Jump up ^ Hicks C, Ramos L, Reekie T, Misagh GH, Narlawar R, Kassiou M, McGregor IS (June 2014). "Body temperature and cardiac changes induced by peripherally administered oxytocin, vasopressin and the non-peptide oxytocin receptor agonist WAY 267,464: a biotelemetry study in rats". British Journal of Pharmacology. 171 (11): 2868–87. doi:10.1111/bph.12613. PMC 4243861. PMID 24641248.
In this study, Tβ4 mRNA down-regulation was detected in in vitro in PDLCs stimulated with the ROS. This down-regulation of Tβ4 was also observed in GCF of periodontitis patient [19] and endotoxin-induced septic shock of rats [39]. ROS were generated predominantly by polymorphonuclear leukocytes (PMN) during an inflammatory response and involved in tissue destruction associated with periodontal diseases [40]. Thus, we chose to use ROS-stimulated PDLCs in this study since ROS, such as superoxide and H2O2, have been proposed as key players in bone resorption [41] and implicated in the pathogenesis of rheumatoid arthritis and periodontitis [29].
“This is a very ancient molecule,” says Sue Carter, a neuroscientist at Indiana University in Bloomington, whose lab pioneered many of the early studies of oxytocin in voles. “It has been used and reused for many purposes across the evolution of modern animals, and almost everybody who's tried to look at an effect of oxytocin on anything like social behaviour has found something.”
Studies demonstrate that TB-500 is a potent, naturally occurring wound repair factor with anti-inflammatory properties. Tß4 is different from other repair factors, such as growth factors, in that it promotes endothelial and keratinocyte migration. It also does not bind to the extracellular matrix and has a very low molecular weight meaning it can travel relatively long distances through tissues. One of TB-500 key mechanisms of action is its ability to regulate the cell-building protein, Actin, a vital component of cell structure and movement. Of the thousands of proteins present in cells, actin represents up to 10% of the total proteins which therefore plays a major role in the genetic makeup of the cell.
5-HTP increases a chemical in the brain. This chemical is called serotonin. Some medications used for depression also increase serotonin. Taking 5-HTP with these medications used for depression might cause there to be too much serotonin. This could cause serious side effects including heart problems, shivering, and anxiety.

Some of these medications used for depression include phenelzine (Nardil), tranylcypromine (Parnate), and others.

A study using an oral cavity spray of 5-HTP (via the plant source of Griffonia Simplicifolia) has noted that 7.68mg of 5-HTP via 30.72mg of Griffonia Simplicifolia extract taken five times daily (total daily dose of around 40mg) has confirmed an increase in urinary 5-HIAA (from 3.71+/-1.27mg/24 hours to 8.80+/-4.02mg/24 hours; a 137% increase) relative to baseline, confirming that 5-HTP can be absorbed sublingually.[3] Similar results have been noted elsewhere with this spray, although it should be noted that it is confounded with other herbs (detailed in the appetite subsection).[2]

Young says that the oxytocin field would benefit from closer collaboration between basic and clinical researchers. If basic scientists can work out how oxytocin helps the brain to process social stimuli, then that might help in the design of stimuli — in the form of behavioural therapies — that could be given alongside the hormone to change behaviour, just as oxytocin and pup calls together affect virgin mice. “I think in the future these two branches need to have more communication,” Young says.
Oxytocin production is controlled by a positive feedback mechanism. This mechanism allows the release of the oxytocin hormone when a trigger occurs. The hormone then causes an action in the body, such as the letdown of milk or the start of labor contractions, which signals more production of oxytocin. The feedback cycle continues until the action, such as childbirth or feeding the baby, is complete.

Oxytocin is a peptide of nine amino acids (a nonapeptide) in the sequence cysteine-tyrosine-isoleucine-glutamine-asparagine-cysteine-proline-leucine-glycine-amide (Cys – Tyr – Ile – Gln – Asn – Cys – Pro – Leu – Gly – NH2, or CYIQNCPLG-NH2); its C-terminus has been converted to a primary amide and a disulfide bridge joins the cysteine moieties.[116] Oxytocin has a molecular mass of 1007 Da, and one international unit (IU) of oxytocin is the equivalent of about 2 μg of pure peptide.
Hi Ben. Have a groin problem which I have had for years and it just won’t go away it’s not a hernia or osteitis pubis I had an MRI and the specialist said they wouldn’t operate. I can still play sport but I’m just less agile and slower than normal and it takes a few days for the groin pain to go away after sport. Would tb500 help to heal it or would bpc157 or something else be better? Thanks :)
The molecule of this peptide is very big, so it isn’t able to completely fit within a receptor. Each area of the molecule has different functions. For instance, TB 500 is responsible for promoting majority of the useful effects, such as the healing, muscle cells, new blood and repair. In some scenarios, TB 500 could be used rather than the whole Thymosin Beta 4 protein. TB 500’s main ability is to regulate Actin, which is a cell-building protein. There are thousands of proteins found inside of cells, but actin makes up to 10 percent of the total amount of proteins, giving it a major role in the cell’s genetic makeup.

5-HTP helps the body to produce more serotonin. Serotonin is a neurotransmitter that plays a key role in regulating mood and sleep-wake cycles. Healthy levels of serotonin contribute to a positive mood and outlook and also promote restful sleep. Serotonin also plays an important role in many other of the body’s functions, including digestion, appetite, and pain perception.

Bonding. In the Prairie Vole, oxytocin released into the brain of the female during sexual activity is important for forming a monogamous pair bond with her sexual partner. Vasopressin appears to have a similar effect in males. In people, plasma concentrations of oxytocin have been reported to be higher amongst people who claim to be falling in love. Oxytocin has a role in social behaviors in many species, and so it seems likely that it has similar roles in humans.6
High and low oxytocin levels are possible, but research has not yet found any implications of these conditions. Men with high levels of oxytocin sometimes develop benign prostatic hyperplasia, or the enlarging of the prostate gland. This condition can cause urinary complaints. A lack of oxytocin can prevent the milk letdown reflex and make breastfeeding difficult. Low oxytocin levels have also been linked to depression, but using oxytocin to treat mental health conditions has not yet been studied sufficiently.

5-HTP can affect a brain chemical called serotonin. Dextromethorphan (Robitussin DM, others) can also affect serotonin. Taking 5-HTP along with dextromethorphan (Robitussin DM, others) might cause too much serotonin in the brain and can result in serious side effects including heart problems, shivering, and anxiety. Do not take 5-HTP if you are taking dextromethorphan (Robitussin DM, and others).
First developed in the 1980s by researchers at the University of Arizona, Melanotan is principally used for the treatment of skin disorders including vitiligo and erythropoietic protoporphyria that affect skin appearance and sensitivity (especially to sunlight). By promoting melanin in the skin, Melanotan can help ease the symptoms of these conditions and enable those diagnosed to live a more normal life.
Jump up ^ Gauquelin G, Geelen G, Louis F, Allevard AM, Meunier C, Cuisinaud G, Benjanet S, Seidah NG, Chretien M, Legros JJ (1983). "Presence of vasopressin, oxytocin and neurophysin in the retina of mammals, effect of light and darkness, comparison with the neuropeptide content of the neurohypophysis and the pineal gland". Peptides. 4 (4): 509–15. doi:10.1016/0196-9781(83)90056-6. PMID 6647119.

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.

These studies demonstrate that in the animal model of TBI, early (6 hours post injury) treatment with Tβ4 i.p. at doses of 6 and 30 mg/kg reduces cortical lesion volume and hippocampal cell loss and improves functional recovery, suggesting its potential as a neuroprotective therapy for TBI. More importantly, delayed (24 hours post injury) treatment with Tβ4 administered i.p. at a dose of 6 mg/kg does not reduce lesion volume but significantly improves functional outcome in rats.34 Tβ4-induced angiogenesis, neurogenesis and oligodendrogenesis may contribute to functional recovery.34 Therefore, our data suggest that promoting endogenous neurorestorative processes using Tβ4 provides a novel therapeutic option for TBI. It should be noted that systemic administration of Tβ4 is safe and well-tolerated by animals and humans.26 Further investigation of the molecular mechanisms underlying Tβ4-mediated neuroprotection and neurorestoration is warranted.

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.
Jump up ^ Vargas-Pinilla P, Paixão-Côrtes VR, Paré P, Tovo-Rodrigues L, Vieira CM, Xavier A, Comas D, Pissinatti A, Sinigaglia M, Rigo MM, Vieira GF, Lucion AB, Salzano FM, Bortolini MC (January 2015). "Evolutionary pattern in the OXT-OXTR system in primates: coevolution and positive selection footprints". Proceedings of the National Academy of Sciences of the United States of America. 112 (1): 88–93. Bibcode:2015PNAS..112...88V. doi:10.1073/pnas.1419399112. PMC 4291646. PMID 25535371.

20 patients (nine from the 5-HTP group and 11 from the Placebo group) completed the study. Brain tryptophan availability in diabetic patients was significantly reduced when compared to a group of healthy controls. Patients receiving 5-HTP significantly decreased their daily energy intake, by reducing carbohydrate and fat intake, and reduced their body weight.”

However, the Food and Drug Administration and its equivalents in other countries have issued repeated advisory notices about Melanotan II, urging consumers to stop using and purchasing this unapproved product. David Carter of the United Kingdom's Medicines and Healthcare Products Regulatory Agency was unequivocal in his denunciation, warning would-be buyers against being "fooled into thinking that Melanotan offers a shortcut to a more even tan." Liverpool John Moores University researcher Michael Evans-Brown cautioned that the peptide may be linked to dyspepsia and various cardiovascular problems, such as increases in blood pressure, while others have noted it appears to stimulate the growth of moles on the body.
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
In the end, despite three years of intense scrutiny, the drug at the centre of the investigation remains poorly understood. In this regard, it could serve as a reflection of the whole ordeal. Everyone has an opinion, often voiced with authority and conviction. The reality is that much of this complex narrative continues to be a mystery. Many would have been well served by the humble words of the Socratic paradox – “I know that I know nothing”.

Unlike previous studies, the trial will include people with a wide range of symptoms — and one of its major aims is to uncover the set of factors that influence whether and how strongly people respond to oxytocin. Sikich will analyse many measures of cognition and social functioning, and collect blood samples to look for biomarkers — such as levels of oxytocin and the receptor it binds to — that are associated with a response. “Lin has really been trying to create conditions under which you could study the potential beneficial effects of oxytocin and really do this right,” says Carter.
I was just diagnosed with achilles tendonosis in both of my achilles. I am an avid lifter as well as city leagues for football and basketball, I live in Montana so I hike a lot and participate In obstacle course races. My achilles have ground me to a halt over the last 3 months months. I have been referred to a surgeon for a Tenex procedure on both achilles. I am only 32 the last thing I want is have both of my achilles cut into. I’m looking at the TB-500 and BPC-157 to hopefully avoid surgery. I have done my research but am getting conflicting numbers as far as dosing. I am roughly 240 pounds and 6’5 could u recommend a dosage and cycle? Also I was wondering where the most effective injection site would be? Do I need it directly into the achilles itself or is local good enough?
Froemke's and Tsien's work fits into a broader theory: that one way oxytocin helps social interaction and recognition is by enhancing the brain's response to socially relevant sights, sounds or other stimuli. Young has shown that the hormone helps mice to recognize and pay attention to the smells of other mice7; others found that it promotes people's ability to recognize faces8.
An estimated 1.4 million people sustain traumatic brain injury (TBI) each year in the United States, and more than 5 million people are coping with disabilities from TBI at an annual cost of more than $56 billion.1 There are no commercially-available pharmacological treatment options available for TBI because all clinical trial strategies have failed.2,3 The disappointing clinical trial results may be due to variability in treatment approaches and heterogeneity of the population of TBI patients.4-9 Another important aspect is that most clinical trial strategies have used drugs that target a single pathophysiological mechanism, although many mechanisms are involved in secondary injury after TBI.4 Neuroprotection approaches have historically been dominated by targeting neuron-based injury mechanisms as the primary or even exclusive focus of the neuroprotective strategy.3 In the vast majority of preclinical studies, the treatment compounds are administered early and, frequently, even before TBI.10,11 Clinically, the administration of a compound early may be problematic because of the difficulty in obtaining informed consent.12

Down syndrome. Some research shows that giving 5-HTP to infants with Down syndrome might improve muscle and activity. Other research shows that it does not improve muscle or development when taken from infancy until 3-4 years of age. Research also shows that taking 5-HTP along with conventional prescription drugs does improve development, social skills, or language skills.