Expanding upon the possible anti-panic effects of 5-HTP, one study using 2mg/kg 5-HTP to children (3.2-10.6 years of age) at bedtime for 20 days noted that 5-HTP was asssociated with beneficial response (more than 50% reduction in night terror frequency) of 93.5% of children relative to 28.6% in placebo.[42] Oddly, 6 months after the initial supplementation period the 5-HTP group still reported less sleep terrors (83.9% reporting improvement).[42]
Oxytocin is a versatile actor, whose resume includes all sorts of jobs in sex, reproduction, social behaviour and emotions.  It can increase trust among people and make them more cooperative (this works in meerkats, too). It can increase the social skills of autistic people. It’s released during orgasm. It affects lactating breasts, contracting wombs and the behaviour of sheep mothers towards their newly born lambs. The list goes on: drug addiction, generosity, depression, empathy, learning, memory.

Autism. A 1998 study found significantly lower levels of oxytocin in blood plasma of autistic children.7 A 2003 study found a decrease in autism spectrum repetitive behaviors when oxytocin was administered intravenously.8 A 2007 study reported that oxytocin helped autistic adults retain the ability to evaluate the emotional significance of speech intonation.9
Drug interaction: Impact on effects of alcohol and other drugs: According to several studies in animals, oxytocin inhibits the development of tolerance to various addictive drugs (opiates, cocaine, alcohol), and reduces withdrawal symptoms.[68] MDMA (ecstasy) may increase feelings of love, empathy, and connection to others by stimulating oxytocin activity primarily via activation of serotonin 5-HT1A receptors, if initial studies in animals apply to humans.[69] The anxiolytic Buspar (buspirone) may produce some of its effects via 5-HT1A receptor-induced oxytocin stimulation as well.[70][71]
Nolen, W. A., van de Putte, J. J., Dijken, W. A., Kamp, J. S., Blansjaar, B. A., Kramer, H. J., and Haffmans, J. Treatment strategy in depression. II. MAO inhibitors in depression resistant to cyclic antidepressants: two controlled crossover studies with tranylcypromine versus L-5-hydroxytryptophan and nomifensine. Acta Psychiatr.Scand 1988;78:676-683. View abstract.
Melanotan II is a synthetic hormone that speeds up the production of melanin, the pigment that absorbs ultraviolet radiation and gives skin its colour. It was originally developed as a potential treatment for female sexual dysfunction and erectile dysfunction, but this research ceased in 2003. In technical terms, Melanotan II is a synthetic analogue of the peptide hormone α-melanocyte-stimulating hormone (α-MSH). Today, there are numbers of sellers on the internet of unlicensed and untested powders sold as Melanotan II.
Evidence accumulated over the past decades has overturned the traditional dogma that the adult mammalian brain cannot generate new neurons. Adult neurogenesis has been identified in all vertebrate species examined thus far including humans.44-49 Newly generated neuronal cells originate from neural stem cells in the adult brain. Neural stem cells are the self-renewing, multipotent cells that generate the neuronal and glial cells of the nervous system.50 The major function of neurogenesis in adult brain seems to replace the neurons that die regularly in certain brain areas. Granule neurons in the DG continuously die and the progenitors in the subgranular zone of the DG may proliferate at the same rate as mature neuronal death to maintain a constant DG cell number.51 Similarly, the newly proliferated cells from the subventricular zone migrate and replenish the dead olfactory bulb neurons.52 Here, we focus on DG neurogenesis which is important for spatial learning and memory. In normal adult rats, newborn neural cells migrate from the subgranular zone of the DG of the hippocampus into the granule cell layer and eventually become mature granule neurons.53 These new granule neurons extend axonal processes to their postsynaptic targets54-57 and receive synaptic input.58 TBI stimulates widespread cellular proliferation in rats and results in focal neurogenesis in the DG of the hippocampus.59,60 Some of the newly generated granule neurons integrate into the hippocampus. The integration of the injury-induced neurogenic population into the existing hippocampal circuitry coincides with the time point when cognitive recovery is observed in injured animals.44

This mother-child bonding is the most glorified myth that is not re-thought as often as it should. Its apparant purpose is just to make a dangerously selfish mother (such frustrated mothers do exist a lot more than we read in the news) to think twice before harming her defenseless child which is oftentimes in her sole custody in our society. Acts of such mothers are branded as mental illness rather than plain cruelty. While most people (men and women alike) tend to protect, and not harm a child, the real bonding can happen beetween two independent, mature adults.


An interesting concept that has emerged from initial findings is that regeneration and fibrosis are competing events in the vertebrate heart. That is, if there is a capacity for injury-stimulated cardiomyocyte hyperplasia beyond a certain threshold, regenerative mechanisms will overcome scarring. Results consistent with this idea came from experiments with zebrafish possessing a ts mutation in the cell-cycle checkpoint kinase Mps1 (Poss et al., 2002b). As mentioned earlier, mps1 mutants were initially identified based on their defects in caudal fin regeneration. Serendipitously, mps1 mutants also showed defects in cardiac regeneration at a temperature restrictive for the mutation (Poss et al., 2002b). Instead of regenerating muscle in response to ventricular resection injury, mps1 mutants repaired wounds by forming large, collagen-rich scars. Inhibition of Fgf signaling also stunts cardiac regeneration and causes scarring (Lepilina et al., 2006). These results indicate that even vertebrates with high cardiac regenerative capacity have a default scarring mechanism; normally, regeneration somehow restricts this pathway (Fig. 8). The implication is exciting; perhaps by stimulating regeneration in a poorly-regenerative system like the mammalian heart, scarring events characteristic of myocardial infarction would be restricted by new muscle formation. Similarly, deterring cardiac scarring mechanisms would perhaps favor regeneration in mammals.

Osteoclast differentiation was assessed by tartrate-resistant acid phosphatase (TRAP) staining and activity. After 5 days of culture, cells were stained for TRAP kit using a leukocyte acid phosphatase kit (Sigma Aldrich, St Louis, MO, USA). Cells with three or more nuclei were counted as multinucleated mature osteoclasts. To measure TRAP activity, cells were fixed with 10% formalin for 10 min and 95% ethanol for 1 min, and then 100 μl of citrate buffer (50 mM, pH 4.6) containing 10 mM sodium tartrate and 5 mM p-nitrophenylphosphate (Sigma-Aldrich) was added to the wells containing fixed cells in the 48-well plates. After incubation for 1 h, enzyme reaction mixtures in the wells were transferred to new plates containing an equal volume of 0.1 N NaOH. Absorbance was measured at 410 nm using a microplate reader.
Tβ4 is not a thymus-specific peptide but also present in most tissue and all cells except red blood cells [35]. High amounts of Tβ4 were detected in human white blood cells, especially in neutrophils and in macrophages [34], expressed in developing mandible (embryonic day 12) [36] and hair follicles (HF) of mice [37]. In addition, the peptide is also detected outside cells, in blood plasma and in wound and blister fluids [34]. Although the mechanism(s) of action of exogenous Tβ4 on anti-inflammatory effects remains unclear, the high levels of Tβ4 present in human wound fluid (13 μg/mL) suggest its importance in wound healing or anti-inflammation [38]. However, the level of Tβ4 is variable (unchanged, decreased, and increased) in GCF or biopsied gingival tissue of periodontal patients [20, 21]. Based on the observations that Tβ4 has anti-inflammatory effects [11–14], the hypothesis is that Tβ4 regulates inflammatory mediators and osteoclastogenesis in osteolytic bone disease, such as periodontitis.
For example, when a mother is nursing her baby, that stimulation from the breast is going into the brain and causing those oxytocin neurons to fire and release oxytocin directly into the brain. That's much more powerful than what happens with a nasal spray. So I think that, you know, in the future, we may have these drugs that can, in a very potent way, tap into this oxytocin system to treat many different kinds of disorders.
Combined treatments of 5-HTP and SSRI seem to have strong synergistic effects on serotonin levels in rats and humans so that some clinicians recommend the use of slow-released 5-HTP in combination with SSRIs (R, R2, R3). However, additional clinical trials are required to demonstrate the safety and effectiveness of this approach, and combinations of 5-HTP and medications should only be used under medical supervision.
In humans, 5-HTP is the nutrient precursor to the neurotransmitter serotonin – widely known as the 'happy neurotransmitter' – meaning 5-HTP converts directly into serotonin in the brain. As well as being in our bodies, it's found naturally in the seeds of a woody shrub native to West Africa. By taking it as a supplement, in theory, you will end up with more serotonin in your brain. Serotonin deficiency is linked to depression, anxiety and a whole host of physical and mental ailments. Raising its levels seems to help brain cells send and receive chemical messages, which in turn boosts mood.
To further determine the potential anti-inflammatory effects of Tβ4 activation, expressions of proinflammatory or osteoclastogenic cytokines were measured by RT-PCR (Fig 4A). The TNF-α, IL-1β, IL-6, IL-8, and IL-17 mRNA levels increased in the H2O2- stimulated PDLCs, and these increases were significantly decreased in a concentration-dependent manner by treatment with the Tβ4 peptide. Since receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) are two important osteoclastogenic factors, we next explored the effects of Tβ4 peptide on RANKL and OPG expressions in PDLCs. Tβ4 peptide reduced H2O2-stimulated up-regulation of RANKL, with a reciprocal increase in OPG mRNA in a dose-dependent manner (Fig 4B).
Much of human behavior is influenced by hormones. There’s cortisol, involved in our stress response and energy balance. Testosterone, a male sex hormone, tends to make men more competitive. Oxytocin has various social and physiological functions in the brain and the body, but is sometimes referred to as the “love hormone” due to its role in social bonding. These are all simplifications, but hormones do underlie many aspects of what we do and what we feel.
Due to its molecular structure and low molecular weight, TB-500 is very versatile, mobile and possesses the ability to travel long distances through tissues. This means that when targeting injured areas (chronic or acute), TB-500 has the ability to circulate through the body and “find” those areas of injury in order to enhance the healing or growth process. Many users have also noted the added benefits of improved flexibility, reduced inflammation in tendons, re-growth of lost hair, and darkening of grayed hair.
My wife has suffered from debilitating leg cramps for years, usually nocturnal. We have spent much money and time trying to find a cure, including every type of magnesium supplement we could find. Nothing has worked. We’ve also tried MSM and DMSO. Sometimes the cramps are in her calves, sometimes her thighs, sometimes her back and even her toes. Sometimes several muscles cramp at once. She has a high tolerance for pain, but these cramps leave her sobbing. I have purchased TB-500 and received it today. Does your research offer any hope that this could help eliminate her muscle spasms?
Oxytocin is relatively safe when used at recommended doses. Potential side effects include: Central nervous system: Subarachnoid hemorrhage, seizures; Cardiovascular: Increased heart rate, blood pressure, systemic venous return, cardiac output, and arrhythmias;Genitourinary: Impaired uterine blood flow, pelvic hematoma, tetanic uterine contractions, uterine rupture, postpartum hemorrhage.

Established immortalized human PDLCs [22] that maintain the characteristics of primary PDLCs by transfecting human telomerase reverse transcriptase (hTERT) were used. These cell line were kindly provided by Professor Takashi Takata (Hiroshima University, Japan). Cells were cultured in α-MEM supplemented with 10% FBS, 100 U/mL penicillin, and 100 μg/mL streptomycin in a humidified atmosphere of 5% CO2 at 37°C. For the experiments, the cells were seeded into culture dishes and then cultured in α-MEM containing 10% FBS for 2 days until 70% confluent, and, then, the media was replaced by serum-free medium in order to minimize any serum-induced effects on PDLCs. Subsequently, the cells were exposed to H2O2 and human Tβ4 peptide (RegeneRx Biopharmaceuticals Inc., Rockville, MD). All treatments were performed in triplicate and approved by the local ethics committee.
Treated cells were washed with PBS and cytosolic protein extracts were prepared using 1X cell lysis buffer (Santa Cruz Biotechnology, CA) supplemented with protease inhibitor cocktail. Protein concentrations were determined using the Bradford assay (Bio-Rad, CA, USA) as per the manufacturer's protocol. Aliquots of protein lysates were separated on sodium dodecyl sulfate–10% polyacrylamide gels and Western blotting was performed. The proteins were transferred onto a polyvinylidene difluoride membrane (Bio-Rad, CA, USA) in transfer buffer (20 mm Tris, 150 mm glycine, 20% methanol, pH 8.0; TBS-T) at 4°C and 100 V for 1 hour. The membrane was blocked with 5% dry milk in TBS-T for 1 hour at room temperature and incubated with primary antibodies (1:1000) and horseradish peroxidase (HRP)-conjugated secondary antibodies. Protein bands were detected using an enhanced chemiluminescence (ECL) system (Amersham Biosciences, Backinghamshire, UK).
Liver fibrosis, a major characteristic of chronic liver disease, is inappropriate tissue remodeling caused by prolonged parenchymal cell injury and inflammation. During liver injury, hepatic stellate cells (HSCs) undergo transdifferentiation from quiescent HSCs into activated HSCs, which promote the deposition of extracellular matrix proteins, leading to liver fibrosis. Thymosin beta 4 (Tβ4), a major actin-sequestering protein, is the most abundant member of the highly conserved β-thymosin family and controls cell morphogenesis and motility by regulating the dynamics of the actin cytoskeleton. Tβ4 is known to be involved in various cellular responses, including antiinflammation, wound healing, angiogenesis, and cancer progression. Emerging evidence suggests that Tβ4 is expressed in the liver; however, its biological roles are poorly understood. Herein, we introduce liver fibrogenesis and recent findings regarding the function of Tβ4 in various tissues and discuss the potential role of Tβ4 in liver fibrosis with a special focus on the effects of exogenous and endogenous Tβ4. Recent studies have revealed that activated HSCs express Tβ4 in vivo and in vitro. Treatment with the exogenous Tβ4 peptide inhibits the proliferation and migration of activated HSCs and reduces liver fibrosis, indicating it has an antifibrotic action. Meanwhile, the endogenously expressed Tβ4 in activated HSCs is shown to promote HSCs activation. Although the role of Tβ4 has not been elucidated, it is apparent that Tβ4 is associated with HSC activation. Therefore, understanding the potential roles and regulatory mechanisms of Tβ4 in liver fibrosis may provide a novel treatment for patients.
Thymosin beta 4 (Tβ4) is a highly conserved, naturally occurring, water-soluble regenerative peptide that is found in all tissues and in all cell types, except red blood cells (Goldstein, Hannappel, Sosne, & Kleinman, 2012; Goldstein & Kleinman, 2015). It is also found in the blood and in other body fluids, including tears, saliva, cerebrospinal fluid, and wound fluids (Badamchian et al., 2007; Huang, Wang, Barnes, & Elmets, 2006; Mohring, Kellmann, Jurgens, & Schrader, 2005). Both platelets and leukocytes release Tβ4 into the wound fluid such that the final concentration is 13 μg/mL (Fromm, Gunne, Bergman, et al., 1996; Hannappel & van Kampen, 1987).
I’ve tried researching this on my own but haven’t been able to find much. I have Hashimoto’s Thyroiditis & my endocrinologist says I barely have any thyroid left. Would TB-500 help regenerate new thyroid growth & if so where would I inject it?? I plan on taking this along with the BPC-157 (orally) for gut inflammation to see if it can repair leaky gut & digestive issues. Thoughts?
RegeneRx is continuing with pre-clinical research, in collaborative arrangements with the National Institutes of Health, accumulating data on the effects of Tb4 and aiming for an IND application (Investigational New drug App-lication) to proceed with clinical studies. Phase I clinical trials will determine the ability of Tb4 to repair ulcers in diabetic patients and to reduce inflammation and accelerate recovery from burns and abrasions to the cornea.
TB-500 was identified as a gene that was up-regulated four-to-six fold during early blood vessel formation and found to promote the growth of new blood cells from the existing vessels. This peptide is present in wound fluid and when administered subcutaneously, it promotes wound healing, muscle building and speeds up recovery time of muscles fibres and their cells. An additional key factor of TB-500 is that it promotes cell migration through a specific interaction with actin in the cell cytoskeleton. It has been demonstrated that a central small amino acid long-actin binding domain has both blood cell reproduction and wound healing characteristics. These characteristics are uncovered by accelerating the migration of endothelial cells and keratinocytes. It also increases the production of extracellular matrix-degrading enzymes.
One study investigating romantic stress that looked at nondepressed youth who went through a recent breakup and were given 60mg of Griffonica Simplicifonia (12.8mg 5-HTP) twice a day for 6 weeks in an open-label study noted reductions in percieved romantic stress when measured at the 3 week mark with no further improvement at 6 weeks; there was no control nor placebo group in this study.[29]

Social behavior[66][111] and wound healing: Oxytocin is also thought to modulate inflammation by decreasing certain cytokines. Thus, the increased release in oxytocin following positive social interactions has the potential to improve wound healing. A study by Marazziti and colleagues used heterosexual couples to investigate this possibility. They found increases in plasma oxytocin following a social interaction were correlated with faster wound healing. They hypothesized this was due to oxytocin reducing inflammation, thus allowing the wound to heal more quickly. This study provides preliminary evidence that positive social interactions may directly influence aspects of health.[112] According to a study published in 2014, silencing of oxytocin receptor interneurons in the medial prefrontal cortex (mPFC) of female mice resulted in loss of social interest in male mice during the sexually receptive phase of the estrous cycle.[113] Oxytocin evokes feelings of contentment, reductions in anxiety, and feelings of calmness and security when in the company of the mate.[101] This suggests oxytocin may be important for the inhibition of the brain regions associated with behavioral control, fear, and anxiety, thus allowing orgasm to occur. Research has also demonstrated that oxytocin can decrease anxiety and protect against stress, particularly in combination with social support.[114] It is found, that endocannabinoid signaling mediates oxytocin-driven social reward.[115]

Due to its molecular structure and low molecular weight, TB-500 is very versatile, mobile and possesses the ability to travel long distances through tissues. This means that when targeting injured areas (chronic or acute), TB-500 has the ability to circulate through the body and “find” those areas of injury in order to enhance the healing or growth process. Many users have also noted the added benefits of improved flexibility, reduced inflammation in tendons, re-growth of lost hair, and darkening of grayed hair.
Cells on the surface of the skin are constantly being replaced by regeneration from below. The repair of a wound is a scaling up of this normal process, with additional complex interactions among cells, formation of new blood vessels, collagen, more extensive cell division and cell migration, as well as strict control of inflammatory cells and the cytokines they release to resolve the inflammation.
Thymosin beta-4 (Tβ4) is a water-soluble, 43-amino acid, and 4.9 kDa protein that was originally isolated from bovine thymus [6]. Since Tβ4 is the major actin-sequestering molecule in eukaryotic cells and is found in all cells [7], Tβ4 has multiple diverse cellular functions, including tissue development, migration, angiogenesis, and wound healing [7]. We previously reported that Tβ4-overexpressing transgenic mice, using a construct on the skin-specific keratin-5 promoter, have abnormal tooth development and enhanced stimulation of hair growth [8]. Moreover, exogenous Tβ4 has anti-inflammatory effects in the bleomycin-induced mouse model of lung fibrosis [9], tooth extraction sockets in rats [10], rat model of myocardial ischemia [11], corneal wound healing [12], wound healing of rat palatal mucosa [13], in vitro model of cultured human gingival fibroblasts [14], and cardiac fibroblasts [15]. However, the effects of Tβ4 over expression or inhibition on differentiation are controversial. Exogenous β4 peptide inhibited osteogenic differentiation but facilitated adipogenic differentiation in human bone marrow-derived-mesenchymal stem cells (MSCs) [16]. In contrast, Tβ4 inhibition by Tβ4 siRNA attenuated odontoblastic differentiation in the odontoblast-like cells, MDPC-23 [17]. Moreover, we recently demonstrated that odontoblastic differentiation was enhanced by activation of Tβ4 by Tβ4 peptide but was decreased by Tβ4 siRNA in human dental pulp cells (HDPCs) [18]. However, the effects of Tβ4 on osteoclastic differentiation have not been reported.
The matters under subsection 52E (1) of the Therapeutic Goods Act 1989 considered relevant by the delegate included: (a) the risks and benefits of the use of the substance; (b) the purposes for which a substance is to be used and the extent of use of a substance; (c) the toxicity of the substance; (d) the dosage, formulation, labelling, packaging and presentation of a substance; (e) the potential for abuse of a substance; and (f) any other matters that the Secretary considers necessary to protect public health.
While all of the effects described above certainly occur in response to oxytocin, doubt has recently been cast on its necessity in parturition and maternal behavior. Mice that are unable to secrete oxytocin due to targeted disruptions of the oxytocin gene will mate, deliver their pups without apparent difficulty and display normal maternal behavior. However, they do show deficits in milk ejection and have subtle derangements in social behavior. It may be best to view oxytocin as a major facilitator of parturition and maternal behavior rather than a necessary component of these processes.

Skin is the largest organ of the body, which makes up 16% of total body weight. It is also the largest organ that provides immune protection and plays a role in inflammation. Composed of specialized epithelial and connective tissue cells, skin is our major interface with the environment, a shield from the outside world and a means of interacting with it. As such, the skin is subjected to insults and injuries: burns from the sun’s ultraviolet radiation that elicit inflammatory reactions, damage from environmental pollutants and wear and tear that comes with aging.


MT 1 and MT 2 are synthetic analogues of the alpha-melanocyte stimulating peptide hormone Alpha-MSH. This hormone aids skin cells to produce greater quantities of Melanin. Therefore MT-1 and MT-2 mimic this hormone and encourage the production of more Melanin. Melanin is a dark pigment in the skin that can provide some protection from the UV rays of the sun.

Ultimately, this lack of literature on the drug best serves to illustrate the recklessness of Stephen Dank in committing to something so experimental in nature. Perhaps he was privy to anecdotal evidence the rest of us weren’t. The drug has been used by amateur athletes and bodybuilders, and reportedly in the equine industry. Nevertheless, any benefits are unsubstantiated, which lends to an exasperation shared by supporters as to why Dank would risk so much for a substance that potentially offers no advantage at all. As a supporter, I would have much preferred a drug that allowed us to hit a target inside 50.

Jump up ^ Rondanelli M, Opizzi A, Faliva M, Bucci M, Perna S (March 2012). "Relationship between the absorption of 5-hydroxytryptophan from an integrated diet, by means of Griffonia simplicifolia extract, and the effect on satiety in overweight females after oral spray administration". Eating and Weight Disorders. 17 (1): e22–8. doi:10.3275/8165. PMID 22142813.
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