{"id":55994,"date":"2024-02-07T05:48:54","date_gmt":"2024-02-07T05:48:54","guid":{"rendered":"https:\/\/medsname.com\/syndopa-cr\/"},"modified":"2026-05-01T10:49:13","modified_gmt":"2026-05-01T10:49:13","slug":"syndopa-cr","status":"publish","type":"product","link":"https:\/\/medsbase.com\/cs\/product\/syndopa-cr\/","title":{"rendered":"Syndopa CR"},"content":{"rendered":"

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\u26a1 Rychl\u00e1 odpov\u011b\u010f<\/h3>\n

Syndopa CR<\/strong> je controlled-release combination tablet of levodopa + carbidopa<\/strong> (125 mg (100 mg levodopa + 25 mg carbidopa, controlled-release)) \u2014 the cornerstone treatment for Parkinsonova choroba<\/strong>. Levodopa is converted to dopamine in the brain to replace what failing nigral neurones can no longer make; carbidopa blocks that conversion outside the brain so more levodopa reaches the central nervous system, with fewer peripheral side effects (nausea, vomiting, postural drops). CR formulation reduces “wearing-off” between doses and is particularly useful at bedtime to manage overnight stiffness and early-morning akinesia. CR bioavailability is about 70–75% of IR, so the effective dose is slightly lower than IR — an IR “top-up” on waking is often added to break early-morning akinesia rapidly. Critical:<\/strong> never stop levodopa abruptly — risk of neuroleptic malignant-like syndrome<\/em>. Dose must be tapered.<\/p>\n<\/div>\n

\nCo z\u00edsk\u00e1te s MedsBase:<\/strong> V\u00fdrobce certifikovan\u00fd WHO-GMP \u00b7 Diskr\u00e9tn\u00ed balen\u00ed \u00b7 Celosv\u011btov\u00e1 doprava \u00b7 V\u00edce ne\u017e 1 400 ov\u011b\u0159en\u00fdch recenz\u00ed z\u00e1kazn\u00edk\u016f<\/a>\n<\/div>\n

\ud83d\udce6 Ka\u017ed\u00e1 objedn\u00e1vka je pokryta na\u0161\u00ed Z\u00e1rukou op\u011btovn\u00e9ho odesl\u00e1n\u00ed<\/strong><\/a> \u2014 pokud va\u0161e z\u00e1silka nedoraz\u00ed do 20 pracovn\u00edch dn\u016f, p\u0159epos\u00edl\u00e1me ji.<\/p>\n

Pro\u010d objedn\u00e1vat z MedsBase<\/h3>\n

Na\u0161e generick\u00e9 l\u00e9ky poch\u00e1zej\u00ed od v\u00fdrobc\u016f certifikovan\u00fdch WHO-GMP a jsou expedov\u00e1ny po cel\u00e9m sv\u011bt\u011b v diskr\u00e9tn\u00edm, nen\u00e1padn\u00e9m balen\u00ed \u2013 na vn\u011bj\u0161\u00ed stran\u011b bal\u00edku nen\u00ed uveden n\u00e1zev l\u00e9ku. Platby kartou jsou sm\u011brov\u00e1ny prost\u0159ednictv\u00edm regulovan\u00e9ho procesoru (popisky na v\u00fdpisu zahrnuj\u00ed regulovan\u00e9ho procesora plateb kartou \u2013 nikdy \u201cMedsBase\u201d nebo n\u00e1zev l\u00e9ku). P\u0159ij\u00edm\u00e1me tak\u00e9 kryptom\u011bny a bankovn\u00ed p\u0159evody SEPA. Ka\u017ed\u00e1 objedn\u00e1vka je zaji\u0161t\u011bna na\u0161\u00ed politikou p\u0159eposl\u00e1n\u00ed.<\/p>\n

What Is Syndopa CR?<\/h2>\n

Syndopa CR is an oral tablet containing levodopa + carbidopa 125 mg (100 mg levodopa + 25 mg carbidopa, controlled-release)<\/strong> v controlled-release<\/strong> formulation. The combination has been the foundation of Parkinson disease therapy since the 1970s and remains the most effective single treatment for motor symptoms (bradykinesia, rigidity, tremor). It was originally marketed as Sinemet<\/strong> \/ Sinemet CR<\/strong>. Syndopa CR is manufactured by a WHO-GMP certified facility and is bioequivalent to the originator brand at the same strength.<\/p>\n

How Does Syndopa CR Work?<\/h2>\n

Parkinson disease results from progressive loss of dopamine-producing neurones in the substantia nigra<\/em>. Levodopa<\/strong> is the immediate biochemical precursor of dopamine; unlike dopamine itself, it crosses the blood–brain barrier. Once inside the brain, surviving neurones decarboxylate it to dopamine, restoring synaptic dopamine levels and improving motor control.<\/p>\n

The problem: when levodopa is given alone, >95% is converted to dopamine in peripheral tissues before it reaches the brain — causing severe nausea, vomiting and orthostatic hypotension, and forcing the use of huge doses. Carbidopa<\/strong> is a peripheral aromatic-amino-acid decarboxylase inhibitor. It does not cross the blood–brain barrier itself, but blocks the breakdown of levodopa in peripheral tissues. The result: a 4–5-fold reduction in the levodopa dose needed for the same brain effect, and far fewer GI\/cardiovascular side effects.<\/p>\n

The controlled-release<\/strong> matrix slows tablet dissolution so levodopa is absorbed over 4–6 hours rather than 1–2. This smooths plasma levels and helps reduce end-of-dose wearing-off<\/em> in patients with motor fluctuations. The trade-off: bioavailability is about 70–75% of the IR tablet, so the effective dose is slightly lower; food (especially protein) further delays absorption. Many patients use a mix — an IR dose first thing in the morning to get a quick “on” period, then CR for daytime smoothness, and an IR top-up before bed if needed.<\/p>\n

Who Is Syndopa CR For?<\/h2>\n

Syndopa CR is appropriate for adults with idiopathic Parkinson disease who need symptomatic motor relief, including:<\/p>\n

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  • Newly diagnosed patients in whom symptoms interfere with daily function (older patients especially — in younger patients, neurologists often start with a dopamine agonist or MAO-B inhibitor first to delay levodopa-related dyskinesia).<\/li>\n
  • Patients on a dopamine agonist or MAO-B inhibitor whose symptoms have progressed and who now need additional motor benefit.<\/li>\n
  • Patients experiencing end-of-dose “wearing-off”<\/strong> on standard immediate-release levodopa — the controlled-release matrix lengthens the duration of effect.<\/li>\n
  • Patients with overnight symptoms<\/strong> — a bedtime CR dose can reduce night-time stiffness and early-morning akinesia.<\/li>\n
  • Some patients with parkinsonism due to other causes (post-encephalitic, manganese intoxication, certain atypical syndromes) — under specialist guidance, with the understanding that response is usually less robust than in idiopathic PD.<\/li>\n<\/ul>\n

    Nevhodn\u00e9 pro:<\/strong> patients with narrow-angle glaucoma, suspected melanoma or undiagnosed skin lesion, severe psychotic disorder, or current use of a non-selective MAO inhibitor (within 14 days).<\/p>\n

    D\u00e1vkov\u00e1n\u00ed a pod\u00e1v\u00e1n\u00ed<\/h2>\n\n\n\n\n\n\n\n\n
    F\u00e1ze<\/th>\nD\u00e1vkovac\u00ed sch\u00e9ma<\/th>\nPozn\u00e1mky<\/th>\n<\/tr>\n<\/thead>\n
    Switching from IR to CR<\/td>\nAdd 10–30% to the total daily levodopa dose; redistribute over 4–8 hours<\/td>\nCR is ~75% bioavailable<\/td>\n<\/tr>\n
    Typical schedule<\/td>\n125 mg every 4–8 hours; 1–2 tablets per dose<\/td>\nPlus IR for first morning dose if needed<\/td>\n<\/tr>\n
    Bedtime dose<\/td>\n125 mg or 250 mg at bedtime<\/td>\nReduces overnight stiffness<\/td>\n<\/tr>\n
    Polykejte cel\u00e9<\/td>\nDo not crush or split (some scored CR formulations can be split into halves; check the tablet)<\/td>\nCrushing destroys the matrix<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

    Syndopa CR is the controlled-release<\/strong> formulation: onset is slower (45–90 minutes vs 30 for IR), peak is lower and later, duration is longer (5–7 hours per dose vs 3–5). This makes it well suited to maintaining steady plasma levels during the day and overnight, but less suitable for the first morning dose where rapid “on” is the priority — many advanced patients use IR for the first dose and CR for the rest of the day. Take ideally 30 minutes before food when possible; food (especially protein) delays and reduces absorption.<\/p>\n

    Take with or away from protein?<\/strong> Levodopa competes for absorption with dietary amino acids (large neutral amino acids — LNAAs — from protein meals). For most patients in the early years, this competition is unimportant; take with food if nausea is a problem. For patients with motor fluctuations<\/strong>, take levodopa 30 minutes before<\/strong> protein meals (or 1 hour after) to maximise absorption. Some specialists recommend a low-protein breakfast\/lunch and shifting most protein to the evening meal.<\/div>\n

    Long-Term Issues: Motor Fluctuations and Dyskinesia<\/h2>\n

    After 5–10 years of levodopa therapy, many patients develop:<\/p>\n

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    • Wearing-off<\/strong> — each dose lasts a shorter time; symptoms return before the next dose. Managed by shorter dose intervals, adding a COMT inhibitor (entacapone) or MAO-B inhibitor (rasagiline, safinamide).<\/li>\n
    • On–off phenomena<\/strong> — sudden unpredictable swings between mobile (“on”) and rigid (“off”) states.<\/li>\n
    • Dyskinesia<\/strong> — involuntary writhing or twisting movements at peak levodopa concentration. Managed by reducing each individual dose, adding amantadine, or changing the formulation.<\/li>\n
    • Freezing of gait<\/strong> — brief inability to start or continue walking. Less responsive to medication; physical-therapy strategies (visual cues, rhythmic music) often help more.<\/li>\n<\/ul>\n

      These problems are easier to delay than to treat once established — one reason younger patients are sometimes started on dopamine agonists or MAO-B inhibitors first.<\/p>\n

      B\u011b\u017en\u00e9 ne\u017e\u00e1douc\u00ed \u00fa\u010dinky<\/h2>\n

      Early in treatment:<\/strong> nausea, vomiting, anorexia, postural hypotension, dizziness, dry mouth. Most settle within 2–4 weeks. Taking with food or domperidone helps.<\/p>\n

      With long-term use:<\/strong> dyskinesia (peak-dose involuntary movements), motor fluctuations (wearing-off, on–off), hallucinations, vivid dreams, impulse-control disorders (less common than with dopamine agonists), insomnia, sudden-onset sleep, harmless reddish-brown discolouration of urine and sweat.<\/p>\n

      M\u00e9n\u011b \u010dast\u00e9:<\/strong> confusion, paranoia, depression, mania, gambling\/hypersexuality, neuroleptic malignant-like syndrome on abrupt withdrawal.<\/p>\n

      ⚠ Never stop levodopa abruptly<\/strong> Sudden discontinuation can precipitate a neuroleptic-malignant-like syndrome<\/em>: high fever, muscle rigidity, autonomic instability, raised CK, altered consciousness. This is a medical emergency. If you must stop levodopa — for surgery, a hospital admission, severe illness — this should be planned and tapered with your neurologist. If you cannot take it orally for any reason, contact your team immediately about transdermal rotigotine or apomorphine as a bridge.<\/div>\n

      Drug and Food Interactions<\/h2>\n