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Noopept was synthesized as a highly bioavailable dipeptide conjugate of Piracetam and is, therefore, more bioavailable than racetams like Aniracetam, Piracetam, and Pramiracetam. It is an acetylcholine containing dipeptide (a compound that contains two amino acids connected by a single peptide bond) that has a large number of acclaimed neuroprotective effects. Noopept was created to imitate the reactions of Piracetam and vasopressin metabolite AVP (4-9). In animal models, it has been observed to produce positive cognitive and nootropic effects. Additionally, it is water soluble and has shown to be undetectable in serum despite injection of high concentrations. Its molecular name is N-phenylacetyl-L-prolylglycine ethyl ester. Noopept has been observed to increase the concentration of Cycloprolylglycine and is, therefore, a Cycloprolylglycine pro-drug. Compared to Piracetam, it is not as extensively researched but the available study statistics indicate that Noopept results in higher levels of efficacy. Noopept is a nootropic agent that scientific studies have shown to have neuroprotective properties. A number of animal studies have proven that it can restore memory and assist with sleep disorders, anxiety levels, emotional instability, and irritability. Its mechanism of action is still not very well known although it’s said to be similar to that of racetams.There are very few human based trials conducted on the effects of Noopept.


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Before you decide to buy Noopept, it is important that you learn the history of it. Noopept was originally synthesized in 1996 by Lekka Laboratories, a Russian pharmaceutical company and had been patented in Russia since 1995. In Russia, this nootropic agent is referred to as GVS-11 or Hooneпт. A patent application made in the U.S. in 1995 was not approved by the FDA. Elsewhere, the European Medicines Agency has not approved its use too. Its synthesis was based from endogenous neuropeptide cycloprolylglycine. It is commonly mistaken to be a racetam, but this is not true because it does not contain a 2-oxo-pyrollidine nucleus. Noopept is closely linked with racetams due to its mechanism of action which relates to that of racetams. Additionally, it is thought to be anxiolytic and psychostimulatory, and additionally it promotes memory and cognitive health.

Noopept acts in a similar manner as Piracetam although it is said to be over1000 times more potent than Piracetam (by weight). This substance has a very high oral bioavailability and has been noted to potentiate its own effects when administered chronically. It has also proven to be a potential medication for various aspects of cognitive deficits, but more research is needed in humans. A number of countries have medically registered and approved the use of this substance as a general nootropic agent although in the United States the FDA has not registered it for any medical use.


Animal-based studies have shown Noopept to be neuroprotective and to assist improve and restore memory. In studies modeled for Alzheimer’s disease, Noopept has been observed to restore spatial memory as well as increase immunoreactivity to amyloid buildup. Its safety margin is very high, and it has a particular bioavailability for the brain according to its pharmacokinetics.

Rat based studies discovered other remarkable benefits of Noopept that correlated to BDNG (brain-derived neurotropic factor), immune system, and NGF (nerve growth factor). In one study where rats received acute and chronic Noopept treatment, in both cases, higher expression of NGF and mRNA BDNF were noted. The treatment did not show any signs of tolerance towards Noopept even after being administered for 28 days, and the results obtained suggested that the effects of Noopept potentiate when administered for longer periods. The other study examined how Noopept exhibited effects in immune deficient mice. The researchers established that Noppept had immune-corrective properties.

In in vivo and in-vitro modeled studies, Noopept was observed to affect positively all memory stages (from learning to recall) and also had anxiolytic effects. The in vitro study indicated that Noopept is neuroprotective against the application of H2O2 in neuronal degradation in brains with Down’s Syndrome and healthy brains when administered in a dose-dependent method. It enhanced memory retention and memory retrieval as well as improved learning as shown using the passive avoidance response test. When rats that had ischemic lesions were administered with Noopept for 9 days and then assessed using the passive avoidance test, the Noopept treated rats performed better compared to the control group. These treated rats also showed that Noopept had neuroprotective effects through antioxidation. Other studies in which rats were administered with a single oral dose of Noopept had positive results indicating that they had improved scores when assessed using the passive avoidance test. In a study that involved rats with Alzheimer’s symptoms as a result of undergoing olfactory bulbectomy, after administration of Noopept for 21 days, Morris Water maze test results showed that their spatial memory had improved significantly.

In a rat study that related the effects of Noopept on learning helplessness in rats to a depression model (because it is associated with extraneous factors), Noopept was able to eliminate the effects. The only human study that evaluated depression established that Noopept led to fewer depressive symptoms in individuals with a cognitive injury. The patients had been administered with 20mg of Noopept for 56 days, and the evaluations were carried out using MMSE, CCSE, and BPRS.

In an Alzheimer’s condition mice model, Noopept was noted to boost immunoreactivity to Aβ amyloid after the mice had undergone olfactory bulbectomy operation. In another animal model study on the symptoms of Alzheimer’s Disease as a result of injections with Aβ amyloid, when Noopept was later administered in doses of 0.5mg/kg as treatment, therapeutic effects were observed.

A clinical trial was conducted for 56 days in which patients suffering from cerebrovascular deficiency were used as subjects. The study found that a dosage of 20gm Noopept had higher efficacy compared to 1200mg Piracetam when subjects’ improvements were assessed using global MMSE scores. It was also effective in individuals suffering from post-traumatic cerebral insufficiency. Piracetam only showed efficacy in individuals with the vascular disease and no effects in trauma patients.

Studies assessing the brain concentrations of Noopept in rats following oral administration peaked within 7 minutes, and this is attributed to the fact that concentrations in serum and neural are the same; therefore, Noopept can navigate the blood-brain barrier rapidly. In a rat study, the half-life of Noopept was found to be approximately 16 minutes although this study did not take into account the serum levels in the bioactive cycloprolylglycine. These metabolites are considered to be crucial since Noopept is not detected in serum within 25 minutes following oral administration. Effects have been observed even 70 minutes after injections yet their (oral and injection) excretion kinetics are similar. Interspecies variations have been noted as rats have a higher metabolism rate of Noopept in serum compared to humans.

Another study observed that Noopept has species-dependent effects in mice. In the study, BALB/c mice, C57BL/6J mice, and DBA/2J mice were assessed. Only two species, BALB/c mice, and C57BL/6J had enhancements in long-term memory after administration with Noopept and they also exhibited improvements in their ability to extrapolate the origin of stimuli. DBA/2J mice did not respond to Noopept treatment, and this can be explained by the fact that they have a cholinergic deficit and modifications in hippocampal function and formation.

In studies seeking to evaluate oral ingestion and dose response of Noopept, rats induced with amnesia (through electroshock therapy) were administered with different dosages. Oral doses of 0.5mg/kg and 10mg/kg had positive effects on memory retention. On the other hand, oral administration of 1.2mg/kg and 30mg/kg did not show any changes. The pattern of results seemed to be bimodal and when correlated with human doses, the two effective doses of 0.5mg/kg and 10mg/kg were projected to be around 0.08mg/kg and 1.6mg/kg respectively in humans.

In a study involving healthy rats and OBX rats, 0.01 mg/kg of Noopept administered via injection for 21 days did seem to increase memory in the healthy rats. In the OBX rats, the injections of Noopept seemed to restore memory. The ability of Noopept to restore memory has been observed in rats that had been subjected to compression damage (this is the research model of concussions), cerebral hypoxia and stroke, scopolamine injections and use of anticholinergics, oxidative stress, excitotoxicity through glutamate, bilateral frontal lobectomy, and prefrontal cortex photothrombosis. Furthermore, it has been noted to have protective effects against oxidative damage at concentrations in the range of 10nM.

A human model study involving 53 patients suffering from cognitive condition compared Noopept to Piracetam. The study sample included 37 individuals with cerebral vascular damage, 17 suffering from post-traumatic damage but only 41 finished this clinical trial. Noppept treatment was administered at 10mg twice a day contrasted with an active control dose of 1200mg Piracetam over a period of 56 weeks. Improvements were noted in cerebral vascular damage, trauma parameters, anxiety, fatigue, apathy, irritability, and affective liability were enhanced in both groups. Additional improvements in sleep, mood, and wakefulness were recorded in individuals suffering from the cognitive condition as a result of vascular damage. Comparatively, Noopept was found to have a higher efficacy within the 56 days of the study in improving the MMSE score of subjects compared to Piracetam, in post-trauma patients Noopept was effective but Piracetam had no effects. However, on comparing all scores from CCSE, BPRS, and MMSE, the differences were insignificant.

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