Cortexin brain boosting amino acid and vitamin complex with RNA 10×10 mg


Available on backorder


ONE OF A KIND nootropic complex with Ribonucleic acid, full spectrum of amino acids, vitamins and minerals! 

Over the last decade, neurologists and other doctors have witnessed the increasing use of Cortexin – a home-produced peptide drug. Its use has become possible after the discovery of low molecular peptides,which convey the information necessary for normal functioning, interaction and development of cells. The discovery of these peptides underlay a search and development of new pharmacological agents. Cortexin use is based on the ability of the drug to provide a normalizing effect on many functions of the brain.

Cortexin is a polypeptide with an optimal, balanced composition of polypeptides and neurotransmitters provider of tissue-specific effects on the cerebral cortex. The drug reduces the toxic effects of neurotrophic substances, improves learning ability of patients improves cognitive performance (nootropic effect), activates the repair processes in the central nervous system. Has also an anticonvulsant and cerebroprotective action. Cortexin contributes to the rapid restoration of the central nervous system after stress influences.

Cortexin normalizes the ratio of excitatory and inhibitory amino acids in the brain regulates dopamine and serotonin. Other mechanisms of action are the restoration of bioelectric activity of brain cells, the effect of oxidative stress (antioxidant effect) and GABAergic influence. Pharmacokinetic parameters can not be determined because the L-amino acids and neuropeptides that are part of the drug had an average half-life of about 3 minutes, making it impossible to identify indicators of absorption, distribution and discretion peptide residues.

Nootropic effect: Improves higher cerebral functions, processes of learning and memory, concentration, attention and tolerance to mental and physical stress;

Neuroprotective effect: protects neurones against different endogenous neurotoxic factors (glutamate, calcium ions and free radicals) and reduces toxic impact of psychotropic agents;

Antioxidant effect: inhibits lipid peroxidation, increases survival of neurones under oxidative stress and hypoxia;

Tissue-specific effect: activates metabolism of neurones of central and peripheral nervous system as well as reparative processes; also, promotes stimulation of cortical function and general improvement of the nervous system.

Cortexin has the following amino acids, vitamins and minerals (ONE OF A KIND on the market):

Amino acids:

Aspartic acid: 446 nmol/mg; Glycine: 298 nmol/mg; Threonine: 212 nmol/mg; Serine: 268 nmol/mg; Glutamic acid: 581 nmol/mg; Proline: 187 nmol/mg; Alanine: 246 nmol/mg; Isoleucine: 356 nmol/mg; Tyrosine: 109 nmol/mg; Phenylalanine: 162 nmol/mg; Histidine: 116 nmol/mg; Lysine: 253 nmol/mg; Arginine and other amino acids: 202 nmol/mg.


Lysine: 253 nmol/mg; Thiamine (Vitamin B1) – 0.08 mcg/10mg; Lysine: 253 nmol/mg; Riboflavin (Vitamin B2) – 0.03 mcg/10 mg; Niacin (Vitamin B3, Vitamin PP) 0.05 mcg/10 mg; Retinol (Vitamin A) – 0.011 mcg/10mg; Alfa-tokoferol (vitamin E) – 0.007 mcg/10mg.


(Cu): 0,2129 mcg/10 mg; (Fe): 2,26 mcg/10 mg; (Ca): 22,93 mcg/10 mg; (Mg): 8,5 mcg/10 mg; (K): 19,83 mcg/10 mg; (Na): 643,2 mcg/10 mg; (S): 152,65 mcg/10 mg; (P): 91,95 mcg/10 mg; (Zn): 4,73 mcg/10 mg; (Mb): 0,0203 mcg/10 mg; (Co): 0,0044 mcg/10 mg; (Mn): 0,0061 mcg/10 mg; (Se): 0,0745 mcg/10 mg; (Al): 0,3104 mcg/10 mg; (Li): 0,0340 mcg/10 mg.

RUSSIAN PACKAGING, 10x 10 ml vials, each vial has 10 mg of Cortexin (5 mg exist as the paediatric version)

Detailed information below


This term is often used in medical publications, media and in the promotional materials. Neuroprotection is inherent in the very nature of the brain: in the genes and at the level of regulatory neuropeptides. The essence of neuroprotection is that the healing process not only contributes to the protection of the affected group of neurons, but also ensures their continued function. The issue of the availability of an adequate pharmacological intervention that can run these natural mechanisms and support them at the appropriate level is important for medicine. In this context, search, development and testing of new pharmaceutical drugs are and will be one of the most important areas of modern pharmacology.

Obviously, the search for new neuroprotectors is a complex process that requires the combined efforts of physicians, biologists and pharmacologists at all stages. In this regard, special attention should be given to peptide drugs. Despite their diversity they share several common characteristics: low dosage, lack of significant toxic effects and soft exposure time. In general it is possible to state that a system of peptides in the body (Koroleva S.V., Ashmarin I.P., 2006) formed within millions of years of evolution. The system provides a multi-level regulation of all functions including the processes that lead eventually to the neuroprotective effect. In terms of the information, the peptides are a universal language that is understandable by living organisms both on the system level and on the cellular level.

Changes in the ischemic stroke zone during Cortexin treatment. According to MRI in the right temporal region of the brain it is possible to determine a lesion with the volume increasing by day 3. With such a lesion on day 28 the formation of a glial scar and poststroke cysts is usually observed. During Cortexin administration, when a patient with ischemic stroke begins to receive the drug in the first hours after the ischemic incident, the volume of brain lesion reduces by 40% on day 28. There is also a noticeable improvement in general health, clinical and neurological patterns. These observations illustrate a striking effect of the Cortexin’s neuroprotective action (Skoromets A.A., Skvortsova V.I., et al, 2008).

Dynamics in the functional recovery during the Cortexin treatment depends on the severity of the ischemic injuryMonitoring of neurological parameters during the Cortexin therapy demonstrates a significant reduction in the neurological deficit on the 11th day after the onset of ischemic stroke (Rankin Scale). As for the stroke with cortical foci there is more of a positive changes compared with the placebo group (Skoromets A.A., Skvortsova V.I., et al, 2008).

Stroke, craniocerebral injury, age or acquired neurodegenerative diseases have different causes and clinical presentation but the attendant loss of nerve cells results from the pathological cascade processes with similar molecular mechanisms. The key process is associated with excitotoxicity caused by excessive activation of glutamate receptors and subsequent entry of calcium ions into the cell. Excessive calcium starts the processes leading to cell death by way of necrosis or apoptosis.

The cascade of pathological processes in the brain during stroke. Terminology: Ischemia is insufficient blood supply to any organ or the tissue area caused by the blockage or narrowing of the appropriate artery; ATP Adenosine triphosphate – nucleotide plays a crucial role in the exchange of energy and substances in the body, first of all the compound is known as a universal source of energy for all biochemical processes occurring in the living systems. Depolarization of the cell membrane is a change in the electrical potential on the cell membrane; Glutamate is an amino acid, the major excitatory neurotransmitter. Glutamate binding to specific receptors on neurons results in excitation of neurons. NMDA and AMPA glutamate receptors – eceptors providing an excitatory impulse conduction by the neurons, which bind glutamate; NO-synthase – intracellular enzymes involved in the processes of cell death and development of oxidative stress.

Neuroprotective anti-apoptosis effect

Cortexin is a neuroprotective agent with therapeutic effects that starts acting within the first hours after the development of an ischemic brain lesion. This means that its main target is the penumbra area – the neural tissue area surrounding the ischemic lesion, which remains alive for up to 6 hours. The outcome of this process influences the possibility of the subsequent recovery of nerve functions, and the life and death of a patient. Cortexin affects all steps in the pathological molecular events resulting in the death of neurons. It is established that Cortexin decreases neuronal apoptosis (programmed cell death), caused by the excessive accumulation of glutamate (Pinelis et al., 2008).

Cortexin have an effect on the survival of neurons, which are subjected to a toxic effect of glutamate. Glutamate is the major excitatory neurotransmitter of the nervous system. During stroke an excessive release of glutamate occurs and leads to the launch of the cascade that underlies neuronal death. In a culture of neurons the introduction of glutamate also results in the death of neurons. If a substance having a neuroprotective effect is introduced simultaneously with glutamate the death of neurons is reduced. This figure shows the study results of the Cortexin neuroprotective properties in vitro. With the simultaneous introduction of glutamate, Cortexin has an intensive neuroprotective effect in the nanogram concentrations compared with the control (Granstrem O.K. et al, 2008).

ATP synthesis recovery

Adenosine triphosphate (ATP) is a nucleotide that plays a crucial role in the exchange of energy and substances in the body, and is a universal source of energy for all cells. Reduction in the ATP content in cells of the brain is a central link of all pathological processes taking place subsequent to cerebral ischemia. Reduction in synthesis and increase in consumption of ATP is reported immediately after the onset of the nervous tissue ischemisation (Sorokin et al, 2007). Recent studies have demonstrated that Cortexin is able to restore the ATP content in neurons.

Cortexin increases the ATP content in neurons after exposure to toxic concentrations of glutamate (*p < 0,05 compared with the control group). This study has demonstrated the ability of Cortexin to initiate the processes of natural regeneration of ATP in the mitochondria of nerve cells. Due to the fact that the fall in the ATP level is one of the main causes leading to the death of neurons in stroke, recovery of this parameter under the influence of Cortexin explains its clinical efficacy (Granstrem O.K. et al, 2008). 

Delayed calcic disregulation (DCD) depression

In cerebral ischemia and stroke an increased penetration of calcium ions into neurons is observed; it results in an irreversible increase in intracellular calcium concentration and the subsequent malfunction of the mitochondria. This is associated with a fall in a mitochondrial potential (ΔΨm) (Khodorov et al, 2001; Krieger C. & Duchen MR , 2002). As a rule, the cells with a collapse ΔΨm after a decrease in glutamate, do not restore the initialpotential and, eventually, die. This is so-called delayed calcium disregulation (DCD) phenomenon (De Wied D., 1997; Sorokina E.G., et al ., 2007).

Studies of the mitochondrial potential (ΔΨm)  by fluorescence microscopy demonstrate that Cortexin significantly slows down the development of calcium deregulation during glutamate action. The recorded mitochondrial potentials of the neurons presented in the figure show a protective effect of Cortexin due to the delay in the onset of calcium disregulation. Thus, this figure demonstrates that the use of Cortexin can extend the therapeutic window when there is an ischemic lesion in nervous tissue (Report on the Study of the neuroprotective effect of Cortexin, SI Children Health Science Center, RAMS, Moscow, 2008).

Neurotrophic effect

Peptides of Cortexin have a direct and indirect neurotrophic effect on the cells. The basic mechanisms of this effect are based on the changes in gene expression of neurotrophic factors such as a brain-derived neurotrophic factor (BDNF) and a nerve growth factor (NGF).

Stimulation of neurite growth in the chick embryo brain culture. In the nerve tissue culture the growth of neurites (nerve cell processes through which nerve impulses run from the cell body to the organs and other nerve cells) occurs only in the presence of neurotrophic factors. In this experiment, the addition of Cortexin allows for the determination of the degree of its neurotrophic effect. On the right photograph the entire field around the island of a nervous tissue is occupied by an extensive neurite network, whereas, in the control group (left photograph) the growth of neuronal processes are few in number. There are results of the drug series testing in the photos. Such testing is regularly carried out in the analytical laboratory of GEROPHARM LLC.

Thus, numerous independent studies convincingly demonstrate that Cortexin has multiple effects which regulate a cascade of proteins involved in apoptosis, expression of neurotrophic factors, energy supply to the nerve cells, mitochondrial potential, functioning of glutamate receptors and regulation of calcium ion concentration in the cell. This, as a whole provides a neuroprotective and neurotrophic effects of the drug, and, as a result, a high treatment efficiency and improvement in the patient’s quality of life. 

Clinical literature:

Cortexin improves attention, perception, memory, thinking, cortical neurodynamic processes. It is well tolerated and has no side effects.

Cortexin effectiveness in circulatory encephalopathy

Clinical efficacy and pharmacoeconomic characteristics of the neuroprotection with low doses of cortexin in the treatment of acute ischemic stroke

Other references:

1.Gerasimova M.M., Petushkov A.Y./Cortexin effect on the cytokine metabolism in lumbosacral radiculopathies. Neuroimmunology -2004- vol.II-#2- p. 26 
2.Granstrem O.K., Sorokina E.G., Storozhevykh T.P., Stuchnaya G.V., Pinelis V.G. Dyakonov M.M. / The latest news on Cortexin (neuroprotection at the molecular level). Terra Medica Nova. – ¹5. – 2008. – p. 40-44. 
3.Koroleva S.V., Ashmarin I.P. / Development and Application of the Expert System for Analysis of the Functional Continuum of Regulatory Peptide / /Bioorganic Chemistry. – 2006. -, 32. – ¹ 3 – p. 249-257 
4.Skoromets A.A., Stakhovskaya L.V., Belkin A.A., Shekhovtsova K.V., Kerbikov O.B., Burenchev D.V., Gavrilova O.V., Skvortsova V.I. / New Possibilities in Neuroprotection in the Treatment of Ischemic Stroke / /Journal of Neurology and Psychiatry named after S.S. Korsakova. 2008. – V. 22. – p.32-38 . 
5.Sorokina E.G., Reutov V.P., Senilova J.E., Khodorov B.I., Pinelis V.G. /Change in ATP Content in Cerebellar Granule Cells During Hyperstimulation of Glutamate Receptors: Possible Involvement of NO and Nitrite Ions / Bull. Experimental. biol. and med. – 2007. – ¹ 4. – p. 419 – 422. 
6.Khodorov B.I., Storozhevykh T.P., Surin A.M., Sorokina E.G., Yuravichus A.I., Borodin A.V., Vinskaya N,P., Khaspekov L.G., Pinelis V. G. / Mitochondrial depolarization plays a dominant role in the mechanism of disturbance of neuronal calcium homeostasis induced by glutamate //Biol. membranes. – 2001. – V. 18, N 6. – p. 421-432. 
7.De Wied D. / Neuropeptides in learning and memory processes. // Behav. Brain. Res. — 1997. — Vol. 83. — P. 83–90.
8.Krieger C. and Duchen MR. / Mitochondria, Ca2+ and neurodegenerative disease. // Eur. J. Pharmacol. — 2002. — Vol. 447. — P. 177–188. 
9.O’Collins VE., Macleod MR., Donnan GA., Horky LL.,. van der Worp BH, and Howells DW. «1,026 Experimental Treatments in Acute Stroke» // Annals of Neurology. — 2006. — 59:467–477. 
10.Pinelis V. G., Storozhevykh T. P., Surin A. M., Senilova Ya.E., Persiyantzeva N. F., Tukhmatova G. R., Andreeva L. A., Myasoedov N. F., Granstrem O. «Neuroprotective effects of cortagen, cortexin and semax on glutamate neurotoxicity» / 30th European Peptide Symposium (30EPS), Helsinki, 30 August — 5 September 2008



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