The reality is that people are always going to self-medicate. Boots, Amazon and H&B all sell 5-HTP, and in theory you could keep buying it and taking it for as long as you like. But it's important to know the facts. It shouldn't be used in conjunction with an SSRI, for example. In that situation, if the body is preventing serotonin breakdown while also getting extra serotonin, which leads to seriously unhealthy levels of serotonin activity.
In the hypothalamus, oxytocin is made in magnocellular neurosecretory cells of the supraoptic and paraventricular nuclei, and is stored in Herring bodies at the axon terminals in the posterior pituitary. It is then released into the blood from the posterior lobe (neurohypophysis) of the pituitary gland. These axons (likely, but dendrites have not been ruled out) have collaterals that innervate neurons in the nucleus accumbens, a brain structure where oxytocin receptors are expressed.[31] The endocrine effects of hormonal oxytocin and the cognitive or behavioral effects of oxytocin neuropeptides are thought to be coordinated through its common release through these collaterals.[31] Oxytocin is also produced by some neurons in the paraventricular nucleus that project to other parts of the brain and to the spinal cord.[32] Depending on the species, oxytocin receptor-expressing cells are located in other areas, including the amygdala and bed nucleus of the stria terminalis.
Work with cell cultures and experiments with animals have shown that administration of thymosin β4 can promote migration of cells, formation of blood vessels, maturation of stem cells, survival of various cell types and lowering of the production of pro-inflammatory cytokines. These multiple properties have provided the impetus for a worldwide series of on-going clinical trials of potential effectiveness of thymosin β4 in promoting repair of wounds in skin, cornea and heart.[17]
Cells were pretreated with indicated concentrations of Tβ4 peptide for 2 hours and then incubated with 200 μM H2O2 for 48 hours (A-E). Cell viability was measured by MTT assay (A). Protein and mRNA expressions were assessed by RT-PCR (B) and Western blot analysis (C), respectively. The production of NO (D) and PGE2 (E) were measured by Griess reaction and ELISA, respectively. Data replicated the quantifications of cytotoxicity, NO, and PGE2 with the standard deviation of at least three experiments (n = 4). The bar graph shows the fold increase in protein or mRNA expression compared with control cells. * Statistically significant differences compared with the control, p<0.05. # Statistically significant difference compared with the H2O2—treated group.

Oxytocin (Oxt; /ˌɒksɪˈtoʊsɪn/) is a peptide hormone and neuropeptide. Oxytocin is normally produced by the paraventricular nucleus of the hypothalamus and released by the posterior pituitary.[3] It plays a role in social bonding, sexual reproduction, and during and after childbirth.[4] Oxytocin is released into the bloodstream as a hormone in response to stretching of the cervix and uterus during labor and with stimulation of the nipples from breastfeeding.[5] This helps with birth, bonding with the baby, and milk production.[5][6] Oxytocin was discovered by Henry Dale in 1906.[7] Its molecular structure was determined in 1952.[8] Oxytocin is also used as a medication to facilitate childbirth.[9][10][11]


Although Tβ4 contains only 43 amino acids, it appears to have a wide range of regenerative activities and specific sites on the molecule have been shown to mediate these effects (Goldstein & Kleinman, 2015; Sosne, Qiu, Goldstein, & Wheater, 2010). Both chemically synthesized and recombinant forms have shown efficacy for dermal healing in preclinical models and in human patients (Ehrlich & Hazard, 2012; Kim & Kwon, 2014, 2015; Malinda et al., 1999; Philp, Badamchian, et al., 2003; Philp & Kleinman, 2010; Philp et al., 2006; Ti et al., 2015; Treadwell et al., 2012). A dimeric form has been found to accelerate the rate of dermal healing in an animal model more rapidly than that of the parent molecule (Xu et al., 2013). Tβ4 has also shown repair and regenerative activity in a number of other injury models, such as traumatic brain injury, spinal cord injury, stroke, a model of multiple sclerosis, ischemic limbs, and cardiac damage due to ischemia (Bock-Marquette, Saxena, White, Dimaio, & Srivastava, 2004; Cheng, Kuang, Zhang, Ju, & Wang, 2014; Dube, Bollini, Smart, & Riley, 2012; Morris, Chopp, Zhang, Lu, & Zhang, 2010; Morris et al., 2014; Philp & Kleinman, 2010; Postrach et al., 2014; Smart et al., 2007; Sopko et al., 2011; Ti et al., 2015, Wang et al., 2012; Wei, Kim, Li, Wu, & Gupta, 2014; Xiong, Mahmood, Meng, et al., 2011; Zhang, Zhang, Morris, et al., 2009; Zuo et al., 2013). The processes and pathways for Tβ4-mediated repair are similar in these various tissues and support the observed promotion of dermal healing.

The group had first identified the thymosin sulfoxide as an active factor in culture fluid of cells responding to treatment with a steroid hormone, suggesting that its formation might form part of the mechanism by which steroids exert anti-inflammatory effects. Extracellular thymosin β4 would be readily oxidised to the sulfoxide in vivo at sites of inflammation, by the respiratory burst.[21]
Thymosin β4 has been tested in multicenter trials sponsored jointly by RegeneRx Biopharmaceuticals Inc (Rockville, MD, USA) and Sigma Tau (Pomezia, Italy) in the United States and Europe in patients with bed sores, ulcers caused by venostasis, and Epidermolysis bullosa simplex and was found to accelerate bed sore and stasis ulcer repair by one month. It has also been tested in patients with chronic neurotrophic corneal epithelial defects and found to promote repair.
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.
The vascular system in the normal adult brain is stable, but is activated in response to certain pathological conditions including injuries.68 Von Willebrand factor (vWF) staining has been used to identify vascular structure in the brain after TBI.69 TBI alone significantly increased vascular density in the injured cortex, CA3, and DG of the ipsilateral hemisphere when examined at day 35 after TBI compared to sham controls.18,34,64,65 Tβ4 treatment significantly increased the vascular density in these regions compared to saline treatment.34 This is in agreement with in vitro and in vivo pro-angiogenic effect of Tβ4.70,71
Evidence for this role of oxytocin come from two types of experiments. First, infusion of oxytocin into the ventricles of the brain of virgin rats or non-pregnant sheep rapidly induces maternal behavior. Second, administration into the brain of antibodies that neutralize oxytocin or of oxytocin antagonists will prevent mother rats from accepting their pups. Other studies support the contention that this behavioral effect of oxytocin is broadly applicable among mammals.
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.
Sexual activity: The relationship between oxytocin and human sexual response is unclear. At least two uncontrolled studies have found increases in plasma oxytocin at orgasm – in both men and women.[103][104] Plasma oxytocin levels are notably increased around the time of self-stimulated orgasm and are still higher than baseline when measured five minutes after self arousal.[103] The authors of one of these studies speculated that oxytocin's effects on muscle contractibility may facilitate sperm and egg transport.[103]
Oxytocin and vasopressin are the only known hormones released by the human posterior pituitary gland to act at a distance. However, oxytocin neurons make other peptides, including corticotropin-releasing hormone and dynorphin, for example, that act locally. The magnocellular neurosecretory cells that make oxytocin are adjacent to magnocellular neurosecretory cells that make vasopressin. These are large neuroendocrine neurons which are excitable and can generate action potentials.[124]
TBI patients frequently suffer from long-term deficits in cognitive and motor performance. No single animal model can adequately mimic all aspects of human TBI owing to the heterogeneity of clinical TBI.11 Some features of cognitive and motor function in humans have been successfully demonstrated in experimental brain trauma models.28-30 The controlled cortical impact (CCI) model is one of the most widely used TBI models. The CCI-TBI model has many clinically relevant features in that CCI causes not only cortical damage but also selective neuronal death in the hippocampus in rodents, leading to sensorimotor dysfunction and spatial learning and memory deficits, respectively.18,31-33

I am not a doctor and this is not to be taken, interpreted or construed as medical advice. Please talk with a licensed medical professional about this. These are just my own personal thoughts and not a prescription or a diagnosis or any form of health care whatsoever. I would take the recommended dosage and see how you feel. Only you can tell whether it's working or not.


Oxytocin has been of keen interest to neuroscientists since the 1970s, when studies started to show that it could drive maternal behaviour and social attachment in various species. Its involvement in a range of social behaviours2, including monogamy in voles, mother–infant bonding in sheep, and even trust between humans, has earned it a reputation as the 'hug hormone'. “People just concluded it was a bonding molecule, a cuddling hormone, and that's the pervasive view in the popular press,” says Larry Young, a neuroscientist at Emory University in Atlanta, Georgia, who has been studying the molecule since the 1990s.
Uterine contraction important for cervical dilation before birth and causes contractions during the second and third stages of labor. Oxytocin release during breastfeeding causes mild but often painful uterine contractions during the first few weeks of lactation. This also serves to assist the uterus in clotting the placental attachment point postpartum. However, in knockout mice lacking the oxytocin receptor, reproductive behavior and parturition is normal.[4]
The CCI model we used causes cortical tissue loss. Traditionally, the target for neuroprotective treatment of TBI is to reduce the lesion volume.39,40 A major limitation of neuroprotection strategies is the short time window between injury and treatment. In the vast majority of preclinical TBI studies, the treatment compounds provide neuroprotection only when administered early (usually several hours after brain injury).11 The administration of a compound early in the clinical setting is not practical.41 The neuroprotective effects demonstrated in rodents may diminish if the treatment compounds are given in the clinical setting beyond the short neuroprotective window. We are able to stimulate recovery of neurological function without altering the lesion volume, which has also been demonstrated in our experimental studies of stroke,19,42,43 and is in essence, enhancement of neurorecovery.19 The extended 24-hour window for treatment which improves neurological recovery, without altering CCI cortical volume, is a major benefit of the neurorestorative therapy. Recently, we evaluated the efficacy of delayed Tβ4 treatment on spatial learning and sensorimotor functional recovery in rats after TBI induced by CCI.34 Briefly, TBI rats received Tβ4 at a dose of 6 mg/kg or a vehicle (saline) administered i.p. starting at 24 hours after injury and then every third day for 2 weeks. The dose of Tβ4 was selected based on our previous studies in animal models of stroke and EAE.25,27 Tβ4 did not alter lesion volume (14.2 ± 3.9% for saline treatment vs. 15.7 ± 3.6% for Tβ4 treatment). TBI caused neuronal cell loss in the ipsilateral CA3 and DG examined 35 days after injury compared to sham controls. Tβ4 treatment initiated 24 hours post injury significantly reduced cell loss in these two regions compared to saline controls. Tβ4-treated TBI rats showed significant improvement in spatial learning (MWM test) and sensorimotor (mNSS test) functional recovery compared to the saline-treated TBI rats.34
Despite this, Tβ4’s place on the banned-substances list is warranted. It reflects the possibility that the effects of the supplement may manifest as a tangible improvement in athletes. However, any time a journalist flippantly declares it “heals damaged tissue and speeds recovery”, it should be noted that such claims are a harmful distortion of the facts.
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Despite this, Tβ4’s place on the banned-substances list is warranted. It reflects the possibility that the effects of the supplement may manifest as a tangible improvement in athletes. However, any time a journalist flippantly declares it “heals damaged tissue and speeds recovery”, it should be noted that such claims are a harmful distortion of the facts.

MAPKs and NF-κB played pivotal roles in the development of osteoclasts downstream of RANK signaling [54]. In this study, we demonstrated that Tβ4 activation by Tβ4 peptide inhibited RANKL-induced p38, ERK, JNK MAPK, and NF-κB signaling pathways. These results suggested that Tβ4 activation might inhibit osteoclast differentiation via inhibition of the signaling cascades MAPK/NF-κB/NFATc1.


In mammals, many mysteries remain. Oxytocin is difficult to measure reliably in the brain, making it hard to know exactly where, when and how much is normally released; nor do scientists understand precisely how it works to alter behaviour. “What we need to start thinking about is the more fundamental role that oxytocin plays in the brain,” Young says. The determination to find out has been strengthened by a growing move in neuroscience to characterize circuits that are important in brain operations. “That's the level that's critical for understanding how the brain is regulating behaviour,” says Thomas Insel, director of the US National Institute of Mental Health in Bethesda, Maryland, who has studied oxytocin in voles.
As reactive oxygen species (ROS) have been implicated in the pathogenesis of periodontitis [24], we examined whether H2O2 could down-regulate or up-regulate Tβ4 expression in PDLCs. As shown in Fig 1A and 1B, Tβ4 mRNA and protein expressions were down-regulated by H2O2 in a time- and concentration-dependent manner. Because maximal Tβ4 mRNA and protein expressions were achieved with 200 μM H2O2 within 48 hours in PDLCs, this concentration was used in subsequent experiments.
18x More C8 than the serve serving of Coconut Oil Product : 1 bottle of Brain Octane™ Oil (473ml) Formulated supplementary sports food to be consumed as part of a nutritious diet and as part of a program of physical activity. OVERVIEW SOURCING INGREDIENTS AND USE SCIENCE AND RESEARCH Brain Octane Oil is the top choice for reaching peak brain performance...
I’m always interested in learning about better supplements for my health. I’ve heard a lot of good things about peptides, but this was the first time I’ve read about TB-500 in particular. It sounds like it can have a major impact on helping you recover from injuries, which is a huge deal in today’s world. I may need to look into it some more before actually buying it, but thank you so much for taking the time to explain it!

For all its positivity, however, oxytocin has a dark side. Or, more accurately, it plays a more complex role in human behavior than is commonly thought. As a facilitator of bonding among those who share similar characteristics, the hormone fosters distinctions between in-group and out-group members, and sets in motion favoritism toward in-group members and prejudice against those in out-groups. Ongoing research on the hormone is a potent reminder of the complexity of biological and psychological systems.
The soluble form of Ac-SDKP peptide, derived from thymosin beta-4, has been described as a natural inhibitor of pluripotent hematopoietic stem cell proliferation and as a stimulator of angiogenesis, both in vitro and in vivo (Koutrafouri et al., 2001; Wang et al., 2004). This peptide has been selectively bound to acrylated hyaluronic acid hydrogels via thiol groups from cysteine residues (Song et al., 2014). Unfortunately, the immobilization process was poorly characterized and the effect of hydrogels on EC function was not tested in vitro. In a mouse model of chronic myocardial infarction, hydrogels with immobilized Ac-SDKP did not show improved regeneration potential. Yet, Ac-SDKP-HA hydrogels with entrapped stem cell homing factor SDF-1 showed a significant increase of myocardial regeneration and recovery of heart function, as compared to groups with only one or none of these factors, suggesting a potentially interesting synergistic effect.
Recent preclinical studies by us and others have revealed that endogenous neurorestoration is present after TBI, including neurogenesis, axonal sprouting, synaptogenesis, and angiogenesis, which may contribute to the spontaneous functional recovery.13-18 In addition, treatments that promote these neurorestorative processes have been demonstrated to improve functional recovery after brain injury.19,20 However, clinical trials in TBI have primarily targeted neuroprotection, and trials directed specifically at neurorestoration have not been conducted. The essential difference between neuroprotective and neurorestorative treatments is that the former target the lesion that is still not irreversibly injured and the latter treat the intact tissue.19 Thus, neurorestorative treatments can be made available for a larger number of TBI patients.
Melanotan peptides are stable and durable when shipped, surviving about 37 degrees temperatures for around a month or more. Even during summer, this peptide can be shipped without hassles. Once they have been received, they ought to be put away in the refrigerator or better still, freezer to avert conceivable deterioration until ready to be mixed, which then the mixed Melanotan is stored in the refrigerator.
"By understanding the oxytocin system's dual role in triggering or reducing anxiety, depending on the social context, we can optimize oxytocin treatments that improve well-being instead of triggering negative reactions," said Jelena Radulovic, the senior author of the study and the Dunbar Professsor of Bipolar Disease at Northwestern University Feinberg School of Medicine. The paper was published July 21 in Nature Neuroscience.

Treatment of patients with hyperbaric oxygen has been shown to improve the healing of chronic lower extremity wounds of diabetic patients (Londahl et al., 2010). In a pilot study, this treatment has been shown to more than double the number of circulating vascular stem/progenitor cells in these patients by a mechanism that elevates platelet NOS activity and to stimulate recruitment of vascular progenitor cells to wounds made in their abdominal skin (Thom et al., 2011). This treatment might be combined with topical agents for even greater efficacy in healing chronic wounds.
For depression: Most commonly, 150-800 mg daily is taken for 2-6 weeks. These doses are sometimes divided up and administered as 50 mg to 100 mg three times a day. Sometimes the dose starts out low and steadily increases every 1-2 weeks until a target dose is reached. Less commonly, higher doses are used. In one study, the dose is steadily increased up to 3 grams per day.
It turns out oxytocin is responsible for a lot more than just love. New science has found that this amazing molecule also influences how sociable each of us is, allowing us to 'tune in' to the social information around us, perceiving it in much higher resolution. Scientists are now applying this new knowledge in the lab, and as reporter Dr Graham Phillips finds out, they're discovering oxytocin's great potential to treat social disorders, like drug addiction and alcoholism.

There are several layers in the skin; the outer epidermis and beneath it the dermis and the subcutaneous layer. Cells in the epidermis include keratinocytes, its major cell type, that move continuously from the lower basal layer where they are formed by cell division. Other cells in the epidermis are the melanocytes that synthesize pigment and transfer it to the keratinocytes, giving our skin its color, and a wide variety of immune cells that maintain immune surveillance and secrete substances called cytokines, like interleukin 1 and 2, which are active in inflammation. The dermis contains connective tissue, mainly collagen, blood vessels, various types of immune white cells and fibroblasts.

TB-500 has been used extensively for race horses to prevent adhesions from forming, although it is not a prescription veterinary drug. It’s an injectable peptide with limited human use. Mostly, it’s limited to humans who like to experiment, although reports of human use of thymosin dates back as far as 1974 – when a young girl became the first person to receive injections of thymosin because she was diagnosed without a functioning thymus gland.
Many early studies of oxytocin for autism were limited because they assessed only a single dose and had relatively few participants, and later experiments with more doses failed to show the same promise. In 2010, clinical psychologist Adam Guastella at the University of Sydney in Australia studied 16 male adolescents with autism spectrum disorder, and found that one dose of oxytocin could improve their ability to gauge the emotions of others by looking at their eyes13. But when he tried giving twice-daily doses of the hormone for two months, he found no significant improvements in social interaction or social cognition14. “Studies to this point have really shown limited benefit of oxytocin in improving psychiatric illnesses over time,” he says. Guastella says that getting to the bottom of oxytocin's complex neurological effects will take time. “If we want a simple answer, we're not going to get it.”
If you were to go on the internet, read the hype, you'd probably think it'll be something like having an ecstasy tablet or having an orgasm or something like that, but the reality is you probably wouldn't be able to distinguish it from placebo. So the effects are extremely subtle. Now, that subtlety isn't necessarily because of oxytocin itself being a subtle hormone, it's just this issue of it penetrating the brain. So when you take it intranasally, we're still trying to work out how much gets into the brain, but probably only a vanishingly small amount.
Like I said, it’s amazing stuff. And it shouldn’t come as a surprise that it affects that amazing part of your brain so intimately involved in keeping you safe…the amygdala. Remember, trust has a lot to do with survival among social animals who depend on each other for safety and protection. Show someone an untrustworthy face, and the amygdala is one of two areas that become more active than anywhere else in the brain.7 It is apparently programmed for reading trust just as it is for snakes or spiders.
Milk ejection reflex/Letdown reflex: in lactating (breastfeeding) mothers, oxytocin acts at the mammary glands, causing milk to be 'let down' into subareolar sinuses, from where it can be excreted via the nipple.[47] Suckling by the infant at the nipple is relayed by spinal nerves to the hypothalamus. The stimulation causes neurons that make oxytocin to fire action potentials in intermittent bursts; these bursts result in the secretion of pulses of oxytocin from the neurosecretory nerve terminals of the pituitary gland.

Touting their discovery as “a great step forward in weight loss history,” the panel were quick to offer up their hard earned cash to back the entrepreneurial pair. “We were shocked. The most we were hoping for was some advice…we weren’t even sure that we would manage to get any investors,” explained Samantha. After outstanding offers from each panel member, the sisters burst into tears.

The enzyme dopamine decarboxylase (aromatic L-amino acid decarboxylase) mediates the conversion of 5-HTP into serotonin, and this enzyme is expressed in stomach tissue.[53] Inhibition of this enzyme in the stomach during 5-HTP ingestion is thought to promote the concentration of 5-HTP that reaches neural tissue, which is supported by a study using 100-200mg Carbidopa (pharmaceutical inhibitor) alongside 5-HTP to increase radioactivity of 5-HTP (indicative of neural accumulation) in humans.[54]
Oxytocin and vasopressin are the only known hormones released by the human posterior pituitary gland to act at a distance. However, oxytocin neurons make other peptides, including corticotropin-releasing hormone and dynorphin, for example, that act locally. The magnocellular neurosecretory cells that make oxytocin are adjacent to magnocellular neurosecretory cells that make vasopressin. These are large neuroendocrine neurons which are excitable and can generate action potentials.[124]
Beta thymosins are a family of proteins which have in common a sequence of about 40 amino acids similar to the small protein thymosin β4. They are found almost exclusively in multicellular animals. Thymosin β4 was originally obtained from the thymus in company with several other small proteins which although named collectively "thymosins" are now known to be structurally and genetically unrelated and present in many different animal tissues.
Melanotan II is a synthetic analogue of the α-melanocyte stimulating hormone (α-MSH). α-MSH is a melanocortin I receptor agonist which has a role in human pigmentation by stimulating production of eumelanin. As melanotan II is a non-specific melanocortin receptor agonist, it has been reported to cause toxicity effects involving the many physiological systems affected by the receptors.
Some differences in cardiac anatomy exist between mammals and teleosts. The zebrafish ventricle has a thin wall of compact muscle surrounding a much larger compartment of myofibers organized into elaborate trabeculae. It is intriguing that this structure is very similar to that of the embryonic mammalian ventricle prior to its septation and fusion of trabeculer myofibers into a thick, vascularized wall (Sedmera et al., 2000). That the mammalian heart has a more differentiated, contractile anatomy is apparent not only in gross cardiac structure, but also in cellular features. Teleost cardiomyocytes are 2–10 times smaller, mononucleated, have a greatly-reduced sarcoplasmic reticulum and lack the T-tubule system found in skeletal muscle and mammalian cardiac muscle (Farrell, 1992). One might speculate that the teleost heart is better designed for growth and regeneration, while the mammalian heart is better designed for sheer contractile force. Nevertheless, none of the mentioned differences between lower and higher vertebrate hearts preclude the idea that the mammalian heart could be stimulated to regenerate, especially if that regeneration is due to mobilization of a progenitor cell population.
At least one study has actively differentiated between 'an increase in satiety' (sensation of fullness from food) and a 'decrease in appetite' (less desire to eat) and noted that 5-HTP causes an increase in satiety without a concomitant decrease in appetite.[9] Additionally, most studies are in exclusively females which may have more significance with interventions pertaining to serotonin metabolism; only one study mentioned above was conducted in men as well[10] but appears to suggest that it benefits both genders.
Injection is the most effective way to administrate the peptide and results are seen the fastest and best. The nasal spray method is effective up to 30 – 40% because the nasal passages have poor absorption rate, you have to apply the nasal spray at least two to three times more than the injection. The injectable product of the Melanotan is very superior as compared to the nasal version. The nasal versions generally take four to five weeks for displaying the results appose to 10 days with the injection.

The promise of repairing sun parched aging skin is alluring, especially if damage control may be attained by applying a substance that is abundant in our body. Thymosin beta 4 (Tb4), a molecule that accelerates wound healing in animals and cultured cells, "may be valuable in repairing skin damage caused by sun or even by the wear and tear of aging?" This hopeful message of Tb4's potential to restore damaged human skin was voiced at the 5th International Symposium on Aging Skin, in California (May 2001), by Dr. Allan Goldstein, Chairman of the Biochemistry Department at George Washington University and founder of RegeneRX Biopharmaceuticals. RegeneRX is carrying out preclinical research on Tb4 as a wound healer, in collaboration with scientists at the National Institutes of Health.

Thymosin β4 has been tested in multicenter trials sponsored jointly by RegeneRx Biopharmaceuticals Inc (Rockville, MD, USA) and Sigma Tau (Pomezia, Italy) in the United States and Europe in patients with bed sores, ulcers caused by venostasis, and Epidermolysis bullosa simplex and was found to accelerate bed sore and stasis ulcer repair by one month. It has also been tested in patients with chronic neurotrophic corneal epithelial defects and found to promote repair.
At first, the mice showed an irregular smattering of neural impulses when they heard the baby's cries. Then, as the oxytocin kicked in, the signal evolved into a more orderly pattern typical of a maternal brain. The study showed in unusual detail how the hormone changed the behaviour of neurons1. “Oxytocin is helping to transform the brain, to make it respond to those pup calls,” Froemke says.
The peripheral actions of oxytocin mainly reflect secretion from the pituitary gland. The behavioral effects of oxytocin are thought to reflect release from centrally projecting oxytocin neurons, different from those that project to the pituitary gland, or that are collaterals from them.[31] Oxytocin receptors are expressed by neurons in many parts of the brain and spinal cord, including the amygdala, ventromedial hypothalamus, septum, nucleus accumbens, and brainstem.[citation needed]

Affecting generosity by increasing empathy during perspective taking. In a neuroeconomics experiment, intranasal oxytocin increased generosity in the Ultimatum Game by 80% but has no effect in the Dictator Game that measures altruism. Perspective-taking is not required in the Dictator Game, but the researchers in this experimental explicitly induced perspective-taking in the Ultimatum Game by not identifying to participants which role they would be in.13


In another study, published in PNAS in 2010, men were given a dose of oxytocin and asked to write about their mothers. Those with secure relationships described their moms as more caring after the hormone dose. Those with troubled relationships actually saw their mothers as less caring. The hormone may help with the formation of social memories, according to the study researchers, so a whiff strengthens previous associations, whether good or bad.


"By understanding the oxytocin system's dual role in triggering or reducing anxiety, depending on the social context, we can optimize oxytocin treatments that improve well-being instead of triggering negative reactions," said Jelena Radulovic, the senior author of the study and the Dunbar Professsor of Bipolar Disease at Northwestern University Feinberg School of Medicine. The paper was published July 21 in Nature Neuroscience.
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.
5-HTP (5-Hydroxytryptophan) is a chemical by-product of the protein building block L-tryptophan. It is also produced commercially from the seeds of an African plant known as Griffonia simplicifolia 5-HTP is used for sleep disorders such as insomnia, depression, anxiety, migraine and tension-type headaches, fibromyalgia, obesity, premenstrual syndrome (PMS), premenstrual dysphoric disorder (PMDD), attention deficit-hyperactivity disorder (ADHD), seizure disorder, and Parkinson's disease..
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