To determine the effects of Tβ4 peptide and H2O2 on cytotoxicity, its cell viability was evaluated. A 48-h exposure to 0.1–5 μg/mL Tβ4 peptide did not affect H2O2-mediated cell viabilities (Fig 2A). In order to examine whether Tβ4 peptide suppressed ROS-induced inflammatory mediators, the ability of Tβ4 peptide on production of NO and PGE2, and expressions of COX-2 and iNOS were measured by RT-PCR, Western blot, and ELISA. Pretreatment with Tβ4 peptide dose-dependently inhibited H2O2-induced mRNA and protein expressions of COX-2 and iNOS, and NO and PGE2 production (Fig 2B–2E).
^ Jump up to: a b Low TL, Hu SK, Goldstein AL (February 1981). "Complete amino acid sequence of bovine thymosin beta 4: a thymic hormone that induces terminal deoxynucleotidyl transferase activity in thymocyte populations". Proceedings of the National Academy of Sciences of the United States of America. 78 (2): 1162–6. Bibcode:1981PNAS...78.1162L. doi:10.1073/pnas.78.2.1162. PMC 319967. PMID 6940133.
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.
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?
Growth factors play an important role is enhancing structural repair of chronic wounds (Robson, 1997). KGF-2 (Robson et al., 2001), TGF-β (Robson et al., 1995), PDGF-BB (Mustoe et al., 1994; Kiritsy et al., 1995; Smiell et al., 1999), β-NGF (Muangman et al., 2004) have been shown to enhance re-epithelialization (Greenalgh, 1996 for review). The KGF-1 gene has been shown to improve cutaneous wound healing in a septic rat model when delivered in a plasmid (Lin et al., 2006). The PDGF-B gene carried in a plasmid mixed with a bovine collagen gel was reported to accelerate closure of patient diabetic ulcers (Mulder et al., 2009; Blume et al., 2011). KGF-2, PDGF-BB and FGF-L are commercially available as RepiferminTM, RegranexTM, and Trafermin to treat human chronic wounds. Data for the effects of PDGF-BB on back wounds of diabetic mice and for the effects of KGF-2 on chronic venous ulcers in patients is tabulated in Tables 10.3 and 10.4. Thymosin β4 accelerated keratinocyte migration in the wounds of old diabetic mice (Philp et al., 2003).
To investigate whether the newborn neurons generated in the DG are capable of projecting their axons into the CA3 region of the hippocampus after TBI, we stereotactically injected a fluorescent tracer, 1,1″-dioleyl-3,3,3″,3″-tetramethylindocarbocyanine methanesulfonate (Dil, Delta 9-DiI; AnaSpec, San Jose, CA) into the ipsilateral CA3 region (stereotaxic coordinates AP, -3.6 mm bregma, ML, 3.6 mm, DV, 3.0 mm, Paxinos and Watson, 1994) at day 28 after TBI. BrdU (100mg/kg, ip) was injected i.p. daily starting at day 1 after TBI for 10 days to label newly generated cells. One week after DiI injection (i.e., 35 days after TBI), the animals were anesthetized and sacrificed. Their brains were fixed in 4% paraformaldehyde. The brain was cut into seven equally spaced 2-mm coronal blocks using a rat brain matrix. The brain blocks containing the hippocampus were processed for vibratome sections (100 μm) followed by BrdU staining. BrdU and DiI labeling in the hippocampus on brain sections was analyzed with a Bio-Rad MRC 1024 (argon and krypton) laser-scanning confocal imaging system mounted onto a Zeiss microscope (Bio-Rad, Cambridge, MA). Co-localization of BrdU-positive nuclei within retrogradely DiI-labeled granule cells was found, indicating that newborn granule neurons extend axons into the CA3 region that are capable of retrogradely transporting DiI from the CA3 to their cell bodies within the DG after TBI (Fig.2). This finding suggests that newborn granule neurons may be incorporated into functional hippocampal circuitry after TBI.

Plain sterile water is the most suitable diluent for TB-500. Alternatively it can be reconstituted with sterile saline (0.9% NaCl) or sterile bacteriostatic water (0.9% sodium chloride). Plain sterile water should be readily available to buy without prescription in any local pharmacy. Alternatively it can also be purchased online. It is even available on ebay.

I am not sure if my original question posted…I was wondering if I could use TB-500 to regenerate thyroid tissue? My endocrinologist said that my Hashimoto’s Thyroiditis has almost completely destroyed my thyroid. If yes, then where do I inject?? Additionally, I was wonder if the BPC-157 would have any benefits on thyroid as I plan to take orally for leaky gut/digestive issues.
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).
The logic behind this trend is that creating tanned skin (by increasing melanin) with minimal to no sun exposure could protect individuals from skin damage, and even potentially lower melanoma risk. More melanin means more protection from UV radiation, and therefore a healthier (and conveniently, deeper) complexion. In this sense, there is perhaps a kernel of truth to the idea of the “healthy glow”.
Toxicity includes renal dysfunction, rhabdomyolysis, sympathomimetic overdrive, change in size and pigmentation of new moles, with one report of melanoma associated with use of melanotan II. Other case reports include posterior reversible encephalopathy syndrome (consisting of seizures, visual disturbance, confusion, headache, vomiting); refractory priapism, stretching and yawning syndrome; shortness of breath, chest pain, abdominal cramping & pain, dizziness and lethargy.
The activity of the PAM enzyme system is dependent upon vitamin C (ascorbate), which is a necessary vitamin cofactor. By chance, sodium ascorbate by itself was found to stimulate the production of oxytocin from ovarian tissue over a range of concentrations in a dose-dependent manner.[23] Many of the same tissues (e.g. ovaries, testes, eyes, adrenals, placenta, thymus, pancreas) where PAM (and oxytocin by default) is found are also known to store higher concentrations of vitamin C.[24]
“People got quite excited,” recalls clinical neuroscientist Evdokia Anagnostou, who co-directs the Autism Research Centre at Holland Bloorview Kids Rehabilitation Hospital in Toronto, Canada. But Anagnostou says that some preliminary steps were skipped over as researchers rushed to test oxytocin as a psychiatric drug. “To be honest, if we had done it properly, we wouldn't have done it the way we did. It went a little bit too fast,” she says. Because oxytocin had cleared the early, standard steps of drug development decades earlier, some researchers did not systematically test a range of doses to see whether they had differing psychological effects.
100mg works well for mood and getting to sleep. Put 100mg in my Pre Workout Powder (Non Stimulant). Don't know if anyone else has tried this or if it was just a coincidence but it made the weights feel considerably lighter and I was able to use more weight than I have in a decade. I will definitely be trying that again. I also cut the bag open and emptied it into an old pill bottle through a small funnel. No wastage. Easy.
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 cornea is the outer thin layer of epithelial cells protecting the eye. After wounding, timely resurfacing of the cornea with new cells is critical, to prevent loss of normal function and loss of vision. Corneal epithelial healing occurs in stages, with cells migrating, dividing and differentiating. Therapies for corneal injury are limited. Therefore, the recent finding that Tb4 promotes corneal wound repair in animal models offers hope for a therapeutic product that will improve the clinical outcome of patients with injured corneas.

^ Jump up to: a b Hurlemann R, Patin A, Onur OA, Cohen MX, Baumgartner T, Metzler S, Dziobek I, Gallinat J, Wagner M, Maier W, Kendrick KM (April 2010). "Oxytocin enhances amygdala-dependent, socially reinforced learning and emotional empathy in humans". The Journal of Neuroscience. 30 (14): 4999–5007. doi:10.1523/JNEUROSCI.5538-09.2010. PMID 20371820.
Studies on diabetic rats indicated significant increases in the amount of collagen and in tensile strength of light-treated wounds over controls (Stadler et al., 2001; Reddy et al., 2001). In combination with hyperbaric oxygen, light-treated skin wounds in rats closed faster (Yu et al., 1997), an effect that was associated with a more uniform rise and fall in VEGF and FGF-2 instead of the sharp peaks at day four and subsequent rapid drop-off observed in control wounds (Whelan et al., 2001). In vitro, proliferation of mouse fibroblasts was increased by over 150% and that of human epithelial cells by 155–171% (Whelan et al., 2001). Whelan et al. (2001) also reported that wound-healing time was decreased by 50% aboard a submarine, where the atmosphere is lower in oxygen and higher in carbon dioxide, and that children suffering from oral mucositis as a result of chemotherapy experienced a 47% reduction in pain. Recently, however, a randomized trial using a 980 nm diode laser to treat venous leg ulcers of 18 patients indicated no difference in reduction of ulcer size compared to the 16 control patients (Leclere et al., 2010).
Hi Jesse, while I cant make specific sarms recommendations as it would be teetering on giving medical advice, I have a ton of resources on this on that you can easily search through. There is also a lot of invaluable discussion on sarms going on in the comments sections of these articles. The Kion Community is also a great place to ask a question like this:
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.

Synthetic oxytocin is sold as medication under the trade names Pitocin and Syntocinon and also as generic oxytocin. Oxytocin is destroyed in the gastrointestinal tract, and therefore must be administered by injection or as nasal spray. Oxytocin has a half-life of typically about three minutes in the blood. Oxytocin given intravenously does not enter the brain in significant quantities - it is excluded from the brain by the blood-brain barrier. There is no evidence for significant CNS entry of oxytocin by nasal spray. Oxytocin nasal sprays have been used to stimulate breastfeeding but the efficacy of this approach is doubtful[24].
This sounds very promising and I have a question I’m sure you haven’t heard before. It’s regarding healing. I’m about 230 and avid lifter as well as running occasionally. But I’ve had severe injuries to my l3-s1 for years a d yes I’ve tried some stuff before as far as lifting. But when I was 2 I had encephalitis. I survived it back in 74 which most didn’t however the treatment had left me with migraines and seizures as a child and was told my adult teeth would be very weak when they grew in. So I’m 44 and most of my teeth have broken and I’ve been looking for alternatives to implants. You said both the products mentioned in this article would improve healing and I’ve heard stem cells are capable of regrowing teeth. Would this work for me and how or where would I inject it or maybe do a oral form and let it sit in my mouth for a bit? Never really thought about this but I’ve tried so many clinical trials and been turned down each time. Any info would be greatly appreciated thank you in advance.
Who is 5-HTP best for? Emotional eaters stand to benefit greatly, of course. So do carb addicts. Carbs help the body make 5-HTP — so when 5-HTP or serotonin are low, carb cravings kick in. Boosting 5-HTP with a supplement has been shown to slash carb cravings by more than 50 percent. And if a “fat gene” runs in your family, early evidence hints that this genetic tendency toward obesity is linked to “decreased activity of an enzyme that helps turn tryptophan into 5-HTP,” explains Michael T. Murray, ND, author of 5-HTP: The Natural Way to Overcome Depression, Obesity and Insomnia ($14.77, Amazon). Though more human research is needed, Dr. Murray believes 5-HTP supplements are a quick fix for the genetic glitch.
5-HTP has been investigated for its role in hot flashes as Selective Serotonin Reuptake Inhibitors (SSRIs) have been noted to reduce the occurrence of hot flashes and menopausal symptoms.[30][31] In a study in menopausal females given 150mg 5-HTP daily (50mg taken thrice a day) for a period of one week failed to quantitivatively reduce the occurrance of hot flashes[32] as assessed by a Flashmark Pro recording device.[33]
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.
In all groups, [intravenous tryptophan] impaired memory and psychomotor performance significantly. In conclusion, cognitive deficits in [bipolar patients] following [intravenous tryptophan] may reflect a central 5-HT vulnerability in frontal brain areas. Independent of [intravenous tryptophan], cognitive deficits in [bipolar patients] provide evidence for a trait marker for [bipolar disorders].
5-HTP is converted by the body to serotonin, a chemical in the brain that plays an important role in mood, sleep, and appetite. Many prescription medications used for the treatment of depression increase serotonin concentrations in the brain. Because of 5-HTP's pathway to serotonin, it has appealed to researchers as well as the public as a "natural" alternative to antidepressants and treatment of depression, insomnia, migraines, obesity, and fibromyalgia.
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".
Loading is not absolutely necessary, it is only done to achieve results faster. Loading means taking doses more frequently to build up initial tan faster thus getting in tan maintenance mode sooner. Typical loading is done by taking 0.5mg once a day until desired skin tone is achieved. Loading dose can slightly vary from person to person, depending on skin type, bodyweight and other factors, but 0.5mg is pretty standard for most

In the prairie vole, oxytocin released into the brain of the female during sexual activity is important for forming a pair bond with her sexual partner. Vasopressin appears to have a similar effect in males.[57] Oxytocin has a role in social behaviors in many species, so it likely also does in humans. In a 2003 study, both humans and dog oxytocin levels in the blood rose after five to 24 minutes of a petting session. This possibly plays a role in the emotional bonding between humans and dogs.[58]
I was kind of scared because I ran across some threads that said TB500 leads to cancer or promotion of benign tumors…most of these were at least 4-5 years old though and it seems there are countless logs online all with good experiences. Nonetheless I was still worried so I did some more research and came across a pharmaceutical company in the US doing clinical trials for thymosin beta 4 to help with dry eye syndrome. I have attached some links. This makes me feel much safer but if you have any more insight I’d really appreciate it.
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
Thymosin Beta 4 is a potent peptide that comes from a family of 16 related molecules that are localized in circulating cells and tissues within the body. These molecules also have a high conservation of sequence. TB 500 conjoins with actin and prevents actin polymerization. It is noted as being the actin-sequestering molecule within eukaryotic cells. It also boosts extracellular matrix-degrading enzyme production.
Thymosin Beta 4 is a potent peptide that comes from a family of 16 related molecules that are localized in circulating cells and tissues within the body. These molecules also have a high conservation of sequence. TB 500 conjoins with actin and prevents actin polymerization. It is noted as being the actin-sequestering molecule within eukaryotic cells. It also boosts extracellular matrix-degrading enzyme production.
Such tissue-regenerating properties of thymosin β4 may ultimately contribute to repair of human heart muscle damaged by heart disease and heart attack. In mice, administration of thymosin β4 has been shown to stimulate formation of new heart muscle cells from otherwise inactive precursor cells present in the outer lining of adult hearts,[18] to induce migration of these cells into heart muscle[19] and recruit new blood vessels within the muscle.[20]
“Shortly after taking the supplement, my vision changes. Colours appear more vivid, I feel lightheaded and generally at ease. My mind calms down and the racing thoughts stop. Today is the 3rd day and I’ve noticed the intensity has gone up and it almost feels like I’m tripping on something. The sky looked absolutely amazing today, colours are so intense but I feel a kind of ungrounded and odd, but still pretty mellow with no anxious thoughts or anything like that which is good.”
The first dosage should be fairly small, as little as 0.3mg in order to gauge the reaction of the user's body. With increased dose first time user will deel warming ensation, flush in face and mild nausea, if these side effects occure dosage can be taken before going to bed, so any unpleasant effects take place while user is asleep. With regular use these side effects disapper and product can be taken at any tome of the day.
Affecting generosity by increasing empathy during perspective taking: In a neuroeconomics experiment, intranasal oxytocin increased generosity in the Ultimatum Game by 80%, but had no effect in the Dictator Game that measures altruism. Perspective-taking is not required in the Dictator Game, but the researchers in this experiment explicitly induced perspective-taking in the Ultimatum Game by not identifying to participants into which role they would be placed.[89] Serious methodological questions have arisen, however, with regard to the role of oxytocin in trust and generosity.[90] Empathy in healthy males has been shown to be increased after intranasal oxytocin[88][91] This is most likely due to the effect of oxytocin in enhancing eye gaze.[92] There is some discussion about which aspect of empathy oxytocin might alter – for example, cognitive vs. emotional empathy.[93] While studying wild chimpanzees, it was noted that after a chimpanzee shared food with a non-kin related chimpanzee, the subjects' levels of oxytocin increased, as measured through their urine. In comparison to other cooperative activities between chimpanzees that were monitored including grooming, food sharing generated higher levels of oxytocin. This comparatively higher level of oxytocin after food sharing parallels the increased level of oxytocin in nursing mothers, sharing nutrients with their kin.[94]
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.
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.
To determine the direct effect of Tβ4 peptide on osteoclastogenesis, mouse BMMs were directly exposed to Tβ4 peptide. Direct treatment with Tβ4 peptide also reduced the number of multinucleated TRAP-positive cells and TRAP activity in a dose-dependent manner (Fig 7A and 7B). Since Tβ4 downregulated H2O2-induced various cytokines expression, the indirect effect of Tβ4 on osteoclast formation through PDLC cells using co-culture system were investigated. After addition of Tβ4 peptide to the BMMs-PDLCs co-culture, the number of osteoclast and TRAP activity were also significantly decreased (Fig 7C and 7D).
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.
If the two things you can't live without are a dark, even tan and a fast-acting, long-lasting erection, then add Melanotan II to your holiday shopping list. This synthetic peptide hormone, which was developed by a research team at the University of Arizona during the late 1990s, darkens skin pigment and may stimulate erectile activity. And despite continued concern and controversy within the medical community regarding its use, it remains available for sale over the internet in a powdered form that can then be reconstituted for subcutaneous injections.
Its unique potential as a healing substance lies in that it interacts with cellular actin and regulates its activity. Tb4 prevents actin from assembling (polymerizing) to form filaments but supplies a pool of actin monomers (unpolymerized actin) when a cell needs filaments for its activity. A cell cannot divide if actin is polymerized. Tb4 therefore serves in vivo to maintain a reservoir of unpolymerized actin that will be put to use when cells divide, move and differentiate.
“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.”
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.
Both the production of oxytocin and response to oxytocin are modulated by circulating levels of sex steroids. The burst of oxytocin released at birth seems to be triggered in part by cervical and vaginal stimulation by the fetus, but also because of abruptly declining concentrations of progesterone. Another well-studied effect of steroid hormones is the marked increase in synthesis of uterine (myometrial) oxytocin receptors late in gestation, resulting from increasing concentrations of circulating estrogen.

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.
In 19 obese females given either placebo or 8mg/kg (weight not actually given, only BMI between 30-40 for women) daily for 5 weeks without any concurrent dietary recommendations, 5-HTP treatment was associated with a decrease in appetite and food intake (resulting in weight loss) without significantly affecting mood state.[9] This study noted that food intake was reduced from an average of 2,903kcal to 1,819kcal (62% of baseline) while placebo only reduced calories to 80%, and the 0.5kg weight loss in placebo was outperformed by a near 1.5kg loss in 5-HTP. These weight loss effects have been noted with 750mg 5-HTP over 2 weeks in overweight diabetics[10] and over 12 weeks in obese persons given 900mg 5-HTP daily (58% of baseline intake); this latter study had a 6 week trial without a diet (in which significant weight loss was only noted at week 6) followed up by coadministration with a diet where weight loss proceeded to reach an additional 3.3kg over the subsequent 6 weeks;[11] this latter study is duplicated in Medline.[12]

To evaluate the indirect effect of Tβ4 peptide on RANKL-induced osteoclastogenesis, mouse BMMs were incubated with RANKL and CM, prepared from HPDLCs treated with H2O2 and different concentrations of Tβ4, and allowed to differentiate into osteoclasts. As shown in Fig 6, Tβ4 peptide dose-dependently decreased the number of osteoclasts and TRAP activity. To determine whether the reduction in osteoclast generation by Tβ4 could be due to effects of Tβ4 peptide on viability of the BMMs, a cytotoxicity assay was performed. The viability of BMMs was not significantly affected by Tβ4 peptide (data not shown).

"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.

To determine the direct effect of Tβ4 peptide on osteoclastogenesis, mouse BMMs were directly exposed to Tβ4 peptide. Direct treatment with Tβ4 peptide also reduced the number of multinucleated TRAP-positive cells and TRAP activity in a dose-dependent manner (Fig 7A and 7B). Since Tβ4 downregulated H2O2-induced various cytokines expression, the indirect effect of Tβ4 on osteoclast formation through PDLC cells using co-culture system were investigated. After addition of Tβ4 peptide to the BMMs-PDLCs co-culture, the number of osteoclast and TRAP activity were also significantly decreased (Fig 7C and 7D).
To identify newborn neurons, double immunofluorescent staining for BrdU/NeuN (mature neuronal marker) was performed (Fig.1). TBI alone significantly increased the number of newborn neurons (NeuN/BrdU-colabeled cells) in the DG of injured hemisphere. Tβ4 treatment significantly further increased the number of newborn neurons compared to saline controls. These data suggest that Tβ4 administration initiated 24 hours after TBI promotes neurogenesis in rats.

In November 2008, the UK Medicines and Healthcare products Regulatory Agency (MHRA) warned the public against melanotan use stating it was an unlicensed medicine that may not be safe. As such, it is illegal to market or supply this product in the UK due to its unlicensed nature. Additionally the MHRA warned 18 companies about selling or advertising the product and closed down 72 websites involving melanotan. By 2013, the MHRA had received 18 reports of 74 separate reactions to the products and reactions have involved stomach and heart problems, as well as blood and eye disorders.
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
The neurotransmitter serotonin is synthesized from the amino acid tryptophan through 5-HTP. In which tryptophan gets converted into 5-HTP via the enzyme tryptophan hydroxylase and 5-HTP gets converted into serotonin via the enzyme L-amino acid decarboxylase.[4] Serotonin is later degraded into 5-hydroxyindoleacetic acid (5-HIAA) by monoamine oxidase.

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.