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.
The uterine-contracting properties of the principle that would later be named oxytocin were discovered by British pharmacologist Sir Henry Hallett Dale in 1906,[125][46] and its milk ejection property was described by Ott and Scott in 1910[126] and by Schafer and Mackenzie in 1911.[127] In the 1920s, oxytocin and vasopressin were isolated from pituitary tissue and given their current names. The word oxytocin was coined from the term oxytocic, Greek ὀξύς, oxys, and τοκετός , toketos, meaning "quick birth".

Serotonin influences sleep and sleep-wake cycles in many ways, and scientists continue to make discoveries about how this important neurochemical affects our sleeping and waking lives. One important way serotonin affects sleep and bio time is through its relationship with the “sleep hormone” melatonin. Melatonin is made from serotonin in the presence of darkness. (Remember, melatonin production in the body is triggered by darkness and suppressed by exposure to natural and artificial light.) Healthy serotonin levels are essential for maintaining healthy melatonin levels—and both serotonin and melatonin are critical to sleep and a well-functioning bio clock. With its ability to increase serotonin, 5-HTP supports a neurochemical process that can enable high-quality sleep and keep the body’s bio clock in sync.
Ingroup bonding: Oxytocin can increase positive attitudes, such as bonding, toward individuals with similar characteristics, who then become classified as "in-group" members, whereas individuals who are dissimilar become classified as "out-group" members. Race can be used as an example of in-group and out-group tendencies because society often categorizes individuals into groups based on race (Caucasian, African American, Latino, etc.). One study that examined race and empathy found that participants receiving nasally administered oxytocin had stronger reactions to pictures of in-group members making pained faces than to pictures of out-group members with the same expression.[62] This shows that oxytocin may be implicated in our ability to empathize with individuals of different races and could potentially translate into willingness to help individuals in pain or stressful situations. Moreover, individuals of one race may be more inclined to help individuals of the same race than individuals of another race when they are experiencing pain. Oxytocin has also been implicated in lying when lying would prove beneficial to other in-group members. In a study where such a relationship was examined, it was found that when individuals were administered oxytocin, rates of dishonesty in the participants' responses increased for their in-group members when a beneficial outcome for their group was expected.[63] Both of these examples show the tendency of individuals to act in ways that benefit those considered to be members of their social group, or in-group.
The uterine-contracting properties of the principle that would later be named oxytocin were discovered by British pharmacologist Sir Henry Hallett Dale in 1906,[125][46] and its milk ejection property was described by Ott and Scott in 1910[126] and by Schafer and Mackenzie in 1911.[127] In the 1920s, oxytocin and vasopressin were isolated from pituitary tissue and given their current names. The word oxytocin was coined from the term oxytocic, Greek ὀξύς, oxys, and τοκετός , toketos, meaning "quick birth".
If cupid had studied neuroscience, he’d know to aim his arrows at the brain rather than the heart. Recent research suggests that for love to last, it’s best he dip those arrows in oxytocin. Although scientists have long known that this hormone is essential for monogamous rodents to stay true to their mates, and that it makes humans more trusting toward one another, they are now finding that it is also crucial to how we form and maintain romantic relationships.
The product can be of unknown quality and subject to contamination and stability concerns with use of multi-dose vials. There is no experience with the product other than through unregulated channels. There are health risks from the substance itself and its route of administration – documented in medical literature, case reports as well as reports from NSW PIC.

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.

To pursue the sexual dysfunction agent, melanotan-II was licensed by Competitive Technologies to Palatin Technologies.[9] Palatin ceased development of melanotan-II in 2000 and synthesized, patented, and began to develop bremelanotide, a likely metabolite of melanotan-II that differs from melanotan-II in that it has a hydroxyl group where melanotan-II has an amide.[6][13] Competitive Technologies sued Palatin for breach of contract and to try to claim ownership of bremelanotide;[13] the parties settled in 2008 with Palatin retaining rights to bremelanotide, returning rights to melanotan-II to Competitive Technologies, and paying $800,000.[14]

The tb-500 has a systematic effect regardless of where it is injected. Some believe that thymosin beta-4 should be injected as close to the injury as possible however there is no evidence to show this would be superior. It can be injected subcutaneously (stomach fat) or intramuscularly (shoulders, thighs, buttocks). Injections should be given in different sites (rotated) each time. Depending on the spot, you can either feel nothing or you can feel slight pain - you will learn your favorite spots in time.
Melanotan II was originally developed as a treatment for sexual dysfunction. However, this was abandoned when the metabolite bremelanotide was developed instead for treatment of haemorrhagic shock. Melanotan II is usually injected subcutaneously for the purposes of sunless tanning, appetite suppression, inducing sexual desire and penile erection and other conditions such as rosacea and fibromyalgia. There are also dose forms available for nasal administration. The therapeutic dose is considered to be 0.01 mg/kg.

Naturalistic studies like ours can help unravel the evolutionary history and function of these hormones. Basically, the fact that hormone mechanisms have been tweaked during evolution suggests that the behaviors they promote have provided fitness benefits in the past. In this case, hunting and sharing meat must have increased men’s reproductive success.
Autism. A 1998 study found significantly lower levels of oxytocin in blood plasma of autistic children.[14] A 2003 study found a decrease in autism spectrum repetitive behaviors when oxytocin was administered intravenously.[15] A 2007 study reported that oxytocin helped autistic adults retain the ability to evaluate the emotional significance of speech intonation.[16]
A Risk Quiz; Let’s say you are one of the volunteers to whom researchers gave $100, and this option: you can either keep the money, or give it to an anonymous trustee who will either invest it and double it to $200 and return half of the extra hundred bucks to you–$50–or keep all the money for herself. So you can either increase your money by 50%, or lose it all. What would you do? Would you trust that anonymous trustee? (Remember Loss Aversion from Chapter Two, where in a similar experiment most people decided to avoid the gamble and take the sure cash.)
Once the baby is born, oxytocin promotes lactation by moving the milk into the breast. When the baby sucks at the mother's breast, oxytocin secretion causes the milk to release so the baby can feed. At the same time, oxytocin is released into the brain to stimulate further oxytocin production. Once the baby stops feeding, the production of the hormone stops until the next feeding.
You can browse Drugs A-Z for a specific prescription or over-the-counter drug or look up drugs based on your specific condition. This information is for educational purposes only, and not meant to provide medical advice, treatment, or diagnosis. Remember to always consult your physician or health care provider before starting, stopping, or altering a treatment or health care regimen.

Why have zebrafish retained the ability to regenerate? It is thought that the capacity for organ regeneration is an ancestral condition that has occasionally been diminished in the course of vertebrate evolution (Scadding, 1977; Goss, 1992; Wagner and Misof, 1992). Thus, most biologists suspect that the molecular machinery to optimize regeneration is present but poorly-utilized in mammals. By this line of reasoning, zebrafish heart regeneration may represent an optimal utilization of universal cardiac machinery.
In September 2007, the FDA issued a public notice advising consumers to stop using melanotan II as it was an unapproved drug with no safety or efficacy data for the advertised indications. Furthermore, the FDA issues a warning notice to a company owner that was illegally selling and marketing the product via a website. This led to subsequent indictment.
With the TB-500 it seems that pain was reduced even more in my shoulder and it appears that I recovered much faster from my workouts. I took the TB-500 on rest days. I have two more 1mg doses of TB-500 and I am going to site inject intramuscularly to the shoulder to see what happens. Then I will stop taking both for a month to see how things work out. Hopefully I won’t need them again.
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.
5-HTP appears to reduce food intake secondary to increasing satiety, although most studies are currently conducted in women (in regards to 5-HTP being related to serotonin, this may be relevant; see our creatine page and the Depression section for more information). At least one study that was mixed gender supports the notion it benefits both genders, however
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
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.
Johansson, A., Westberg, L., Sandnabba, K., Jern, P., Salo, B., & Santtila, P. (2012). Associations between oxytocin receptor gene (OXTR) polymorphisms and self-reported aggressive behavior and anger: Interactions with alcohol consumption [Abstract]. Psychoneuroendocrinology 37(9), 1546-56. Retrieved from

RegeneRX Biopharmaceuticals is focusing on the commercialization of Tb4 “For the treatment of injured tissue and non-healing wounds, to enable more rapid repair and/or tissue regeneration.” Especially needy are diabetics who suffer from poor blood circulation and loss of sensation of pain that keeps their wounds unnoticed and unattended for days, leading to ulcers that may not heal. Other hard healing wounds are pressure ulcers in patients who are bed ridden and often receive skin grafts as treatment, or reconstructive surgery.
Thymosin beta 4, developed by RegeneRx Biopharmaceuticals as a pharmaceutical for the healing of wounds, is a synthetic version of the natural peptide. As Dr. Allan Goldstein emphasizes, “Tb4 represents a new class of wound healing compounds. It is not a growth factor or cytokine, but rather exhibits a number of physiological properties which include the ability to sequester and regulate actin, its potent chemotactic properties. . . and its capability to downregulate a number of inflammatory cytokines that are present in chronic wounds.” When a wound heals there are many growth factors produced in the area so that additional factors, such as those currently on the market for wound healing, may help but are not necessarily lacking. Tb4 treatment, however, adds a new dimension to wound repair by providing cells with actin as needed, for cell migration, replication and differentiation.

5-HTP is very reliable in increasing serotonin levels. 5-HTP is actually used as a clinical test to judge the potency of drugs that affect serotonin levels (by pairing an experimental drug with 5-HTP to induce 'serotonin syndrome', or serotonin toxicity, one can see how much that drug exacerbates serotonin biosynthesis or bioavailability by seeing how much of a 5-HTP dose is required to induce the syndrome; the lower dose indicative of higher drug potency). This test is known as the 5-HTP induced syndrome test.[8]
What is serotonin and what does it do? Serotonin is a chemical that transmits messages between nerve cells. Known as the happy chemical, serotonin plays a major role in the body by contributing to well-being, good mood, appetite, memory, and sleep. This article looks at what happens when a person is deficient in serotonin, and whether it can aid depression. Read now
Oxytocin was also correlated with the longevity of a relationship. Couples with the highest levels were the ones still together six months later. They were also more attuned to each other than the low-oxytocin couples when Feldman asked them to talk about a shared positive experience. The high-oxytocin couples finished each other’s sentences, laughed together and touched each other more often. Feldman says it’s still not clear whether oxytocin was responsible for the stability of the couple’s bond six months later or if couples who weren’t as connected failed to trigger the oxytocin system.

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]

Last month, in the article “How To Use BPC-157: A Complete Dummies Guide To Healing The Body Like Wolverine“, I introduced the little-known concept of using BPC-157 peptide self-injections and oral BPC-157 peptide consumption (currently completely legal and not banned by sporting organizations) for everything from rapidly healing leaky gut to fixing tendon, ligament and muscle injuries.
The RANKL and OPG have been identified as a key regulatory component of alveolar bone loss associated with inflammatory periodontal disease [52]. Moreover, PDLCs were shown to express several osteoclastogenic cytokines, including both OPG and RANKL [30, 31]. Our data demonstrated that Tβ4 peptide abolished H2O2-induced RANKL expression and restored OPG expression. Osteoclasts, bone-resorptive multinucleated cells derived from hematopoietic stem cells, are associated with osteolytic diseases. Furthermore, NFATc1, a master modulator of osteoclastogenesis, regulates target genes, such as cathepsin K and calcitonin receptor or Calcr [53]. In our in vitro study using BMMs, Tβ4 peptide directly and indirectly inhibited RANKL-induced osteoclast differentiation and expression of osteoclast markers, such as cathepsin-K, calcitonin receptor or Calcr, NFATc1, and RANK in BMM cells. These results indicated that Tβ4 was a key therapeutic target in controlling inflammation-induced bone loss.
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.
If you’re looking for hard proof that taking 5-HTP to lose weight works, we’ve got it: In a University of Rome study, obese women who took 5-HTP began eating between 1,000 to 2,000 fewer calories per day. And even as their caloric intake plummeted to a level that would leave many dieters irritable, serotonin was soothing these ladies — and not one reported hunger or diet crankiness. Further boosting spirits: The supplements quadrupled their weight loss, compared to folks given a placebo pill. “They ate a lot less than they normally would because it was easy for them,” Dr. Bhatia notes. Hearing about such an easy way to lose weight might be enough to inspire you to try the supplement for yourself. So, we went ahead and rounded up everything you need to know to get started.
Tβ4 was down-regulated in H2O2-exposed PDLCs in dose- and time-dependent manners. Tβ4 activation with a Tβ4 peptide attenuated the H2O2-induced production of NO and PGE2 and up-regulated iNOS, COX-2, and osteoclastogenic cytokines (TNF-α, IL-1β, IL-6, IL-8, and IL-17) as well as reversed the effect on RANKL and OPG in PDLCs. Tβ4 peptide inhibited the effects of H2O2 on the activation of ERK and JNK MAPK, and NF-κB in PDLCs. Furthermore, Tβ4 peptide inhibited osteoclast differentiation, osteoclast-specific gene expression, and p38, ERK, and JNK phosphorylation and NF-κB activation in RANKL-stimulated BMMs. In addition, H2O2 up-regulated Wnt5a and its cell surface receptors, Frizzled and Ror2 in PDLCs. Wnt5a inhibition by Wnt5a siRNA enhanced the effects of Tβ4 on H2O2-mediated induction of pro-inflammatory cytokines and osteoclastogenic cytokines as well as helping osteoclastic differentiation whereas Wnt5a activation by Wnt5a peptide reversed it.

In the experiments, an epithelial wound was made in the corneas of sedated rats. A Tb4 solution was applied at several concentrations to the injured eyes in one group of rats while another group was treated with a solution without Tb4. Following 12, 24 and 36 hours, the eyes were tested by microscopic observation for epithelial growth over the injured site. Investigators found the Tb4 accelerated corneal wound repair at doses of Tb4 similar to those found to repair skin wounds. When tested 24 hours after treatment, the rate of accelerated repair was proportional to the concentration of Tb4, with the highest dose (25 microgram) showing a threefold acceleration of epithelial cell migration, compared to untreated. Treatment with Tb4 showed anti-inflammatory effects, helping resolve the injury. An application to human cells in a model of human corneal cells in culture showed that Tb4 enhanced epithelial cell migration in vitro.

How not surprising on one level that a hormone involved in the formation of primary bonds, those that can have serious impacts on your survival, would be discerning. After all, if you had a mother who was dangerous, abusive, etc., how counter productive would it be for you to bond so tightly to her that you were all over her all the time, increasing your chances of pissing her off and killing you. And, how beneficial for you to be more bonded to a mother figure who was good to you, and provided you with nurture.
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The pamphlet, titled "Melanotan-2: Safe enhanced tanning" says although the drug is not approved by the Therapeutic Goods Administration (Australia's drug watchdog) and that studies into its effects are under way, it "is safe" and and its use "well documented". It says people can be referred to a "suitable doctor who is trained to prescribe MT2" so the pharmacy can dispense it to them.
Cells that line blood vessels (endothelial cells), taken from human umbilical chord veins, were grown in culture and the layer of cells subjected to a scratch wound. Cultures were then treated with Tb4 or kept in growth medium without Tb4. When examined four hours later, Tb4 treatment attracted cells to migrate into the wound and accelerated their movement, showing it is a chemoattractant. Cell migration was four to six times faster in the presence of Tb4 compared to the migration of untreated cells. Tb4 also hastened wound closure and increased the production of enzymes, called metalloproteases, that could pave the way for angiogenesis by breaking down barrier membranes and facilitating the invasion of new cells to the needy area, to form new vessels. Other experiments showed Tb4 acts in vivo. When endothelial cells were implanted under the skin in a gel supplemented with Tb4, the cells formed vessel-like structures containing red blood cells, indicating the ability to stimulate angiogenesis in the animals.
Anxiety. Evidence on the effects of 5-HTP for anxiety is unclear. Early research shows that taking 25-150 mg of 5-HTP by mouth daily along with carbidopa seems to reduce anxiety symptoms in people with anxiety disorders. However, other early research shows that taking higher doses of 5-HTP, 225 mg daily or more, seems to make anxiety worse. Also, taking 60 mg of 5-HTP daily through the vein does not reduce anxiety in people with panic disorders.