In December 2010, the delegate made a delegate only decision to include afamelanotide (also known as melanotan I) with a cross-reference to melanocyte stimulating hormone (MSH) for inclusion into the current Poisons Standard. It was noted that afamelanotide should not be confused with a similar substance commonly known as Melanotan-II, which is a cyclic lactam synthetic analogue of α-MSH. It was noted that melanotan-II was under investigation for treating sexual dysfunction, although this has been abandoned due to side effects associated with the immune and cardiovascular systems. Its metabolite, bremelanotide, is under investigation for treating haemorrhagic shock.
Surgery: 5-HTP can affect a brain chemical called serotonin. Some drugs administered during surgery can also affect serotonin. Taking 5-HTP before surgery might cause too much serotonin in the brain and can result in serious side effects including heart problems, shivering, and anxiety. Tell patients to stop taking 5-HTP at least 2 weeks before surgery.

Melanotan II tanning injections have received media attention over the past few years and have been dubbed the "barbie drug" by XXXXXX. The XXXXXX website states that all products are manufactured and compounded in pharmacies in Australia and, pending the satisfactory completion of a short medical assessment, will express post products to a nominated shipping address. The XXXXXX website also states that melanotan II is defined as a 'more potent peptide' when compared to melanotan I, offering a greater density in peptide chain with noticeable results in a shorter timeframe. There are also claims of enhancing male libido, sexual performance, curing erectile dysfunction and as an appetite suppressant.


Reconstituting tanning peptide is a part of the process required for use of the product and will require full attention to get proper results. 1 or 2ml sterile water is usually used, diluting with more water will improve dosing accuracy. Lovemelanotan peptide calculator is ideal tool for anyone just starting out and not sure how to reconstitute or dose the product properly.

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.
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.
Delayed Tβ4 treatment increases vascular density in the injured cortex, ipsilateral dentate gyrus, and CA3 region 35 days after TBI. Arrows show vWF-stained vascular structure. TBI alone (B) significantly increases the vascular density in the injured cortex compared to sham controls (A, P < 0.05). Tβ4 treatment (C) further enhances angiogenesis after TBI compared to the saline-treated groups (P < 0.05). The density of vWF-stained vasculature in different regions is shown in (D). Scale bar = 25 μm (C). Data represent mean + SD. *P < 0.05 vs Sham group. #P < 0.05 vs Saline group. N (rats/group) = 6 (Sham); 9 (Saline); and 10 (Tβ4).
The reality is that people are always going to self-medicate. Boots, Amazon and H&B all sell 5-HTP, and in theory you could keep buying it and taking it for as long as you like. But it's important to know the facts. It shouldn't be used in conjunction with an SSRI, for example. In that situation, if the body is preventing serotonin breakdown while also getting extra serotonin, which leads to seriously unhealthy levels of serotonin activity.
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.
Thymosin is a hormone secreted from the thymus. Its primary function is to stimulate the production of T cells, which are an important part of the immune system. Thymosin also assists in the development of B cells to plasma cells to produce antibodies. The predominant form of thymosin, thymosin b4, is a member of a highly conserved family of actin monomer-sequestering proteins. b-thymosins are the primary regulators of unpolymerized actin, and are essential for maintaining the small cytoplasmic pool of free G-actin monomers required for rapid filament elongation and allowing for the flux of monomers between the thymosin-bound pool and F-actin.
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.
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]

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]

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”.
In 2015 I found my self bed ridden for 8 weeks with an issue all the doctors I had been to we’re unable to diagnose. I discovered, after much research, that what I was suffering from was damaged facia in my left and right gluteus muscles, which left me unable to do anything. I was in excruciating pain and couldn’t do anything except lay in bed on my back. Then my husband found TB 500. Initially I was against using it but after deteriorating to the point of being bed ridden I broke down and ordered some. As soon as I received it my husband injected me in the gluteus muscle. Within 30 minutes I started getting relief from the TB-500, within 8 weeks I was out of bed and the pain was gone! It healed the damaged fascia covering the gluteus. If I had not done this I don’t know where I would be today. For me, TB-500 was a life saver and if I had to I would use it again. I have suffered no side affects then or now.
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.

As shown in Figure 1, thymic hormones also modulate the production of hypothalamus pituitary hormones and neuropeptides. Initial experiments revealed that neonatal thymectomy promotes a decrease in the number of secretory granules in acidophic cells of the adenopituitary [44]. In the same vein, athymic nude mice display low levels of various pituitary hormones, such as PRL, GH, LH and FSH [45]. With regard to thymic peptides, thymosin beta-4, when perfused intraventricularly, stimulates LH and LHRH secretion [46]. Similar results were obtained with another thymic peptide, thymulin, in perfused or fragmented pituitary preparations [47]. The administration of thymopoietin (another chemically-defined thymic hormone) in children with Hodgkin’s disease increased GH and cortisol serum levels [48]. Moreover, thymopentin (the synthetic biologically active peptide of thymopoietin) enhances in vitro the production of ACTH and beta-endorphin [49]. In addition, thymulin exhibits an in vitro stimulatory effect on perfused rat pituitaries, enhancing PRL, GH, TSH and LH release [50]. Using short-term cultures of pituitary fragments, an increase in ACTH secretion occurs after in vitro thymulin addition, with no changes in GH levels and significant reductions in PRL release [47]. A further thymosin peptide was recently isolated with the task in stimulating IL-6 release from rat glioma cells [51]. By contrast, thymosin alpha-1 is apparently able to down regulate TSH, ACTH and PRL secretion in vivo with no modifications on GH levels [52]. These inhibitory effects seem to occur through hypothalamic pathways. Indeed, the production of the corresponding releasing hormones by hypothalamic neurones decreased after in vitro addition of thymosin alpha-1 in medial basal hypothalamic fragments [52].

Tβ4 is not a thymus-specific peptide but also present in most tissue and all cells except red blood cells [35]. High amounts of Tβ4 were detected in human white blood cells, especially in neutrophils and in macrophages [34], expressed in developing mandible (embryonic day 12) [36] and hair follicles (HF) of mice [37]. In addition, the peptide is also detected outside cells, in blood plasma and in wound and blister fluids [34]. Although the mechanism(s) of action of exogenous Tβ4 on anti-inflammatory effects remains unclear, the high levels of Tβ4 present in human wound fluid (13 μg/mL) suggest its importance in wound healing or anti-inflammation [38]. However, the level of Tβ4 is variable (unchanged, decreased, and increased) in GCF or biopsied gingival tissue of periodontal patients [20, 21]. Based on the observations that Tβ4 has anti-inflammatory effects [11–14], the hypothesis is that Tβ4 regulates inflammatory mediators and osteoclastogenesis in osteolytic bone disease, such as periodontitis.
“Ultimately you’re body is going to down-regulate the enzymes needed to convert the tyrosine/l-phenylalanine into dopamine and norepinephrine; this also counts for 5 -htp being converted into serotonin. As far as I’m aware when simply supplementing amino acids to improve neurotransmitter prevalence in the brain, tolerance will build very rapidly within a one week to two week period (from personal experience). Not saying it’s not viable to help out with mood when used sparingly, just saying there’s most likely better ways for continued treatment.”
Letdown reflex in lactating (breastfeeding) mothers, oxytocin acts at the mammary glands, causing milk to be 'let down' into a collecting chamber, from where it can be extracted by sucking at the nipple. Sucking 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.
Thymosins were discovered in the mid 1960’s, when Allan Goldstein from the Laboratory of Abraham White at the Albert Einstein College of Medicine in New York studied the role of the thymus in development of the vertebrate immune system. Since then, Dr. Goldstein founded a company that creates thymosin alpha 1 for the purpose of increasing immune cell activity, and thymosin beta 4 (TB-500) to promote wound repair and healing.
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.
Good quality Griffonia Simplicifonia, however the pouch is a very inconvenient packaging choice! Why not use the small 25-50gm pill bottle type? I used to be a quality controller in food additives and it would be so perfect to take doses from and fairly cheap and easy to source. I can understand if this is a new product for your line however but you should invest in this for 5htp alone perhaps. Thank you though will be ordering more down the track!
RegeneRX Biopharmaceuticals is focusing on the commercialization of Tb4 “For the treatment of injured tissue and non-healing wounds, to enable more rapid repair and/or tissue regeneration.” Especially needy are diabetics who suffer from poor blood circulation and loss of sensation of pain that keeps their wounds unnoticed and unattended for days, leading to ulcers that may not heal. Other hard healing wounds are pressure ulcers in patients who are bed ridden and often receive skin grafts as treatment, or reconstructive surgery.
All of this becomes heavily ironic when you consider that the chemical in question – a hormone called oxytocin – is often billed as the “hormone of love”, and even marketed as “Liquid Trust”. As a new study shows, the reality is much more complicated. Describing oxytocin as the “hormone of love” is like describing a computer as a “writing tool” – it does other things too, some of which aren’t pleasant.

The matters under subsection 52E (1) of the Therapeutic Goods Act 1989 considered relevant by the delegate included: (a) the risks and benefits of the use of the substance; (b) the purposes for which a substance is to be used and the extent of use of a substance; (c) the toxicity of the substance; (d) the dosage, formulation, labelling, packaging and presentation of a substance; (e) the potential for abuse of a substance; and (f) any other matters that the Secretary considers necessary to protect public health.
While all of the effects described above certainly occur in response to oxytocin, doubt has recently been cast on its necessity in parturition and maternal behavior. Mice that are unable to secrete oxytocin due to targeted disruptions of the oxytocin gene will mate, deliver their pups without apparent difficulty and display normal maternal behavior. However, they do show deficits in milk ejection and have subtle derangements in social behavior. It may be best to view oxytocin as a major facilitator of parturition and maternal behavior rather than a necessary component of these processes.
It is highly important to understand that MT2 itself does not protect skin from burning, tan protects your skin. Until some base tan is developed users should still take care not to over-expose skin to uv rays. Starting only with the amount of exposure that the user's skin can handle without burning. It should not take long before the user can handle longer exposures to strong sunlight without adverse effects.
Oxytocin and vasopressin are the only known hormones released by the human posterior pituitary gland to act at a distance. However, oxytocin neurons make other peptides, including corticotropin-releasing hormone (CRH) and dynorphin, for example, that act locally. The magnocellular neurons that make oxytocin are adjacent to magnocellular neurons that make vasopressin, and are similar in many respects.
Froemke's study1, published in April, showed that oxytocin temporarily suppresses inhibitory neurons — those that dampen neural activity — which allows excitatory cells to respond more strongly and reliably. “Our hypothesis is that the virgin brain is a blanket of inhibition, and that pairing the pup calls with oxytocin allows the network to be reconfigured,” says Froemke. The hormone may serve to amplify incoming signals and allow them to be recognized as behaviourally important. (It is at least possible, he says, that this same mechanism could explain why some human mothers feel they are uniquely tuned to a baby's cries.)
You can browse Drugs A-Z for a specific prescription or over-the-counter drug or look up drugs based on your specific condition. This information is for educational purposes only, and not meant to provide medical advice, treatment, or diagnosis. Remember to always consult your physician or health care provider before starting, stopping, or altering a treatment or health care regimen.

Stimulation of uterine smooth muscle contraction at birth: At the end of gestation, the uterus must contract vigorously and for a prolonged period of time in order to deliver the fetus. During the later stages of gestation, there is an increase in abundance of oxytocin receptors on uterine smooth muscle cells, which is associated with increased "irritability" of the uterus (and sometimes the mother as well). Oxytocin is released during labor when the fetus stimulates the cervix and vagina, and it enhances contraction of uterine smooth muscle to facilitate parturition or birth.
The pore-forming subunit of the cardiac sodium channel Nav1.5 encoded by SCN5A is a critical determinant of myocardial excitability and conduction. Loss-of-function mutations in SCN5A can clinically manifest as progressive cardiac conduction disorders or as arrhythmic syndromes, such as Brugada syndrome. In addition to electrophysiological dysfunction, SCN5A mutations are also associated with myocardial fibrosis manifesting as global cardiomyopathy. In a 10-year old child exhibiting Brugada syndrome, the mutation SCN5AE555X was discovered. Therefore, cardiac sodium channelopathy pig models were generated by homologous recombination in the genetic background of outbred Yucatan minipigs via SCNT exhibiting the orthologous porcine heterozygous mutation SCN5AE558X. The heterozygous mutant animals were viable and fertile, and showed no sudden death over a 2-year monitoring period. They showed reduced SCN5A protein expression, which resulted in diminished total sodium conductance. The heterozygous mutant hearts showed slowed conduction and increased susceptibility for ventricular arrhythmias in the absence of structural defects of the myocardium or specialized conduction system. In total, a novel animal model was established for understanding the mechanisms linking sodium channel dysfunction to cardiac pathophysiology (Park et al., 2015b).
Evidence accumulated over the past decades has overturned the traditional dogma that the adult mammalian brain cannot generate new neurons. Adult neurogenesis has been identified in all vertebrate species examined thus far including humans.44-49 Newly generated neuronal cells originate from neural stem cells in the adult brain. Neural stem cells are the self-renewing, multipotent cells that generate the neuronal and glial cells of the nervous system.50 The major function of neurogenesis in adult brain seems to replace the neurons that die regularly in certain brain areas. Granule neurons in the DG continuously die and the progenitors in the subgranular zone of the DG may proliferate at the same rate as mature neuronal death to maintain a constant DG cell number.51 Similarly, the newly proliferated cells from the subventricular zone migrate and replenish the dead olfactory bulb neurons.52 Here, we focus on DG neurogenesis which is important for spatial learning and memory. In normal adult rats, newborn neural cells migrate from the subgranular zone of the DG of the hippocampus into the granule cell layer and eventually become mature granule neurons.53 These new granule neurons extend axonal processes to their postsynaptic targets54-57 and receive synaptic input.58 TBI stimulates widespread cellular proliferation in rats and results in focal neurogenesis in the DG of the hippocampus.59,60 Some of the newly generated granule neurons integrate into the hippocampus. The integration of the injury-induced neurogenic population into the existing hippocampal circuitry coincides with the time point when cognitive recovery is observed in injured animals.44

The first study to show that Tβ4-promoted tissue repair was a dermal study performed in rats (Malinda et al., 1999). It had previously been found to promote angiogenesis and was reported to be high in platelets (Grant et al., 1995; Hannappel & van Kampen, 1987; Malinda, Goldstein, & Kleinman, 1997; Philp, Huff, Gho, Hannappel, & Kleinman, 2003). Since platelets are the first cells to enter a wound, it was clear that Tβ4 should be tested in dermal wounds in an animal model (Malinda et al., 1997, 1999; Philp, Badamchian, et al., 2003). In the first dermal study using 8 mm full-thickness punch wounds in rats, Tβ4 at 5 μg/50 μL of phosphate-buffered saline was found to accelerate wound closure, increase angiogenesis, and accelerate collagen deposition (Malinda et al., 1999). Tβ4 was only applied at the time of injury and at 48 h since after that the crust had formed. Visible macroscopic improvement was seen in the treated group by day 4. The study also found that Tβ4 promoted keratinocyte migration in vitro with activity in the picogram range. The findings were confirmed in various additional animal models (Table 1) and led to the clinical trials for hard to heal wound in patients as detailed in Table 2.

Increasing trust and reducing fear. In a risky investment game, experimental subjects given nasally administered oxytocin displayed "the highest level of trust" twice as often as the control group. Subjects who were told that they were interacting with a computer showed no such reaction, leading to the conclusion that oxytocin was not merely affecting risk-aversion.[18] Nasally administered oxytocin has also been reported to reduce fear, possibly by inhibiting the amygdala (which is thought to be responsible for fear responses).[19] There is no conclusive evidence for access of oxytocin to the brain through intranasal administration, however.
Cells on the surface of the skin are constantly being replaced by regeneration from below. The repair of a wound is a scaling up of this normal process, with additional complex interactions among cells, formation of new blood vessels, collagen, more extensive cell division and cell migration, as well as strict control of inflammatory cells and the cytokines they release to resolve the inflammation.
Friedman, J., Roze, E., Abdenur, J. E., Chang, R., Gasperini, S., Saletti, V., Wali, G. M., Eiroa, H., Neville, B., Felice, A., Parascandalo, R., Zafeiriou, D. I., Arrabal-Fernandez, L., Dill, P., Eichler, F. S., Echenne, B., Gutierrez-Solana, L. G., Hoffmann, G. F., Hyland, K., Kusmierska, K., Tijssen, M. A., Lutz, T., Mazzuca, M., Penzien, J., Poll-The BT, Sykut-Cegielska, J., Szymanska, K., Thony, B., and Blau, N. Sepiapterin reductase deficiency: a treatable mimic of cerebral palsy. Ann Neurol. 2012;71(4):520-530. View abstract.
×