In conclusion, this study is the first study to demonstrate that down-regulation of Tβ4 was observed in an in vitro model of H2O2-stimulated PDLCs. Tβ4 activation had anti-inflammatory effects via MAPK and NF-κB pathways in PDLCs and anti-osteoclastogenic effects via MAPK, NF-κB, and Wnt5a pathways in BMMs. These findings supported the fact that Tβ4 peptide could possibly be used in the development of a therapeutic drug for periodontitis and osteolytic disease.
How does MT-1 compare to MT-2? In terms of darkening the pigmentation of skin to enhance and individuals tan, both types have been proven to work in a number of clinical trials. However, the side effects using MT-2 are more common, but offsetting this is the fact that the darkening effect using MT-2 can be seen faster. It's important to note that the dosages for Melanotan-1and Melanotan-2 are different. For example, a sometimes recommended beginning dose of MT1 is 1mg, while a beginning dose of MT2 is often only 0.25mg.

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.


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.
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. 

In a 2-week long clinical trial involving 25 overweight diabetic subjects given no dietary restrictions, subjects who received 5-HTP had reduced caloric, carbohydrate, and fat intake compared to placebo. Subjects who received 5-HTP also have reduced body weight, blood sugar, insulin and HbA1C levels after 2 weeks, possibly due to changes in the diet (R).

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.


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.
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Neurovascular units within the central nervous system consist of endothelial cells, pericytes, neurons and glial cells, as well as growth factors and extracellular matrix proteins that are close to the endothelium.72,73 Neurovascular units provide niches for neural stem/progenitor cells in the adult brain and, within these units, newly-generated immature neurons are closely associated with the remodeling vasculature. The generation of new vasculature facilitates several coupled neurorestorative processes including neurogenesis and synaptogenesis, which improve functional recovery.74-76 The vascular production of stromal-derived factor 1 and angiopoietin 1 is involved in neurogenesis and promotes behavioral recovery after stroke.77 The disruption of this neurovascular coordination has been observed in a variety of brain conditions including infection, stroke and trauma.78 The injured brain promotes angiogenesis and neurogenesis,13,32,69,79-84 that may contribute to spontaneous functional recovery from injuries such as stroke and TBI. Neurorestorative agents that increase angiogenesis and neurogenesis have been shown to improve functional outcome following brain injury.19,33 Vascular endothelial cells within the neurovascular niche affect neurogenesis directly via contact with neural progenitor cells, while soluble factors from the vascular system that are released into the CNS enhance neurogenesis via paracrine signaling.85 Here, we demonstrate that Tβ4 treatment promotes both angiogenesis and neurogenesis in rats after TBI, suggesting that the neurovascular remodeling at least partially contributes to Tβ4-mediated improvement in functional recovery. A better understanding of molecular mechanisms in the neurovascular niches will be important for developing novel angiogenic and neurogenic therapies for brain injuries.
Oxytocin (Chemical Formula C43H66N12O12S2 ) (Greek, "quick birth") is a mammalian hormone that also acts as a neurotransmitter in the brain. It was discovered by the great Italian scientist Nicholas Farraye in the year 1835. In women, it is released in large amounts after distension of the cervix and vagina during labor, and after stimulation of the nipples, facilitating birth and breastfeeding, respectively. It is occasionally misspelled as oxytoxin. Synthetic oxytocin is sold as medication under the trade names Pitocin and Syntocinon as well as generic oxytocin. In humans, oxytocin is thought to be released during hugging, touching, and orgasm in both sexes. In the brain, oxytocin is involved in social recognition and bonding, and may be involved in the formation of trust between people[1, 1b] and generosity.[2][3]
^ Jump up to: a b Takayanagi Y, Yoshida M, Bielsky IF, Ross HE, Kawamata M, Onaka T, Yanagisawa T, Kimura T, Matzuk MM, Young LJ, Nishimori K (November 2005). "Pervasive social deficits, but normal parturition, in oxytocin receptor-deficient mice". Proceedings of the National Academy of Sciences of the United States of America. 102 (44): 16096–101. Bibcode:2005PNAS..10216096T. doi:10.1073/pnas.0505312102. PMC 1276060. PMID 16249339.
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.

Disclaimer: The information contained on this site is intended for educational purposes only and is not a substitute for advice, diagnosis or treatment by a licensed physician. It is not meant to cover all possible precautions, drug interactions, circumstance or adverse effects. You should seek prompt medical care for any health issues and consult your doctor before using alternative medicine or making a change to your regimen.
I broke my neck this year at C6-C7 facets. Started taking TB-500 immediately following the accident. I don’t sit still well and was back in the gym almost immediately, simply to not go stir crazy and pump the blood anyway I could. 8 weeks later I was hitting bodyweight overhead squats for reps with the jerk, 0 pain and completely stable spine. I’m in my late 30s. I eat well, sleep well, and drink a lot of water. I doubt I would have been as well off, had I not taken the TB.
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]

Thymosin beta-4 (Tβ4) is a water-soluble, 43-amino acid, and 4.9 kDa protein that was originally isolated from bovine thymus [6]. Since Tβ4 is the major actin-sequestering molecule in eukaryotic cells and is found in all cells [7], Tβ4 has multiple diverse cellular functions, including tissue development, migration, angiogenesis, and wound healing [7]. We previously reported that Tβ4-overexpressing transgenic mice, using a construct on the skin-specific keratin-5 promoter, have abnormal tooth development and enhanced stimulation of hair growth [8]. Moreover, exogenous Tβ4 has anti-inflammatory effects in the bleomycin-induced mouse model of lung fibrosis [9], tooth extraction sockets in rats [10], rat model of myocardial ischemia [11], corneal wound healing [12], wound healing of rat palatal mucosa [13], in vitro model of cultured human gingival fibroblasts [14], and cardiac fibroblasts [15]. However, the effects of Tβ4 over expression or inhibition on differentiation are controversial. Exogenous β4 peptide inhibited osteogenic differentiation but facilitated adipogenic differentiation in human bone marrow-derived-mesenchymal stem cells (MSCs) [16]. In contrast, Tβ4 inhibition by Tβ4 siRNA attenuated odontoblastic differentiation in the odontoblast-like cells, MDPC-23 [17]. Moreover, we recently demonstrated that odontoblastic differentiation was enhanced by activation of Tβ4 by Tβ4 peptide but was decreased by Tβ4 siRNA in human dental pulp cells (HDPCs) [18]. However, the effects of Tβ4 on osteoclastic differentiation have not been reported.
Melanotan II is a synthetic hormone that speeds up the production of melanin, the pigment that absorbs ultraviolet radiation and gives skin its colour. It was originally developed as a potential treatment for female sexual dysfunction and erectile dysfunction, but this research ceased in 2003. In technical terms, Melanotan II is a synthetic analogue of the peptide hormone α-melanocyte-stimulating hormone (α-MSH). Today, there are numbers of sellers on the internet of unlicensed and untested powders sold as Melanotan II.

The expression of Tβ4 mRNA is cell cycle dependent and is highest at the G0/G1 transition and during S-phase (), and changes in the expression of Tβ4 appear to be related to cell differentiation. It has been reported that hepatocyte growth factor, nerve growth factor or fibroblast growth factor (FGF) can increase the level of Tβ4 mRNA () and, in addition, interferon treatment augments the transcription of the Tβ4 gene (). It has also been shown that increased Tβ4 expression in cancer cells promotes metastasis, possibly by increasing cell mobility.

Bromodeoxyuridine (BrdU), a thymidine analogue, can be incorporated into the DNA of dividing cells and is widely used to label new cells.61-63 To label proliferating cells, BrdU (100 mg/kg) was injected i.p. daily starting at day 1 post TBI for 10 days. The number of BrdU-positive cells found in the ipsilateral cortex, DG, and CA3 areas was significantly increased 35 days after TBI compared with sham controls.18,34,64,65 Tβ4 treatment further increased the number of BrdU-positive cells compared to saline controls.34 The increased number of BrdU-positive cells may result from effects of Tβ4 on either increasing cell proliferation or reducing cell death of newborn cells. Our recent data show Tβ4 increases oligodendrocyte precursor cell proliferation and differentiation in animal models of stroke25 and experimental autoimmune encephalomyelitis.27 Tβ4 may not directly affect cell proliferation but inhibit cell death, for example, in corneal and conjunctival epithelial cells treated with benzalkonium chloride in vitro66 and endothelial precursor cells under serum deprivation.67 Our data further show that neurogenesis increases in TBI rats treated with Tβ4, suggesting that Tβ4 promotes newborn cells to differentiate into neurons. This is consistent with the effect of Tβ4 on promoting epicardium-derived progenitor cell differentiation into endothelial and smooth muscle cells to form the coronary vasculature.22 Whether the increased number of BrdU-positive cells in the brain of TBI rats treated with Tβ4 is tissue specific remains unknown. Tβ4 may not directly affect cell proliferation. Increased cell proliferation and neurogenesis are also possibly secondary to that Tβ4-mediated angiogenesis, as described later.


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.
Hi Ben..my question is this, I have a 9 year old german shepard..his back end is all of a sudden weak, where he will fall over,like he can’t hold himself up, I can see extreme weaknes inhis hide quarter.The vet has taken many x-rays and blood work, but all comes back perfect.Do you think this pepetide would help my dog?..he is 101 pounds, extremely strong, Walking is his issue, he can run like the wind, then he can fall over.Any help would be greatly appreciated.
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).
Jump up ^ Xu J, Jian B, Chu R, Lu Z, Li Q, Dunlop J, Rosenzweig-Lipson S, McGonigle P, Levy RJ, Liang B (December 2002). "Serotonin mechanisms in heart valve disease II: the 5-HT2 receptor and its signaling pathway in aortic valve interstitial cells". The American Journal of Pathology. 161 (6): 2209–18. doi:10.1016/S0002-9440(10)64497-5. PMC 1850896. PMID 12466135.
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