Dihexa Nootropics

Dihexa: The Story and Science of a Neurogenic Wonder-Drug

If you have spent any respectable amount of time studying the more extreme margins of nootropics lore, then you have likely stumbled upon accounts of Dihexa, the neigh-legendary Alzheimer’s drug that is purportedly “10,000,000 times stronger than BDNF for new synapse formation”.[1]

In the past Dihexa has been notoriously difficult to find, and even now it is far from accessible to budding body hackers, but with increasingly regular group buys and even a straightforward FAQ popping up, it would seem that Dihexa has made a stable arrival on the fringe of the Nootropics community, and is here to stay.

But despite the increase in access, Dihexa’s mechanism of action is still shrouded in a veil of mystery unperturbed by a mere Google search. Fortunately, the history and pharmacokinetics of Dihexa are as fascinating and tantalizing as the fabled experience reports and research studies purporting its potency.

History of Dihexa

As with many great drugs, the idea for Dihexa was conceived by the inspiration of serendipity and circumstance. In the early ‘90s, the laboratory of Joseph W. Harding was mainly focused on the cerebral control of vascular function, which is heavily influenced by the neuropeptide angiotensin. The lab’s work originally involved angiotensin blockers, specifically ACE inhibitors[2], as a novel means of cancer prevention through the lowering of prostaglandin[3] levels.

But in their tests was an anomaly: a specific sequence of angiotensin, specifically angiotensin IV (Val-Tyr-Ile-His-Pro-Phe), did not exert hypertensive effects unlike its precursor, angiotensin II. Harding’s interest in the compound was further piqued when a colleague’s paper on angiostatin, which is essentially the opposing hormone of angiotensin, had the angiotensin IV peptide sequence incorporated into its structure. Upon testing it for binding sites, Ang-IV was found significantly in the hippocampus, suggesting it had a potential connection to memory formation. With the acquisition of funding from the pharmaceutical giant Eli Lily & Co. (the same company responsible for Cialis, Prozac, and Cymbalta), Harding was able to synthesize an unlimited number of Angiotensin IV analogues for his work. Big Pharma had just given the hunt for Dihexa the huge boost it needed.

3D structure of Dihexa
The 3D structure of Dihexa, with labelled amino acid groups and modifications to encourage lipophilicity and stability.

Work with the Ang-IV analogues was nothing short of miraculous: in every model of cognitive decline, that the analogues of Ang-IV that Harding had developed were able to completely reverse impairment when intraperitoneally injected. (This even included such the reversal of damage from kainic acid brain injections that destroyed up to 60% of cerebral neurons![4]) Yet despite these remarkable findings, none of the tested analogues could pass the blood-brain barrier, and their half-lives in the brain lasted a handful of minutes, at most: none of these candidates could pass muster as a pharmaceutical drug. Unfortunately, before a more functional analogue could be found, Eli Lily was forced to cut off funding: the company had been plunged into a financial crisis when it failed to warn patients about the possible birth defects that can be caused by Prozac, launching a legion of lawsuits against the pharmaceutical giant. The strain and frustration of the period were so great that the company’s vice president actually resigned, and a happy byproduct of the resignation was the return of Harding’s intellectual property. The significant reduction of funds, however, had stopped progress with the Ang-IV analogues in its tracks.

In the early 2000s, the work began anew. Harding and his colleagues began to zero in on the precise peptides necessary for the procognitive properties of a particularly promising analogue, Nle-Angiotensin-IV and arrived at the tripeptide sequence Nle-Tyr-Ile. This sequence was then modified to increase its stability and lipophilicity. This progress attracted the attention of ADDF and WSU, which have been funding the project since. Eventually, one particular modified analogue, MM-201, later known as Dihexa, distinguished itself from the rest of the pack, even going as far as to boost the performance of impaired mice beyond that of non-impaired controls.

Dihexa compared with Ang-IV
Rodent hippocampal neurons were treated for 5 days in vitro with A) water B) Dihexa C) Nle1-Ang-IV. The images show the representative dendritic arbors from each sample, with glowing dots marking synapses. D) and E) show the number of dendritic spines per 50µm of dendrite following 5 days of stimulation and 30 minutes of stimulation with solutions, respectively. [5]
How does something this incredible happen on a chemical level? What miracles is Dihexa performing in our minds? The details are as complicated and interesting as anyone could hope for, and portray Dihexa as a very powerful drug that may also be very dangerous.

Dimerization: a novel mechanism of action

The major term to understand in comprehending Dihexa’s MOA is dimerization, coming from di-, or “two”, and -mer, or “part” (as in merman). Recent science has revealed that many growth factors actually come in two parts that remain apart in the cell, until conditions demand that they activate, at which point they will dimerize into a two-part complex that can then cause a signal cascade resulting in growth, survival, and regeneration of the factor’s target cells. Dihexa works with hepatocyte growth factor (HGF), which has been found in elevated levels in the cortex during the early stages of neurodegenerative disease, suggesting it is being released by the brain in an attempt to facilitate a recovery from damage.

The dimerization of hepatocyte growth factor involves the membrane-bound enzyme c-MET, a tyrosine kinase that is involved in the expression of certain genes by managing the proteins that bind onto DNA strands, preventing or enabling other enzymes to “read” the genes and produce the corresponding proteins from that code (this is the basis for changes in “gene expression”).

This is where the monumental potential of this drug becomes apparent: the current understanding that the dimerized form of growth factors is the activated form, Dihexa both increases HGF activity and lowers dimerization. This suggests that the allosteric modulation of HGF is actually producing an active monomer complex, theoretically doubling the capacity of the available factors to promote signaling cascades and exert changes on cell development. Here is the change in effect worked out as an equation:

Normal HGF/c-MET function: (HGF + HGF) + (c-MET) = Activation

HGF/c-MET function with Dihexa: (HGF + Dihexa) + (c-MET) = Activation

For analogy, imagine that the normal dimerized growth factor activity is like typing: you have to use both hands to do it properly. By allosterically binding to HGF, Dihexa is basically coming along and making it so you only need one hand to do a two-handed job, freeing the other hand to do another two-handed job.

c-MET pathway
An overview of the c-MET pathway. Note the dimerized c-MET complex protruding from the cell membrane.[6]
Before Dihexa, there were no drugs looking at managing the dimerization of growth factors to restore cognition. In fact, most contemporary dimerization work focuses on its prevention. This is where some very real concerns arise concerning the use of Dihexa in healthy subjects: the contemporary work to which I am referring is anti-cancer research. As much help as these performance-enhancing growth factors are for enhancing neuroplasticity and long-term potentiation, they give just as much of a leg up to any latent tumors developing in the body. The HGF/c-MET complex is actually an explicit target for antagonism in anti-cancer research, as this illustrative video reviewing the function of the factor shows.

Due to this implied cancer risk, one could liken the use of Dihexa to the use of nuclear power: rare but incredible power married to rare but incredible risks. But what power, indeed, we have yet to test the limits of. As suggested by its pro-tumor capacities, the HGF/c-MET pathway extends far beyond neurogenesis alone: c-MET receptors are expressed on the endothelial cells of many major organs, including the liver, kidneys, skeletal muscle, bone marrow, pancreas, and prostate. Dihexa could perhaps be used to accelerate wound healing, promote improvement of circulation, and perhaps even enhance anabolic development and prevent muscular atrophy from wasting disease. It could also facilitate recovery from diabetic neuropathy and circular dysfunction, liver cirrhosis/scarification, other types of organ damage, anemia, and perhaps even metabolic and mitochondrial disorders.

So why is such a remarkable drug so understudied and underdeveloped? The answer can be found in several endpoints, but the biggest one is the dollar: without the support of deep pockets like Eli Lily, there is no realistic scenario in which Dihexa becomes FDA approved, a process that can easily cost hundreds of millions, if not billions, of dollars. NIH, one of the major bodies giving research grants for Alzheimer’s treatments, only cares about working with amyloid beta to manage the disease.

The second reason is the sheer novelty of the drug means that it is not even on the radar for most organizations. In scientific research, being remarkable and unique is as much a blessing as a curse, because researchers prefer to build off of established knowledge bases, specifically the ones for which they have established a knowledge base. With the exception of some anti-cancer treatments, Dihexa is one of the only Alzheimer’s research chemicals that modulates HGF, an MOA most doctors know nothing about.

The pharmacology of Dihexa in animals is well-documented: in vitro, the synaptogenesis of Dihexa begins at T+30:00, maximizes at +48:00:00[7]. The overall half-life of the drug is currently charted at approximately a week: longer than just about any other neurogenic compound. While the major observed effect is synaptogenesis, in models of impairment the drug also revived production of tyrosine hydroxylase (the enzyme essential for the production of catecholamines such as dopamine and noradrenaline) in the substantia nigra (one of the largest concentrations of dopaminergic neurons in the brain).

Dihexa experiences

Discussion of history, MOA, pharmacokinetics, and obscurity aside, one question still remains: “What does it do when a healthy human takes it?” As with many neurogenic substances, the answer to such a question is predicted heavily on the existing neurochemical environment (including other drugs in the system), route of administration, and genetic predisposition. In the absence of neurological insult (science speak for “brain damage), which gives a firm basis for improvement, these conditions have a heavy bearing on whether such a substance will influence development at all. Formal testing of Dihexa in human trials has yet to even begin, due to the lack of funding for such research, and anecdotal reports are varied. Adventurous guinea pigs on different forums have listed dosages everywhere from 8 to 45 mg per day and report a variety of benefits, from increased mental stamina to heightened articulation. Users have reported increases in creative thinking, social intuition, and problem-solving skills. There has also been a fair deal of non-responders who haven’t felt anything at all.

Dihexa experienceThe author has personally experimented with a DMSO+Dihexa solution with a 16.67mg/mL concentration, applying .5mL to clean, exfoliated inner forearms every other evening for a week (3 doses, total). The experience was transformative in many of the ways purported by anecdote, including an increase in creativity, articulation, and problem-solving. What really distinguished the drug from other neurogenic substances in the author’s personal repertoire was how well it accelerated deliberation of social conflict. Remarkably large and fast leaps in logic allowed for prompt and thorough insight into the dynamics of ethical quandaries, suggesting a boost in critical thinking via the anterior cingulate cortex, the malfunction of which has been associated with such mental disabilities as ADHD[8] and ASD.[9]

Of course, this is only an informal study, complete with exposure to a multitude of confounding factors. Despite the promise already posed by Dihexa, poor funding and a lack of interest from much of the scientific community means that the chemical has a long way to go before human trials, let alone becoming an FDA-approved pharmaceutical, and if the view of the HGF/c-MET system as a vehicle for tumor growth persists, it may always be reserved for only the most severe cases of cognitive decline and physical distress. Still, for those determined few transhumanists willing to go to any lengths to transcend their normal limitations, Dihexa holds great promise and, despite its difficult procurement, doesn’t seem to be disappearing anytime soon. It is the imposing poster child of a new frontier in medicine, where the hopes of expectations met are to meet our expectations of ourselves.

References   [ + ]


Is Berberine the New Resveratrol?

There are very few supplements that have a list of potential benefits as impressive as berberine. Despite the fact that berberine is not all that well known compared to many other supplements, it is extremely well researched. While not all of these benefits are guaranteed to occur for every single user, berberine has been found to

  1. Reduce inflammation
  2. Improve gastrointestinal health
  3. Reduce glucose production in the liver
  4. Improve markers of insulin resistance
  5. Lower cholesterol
  6. Lower oxidative stress
  7. Help in losing body fat
  8. Slow down aging
  9. Suppress chemical-induced carcinogenesis, clastogenesis, tumor promotion and tumor invasion
  10. Exert antiarrhythmic effects
  11. Exert anti-microbial activity against a wide range of microorganisms.
  12. Exert minor antidepressant effects, as well as work in a synergistic fashion with existing antidepressants

While this list of touted benefits is certainly impressive, berberine also carries with it a number medication interactions, which must be noted with caution (more on this later).

What is Berberine?


Berberine is an isoquinoline alkaloid and ammonium salt of a bright yellow color that is found in and extracted from a variety of plants from the genus berberis, as well as Coptis chinensisPhellodendron amurense, and Hydrastis canadensis (Goldenseal) and many others. These plants have a history of being used in both traditional Chinese Medicine and Indian Ayurveda as an anti-microbial agent. Berberine appears to be effective in fighting bacteria, fungi, and protozoa. [1] However, these traditional uses of berberine barely scratch the surface of its full capability.

When berberine is ingested orally, it has a relatively low bioavailability of 5% or less. [2] Berberine increases the action of P-Glycoprotein, a substance which actually makes berberine more difficult for the intestines to absorb. Because of this, taking a P-Glycoprotein inhibitor (such as Milk Thistle) can possibly make smaller doses of berberine more effective.[3] Another option is to take Berberine with Coconut oil that contains a fatty acid known as Sodium Caprate which significantly increases the absorption and the efficacy of Berberine.[4][5]

AMPK Modulation

One of berberine’s main mechanisms of action is its ability to activate an enzyme called Adenosine Monophosphate Kinase (AMPK). AMPK is crucial for maintaining energy homeostasis in cells. It is responsible for regulating glucose and other nutrients by sensing their concentrations within cells. [6] The activation of AMPK caused by berberine has multiple different effects. First, the AMPK activation causes an increased uptake of glucose into adipocytes (fat cells). This is one of the major methods through which berberine reduces glucose levels in the blood.[7] In fact, berberine’s antidiabetic effect is so effective that it is regarded as one of the few supplements to be as strong as a pharmaceutical drug. When taken correctly, berberine can be as effective (or even more effective[8] as the popular type II diabetes drug metformin.[9]

Molecular structure of BerberineBerberine also appears to have various positive effects on the heart and the cardiovascular system as a whole. Activated AMPK located in liver cells causes an inhibition of cholesterol and triglyceride synthesis.[10] This change is also linked to a lowering of low-density lipoproteins (“bad” cholesterol) and raising of high-density lipoproteins (“good” cholesterol). Additionally, berberine can lower the levels of LDL by stimulating the synthesis of LDL receptors, which are responsible for removing LDL from the blood.[11] The activation of AMPK induced by berberine also appears to inhibit the synthesis of lipids and lower triglyceride levels, which is useful for individuals who are attempting to lose weight.[12]

In one study, reperfusion (oxidative stress) was induced in rats who had been pre-treated with berberine. The rats treated with berberine displayed significantly less heart damage than those who had not been treated.[13] One study conducted on 24 overweight or obese subjects concluded that berberine was able to reduce blood pressure significantly more than placebo. [14] These effects of berberine—the inhibition of LDL cholesterol and triglyceride synthesis, increase in HDL cholesterol, decrease in lipid production, protection from oxidative stress, and the decrease in blood pressure—all work together to contribute to berberine’s overall positive effect on heart health and weight loss. But that’s not all…

Anti-aging & Anti-cancer

There is some early research evidence that seems to suggest berberine’s efficacy as telomerase inhibitor.[15] Telomerase is a protein that is intricately linked with cell proliferation and the life cycle of cells. Telomeres (the region that telomerase acts upon) are a portion of DNA sequences located at the ends of chromosomes that keep them from deteriorating.

Essentially, the inhibition of telomerase by berberine has potential applications in the area of life extension & longevity as well as a chemopreventive supplement or in conjunction with existing cancer treatments to increase their efficacy.[16]

fight cancerBesides telomerase inhibition, berberine has also been found to suppress the growth of a wide variety of tumor cells[17][18], including breast cancer,[19] leukemia[20], melanoma,[21] epidermoid carcinoma, hepatoma[22], pancreatic cancer[23], oral carcinoma, tongue carcinoma[24], glioblastoma, neuroblastoma[25], prostate[26][27][28] and gastric carcinoma.

Mental Health

Berberine also exhibits minor to moderate antidepressant effects. One study conducted on mice discovered that berberine administration reduced the immobility time of mice in a swim test, which is indicative of antidepressant effects. The same study also concluded that berberine caused significant increases in the levels of dopamine, serotonin, and norepinephrine in the whole brain. It was also discovered that berberine works synergistically with certain antidepressant medications, such as fluoxetine, imipramine, tranylcypromine, and venlafaxine.[29]

New studies suggest berberine may have a potential for inhibition and prevention of Alzheimer’s disease through inhibition of β-amyloids pathways and cholinesterase[30] and through antioxidant capacities. Berberine derivatives are currently being developed as potent acetylcholinesterase (AChE) inhibitors.[31]

As a PCOS treatment

In a 2012 human study[32], 89 Chinese women of reproductive age who met the diagnostic criteria for polycystic ovarian syndrome (PCOS) and insulin resistance, were recruited and prescribed the anti-androgen compound cyproterone acetate (2.0 mg/day) in a combined oral contraceptive pill with 35 mcg ethinyl estradiol, taken in a cyclic fashion. They also received advice from a nutritionist to limit dietary fat and carbohydrates without restricting calories.

They were then assigned to one out of three treatment groups:

  1. Berberine hydrochloride, 500 mg 3 times/day (n=31)
  2. Metformin, 500 mg 2 times/day for the first week, then 3 times/day for the remainder of the study (n=30)
  3. Placebo tablet 2 times/day (n=28)

Results of the study were:[33]

  • After 3 months, all the treatment groups showed a significant reduction in body weight and BMI.
  • Waist circumference and waist-to-hip ratio were reduced in all 3 groups. However, the berberine group showed a significantly greater reduction in these measures.
  • All 3 treatment groups showed a significant reduction in fasting insulin. However, in the placebo group, fasting plasma glucose and fasting glucose/insulin ratio remained unchanged.
  • Fasting plasma glucose decreased and fasting glucose/insulin ratio increased in the berberine and metformin groups. There was no significant difference between them.
  • The berberine and metformin groups showed comparable changes in total testosterone and free androgen index, which were significantly greater than placebo. However, sex hormone–binding globulin increased significantly in the berberine group when compared with both metformin and placebo.
  • All 3 groups had reductions in total cholesterol and triglycerides. The berberine group had a significantly greater decrease in triglycerides, total cholesterol, and LDL (“bad” cholesterol”), and a significantly greater increase in HDL (“good” cholesterol) when compared to metformin.
  • Adverse effects were minimal and fewer compared to metformin. Nine subjects who received metformin complained of transient abdominal discomfort including nausea, vomiting, mild diarrhea, and flatulence, while 3 who received berberine complained of a bitter taste in the mouth.

As a result of this study, the researchers conclude that berberine may prove a viable alternative to metformin in optimizing the health outcomes of women with PCOS.
Another study[34] on 102 anovulatory Chinese women was published in 2015 found that administration of berberine alone may improve the menstrual pattern and ovulation rate in anovulatory Chinese women with polycystic ovary syndrome, as well as decrease sex hormone binding globulin, insulin resistance, total cholesterol, triglycerides and low-density lipoprotein cholesterol in normal weight polycystic ovary syndrome women.

Side Effects & Interactions

Berberine is absorbed slowly by the intestine, meaning that high doses can cause diarrhea and cramping. For this reason, berberine is typically taken in various smaller doses throughout the day.

In terms of interactions, the most noteworthy is the potential interaction with macrolide antibiotics like azithromycin (Zithromax) and clarithromycin (Biaxin). The interaction between the two has the possibility of causing cardiotoxicity. Berberine also inhibits enzymes CYP2D6 and CYP3A4 which has the potential to affect how many other drugs are metabolized by the body.[35] For this reason, it is very important to discuss berberine supplementation with a healthcare professional to ensure no dangerous interactions will take place.

Goldenseal vs Berberine Hcl

berberine supplement
Berberine hydrochloride powder

The two most common ways to supplement Berberine are to take either Berberine hydrochloride (hcl) or Goldenseal root powder. This is extremely important and I’ll explain why.

Goldenseal, – which contains a number of other compounds besides berberine – has been shown to cause DNA damage in prokaryotic and eukaryotic organisms[36] as well as promote liver cancer in rats.[37]

Therefore, I strongly advise against using goldenseal root and to take Berberine Hcl instead, the same way it was used in the PCOS studies. If you’re taking goldenseal supplements, stop taking them as soon as possible!


Berberine is certainly unique among supplements in the fact that it is equally as effective as some prescription medications. It also boasts a myriad of benefits that impact a variety of systems throughout the body. This article has only scratched the surface of the researched benefits of berberine. A collation of the large body of evidence concerning berberine can be found here for anyone who wants to learn more about this fascinating supplement. While there are some potential side effects and medication interactions, berberine is still well worth checking out. Berberine stands as a hidden gem among supplements – one that has the potential to greatly improve one’s quality of life.

Berberine Hcl can be bought relatively cheap at PowderCity and other supplement and vitamins shop.

References   [ + ]

1. Berberine at
2. Bioavailability study of berberine and the enhancing effects of TPGS on intestinal absorption in rats.
3. Effect of berberine on the pharmacokinetics of substrates of CYP3A and P-gp.
4. Sodium caprate augments the hypoglycemic effect of berberine via AMPK in inhibiting hepatic gluconeogenesis (2012)
5. Enhancement of Sodium Caprate on Intestine Absorption and Antidiabetic Action of Berberine (2010)
6. Effect of AMPK activation on muscle glucose metabolism in conscious rats.
7. Berberine inhibits PTP1B activity and mimics insulin action.
8. Berberine Compared to Metformin in Women with PCOS | Natural Medicine Journal
9, 35. Berberine at
10. Inhibition of lipid synthesis through activation of AMP kinase: an additional mechanism for the hypolipidemic effects of berberine.
11. Berberine inhibits dyslipidemia in C57BL/6 mice with lipopolysaccharide induced inflammation.
12. Inhibition of lipid synthesis through activation of AMP kinase: an additional mechanism for the hypolipidemic effects of berberine
13. Berberine attenuates ischemia-reperfusion injury via regulation of adenosine-5′-monophosphate kinase activity in both non-ischemic and ischemic areas of the rat heart.
14. Effect of berberine administration on metabolic syndrome, insulin sensitivity, and insulin secretion.
15. Human telomeric G-quadruplex: the current status of telomeric G-quadruplexes as therapeutic targets in human cancer.
16. Human telomeric G-quadruplex: the current status of telomeric G-quadruplexes as therapeutic targets in human cancer.
17. A systematic review of the anticancer properties of berberine, a natural product from Chinese herbs (2009)
18. Berberine and Coptidis Rhizoma as novel antineoplastic agents: a review of traditional use and biomedical investigations (2009)
19. The alkaloid Berberine inhibits the growth of Anoikis-resistant MCF-7 and MDA-MB-231 breast cancer cell lines by inducing cell cycle arrest (2009)
20. Down-regulation of cyclin B1 and up-regulation of Wee1 by berberine promotes entry of leukemia cells into the G2/M-phase of the cell cycle (2006)
21. Different concentrations of berberine result in distinct cellular localization patterns and cell cycle effects in a melanoma cell line (2008)
22. Coptis chinensis inhibits hepatocellular carcinoma cell growth through nonsteroidal anti-inflammatory drug-activated gene activation (2009)
23. Berberine Inhibits Cell Growth and Mediates Caspase-Independent Cell Death in Human Pancreatic Cancer Cells (2010)
24. Berberine induced apoptosis via promoting the expression of caspase-8, -9 and -3, apoptosis-inducing factor and endonuclease G in SCC-4 human tongue squamous carcinoma cancer cells (2009)
25. Berberine inhibits human neuroblastoma cell growth through induction of p53-dependent apoptosis (2008)
26. Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells (2006)
27. Butanol fraction containing berberine or related compound from nexrutine inhibits NFκB signaling and induces apoptosis in prostate cancer cells (2009)
28. Berberine inhibits p53-dependent cell growth through induction of apoptosis of prostate cancer cells (2009)
29. On the mechanism of antidepressant-like action of berberine chloride.
30. Conformation-activity studies on the interaction of berberine with acetylcholinesterase: Physical chemistry approach (2009)
31. Synthesis, biological evaluation, and molecular modeling of berberine derivatives as potent acetylcholinesterase inhibitors (2009)
32, 33. Effect of berberine on insulin resistance in women with polycystic ovary syndrome: study protocol for a randomized multicenter controlled trial
34. A Single Arm Pilot Study of Effects of Berberine on the Menstrual Pattern, Ovulation Rate, Hormonal and Metabolic Profiles in Anovulatory Chinese Women with Polycystic Ovary Syndrome
36. Genotoxicity of the isoquinoline alkaloid berberine in prokaryotic and eukaryotic organisms
37. Toxicology and carcinogenesis studies of goldenseal root powder (Hydrastis Canadensis) in F344/N rats and B6C3F1 mice
Nootropics Selank

My Experience with Selank, the Anxiolytic Peptide

It’s becoming a given — whether you’re stuck in a traffic jam on your way to work, arguing with your partner over finances, coordinating the family’s busy schedule, or having difficulty turning down your racing thoughts at night, most of us encounter daily stresses. According to the National Institute of Health, 40 million adults in the US have anxiety disorders. [1] These can range in severity from Generalized Anxiety Disorder and Social Phobia to more extreme versions including Panic Disorder, OCD, and Post Traumatic Stress Disorder.

Traditional treatments for anxiety disorders have included a class of medications known as benzodiazepines (Xanax, Valium). However, many clinicians have growing concern over prescribing such medications due to their addictive nature and impact on cognition. New reports are emerging that demonstrate a direct correlation of benzo use to an increased risk of Alzheimer’s Disease. A recent study published in the British Medical Journal showed “the risk of Alzheimer’s disease was increased by 43-51% among those who had used benzodiazepines in the past. Risk increased with density of exposure and when long acting benzodiazepines were used”. [2]

With these statistics in mind, many Nootropic enthusiasts have focused attention for anxiety relief on a particular class of Nootropics, peptides.

A peptide is a chemical compound containing two or more amino acids that are coupled by a peptide bond. There are 20 naturally-occuring amino acids and they can be combined together to form new molecules. When a molecule consists of 2-50 amino acids it is called a peptide, whereas a chain of 50 or more amino acids is referred to as a protein.[3]

Discovery of Selank

Research on peptides began in the 1970’s in Russia following the UN “Convention on Psychotrophic Substances” that essentially banned drugs traditionally used by militaries worldwide.[4] This ban included amphetamines, a widely employed wakeful and focusing drug. The Ministry of Russian defense tasked the Research Institute of Molecular Genetics in Moscow to develop comparable chemical agents. It was at this time Nikolai Myasoedov, a researcher at the institute, focused his attention on endogenous compounds, peptides, to provide harmless stimulation.[5]

Tuftsin and Selank

Dozens of molecules previously unexplored came to light out of this research, including Tuftsin (aka TP-1), a tetrapeptide produced primarily in the spleen.[6] The researchers discovered that this peptide had nootropic, anxiolytic and immunostimulating effects[7]

The researchers found out that they could prevent premature decomposition of the molecule by attaching a ‘tail’ of amino acids to the tuftsin molecule. Selank (formerly TP-7) is born.[8][9]

Clinical trials on this novel compound concluded in 2004 and Selank was proven effective for treating an array of anxiety disorders. In addition, many patients were able to conquer their fears coupled with “improved mood, mental and motor activity, and most importantly, Selank was demonstrated as not addictive”. [10]

The benefits of Selank summarized
The benefits of Selank summarized

According to research provided by the Institute of Molecular Genetics, drops “that must be instilled into the nose” is still considered the best way to take neuropeptides.[11] With this in mind, a >1% solution of Selank can be prepared for sterile instillation.

My experience with Selank

I have personally tried Selank on several occasions to help quell feelings of anxiety and have found it to be quite effective. 400 mcg instilled intranasal provided me with several hours of great clarity, focus, and organized thought. My mind doesn’t feel cloudy or groggy like I’ve experienced from other anxiolytics, mood is noticeably improved, and a slight energy lift is detectable. In my opinion, Selank is a viable treatment option for those suffering from anxiety and for certain aspects of motivation especially those with an inability to see projects through to completion.

Reviewer 8.2

References   [ + ]