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]


Due to its molecular structure and low molecular weight, TB-500 is very versatile, mobile and possesses the ability to travel long distances through tissues. This means that when targeting injured areas (chronic or acute), TB-500 has the ability to circulate through the body and “find” those areas of injury in order to enhance the healing or growth process. Many users have also noted the added benefits of improved flexibility, reduced inflammation in tendons, re-growth of lost hair, and darkening of grayed hair.

Hey I have used Tb 500 alot and can tell you injecting it in your fat around your stomach or in your large muscles near the injury is fine. I would never inject it into a wounded area because of possiblity of making the area worse by infection or trama from the needle. Dosage is tough I would say for a 200 pound person you need at least 5mg twice a week. Mixing it with GH releasing peptides seems to make it stronger as well. It’s definitely worth the month just finding legit stuff can be tricky.


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).
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.

Because of its role in creating serotonin, 5-HTP is indirectly involved in producing melatonin, a hormone that is critical for sleep. Melatonin helps the body’s bio clock stay in sync, and regulates daily sleep-wake cycles. A strong bio clock and regular sleep-wake routines are the cornerstone of healthy, restful, rejuvenating sleep. Research suggests that 5-HTP may help shorten the time it takes to fall asleep and increase sleep amounts.
Thymosin beta(4), a small ubiquitous protein containing 43 aa, has structure/function activity via its actin-binding domain and numerous biological affects on cells. Since it is the major actin-sequestering molecule in eukaryotic cells and is found essentially in all cells and body fluids, thymosin beta(4) has the potential for significant roles in tissue development, maintenance, repair, and pathology. Several active sites with unique functions have been identified, including the amino-terminal site containing 4 aa (Ac-SDKP) that generally blocks inflammation and reduces fibrosis. Another active site at the amino terminus contains 15 aa, including Ac-SDKP, and promotes cell survival and blocks apoptosis, while a short sequence containing LKKTETQ, the central actin-binding domain (aa 17-23) plus 1 additional amino acid (Q), promotes angiogenesis, wound healing, and cell migration. Several additional biological activities have been identified but not yet localized in the molecule, including its antimicrobial activity, the induction of various genes (including laminin-5, MMPs, TGF beta, zyxin, terminal deoxynucleotidyl transferase, and angiogenesis-related proteins), and the ability to activate ILK/PINCH/Akt, and other signaling molecules important in both apoptosis and inflammatory pathways. This review details these important physiologically and pathologically active sites and their potential therapeutic uses.
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
Mouse bone marrow macrophage (BMMs) of 5-week-old female ICR mice (Charles River Laboratories, Seoul, South Korea) were used as previously described [23]. Animals were maintained in accordance with the National Institute of Toxicological Research of the Korea Food and Drug Administration guideline for the humane care and use of laboratory animals Institutional Animal Care and Use Committee (IACUC) approval was obtained from Kyung Hee University (Seoul, Korea). Briefly, bone marrow of tibiae and femurs of mice were flushed with α-MEM. After removing erythrocytes with hypotonic buffer, cells were cultured in α-MEM containing 10% FBS for 24 h and adherent cells were discarded. Non-adherent bone marrow cells were transferred onto 100-mm non-coated petri dishes at 5×106 cells per dish and cultured in the presence of M-CSF (30 ng/ml) for 3 days. Condition medium (CM) was obtained from HPDLCs treated with 200 μM H2O2 or Tβ4 (0.5, 1 and 5 μg/mL) for 2 days. To evaluate the osteoclastogenic activity of CM from HPDLCs, we added the CM mixture (60% CM plus 40% fresh α-MEM without M-CSF or RANKL) or rh-Tβ4 to pre-osteoclast-stage cells and further cultured the cells for up to 5 days to achieve mature osteoclast differentiation BMMs (1.5 × 105 cells/well) and PDLCs (1.5 × 104 cells/well) were co-cultured for 7 days in the presence of M-CSF (30 ng/ml), RANKL (100 ng/mL), H2O2 (200 μM) or Tβ4 (0.5, 1 and 5 μg/mL) in α-MEM, supplemented with10% in 48-well plates under 5% CO2 atmosphere.

Monomeric β-thymosins, i.e. those of molecular weight similar to the peptides originally isolated from thymus by Goldstein, are found almost exclusively in cells of multicellular animals.[4] Known exceptions are monomeric thymosins found in a few single-celled organisms, significantly those currently regarded as the closest relatives of multicellular animals:[5] choanoflagellates [6] and filastereans.[7] Although found in very early-diverged animals such as sponges, monomeric thymosins are absent from arthropods and nematodes, which do nevertheless possess "β-thymosin repeat proteins" which are constructed from several end-to-end repeats of β-thymosin sequences.[8] Genomics has shown that tetrapods (land vertebrates) each express three monomeric β-thymosins, which are the animal species' equivalents (orthologues) of human β4, β10 and β15 thymosins, respectively. The human thymosins are encoded by the genes TMSB4X, TMSB10 and TMSB15A and TMSB15B. (In humans, the proteins encoded by the two TMSB15 genes are identical.) Bony fish in general express orthologues of these same three, plus an additional copy of the β4 orthologue.[9]


In regards to interventions, one study in treatment resistant depressed persons that combination therapy of 5-HTP with Carbidopa noted that 43 out of 99 (43.4%) patients improved with an average 200mg (variable 50-600mg) dosage of 5-HTP.[24] It has been noted[25] that since Cardidopa is a peripheral decarboxylase inhibitor that can prevent metabolism of monoamines including serotonin[26] that these results are unlikely to reflect monotherapy with 5-HTP, despite being within the 30-45% range sometimes seen with the placebo effect.[25][27]

“The study is kind of a high-water mark for the field, putting different levels all together: a robust behaviour, a brain region, and a cellular basis for it,” says Richard Tsien, a neuroscientist also at Langone. Tsien has been studying the action of oxytocin on neuronal circuits in detail, by examining slices of the hippocampus, a region involved in learning and memory. In a 2013 study6 of rats, Tsien's team found that oxytocin selectively acts on a type of cell called an inhibitory interneuron in a way that quiets background chatter within the neuronal circuit. “Oxytocin improved signal transmission, almost doubling the ability of information to flow through the system,” Tsien says. In effect, it is producing more signal and less noise.


I was in a bad accident 5 years ago and was feeling better until my Dr. gave me levaquin which damages your mitochondria, gut, tendons And ligaments. I was going to order BPC 157 but see where you think TB500 is stronger. Do you know if it shows up on an employee drug test as i get tested occasionally? Also, your thoughts on fragment 176-191, a friend of mine uses it and suggested it for me. I understand you’re not a Dr, but just looking for your personal opinion. Thank you
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.

There is one glaring problem, however: the supplements come with a disclaimer that recommends not taking them for more than three months. Most of the information out there on 5-HTP is anecdotal, and most of them are stories of it helping people, rather than hard facts about its scientific properties. I approached neurologists, psychologists and experimental doctors about 5-HTP, and many responses were strange. Not many people were willing to speak about it, saying they weren't qualified or hadn't read the relevant material, but there isn't much material to speak of. The main source of legitimate scientific evidence came from the University of Maryland Medical Center website, who stated that 5-HTP may work as well as certain antidepressant drugs to treat people with mild-to-moderate depression. But all the studies that support that statement were done in the 1980s and 1990s. I wanted to know if 5-HTP was a realistic alternative to SSRIs. Could I stay on 5-HTP forever, basking in its natural glory?


I found this to be an excellent supplement for myself, which overcomes the rate limiting step when the body converts tryptophan to 5-HTP. I am sleeping much better and handling life's normal stresses better. If you haven't already, become familiar with how/why the body converts L-Tryptophan > 5-HTP > Serotonin > Melatonin. Very interesting! Thank you Bulk Nutrients for making this available.
I went to a neurologist, He said it was just in my head because I have depression–the exact reason why I took 5HTP. Not satisfied with that doctor, I went to an immunologist. He said I got myositis. Eosinophilic Myositis. From my blood test, I got positive ANA IF, very high number of IgE, elevated Creatine Kinase, and very low Vitamin D 25(OH)D. But my ANA Profile test showed negative.
Therefore, this study was designed to investigate whether Tβ4 was up-regulated in patients with periodontitis, and this study was also designed to investigate whether Tβ4 inhibition or activation suppressed the osteoclastic differentiation in mouse bone marrow-derived macrophages (BMMs) and inflammatory response in periodontal ligament cells (PDLCs) as well as on their signaling pathways.
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
This is a great product, I have been having digestive problems after 13 major surgeries and suffering from Crohn's Disease my whole life. Currently I can only tolerate a liquid diet. Was very depressed, found this and started taking it and it has made a HUGE difference to my life. Only have very mild depression symptoms now, and sleep better at night. Bought the powder to get the dose right, looks like 100mg suits my 50 kg frame. Only bad thing is the packaging. The 10 grams of powder is lost in the large packet, very hard to get it out and measure the same dose every night. I purchased miniature measuring spoons from ebay and they make life much easier. Sort out the correct spoon for your dosage with the scales then off you go. Can be tricky getting it in and out of the bag, often get powder everywhere, but usually just lick it off. A pill container would work much better for this power.
Tβ4 is the major monomeric actin-sequestering peptide in human tissues, and can bind globular actin (G-actin) in a 1:1 ratio and consequently involved in cytoskeletal regulation by inhibiting the polymerization of G-actin into fibrous actin (F-actin) [7]. In addition, Tβ4 is an ubiquitous naturally occurring molecule and is found at concentrations of 1 × 10−5 to 5.6 × 10−1 M in a variety of tissues and cell types, yet, no receptors for the protein have been identified [33]. A recent study suggests that internalization of exogenous Tβ4 is essential for its subsequent cellular functions [34]. Moreover, Tβ4 has been shown to be associated with, wound healing, hair growth, immunomodulation, and angiogenesis [7–9].
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.

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 :)

Robert Love, a urologist in Dallas, understands why there is such back-channel demand for a product like Melanotan II. "People sometimes want to handle performance issues on their own, without a physician involved, either because they are embarrassed or because they may be uninsured or lack adequate insurance," he told Motherboard. "Handling things this way is not advisable. We have prescription drugs that address erectile dysfunction issues. And although this isn't my area, there are alternative ways of getting suntans—tanning beds, spray tans—though of course extended outdoor sun exposure should be avoided if possible."
Melanotans include melanotan I (afamelanotide) and melanotan II. Both melanotan I and II are widely abused to obtain a cosmetic tan. The melanotans are potent, non-selective melanocortin receptor agonists affecting MC1, MC3, MC4 and MC5 receptors. These receptors are responsible for many physiological systems including: pigmentation, energy, sexual function, immune system, inflammation and the cardiovascular system.

Thymosin β4 (TMSB4X, Tβ4) is the most abundant G-actin binding peptide of the cytosol and is a potent proangiogenic factor. The role of myocardin-related transcription factors (MRTF) and serum response factor (SRF) for this function was examined in experimentally induced prolonged ischemic myocardium areas of transgenic pigs ubiquitously and constitutively overexpressing Tβ4 driven by the cytomegalovirus promoter. Upon induction of a reversible loss of cardiomyocyte function which is amenable to therapeutic neovascularization, transgenic pigs did not experience a significant loss of perfusion nor myocardial function at rest or under rapid pacing. Functional vascular regeneration by induced capillary growth and maturation was found in the transgenic pigs (Hinkel et al., 2014).
Osteoclast differentiation was assessed by tartrate-resistant acid phosphatase (TRAP) staining and activity. After 5 days of culture, cells were stained for TRAP kit using a leukocyte acid phosphatase kit (Sigma Aldrich, St Louis, MO, USA). Cells with three or more nuclei were counted as multinucleated mature osteoclasts. To measure TRAP activity, cells were fixed with 10% formalin for 10 min and 95% ethanol for 1 min, and then 100 μl of citrate buffer (50 mM, pH 4.6) containing 10 mM sodium tartrate and 5 mM p-nitrophenylphosphate (Sigma-Aldrich) was added to the wells containing fixed cells in the 48-well plates. After incubation for 1 h, enzyme reaction mixtures in the wells were transferred to new plates containing an equal volume of 0.1 N NaOH. Absorbance was measured at 410 nm using a microplate reader.

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
But this isn’t the only study to show the subtle side of oxytocin. Just three months ago, I wrote about research from Heejung Kim at the University of California, which showed how oxytocin’s effects vary across different cultures. To fulfil its many roles, oxytocin has to dock at a protein called the ‘oxytocin receptor’, encoded by a gene called OXTR.
Maintenance doses are taken once the desired pigmentation has been reached and requires much less frequent dosing. Unfortunately, this is where too many variables come into play to give exact instructions. Skin type, bodyweight, metabolism regulating speed of skin fading, uv ray exposure, preferred tan level – all that makes impossible to give correct advice on maintenance dose. Everyone will find their own perfect dose and dosing frequency through some trial and error. To not leave you completely disinformed on this subject here is example of loading and maintenance which can be used as starting point where to adjust from:
Oxytocin affects social distance between adult males and females, and may be responsible at least in part for romantic attraction and subsequent monogamous pair bonding. An oxytocin nasal spray caused men in a monogamous relationship, but not single men, to increase the distance between themselves and an attractive woman during a first encounter by 10 to 15 centimeters. The researchers suggested that oxytocin may help promote fidelity within monogamous relationships.[109] For this reason, it is sometimes referred to as the "bonding hormone". There is some evidence that oxytocin promotes ethnocentric behavior, incorporating the trust and empathy of in-groups with their suspicion and rejection of outsiders.[66] Furthermore, genetic differences in the oxytocin receptor gene (OXTR) have been associated with maladaptive social traits such as aggressive behavior.[110]
Maintenance doses are taken once the desired pigmentation has been reached and requires much less frequent dosing. Unfortunately, this is where too many variables come into play to give exact instructions. Skin type, bodyweight, metabolism regulating speed of skin fading, uv ray exposure, preferred tan level – all that makes impossible to give correct advice on maintenance dose. Everyone will find their own perfect dose and dosing frequency through some trial and error. To not leave you completely disinformed on this subject here is example of loading and maintenance which can be used as starting point where to adjust from:
In persons with Panic Disorders (versus persons without as control) ingesting 200mg of 5-HTP, both groups experienced an increase in salivary cortisol within 3 hours but the persons with Panic Attacks continued to have greater increases after the 3 hour mark; this increased cortisol was independent of any percieved side-effects such as headache, fatigue, perspiration, nausea, etc.[43]

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.
I have bee suffering from severe symptoms of post concussion syndrome for several.months after a car accident. The use of TB500 has been the only trratment ease my symptoms and give me my life back. I ceased use last week after 3 weeks and had reoccuring concussion symptoms. As such? I recommenced injections as of last night. Have you read much about the impact of TB500 on brain injury as I’d love to know if more prolonged use would have a permanent impact/remedy for me? Thanks for your time and interest.
When looking at studies that investigate carbohydrates per se, one study in overweight women given 8mg/kg 5-HTP for 5 weeks noted that while placebo did not reduce carbohydrate ingested (calories were reduced in placebo, but carbohdyrate remained at 38% of voluntary calorie intake) that 5-HTP also retained 38% of intake as carbohydrates despite consuming less calories and carbohydrates in total.[9] A decrease in both carbohydrate and dietary fat has been noted with 750mg 5-HTP daily for 2 weeks in diabetics (with no dietary guidelines given), but appeared to be reduced to a similar degree as calories overall.[10] Only one study supports these anecdotes, where the reduction in calories seemed to be acounted mostly for by carbohydrates (75% of observed reduction) and then fats (25%).[10]
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!
But we have to be just as good at recognizing who we can trust, so the system needs fine-tuned control. That’s apparently where oxytocin comes in. The amygdala, that critical organ for our biological risk response, has a high concentration of receptors for oxytocin. In the second set of those gambling experiments with the volunteers and the trustees, researchers used fMRI to watch the brains of the volunteers as they made their choices. As the levels of oxytocin in the brain went up compared with the placebo group, activity in the amygdala went down! Oxytocin diminishes the amygdala’s ability to send out the message “Warning! Warning! I don’t trust this guy.”
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 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”.

Serotonin syndrome (Serotonin toxicity) is caused by an excess of serotonin in the brain. It is most often caused by taking more than one Serotonin-enhancing substance at the same time, such as 5-HTP and an antidepressant medication. Symptoms range in severity according to the level of intoxication and may include increased heart rate, tremor, sweating, mental agitation, seizures, shock, organ failure and death (9).


To further determine the potential anti-inflammatory effects of Tβ4 activation, expressions of proinflammatory or osteoclastogenic cytokines were measured by RT-PCR (Fig 4A). The TNF-α, IL-1β, IL-6, IL-8, and IL-17 mRNA levels increased in the H2O2- stimulated PDLCs, and these increases were significantly decreased in a concentration-dependent manner by treatment with the Tβ4 peptide. Since receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) are two important osteoclastogenic factors, we next explored the effects of Tβ4 peptide on RANKL and OPG expressions in PDLCs. Tβ4 peptide reduced H2O2-stimulated up-regulation of RANKL, with a reciprocal increase in OPG mRNA in a dose-dependent manner (Fig 4B).
We are proud to offer 99.9% Pure Pharmaceutical  Grade Melanotan 2, produced in the USA!  Our state of the art labs individually vacuum seal sterile vials of 99.9% Pure Pharmaceutical Grade Peptides as a lyophilized solid, with no added fillers like mannitol.  We strongly believe in bringing you quality MT2 that is free from fillers and additives like mannitol, unlike many cheap Chinese imports that are flooding the market.   In addition, we want you to know that many overseas imports are subject to potentially hazardous chemical degradation.  This is due to long transportation time and fluctuating temperatures that can reduce the effectiveness and even potentially increase the side effects of MT2.   Our supplies are always fresh and kept in climate controlled storage until it is sent to your door. 
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.
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.
That view has led some clinicians to try oxytocin as a treatment for psychiatric conditions such as autism spectrum disorder. But the early trials have had mixed results, and scientists are now seeking a deeper understanding of oxytocin and how it works in the brain. Researchers such as Froemke are showing that the hormone boosts neuronal signals in a way that could accentuate socially relevant input such as distress calls or possibly facial expressions. And clinical researchers are starting a wave of more ambitious trials to test whether oxytocin can help some types of autism.
The structure of oxytocin is very similar to that of vasopressin. Both are nonapeptides with a single disulfide bridge, differing only by two substitutions in the amino acid sequence (differences from oxytocin bolded for clarity): Cys – Tyr – Phe – Gln – Asn – Cys – Pro – Arg – Gly – NH2.[116] A table showing the sequences of members of the vasopressin/oxytocin superfamily and the species expressing them is present in the vasopressin article. Oxytocin and vasopressin were isolated and their total synthesis reported in 1954,[122] work for which Vincent du Vigneaud was awarded the 1955 Nobel Prize in Chemistry with the citation: "for his work on biochemically important sulphur compounds, especially for the first synthesis of a polypeptide hormone."[123]
Oxytocin is known as the hormone that promotes feelings of love, bonding and well-being. It's even being tested as an anti-anxiety drug. But new research shows oxytocin also can cause emotional pain. Oxytocin appears to be the reason stressful social situations, perhaps being bullied at school or tormented by a boss, reverberate long past the event and can trigger fear and anxiety in the future. That's because the hormone actually strengthens social memory in the brain.
Chae, H. S., Kang, O. H., Choi, J. G., Oh, Y. C., Lee, Y. S., Jang, H. J., Kim, J. H., Park, H., Jung, K. Y., Sohn, D. H., and Kwon, D. Y. 5-hydroxytryptophan acts on the mitogen-activated protein kinase extracellular-signal regulated protein kinase pathway to modulate cyclooxygenase-2 and inducible nitric oxide synthase expression in RAW 264.7 cells. Biol Pharm Bull 2009;32(4):553-557. View abstract.
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