I am not a doctor and nothing I say should be taken as medical advice. If you have a read through the article, I would suggest following the recommendations there. If you want to go into detail book a consult at

"Just that it is completely false that these particular substances and the program wasn't discussed through the highest levels of the club. We have been very firm in terms of our belief in what ASADA, the AFL and Essendon know and for them to remotely suggest that no one knew, to be really blunt, is completely wrong and in some ways offending the process we set up at Essendon Football Club. We were very strict in the protocols we set up."


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.

Actual injection can be done Subq or IM that is - subcutaneous or intramuscular. Injection site does not matter, there is no one site better than others so use one which is more comfortabe to reach, after injection product is absorbed into bloodstream and spread through the body evenly. Subq injection takes place by pinching the skin loose from the muscle and raising it so the needle can be inserted in the fat layer of skin.
I am not a doctor and this is not to be taken, interpreted or construed as medical advice. Please talk with a licensed medical professional about this. I would say yes though. Just because you dont “know” or “feel” any injury, you might be one functional movement away from a weakened tendon or muscle – snap, crackle and POP! These are just my own personal thoughts and not a prescription or a diagnosis or any form of health care whatsoever.
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.
I’m curious to know where you got your reconstitution calculation from; you recommend putting approx 3 cc’s in a 5 mg TB-500 which ‘almost fills’ the vial. I have been doing a ton of research on TB-500 and finding contradictory recommendations on how to reconstitute. Because the dosing for TB-500 is higher than what I’m used to with GHRH & GHRP – I felt a lower reconstitution mixture would reduce the amount I needed to take (but now I’m wondering if I’ve been over dosing based on your formula). Would really appreciate knowing how you arrived at filling an insulin syringe ‘three times’ equal to 3 cc’s – just want to make sure i’m dosing correctly
Thymosin Beta 4 is a protein that is made up of 43 amino acids. The TMSB4X gene found in the test subject's body encodes the peptide. There have been a variety of clinical trials that have been performed using this peptide. In the research, it’s been found that the Thymosin Beta 4 may be used after a heart attack takes place in order to reactivate the cells in the cardiac progenitor, so that repair can be done to the damaged tissue in the heart.
Hi Ben, I have been using TB-500 for minor injury repair assistance for more than 2 years. I have found it to be extremely effective for minor strains to calves, hamstring, shoulder etc. Luckily I have not had to try it for any major injuries. When I first used it I was blown away by how effectively it worked – even to the point that I began to doubt the seriousness of the original injury. When injured I dose at 5mg per week for four weeks then take at least four weeks break. The only side affect I have noticed is a little light headed feeling which passes pretty quickly. I am in my late 40’s and I train hard. TB-500 allows me to train through minor injuries which is great. Love your work
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.
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]
Uterine contraction important for cervical dilation before birth and causes contractions during the second and third stages of labor. Oxytocin release during breastfeeding causes mild but often painful uterine contractions during the first few weeks of lactation. This also serves to assist the uterus in clotting the placental attachment point postpartum. However, in knockout mice lacking the oxytocin receptor, reproductive behavior and parturition is normal.[4]
But Carter and other scientists are concerned by reports from the physicians and parents of children with autism spectrum disorder who say that they are already using oxytocin off-label — before it has been thoroughly tested. “We do not understand how the hormone works yet, or have enough information about what happens when it's given repeatedly,” Carter says. “This is not a molecule that people should be self-administering or playing with.”
Before the treatment, the female mice were largely indifferent to the cries of a distressed baby, and were even known to trample over them. But after an injection of oxytocin, the mice started to respond more like mothers, picking up the mewling pup in their mouths. Froemke, a neuroscientist at New York University's Langone Medical Center in New York City, was monitoring the animals' brains to find out why that happened.
Outside the brain, oxytocin-containing cells have been identified in several diverse tissues, including in females in the corpus luteum[34][35] and the placenta;[36] in males in the testicles' interstitial cells of Leydig;[37] and in both sexes in the retina,[38] the adrenal medulla,[39] the thymus[40] and the pancreas.[41] The finding of significant amounts of this classically "neurohypophysial" hormone outside the central nervous system raises many questions regarding its possible importance in these different tissues.

Jump up ^ Grottesi A, Sette M, Palamara T, Rotilio G, Garaci E, Paci M (1998). "The conformation of peptide thymosin alpha 1 in solution and in a membrane-like environment by circular dichroism and NMR spectroscopy. A possible model for its interaction with the lymphocyte membrane". Peptides. 19 (10): 1731–8. doi:10.1016/S0196-9781(98)00132-6. PMID 9880079.


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.
Horvath, G. A., Stockler-Ipsiroglu, S. G., Salvarinova-Zivkovic, R., Lillquist, Y. P., Connolly, M., Hyland, K., Blau, N., Rupar, T., and Waters, P. J. Autosomal recessive GTP cyclohydrolase I deficiency without hyperphenylalaninemia: evidence of a phenotypic continuum between dominant and recessive forms. Mol.Genet.Metab 2008;94(1):127-131. View abstract.
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]
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.
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 http://www.ncbi.nlm.nih.gov/pubmed/22421562

What we noticed was that all the rats that had received oxytocin straight into their brain immediately prior to being given alcohol, were up and moving about and seemed to be completely sober. Whereas all of the rats that had just been given the alcohol were, as we would predict from the dose that we were giving them, quite drunk. And so we thought, 'Wow, what's going on here?' It was almost as though the oxytocin was blocking the intoxicating effects of the alcohol.
“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.”

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.
In addition to angiogenesis and neurogenesis, cell- and pharmacologically based therapies substantially remodel white matter in the ischemic brain. Treatment of experimental stroke with MCSs, rhEPO, or sildenafil significantly increases axonal density encapsulating the ischemic lesion. Dynamic changes of white matter structure along the ischemic boundary have been imaged in living animals by diffusion tensor imaging (DTI) and fractional anisotropy (FA) measurements. Data from these MRI indices demonstrate that administration of rhEPO or sildenafil augments axonal remodeling and angiogenesis and that both of them are spatially and temporally correlated. Administration of MSCs, rhEPO, and thymosin beta 4 (Tβ4) dramatically increases the number of oligodendrocyte progenitor cells in the corpus callosum, the striatum, and the V/SVZ of the ischemic hemisphere and mature oligodendrocytes in the ischemic boundary adjacent to myelinated axons. These findings suggest that cell- and pharmacologically based therapies promote generation of oligodendrocyte progenitor cells in the ischemic brain that migrate to target axons, where they extend their processes myelinating the axons.
MT 1 and MT 2 are synthetic analogues of the alpha-melanocyte stimulating peptide hormone Alpha-MSH. This hormone aids skin cells to produce greater quantities of Melanin. Therefore MT-1 and MT-2 mimic this hormone and encourage the production of more Melanin. Melanin is a dark pigment in the skin that can provide some protection from the UV rays of the sun.
Milk ejection reflex/Letdown reflex: in lactating (breastfeeding) mothers, oxytocin acts at the mammary glands, causing milk to be 'let down' into subareolar sinuses, from where it can be excreted via the nipple.[47] Suckling by the infant at the nipple is relayed by spinal nerves to the hypothalamus. The stimulation causes neurons that make oxytocin to fire action potentials in intermittent bursts; these bursts result in the secretion of pulses of oxytocin from the neurosecretory nerve terminals of the pituitary gland.
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
5-HTP has been shown in scientific studies to promote relaxation and alleviate stress and anxiety. The relaxation and anti-anxiety properties of 5-HTP appear to come from its ability to elevate levels of serotonin. Research has demonstrated that 5-HTP may reduce the risks of panic attacks and symptoms of panic, as well as anxiety and emotional stress. Research also indicates 5-HTP may be effective in helping to alleviate depression.