selectivity is dose-dependent — selegiline above 10 mg\/day, rasagiline above 1 mg\/day, and safinamide above 100 mg\/day lose selectivity and inhibit peripheral MAO-A as well. At those doses, tyramine-rich foods (aged cheeses, cured meats, broad beans, fermented soya, draught beer) can trigger a hypertensive crisis. Stay within prescribed doses to avoid this risk.<\/div>\n

Vanliga biverkningar<\/h2>\n

Insomnia (very common — the most common reason for discontinuation), headache, nausea, dizziness, postural hypotension, dry mouth, increased liver enzymes. Less common: confusion, hallucinations, agitation, mood changes. With levodopa: increased dyskinesia, may need to lower the levodopa dose by 10–30%.<\/p>\n

⚠ Serotonin syndrome — dangerous interactions<\/strong> Combining a MAO-B inhibitor with serotonergic drugs can cause serotoninsyndrom<\/em>: agitation, sweating, tremor, hyperreflexia, fever, diarrhoea, in severe cases seizures and death. Avoid:<\/strong> SSRIs (fluoxetine, sertraline, paroxetine, citalopram, escitalopram), SNRIs (venlafaxine, duloxetine), tricyclics (amitriptyline, imipramine), pethidine (meperidine), tramadol, dextromethorphan, methadone, St John’s wort, MDMA. Wash-out periods:<\/strong> stop fluoxetine 5 weeks before starting MAO-B inhibitor; stop other SSRIs\/SNRIs at least 2 weeks before; do not start fluoxetine within 2 weeks of stopping the MAO-B inhibitor.<\/div>\n

L\u00e4kemedels- och matinteraktioner<\/h2>\n