Thymosin beta-4 is a naturally occurring peptide, and is found ubiquitously in our cells. A range of studies on animal models have indicated several key biological activities for Tβ4, such as “promot[ing] wound repair, tissue protection, and regeneration in the skin, eye, heart and central nervous system”. Only a handful of clinical trials in humans have attempted to explore these roles practically.
Hey Adrian, thanks for reaching out. Firstly, I am not a doctor and nothing I say should be taken as medical advice. For something like this I suggest you book a consult at
Kim found that when Americans who carry a particular version of the OXTR gene are more likely to turn to their friends for support when they are distressed. But Koreans react to social stress in a different way – for them, it’s less socially acceptable to turn to friends for support during tough times. And distressed Koreans who carry the same version of OXTR are less likely to seek support from their friends.
I had tennis elbow on both arms for over 3 years now. Had one surgery on the R, countless PRPs, and a stem cell treatment on both but still to no avail. Pain on the L never eased up and I just had my 3rd PRP booster injections yesterday after having my stem cells 2 months ago. So can you tell me if BPC 157 or TB 500 better suits my situation. Many thanks!
Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity worldwide. No effective pharmacological treatments are available for TBI because all Phase II/III TBI clinical trials have failed. This highlights a compelling need to develop effective treatments for TBI. Endogenous neurorestoration occurs in the brain after TBI, including angiogenesis, neurogenesis, synaptogenesis, oligodendrogenesis and axonal remodeling, which may be associated with spontaneous functional recovery after TBI. However, the endogenous neurorestoration following TBI is limited. Treatments amplifying these neurorestorative processes may promote functional recovery after TBI. Thymosin beta4 (Tβ4) is the major G-actin-sequestering molecule in eukaryotic cells. In addition, Tβ4 has other properties including anti-apoptosis and anti-inflammation, promotion of angiogenesis, wound healing, stem/progenitor cell differentiation, and cell migration and survival, which provide the scientific foundation for the corneal, dermal, and cardiac wound repair multicenter clinical trials. Here, we describe Tβ4 as a neuroprotective and neurorestorative candidate for treatment of TBI.
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]
There is also a positive feedback involved in the milk-ejection reflex. When a baby sucks at the breast of its mother, the stimulation leads to oxytocin secretion into the blood, which then causes milk to be let down into the breast. Oxytocin is also released into the brain to help stimulate further oxytocin secretion. These processes are self-limiting; production of the hormone is stopped after the baby is delivered or when the baby stops feeding.
The peripheral actions of oxytocin mainly reflect secretion from the pituitary gland. The behavioral effects of oxytocin are thought to reflect release from centrally projecting oxytocin neurons, different from those that project to the pituitary gland, or that are collaterals from them.[31] Oxytocin receptors are expressed by neurons in many parts of the brain and spinal cord, including the amygdala, ventromedial hypothalamus, septum, nucleus accumbens, and brainstem.[citation needed]
MAPKs and NF-κB played pivotal roles in the development of osteoclasts downstream of RANK signaling [54]. In this study, we demonstrated that Tβ4 activation by Tβ4 peptide inhibited RANKL-induced p38, ERK, JNK MAPK, and NF-κB signaling pathways. These results suggested that Tβ4 activation might inhibit osteoclast differentiation via inhibition of the signaling cascades MAPK/NF-κB/NFATc1.
But long before that, say researchers, oxytocin could use a rebranding. “It doesn't induce love; it doesn't induce massive amounts of trust,” Guastella says. “The problem we've got ourselves into is that we're trying to look for a simple answer: either oxytocin does or does not work in a patient population, or it does or does not enhance a certain social process.”
But what about the three-month warning? Dr Rush, while an advocate for the supplement, sees it as a short-term solution, and not something to rely on long-term, for good reason. "Technically taking 5-HTP alone can deplete important brain chemicals such as dopamine and adrenaline. While 5-HTP is aimed at increasing the amount of serotonin in the body, dopamine and adrenaline are also important for positive mental health states. In order to prevent the depletion of important brain chemicals, taking 5-HTP would need to be balanced with amino acids that support the production of dopamine and adrenaline." That's L-Tyrosine, which you eat in soy, chicken and beef, and can also be found in health food shops as a supplement.
TB-500 is a synthetic version of the naturally occurring peptide present in virtually all human and animal cells, Thymosin Beta-4. This potent peptide is a member of a ubiquitous family of 16 related molecules with a high conservation of sequence and localization in most tissues and circulating cells in the body. TB-500 not only binds to actin, but also blocks actin polymerization and is the actin-sequestering molecule in eukaryotic cells.
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].

An estimated 1.4 million people sustain traumatic brain injury (TBI) each year in the United States, and more than 5 million people are coping with disabilities from TBI at an annual cost of more than $56 billion.1 There are no commercially-available pharmacological treatment options available for TBI because all clinical trial strategies have failed.2,3 The disappointing clinical trial results may be due to variability in treatment approaches and heterogeneity of the population of TBI patients.4-9 Another important aspect is that most clinical trial strategies have used drugs that target a single pathophysiological mechanism, although many mechanisms are involved in secondary injury after TBI.4 Neuroprotection approaches have historically been dominated by targeting neuron-based injury mechanisms as the primary or even exclusive focus of the neuroprotective strategy.3 In the vast majority of preclinical studies, the treatment compounds are administered early and, frequently, even before TBI.10,11 Clinically, the administration of a compound early may be problematic because of the difficulty in obtaining informed consent.12
5-HTP increases a brain chemical called serotonin. Some medications for depression also increase serotonin. Taking 5-HTP along with these medications for depression might increase serotonin too much and cause serious side effects including heart problems, shivering, and anxiety. Do not take 5-HTP if you are taking medications for depression.

Some of these medications for depression include fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft), amitriptyline (Elavil), clomipramine (Anafranil), imipramine (Tofranil), and others.