TOP 9 cheap analogues of Tanakan - Russian substitutes for the drug

Prohibited during pregnancy

Prohibited during breastfeeding

Not suitable for children

Has limitations for liver problems

Tanakan is a drug that improves microcirculation and cerebral circulation. Contains the active ingredient - ginkgo biloba leaf extract. Available in the form of drops and tablets for oral administration.

The drug has a relatively quick action (1-2 hours after administration) and a long-lasting effect (about 10 hours).

Packaging of the drug Tanakan

Its use is advisable for intermittent claudication, cognitive and neurosensory deficits of various etiologies, decreased visual acuity, and hearing impairment, including ringing and tinnitus. Tanakan is widely used to treat Raynaud's disease or syndrome.

The drug is not used to treat patients with individual intolerance to its components, pregnant women, nursing mothers (except for cases of cessation of lactation while taking the pills), patients with erosive gastritis. It is forbidden to use the medicine in cases of aggravated gastric or duodenal ulcers, acute myocardial infarction, or decreased blood clotting. The drug is also contraindicated for minor children.

The cost of the medicine is relatively low, but sometimes there is a need to look for analogues of Tanakan. The list of generics and drug substitutes is wide enough to choose the best option.

pharmachologic effect

Manufacturer: IPSEN, France
Release form: tablets, oral solution

Active ingredient: ginkgo biloba leaf extract

Tanakan is an angioprotective drug that contains a natural herbal component. It affects metabolism in cells, rheological properties of blood, vasomotor reactions of blood vessels. It also saturates the brain with oxygen and glucose and improves microcirculation. The drug reduces the production of red blood cells and prevents the formation of platelets. At the same time, it has an antihypoxic effect. The product has a high degree of bioavailability. It is excreted along with urine.

Indications for use of Tanakan

Tanakan is prescribed to patients when the following disorders and pathologies are detected:

• cognitive and sensorineural deficits;
• chronic obliterating arteriopathy of the legs;
• impairment of visual and auditory function;
• noise in ears;
• dizziness;
• lack of coordination;
• Rhine's disease.

Helpful information! The product has a significant list of contraindications, which are recommended to be taken into account before starting the course. If necessary, you should consult a specialist. Self-medication should be completely excluded.

Tanakan - instructions for use

According to the instructions for use, Tanakan is intended for oral administration. The drug is recommended to be taken during meals. The dosage and duration of the course are adjusted depending on the condition and diagnosis.

Prescribed for patients of the older age category: 1 tablet. or 1 ml of Tanakan solution no more than three times a day. It is recommended to take the tablets with a sufficient amount of liquid. The solution must first be dissolved in 100–150 ml of water. The average duration of therapy is at least 90 days. Extension of the course and repeated completion is possible on the recommendation of a specialist.

Tanakan's analogs

In pharmacies, analogues presented that are cheaper than Tanakan and have the same effect should be prescribed after prior consultation with a specialist. Taking these medications on your own is not allowed, as this will lead to negative consequences. Products may differ in composition, pharmacology, price category, manufacturer, as well as age restrictions. Many substitutes are dietary supplements - dietary supplements, but drugs.

List of analogues of the drug Tanakan with prices

Helpful information! The cost of drugs depends on the composition, packaging, release form and manufacturer. It is recommended that you read this information in detail before purchasing.

Cost of Tanakan and its analogues

The cost of different forms of the drug is shown in the table:

For comparison: the table below shows the estimated prices for the most affordable and popular analogues of the medicine in question.

Important! The above-described drugs can only be purchased with a prescription certified by the signature and seal of a doctor. Other methods of acquisition are illegal.

See also:

TOP 7 analogues of Picamilon - Russian and foreign substitutes for the drug

Tanakan or Cavinton

Manufacturer: Gedeon Richter, Hungary
Release form: concentrate for infusion, tablets

Active ingredient: vinpocetine

Cavinton is a foreign prescription substitute for Tanakan in tablets. Refers to a psychostimulant and nootropic drug. Prescribed for patients over 18 years of age. The drug has neuroprojector and antioxidant, cerebroprotective effects. Reduces increased blood viscosity and cerebral vascular resistance.

The Tanakan analogue Cavinton is prescribed for the following disorders, depending on the area of ​​application:

• neurology - atherosclerosis of cerebral vessels, previous ischemic stroke, vertebrobasilar insufficiency, vascular dementia, encephalopathy that arose as a result of high blood pressure or after brain injury, impaired blood supply to the brain;
• ophthalmology – vascular pathologies of the chronic stage retina and choroid;
• otorhinolaryngology – deterioration of hearing function, tinnitus.

When should you look for a replacement?

Tanakan is prescribed 40 mg three times a day. The first results are noticeable after a month of use. But you need to drink it for at least 3 months, usually the course of treatment is six months. A package of tablets for a month costs about one and a half thousand rubles. Not all patients, especially the elderly, can afford it. Therefore, they are looking for cheaper substitutes for the drug.

It is also recommended to choose an analogue if the drug causes side effects. They can be caused by individual intolerance to the components of the product or a violation of the dosage regimen. Sometimes the following reactions occur:

• dizziness, headache;
• nausea, vomiting, diarrhea, abdominal pain;
• urticaria, itching, swelling;
• increased risk of bleeding.

Tanakan should not be taken in case of acute cerebrovascular accidents, heart attack, or bleeding disorders. The drug is contraindicated for erosive gastritis and peptic ulcers. It is also not used during pregnancy, breastfeeding and under the age of 18 years. In these cases, it is recommended to look for safer analogues.

Tanakan or Noopept

Manufacturer: Pharmstandard, Russia
Release form: tablets

Active ingredient: omberacetam

Noopept is a domestic over-the-counter analogue of Tanakan, which has nootropic and neuroprotective, antioxidant effects. For memory, it is better to take this particular drug, as it affects all phases of processing. Prevents the development of amnesia that was triggered by disturbances or interventions. Improves the rheological properties of blood.

The drug also has antiplatelet, fibrinolytic and anticoagulant properties. The therapeutic effect is achieved after a week's course. The Tanakan analogue Noopept is prescribed for memory impairment, attention and other cognitive disorders, after a head injury, coma, cerebral vascular insufficiency, asthenia.

Ginkgo biloba (ginkgo biloba) is a relict plant, the only surviving representative of the “Ginkgoaceae” class from the previously existing several dozen species. It grows wild in eastern China. Ginkgo is the oldest surviving tree species, dating back about 300 million years. Preparations obtained from the leaves of the ginkgo biloba plant have been used in traditional medicine in China and Japan for several thousand years. The amazing properties of the plant, its ability to withstand natural adverse factors were one of the reasons that this tree became one of the symbols of Tokyo.

It should be noted that on the modern international pharmaceutical market there are several dozen preparations made from ginkgo biloba leaves, both in the form of dosage forms and food additives, vitamin complexes, teas, gels, ointments, etc. More than 10 ginkgo preparations are presented on the Russian market alone . It is very important to know that ginkgo leaves, in addition to biologically active protective ingredients (which will be discussed below), also contain toxic ginkgolic acids, the minimum permissible concentrations of which may not be maintained in all preparations. The most studied and safest is the standardized extract - EGb761 (tanakan), produced for more than 40 years, the medicinal properties of which are studied by famous medical schools in Europe, Asia and America. A very popular marketing technique is to transfer the proven effectiveness and safety of one drug to all others that have the same starting raw materials. It is important for specialists to know that the production of EGb761 is a patented 27-step process of extraction of all components of ginkgo leaves, subsequent purification from ballast components and toxins, concentration of biologically active components, which makes the substrate a unique drug in terms of effectiveness and safety.

The history of modern research into the mechanisms of action of EGb761 goes back several decades, the amount of research conducted and accumulated material is very large, so the authors presented mainly materials from the last five years, without excluding, of course, key data from an earlier period.

It is known that one of the mechanisms of cell death is apoptosis, which can be accelerated by various factors. Summarizing the data accumulated to date on the mechanisms of action of the components of EGb761, obtained using unique methods of histology, histochemistry, DNA diagnostics, and enzyme-linked immunosorbent assay in laboratories in different countries, we can state the fact of a truly multimodal cytoprotective anti-apoptotic effect of the extract [1]. Action of EGb761: inhibition of apoptosis and apoptosis ligands (Fas mRNA), stabilization of the transmembrane potential of mitochondria, activation of metabolism, increase in the concentration of anti-apoptotic Bcl-2 protein, prevention of DNA fragmentation, inhibition of cytokine production, including TNF-α, IL-2, IL-4, interferon -gamma, activity as a “trap” of free radicals, activation of antioxidant defense components (mitochondrial superoxide dismutase, gamma-glutamylcysteine ​​synthetase, glutathione transferase, NADP dehydrogenase), increased induction of a transcription factor that regulates the expression of antioxidant proteins, activation of genes encoding proteins that determine cell sensitivity to insulin.

Neuroplasticity can be defined as the ability of synapses to undergo structural adaptation in response to functional demands or dysfunction [2, 3]. EGb761 has been shown in preclinical studies to influence almost all aspects of improving neuroplasticity (long-term potentiation, spinal neuron density, neuritogenesis and neuronogenesis). According to the authors of the studies, of the three fractions of EGb761 (ginkgolides, flavonoids, bilobalides), the most active in relation to neuroplasticity are flavonoids, especially the aglycone isoramenthin [4].

Cognitive impairment

Cognitive functions include the most complex functions of the brain, through which the processes of cognition and interaction with the outside world are carried out. This is primarily memory, attention, as well as gnosis, thinking, speech and praxis. Among the main causes of cognitive disorders are neurodegenerative, vascular diseases, mixed vascular-degenerative disorders, dysmetabolic disorders, neuroinfections, demyelinating diseases, traumatic brain injuries, tumors, as well as liquorodynamic disorders [5].

EGb761 has been proven to be effective in the treatment of a wide range of brain dysfunctions, from neurodynamic to degenerative, vascular and mixed diseases. The main effects are associated with improved cerebral circulation, activation of mitochondrial function and protection of nervous tissue through neuroprotection [6].

Alzheimer's disease (AD) is known to be characterized by extracellular accumulation of beta-amyloid and microglial inflammation. The anti-inflammatory effect and mechanisms of this effect of EGb761 were studied using TgCRND8 transgenic mice with overexpression of amyloid precursor protein. The drug was given in food for 2-5 months, and plasma drug concentrations were maintained similar to those in humans taking the drug at a dose of 240 mg per day. A five-month course of treatment significantly improved the cognitive functions of mice, determined by the Barnes Maze test, reduced the loss of synaptic proteins (PSD-95, Munc18−1, SNAP25), and suppressed microglial inflammation. The secretion of pro-inflammatory cytokines (TNF-α, IL-1β) by microglial cells also decreased, and microglial autophages were suppressed. Two months of treatment did not have a statistically significant effect; moreover, EGb761 activated microglial macrophages. Additionally, EGb761 was found to reduce amyloidogenesis by inhibiting beta-secretase and beta-amyloid aggregation [7]. Another study [8] confirmed that catechins and procyanidin, which are one of the active components of EGb761, have the ability to inhibit amyloid A-beta aggregation and destabilize formed fibrils. A study was carried out on isolated components of EGb761, which showed the ability of its individual components to inhibit the aggregation of amyloid A-beta. It has been established that flavonoids 1, 3 and 4 have the greatest activity in this regard [9].

Considering the known cytoprotective properties of EGb761, the authors of another study [10] suggested its possible effectiveness in so-called conformation diseases, the key point of which is disturbances in the tertiary and quaternary structure of cellular proteins with the formation of intracellular deposits. The utilization of such abnormal molecules occurs in the cell's proteasomes, the activity of which may be reduced. The effectiveness of EGb761 was studied in a cell model of Huntington's disease with the expression of a pathological variant of polyglutamine protein (polyQ protein). It has been shown that EGb761 acts on these cells in two ways: it increases proteasome activity and induces more efficient degradation of protein aggregates. This study demonstrates a novel mechanism of EGb761's neuroprotective action through its ability to activate proteasomes and disaggregate protein deposits, which may be useful in the treatment of neurodegenerative diseases that are based on protein homeostasis.

New facts about brain aging were obtained in two prospective cohort studies, which showed that neurobiological changes in the brain begin at age 27 [11], with clear cognitive decline observed from age 37. Moreover, if cognitive changes in men and women under the age of 50 were similar, then after 60 years the percentage of changes was higher in the male group [12]. Interesting results were obtained in a prospective 20-year study of 3612 non-demented participants 65 years of age and older, 589 of whom had ever taken EGb761, 149 had ever taken piracetam, and the rest had never taken either drug [13]. Cognitive decline was observed less frequently in the group taking EGb761 than in the group not taking it. The authors conclude that this is a specific effect of EGb761, as it was not observed with piracetam.

Austrian researchers provide interesting results of pharmacoeconomic analysis [14]. They conducted a meta-analysis of the daily activities of 1201 patients with dementia who received EGb761 or placebo for 22-24 weeks in a double-blind manner. The delay in progression of impairment in activities of daily living was calculated. All costs of patient care were also assessed, including the cost of medications, doctor costs, government subsidies, and nurse costs. Data from the Cochrane Clinical Global Impression Scale for cholinesterase inhibitors were compared with corresponding data from this EGb761 study. Treatment with EGb761 resulted in a delay of 22.3 months in worsening activities of daily living scores compared with placebo. Total savings with EGb761 treatment ranged from EUR 3,692 to EUR 29,577, mainly due to slowing disease progression before additional nursing costs became necessary. According to preliminary calculations, the use of cholinesterase inhibitors requires higher treatment costs.

The monograph by A. Farooqui [15] (Department of Molecular and Cellular Biochemistry of Ohio University), dedicated to Ginkgo biloba [15], describes the effects of the drug in neurological practice: improving memory, concentration, reducing the manifestations of asthenia due to the specific antagonist to the factor produced by the components of the drug platelet activation, endogenous mediators of inflammation and nociception; dilation of blood vessels, activation of the release of endothelium relaxing factor and prostacyclin from vascular endothelial cells, reduction of platelet activation.

Among bioactive drugs, EGb761 is the most intensively clinically studied herbal agent. The goal is to identify treatment options for cognitive decline, dementia, and AD. Although some meta-analyses performed over the past 3 years have been negative for the prevention of AD, other randomized controlled trials of AD dementia and mild cognitive impairment (including patients with neuropsychiatric symptoms) have confirmed the beneficial role of EGb761 in cognitive impairment and dementia. The safety and tolerability of EGb761 are exceptional at all dosages. Analysis in subgroups of patients showed the clinical effectiveness of EGb761 mainly at a dosage of 240 mg per day and also confirmed a decrease in anxiety and depressive symptoms in a subgroup of patients with AD [16].

A meta-analysis conducted by R. Kaschel [17] analyzed 29 randomized placebo-controlled studies examining the effect of EGb761 on cognitive processes in mild cognitive impairment, depression, and multiple sclerosis in young and elderly people. Evidence has been obtained that long-term administration of the drug improves attention, performance and long-term memory in the assimilation of verbal and non-verbal information. One of the latest meta-analyses of randomized controlled trials showed the effectiveness of EGb 761 in the treatment of various types of dementia in patients over 60 years of age [18].

Another meta-analysis of studies was conducted to clarify the effectiveness of EGb761 in dementia. Of the 15 randomized controlled trials, 7 met the inclusion criteria for the meta-analysis. In these studies, patients received 120–240 mg per day of EGb761 or placebo. Efficacy was assessed using validated rating scales of cognitive impairment, functional functioning (activities of daily living), and clinical global impression. Data from 2625 outpatients were analyzed. Statistically significant differences in the EGb761 therapy group from the placebo group were obtained on cognitive scales, scales of daily activities and clinical global impression. Statistically highly significant differences were found in patients with dementia and neuropsychiatric symptoms (anxiety and depression). Side effects and rates of premature treatment discontinuation did not differ between subgroups [19].

Another meta-analysis of data from Cochrane and other relevant databases (as of March 2014) on the effectiveness of EGb761 in the treatment of dementia and possible side effects was carried out by a group of scientists from medical schools in the USA and China [20]; 9 studies met the required criteria. These studies lasted 22–26 weeks and included 2561 patients. According to the results of the meta-analysis, the treatment results of patients taking EGb761 were better than those in the placebo group (cognitive scales, daily activities), and on the Clinical Global Impression scale they were statistically significantly superior to placebo. In a subgroup of patients with neuropsychiatric symptoms (anxiety and depression), EGb761 had a statistically significant effect on improvements in cognitive function, activities of daily living, and Clinical Global Impression scores. In the subgroup of patients with diagnosed asthma, the results did not differ significantly from the general group. The drug was well tolerated, no serious side effects were noted. The authors concluded that EGb761 at a dose of 240 mg per day may stabilize or slow decline in cognitive function, activities of daily living, behavioral disturbances, and global assessment after 22 to 26 weeks of dosing in cognitive impairment or dementia, especially in patients with neuropsychiatric symptoms.

The GINDEM-NP, GOTADAY and GOT-IT studies showed that a dose of 240 mg per day of EGb761 was significantly more effective than placebo in reducing the severity of neuropsychiatric symptoms, improving cognitive function, activities of daily living and quality of life in patients with mild to moderate dementia. The combination of EGb761 with donepezil (10 mg per day) was more effective than monotherapy with these drugs. Cross-comparison of studies of various antidementia drugs allowed the author to conclude that EGb761 is at least as effective as memantine, galantamine and donepezil [21].

Positive experience with the use of EGb761 for cognitive decline in patients with chronic vascular lesions of the brain was obtained by domestic researchers. In an open-label, multicenter study, 108 middle-aged and elderly patients with early stages of cerebrovascular insufficiency received EGb761 120 mg per day for 90 days. The severity of subjective and objective neurological symptoms, the degree of cognitive and behavioral impairments were assessed [22]. As a result of the treatment, the volume of memorization and reproduction of information increased, concentration and stability of attention improved, positive dynamics concerned associative processes and psychomotor functions. An improvement in well-being was also noted in the form of a decrease in the frequency and severity of headaches, dizziness, noise in the head, and restoration of sleep structure.

In a review on the prevention of cognitive impairment in elderly patients using tanakan [23], it was suggested that the preventive effect of the drug is associated with its effect on vascular risk factors for cognitive impairment. The summarized data made it possible to determine predictors of the effectiveness of the drug, namely: male gender, the presence of arterial hypertension and obesity.

Cerebrovascular diseases

Numerous experimental studies have revealed many of the molecular mechanisms of the neuroprotective effect of EGb761[6]. It was found that in rats with a model of non-traumatic subarachnoid hemorrhage, the use of EGb761 is accompanied by an increase in the expression of endothelial growth factor, the concentration of which (as well as the concentration of the corresponding mRNA) significantly increases 24 and 72 hours after the start of treatment. Thus, the use of EGb 761 has a protective effect on tissues by increasing the expression of growth factors [24].

Evaluation of the effect of EGb761 on a model of ischemic brain injury in rats using MRI (diffusion-weighted imaging), behavioral tests and immunochemical analysis of brain tissue showed that EGb761 significantly increases the diffusion coefficient in the central and peripheral areas of ischemia, improves behavioral reactions, and enhances the expression of brain nerve growth factor [25].

EGb761 is known to provide neuroprotection against ischemic brain injury through several mechanisms. Some of these mechanisms are related to calcium metabolism.

Hypocalcin is a calcium-binding protein that belongs to a family of neuronal calcium sensors that regulate many cellular processes, including ion channel modulation and permeability, neurotransmitter release, synaptic plasticity, apoptosis, and gene expression. Information has been obtained on the connection between neuronal calcium sensors and diseases such as cancer, schizophrenia and AD. A study in a mouse model of ischemic stroke by middle cerebral artery (MCA) occlusion showed that EGb761 has a neuroprotective effect in ischemic damage, including by maintaining normal hypocalcin expression [26]. Parvalbumin is a calcium-binding protein that regulates intracellular calcium concentration and thus influences apoptosis. The effect of EGb761 on the expression of parvalbumin in ischemic brain damage was studied. A model of ischemic stroke was created in rats by clamping the MCA. One group of animals received EGb761 before clamping, the other received an inert substance. Rats treated with EGb761 showed a less significant decrease in parvalbumin expression. This study revealed another mechanism of the neuroprotective and antiapoptotic effect of EGb761—maintenance of normal parvalbumin expression in the ischemic brain [27].

Another study was conducted at the Texas Tech University Health Center to determine the neuroprotective properties of EGb761 in an experimental stroke model by measuring glucose and glutamate concentrations in the striatum using microdialysis. The method of glucose-oxygen deprivation of brain slices in
vitro
and MCA occlusion in mice
in vivo
.
EGb761 reduced ischemic cell swelling in hippocampal slices by 60%. In vivo,
EGb761(300 mg/kg) reduced cellular degeneration and swelling after MCA clamping by 35-50%. Immediately after MCA clamping, glucose levels in the striatum dropped by 25%, and this was not corrected by the use of EGb761. In contrast, the level of glutamate in the striatum increased 15-fold after clamping the MCA, and with prior administration of EGb761, the glutamate level increased only 4-5-fold. The authors concluded that pretreatment with EGb761 significantly reduced cellular swelling and neurodegeneration during ischemia. The mechanism for this phenomenon may be a reduction in glutamate excitotoxicity, since ischemia-induced glutamate secretion was significantly suppressed. The authors believe that EGb761 may be a valuable tool for preventing brain damage in patients predisposed to stroke [28].

In patients with vertebrobasilar insufficiency, administration of EGb761 had an effect in the form of improvement in cognitive function according to psychometric tests [29].

Follow-up observation of patients with initial signs of cerebral circulatory failure allowed us to establish the long-term positive effect of EGb761, the severity of which persists for a long time after the end of the course of treatment [30]. The results of other domestic studies also confirm the high effectiveness of tanakan in the treatment and prevention of the progression of encephalopathy in patients suffering from vascular diseases [22,31,32].

Conclusion

The experimental and clinical data accumulated to date allow us to qualify EGb761 (tanakan) as a universal cytoprotector of many systems (brain and spinal cord, myocardium, retina, lens, intestines, kidneys, reproductive system).

Available data allow us to conclude that EGb761(tanakan) has a cytoprotective effect by activating the cell genome and the expression of cellular defense factors against ischemic damage, energy depletion and free radicals.

The vast majority of studies (experimental and clinical) were carried out using tanakan, which leads to an unambiguous conclusion about the incorrectness of transferring the positive results of tanakan studies to other ginkgo preparations, as well as the incorrectness of transferring data on the ineffectiveness of other ginkgo preparations or their side effects to tanakan.

Based on modern data on the subclinical (much earlier than previously thought) debut of many vascular, neurodegenerative, metabolic, stress-induced damage to the nervous system, it can be considered advisable to prescribe tanakan for the purpose of neuroprotection at a young age when the first signs of maladaptation syndrome appear (“ “vegetative dystonia syndrome” in domestic practice), one of the symptoms of which is memory impairment (decreased tolerance to intellectual stress).

It is advisable to determine the duration of treatment based on the clinical situation. At a young age, this may be “situational” (1-3 months) treatment, depending on the duration of symptoms. At an older age and/or in the presence of persistent symptoms or their rapid return after treatment, constant use of Tanakan is advisable (similar to constant treatment with antihypertensive drugs, antiplatelet agents, hypoglycemic and other drugs for the treatment of chronic diseases).

Tanakan or Bilobil

Manufacturer: KRKA, Slovenia
Release form: capsules

Active ingredient: ginkgo biloba leaf extract

Bilobil is a herbal over-the-counter analogue of Tanakan, which contains the same active ingredient. The drug increases the body's resistance to hypoxia, stops the development of cerebral edema, improves blood flow in this area and the rheological properties of blood. Prescribed to patients over 18 years of age to combat insomnia and increased nervous excitability.

Analogues and generics

Sometimes it happens that a drug prescribed by a doctor is not on sale or is not affordable for the patient. In this case, the pharmacist may offer a generic or analogue of the medicine. Not everyone knows how they differ.

• A synonym for a drug
  is a product with the same active ingredient. It has the same release form, but a different name. The dosage may also differ.
• A generic
  is a copy of a drug and has the same composition, dosage and release form. But it is not produced under a patent.
• Analogs
  are similar drugs with the same effect. May have a different active ingredient.

When Tanakan is prescribed, if necessary, it should be replaced only with drugs with the same active ingredient. If the active ingredient is different, the drug may have a different effect or may not work at all. When treating vascular disorders, this is unacceptable, as it can lead to serious consequences.

Tanakan or Ginkgo Biloba

Manufacturer: EVALAR, Russia
Release form: tablets

Active ingredient: ginkgo biloba leaf extract

Ginkgo Biloba is an over-the-counter analogue of Tanakan produced in Russia. Is a dietary supplement. A herbal preparation that has a vasodilator and antihypoxic, as well as anti-edematous effect. Prevents the formation of platelets and free radicals, swelling of the brain and peripheral tissues. Prescribed to patients over 18 years of age with the following conditions:

• increased sensitivity of the body to magnetic storms;
• reduced mental and physical performance;
• impaired blood supply to the brain, retina and myocardium;
• atherosclerosis;
• increased formation of blood clots.

What to choose for treatment instead of Tanakan?

Some drugs belonging to the nootropic group also have a similar effect. They may have a natural composition: Actovegin, Vertigohel, Vinpocetine, Cortexin, Cocculin. But synthetic agents are considered more effective: Lucetam, Hypoxen, Picamilon, Cinnaresin, Vazonit, Dramamine.

Tanakan is a drug with proven effectiveness. It is safe and easy to carry. The advantage is the natural composition and guaranteed quality of the active ingredient. It rarely causes side effects and has almost no contraindications. Therefore, it is often prescribed to patients with cerebrovascular accidents. If necessary, you can replace it with medications or dietary supplements with the same composition. For those patients who are intolerant to ginkgo biloba, it is better to choose nootropic drugs with other active ingredients, for example, Noopept.

Tanakan or Ginkum - which is more effective?

Manufacturer: EVALAR, Russia
Release form: capsules

Active ingredient: ginkgo biloba leaf extract

What else can replace Tanakan? Ginkoum is a herbal over-the-counter analogue of Tanakan, which improves blood supply to the brain, thereby increasing mental performance. After completing the course, the patient noted an improvement in memory, thinking, and attention. The drug is also used as a prophylactic against heart attack and stroke, and cephalalgia. Prescribed for patients of older age category. Like most products in this category, it is recommended to take it according to the instructions without exceeding the specified dosage. Can be prescribed for the symptomatic treatment of tinnitus and vestibular rehabilitation.