Selank which was developed in Russia, is a short peptide with nootropic and anxiolytic properties. It is a synthetic analogue of naturally occurring Tuftsin, an immunomodulatory peptide that modulates IL-6, T helper cells, monoamine neurotransmitters, and brain derived neurotropic factor (BDNF). In fact, Selank and Tuftsin are essentially the same except that Selank has an additional four amino acids in its chain that help to improve metabolic stability and half-life.

Numerous clinical studies have shown that Selank has strong anti-anxiety and neuroprotective effects in the treatment of anxiety. The clinical effects of Selank are similar to those of classical anti-anxiety medications such as benzodiazepines, which are allosteric modulators of GABAA receptors and increase the inhibitory action of GABA. Selank’s effects include reducing anxiety, improving mood, lower stress levels, and positively influencing memory and learning. Unlide benzodiazepines, Selank does not appear to be habit-forming and does not lead to symptoms of withdrawl or amnesia.

Significantly improves memory and attention under extreme conditions of activities. Improves recovery of stroke clinically and by EEG Neuroprotective- helps with glutamate toxicity, has a high affinity for copper and may be a chelating agent

Cerebrolysin is currently a drug approved in 44 countries, including Austria, China, Germany, Russia and South Korea, for treatment of dementia, stroke and TBI. It is a synthetic nootropicdrug that consists of low-molecular peptides and possesses neuroprotective and neurotrophic repair properties. The active fragment of cerebrolysin is made of proteins which molecular masses do not exceed 10.000 daltons, so they can penetrate blood-brain (or blood-SCF) barrier and reach neurons directly which in turn makes the drug to be able to show organo-specific combined effects towards brain. Cerebrolysin has been proven to have neurotrophic action similar to nerve growth factors causing peripheral and central neuronal stimulation. It improves efficiency within the brain’s aerobic metabolic processes and improves intracellular peptide synthesis. The neuroprotective properties of this nootropic agent help to shield neurons from lactocidosis, to prevent formation of free radicals and to decrease neurotoxic action of certain amino acids.

Dihexa is an oligopeptide drug derived from angiotensin IV that binds with high affinity to hepatocyte growth factor (HGF) and potentiates its activity at its receptor, c-Met. Dihexa is a nooptropic and a small peptide that has been developed by researchers from Washington State University to potently improve certain cognitive function of potential trauma-based brain disorders and neurodegenerative conditions such as Alzheimer’s through increased synaptogenesis. In an assay of neurotrophic activity, Dihexa was found to be seven orders of magnitude more potent than brain-derived neurotrophic factor. Dihexa has also been called a “neurogenic wonder-drug” and the drug can be ten million times stronger than BDNF (Brain-derived neurotrophic factor), one of the leading medications for new synapse formation.Unlike current Alzheimer’s treatments which either slow the process of cell death or inhibit cholinesterase, an enzyme believed to break down a key neurotransmitter involved in learning and memory development, Dihexa is a neuropeptide that is intended to repair brain damage that has already occurred. Dihexa (N-hexanoic-Tyr-Ile-(6) aminohexanoic amide) is a neuropeptide that has been shown to dramatically improve cognitive function in animal models of Alzheimer’s disease-like mental impairment. FGL (l) FGL(I) is a peptide with neurotrophic and memory enhancing properties. FGL peptide is a variant of the natural neural cell adhesion molecule. Neural cell adhesion molecule (NCAM) is a membrane-bound glycoprotein expressed on the surface of neuronal and glial cells. FGL(L) was directly created as a fibroblast growth factor receptor agonist. FG loop (FGL) peptide, that is derived from the second F3 module of NCAM has been found to activate FGFR1. Activating the NCAM–FGFR signaling pathways result in increased neurite outgrowth and survival and leads to its effects in memory. In addition to its effects on memory, FGL was found to have a positive impact on the healing of neuronal tissues subjected to ischemia by decreasing oxidative stress-induced neuronal cell death. FGL was also demonstrated to affect neuropathological symptoms related to Alzheimer’s disease by inhibiting neuronal degeneration and death. Its potential effect on memory and neurodegenerative disease progression have excited many people and it was awarded a 60 million dollar grant in 2016 for further exploration. In addition to its effects on neurodegenerative disease, it also has been viewed as a targeted treatment for TBI, stroke, depression, and general improvement of cognitive function.