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High testosterone at this stage will accelerate the process. The SARMs are not testosterone, and don’t get metabolised into DHT (nor estradiol). The SARMs selectively bind to the androgen receptor in muscle and bone and amplify the effect of testosterone and DHT there, while not amplifying the effect on other tissue ie skin, prostate. However, through inheritance, if you have hair androgen receptors that are similar to muscle/bone androgen receptors, then SARMs can amplify the androgen message in the hair follicles, and if the inherited androgen sensitivity is activated, it could lead to accelerated male pattern baldness. This is a very rare variation, and while possible, is uncommon. There are no tests available to determine SARMs effect on your hair follicles, nor to determine when your genetic androgen sensitivity in hair follicles will activate.
Growth hormone-releasing peptides (GHRPs) constitute a group of small synthetic peptides that stimulate the growth hormone secretion and the downstream axis activity. Mounting evidences since the early 1980s delineated unexpected pharmacological cardioprotective and cytoprotective properties for the GHRPs. However, despite intense basic pharmacological research, alternatives to prevent cell and tissue demise before lethal insults have remained as an empty niche in the clinical armamentarium. Here, we have rigorously reviewed the investigational development of GHRPs and their clinical niching perspectives.

As previously explained, multiple GHRP-6 doses are required throughout the day due to the pulsatile nature of the HGH release, and the administration of these doses are typically administered on average 3 times daily spaced evenly apart. More administrations are acceptable for greater effects on physique and performance, but it is advised that approximately 3 hours in between each injection is ensured so as to allow the pituitary gland to restore its storage of HGH. The most common protocol is as follows:

Additionally and not less relevant, GHRP-6 appears as an excellent partner to combine with other molecules (ie, epidermal growth factor [EGF]) because their exclusive actions seem to achieve a kind of synergism, useful to target the multiples nodes of complex pathophysiological processes, and thus to enhance tissue repair processes.56 Garcia del Barco and coworkers in our group have opened unprecedented avenues, by combining GHRP-6 and EGF as a therapeutic approach to ameliorate the damages of multiple sclerosis,57 peripheral axonal pathology,58 and brain ischemia in animal models.59,60 They have demonstrated that in all these experimental substrates the combined action of GHRP-6 and EGF is associated with a better outcome in both clinical and pathological fields.


The delegates' reasons for the final decision to exempt from the proposed Appendix C entries, teeth whitening preparations containing more than18 per cent of carbamide peroxide and more than 6 per cent of hydrogen peroxide manufactured for and supplied solely by registered dental practitioners as part of their dental practice, comprise of the following.
In June 2011, the delegate considered a request to restrict the use of chloramphenicol (Schedule 3) to ophthalmic use for the treatment of bacterial conjunctivitis only. The delegate decided that a more restrictive wording of the Schedule 3 chloramphenicol entry would not result in further benefits concerning its ophthalmic use, therefore the wording of the entry remained unchanged.
Studies have shown that individuals fighting infection have a lower amount of circulating T α 1 and suppressed helper T cell numbers compared to healthy individuals. This is problematic, as optimal immune function is vital to recovery from infection. Supplementation with T α 1 has the potential for great therapeutic benefit for patients suffering from infection or autoimmune disease.
When using any GHRH, it should always be remembered that positive results cannot be achieved overnight. These compounds act steadily over time, and the best results can be achieved slowly, and with a nutritious diet and a proper exercise regime. Also, these peptides are not sex-specific, so they do not have any androgenic effects. They can be used by women in the same dosages that men do.
TGA evaluator concluded that the consistent absence of any clinically meaningful effects on blood pressure (BP) or heart rate (HR) in the applicant's bioavailability studies, and the absence of any ADR reports of BP, HR or other cardiovascular problems, indicate that "there is no valid reason for concern and no need to take any regulatory against the combination products currently in the ARTG and available in the Australian market", i.e. no demonstrated safety risk, and no evidence provided of efficacy of paracetamol 1000 mg / phenylephrine HCl 5 mg adult dose.

The scheduling of paracetamol and caffeine when combined in a compound analgesic as the only two active ingredients was amended from Schedule 4 to Schedule 2 by the NDPSC at its 50th Meeting in June 2007. Evidence reviewed by the Committee at that time conclusively demonstrated that the key ingredient in terms of analgesic overuse and nephropathy was phenacetin and not caffeine. It was agreed that the indications for use, safety profile and potential for misuse met the criteria for a Schedule 2 medicine.
It is both impractical and impossible to categorize GHRP-6 doses into the typical three tiers of users (beginner, intermediate, and advanced) due to the inherent nature of the type of substance and hormone. The saturation doses of GHRP-6 should elicit significant increases in HGH levels in the body in a pulsatile manner that is adequate enough to ensure any performance and physique enhancing goals desired by any individual. The difference in which goals might be more attainable than others is the frequency of dosing. GHRP-6 exhibits a varying half-life of approximately 15 – 60 minutes after injection, and will stimulate a large pulse of HGH from the pituitary gland that will last several hours but is most intense and achieves its peak at approximately 30 minutes. Therefore, in order to simulate higher and steadier blood plasma levels of HGH, it is necessary to administer GHRP-6 doses multiple times daily (depending on the user’s goals).
Thymosin alpha-1 (T α 1) is a peptide, or small protein, consisting of 28 amino acids. T α 1 is produced naturally by the thymus gland. The thymus is located behind the sternum and between the lungs, and is where immune cells known as T cells mature and are released, prompted to do so by the T α 1 peptide. T cell production and action within the body is vital to adaptive immunity—the mode by which immune cells are able to recognize and eradicate foreign invaders.
ADV Research ADV-033 (Ligandrol LGD-4033 SARM Alternative) PRODUCT STRENGTH (CONCENTRATION): 30MG/ML KEY BENEFITS ADV-033 is the best-in-class for bulking Highly anabolic, with “Anabolics-like” results Excellent for re composition Fast recover Protects muscle and prevents wasting Promotes healing and repair Nontoxic, so it doesn’t harm the liver or prostate. Enhances strength, power, and performance GENDER SUITABILITY ADV-033 is suitable for use…
For increasing GH levels, GHRP-6 is less effective in the presence of high blood glucose levels or high somatostatin levels, which result from high IGF-1 levels. For this reason, for best effect GHRP-6 should be taken while blood sugar is relatively low, for example about 30-60 minutes before a meal. GHRP-6 will have reduced effect if GH is being taken by injection, because GH increases IGF-1. Where GH use is limited to no more than about 14 IU per week, simultaneous GHRP-6 use probably still will increase GH somewhat further, but if GH use is greater than this then likely GHRP-6 injections will do little to nothing towards increasing GH levels any further.

Five of the submissions did not support the proposal while the sixth submission did. The former contend that potential risks of inadvertent use of caffeine in those at risk of an adverse event will be increased if selection of an analgesic is made without the assistance or intervention of a healthcare professional. There was also concern that the proposed exemption may result in an increase in liver damage due to excessive consumption of such a product. This was likely to result from people abusing these products as a source of stimulants.
In 2005, we undertook a porcine model of AMI via left circumflex artery occlusion for 1 hour followed by a 72-hour reperfusion period. GHRP-6 rescued ischemic myocardium from death for over 70% of the area at risk (Figure 3), and that in addition to enhance survival signaling pathways/gene expression of the PI-3K, AKT1, and BCL2 pathways, GHRP-6 decreased reactive oxygen species (ROS) spillover, the inflammatory marker CRP, and preserved the antioxidant defenses.45 These antioxidant and anti-inflammatory properties have also been attributed to GHRP-2 when its antiatherogenic potential was examined in ApoE(−/−) mice so that 12/15-lipoxygenase, interferon gamma, and macrophage migration inhibitory factor (MMF) gene expression were accounted. Furthermore, in cultured aortic smooth muscle cells, GHRP-2 prevented the generation of peroxides, the downregulation of IGF-1 receptor, and the commitment of apoptosis.46
If using it with CJC 1295, you can experience a correlation in increased muscle mass levels. With longer release periods, greater results are achievable. So, if you want to gain more muscle mass, or if you simply want to increase levels of lean muscle mass, you are going to realize these possibilities when you incorporate the use of Ipamorelin into your daily regimen.
GHRP mechanism of action. GHRPs are endowed with the ability to bind two different receptors that seem to mediate its cytoprotective and other pharmacological properties (GHS-R1a and CD36). The main biological properties/pharmacological actions of GHRP-6 as cyto- and cardioprotective candidates are summarized as follows: Inotropic: mediated by an elevation of Ca2+ influx via PLC/DAG/PKC, through the voltage-gated calcium channel, triggering Ca2+ release from thapsigargin-sensitive intracellular stores, which translated in a positive inotropic response without a chronotropic effect. Anti-fibrotic: via upregulation of PPARγ, which is followed by a transforming growth factor-beta (TGF-β), CTGF, and platelet-derived growth factor (PDGF) downregulation. Anti-inflammatory: blunts NFκB expression and activation. Cell survival: it involves the phosphatidylinositol 3-kinase/RAC-alpha serine/threonine-protein kinase (PI-3K/AKT1) pathway, as the induction of the hypoxia-inducible factor-1 alpha (HIF-1α). Cardioprotective: as shown, it involves different biological actions that converge to enhance cardiomyocytes survival. Vasodilatory: it seems to involve e-NOS upregulation and endothelin activity reduction. Anabolic: it is mediated by the IGF-1/AKT1 and mTOR pathway activity.

Peptide therapy, or the use of specific peptides in treatment, has gained great popularity in recent years. This is due largely to the fact that these peptides are highly specific (i.e., only do what you want them to do) while also being well-tolerated and safe. As of January 2015, there were over 60 US FDA-approved peptide medications, 140 peptide drugs being evaluated in clinical trials, and 500 in pre-clinical development.
In 2005, we undertook a porcine model of AMI via left circumflex artery occlusion for 1 hour followed by a 72-hour reperfusion period. GHRP-6 rescued ischemic myocardium from death for over 70% of the area at risk (Figure 3), and that in addition to enhance survival signaling pathways/gene expression of the PI-3K, AKT1, and BCL2 pathways, GHRP-6 decreased reactive oxygen species (ROS) spillover, the inflammatory marker CRP, and preserved the antioxidant defenses.45 These antioxidant and anti-inflammatory properties have also been attributed to GHRP-2 when its antiatherogenic potential was examined in ApoE(−/−) mice so that 12/15-lipoxygenase, interferon gamma, and macrophage migration inhibitory factor (MMF) gene expression were accounted. Furthermore, in cultured aortic smooth muscle cells, GHRP-2 prevented the generation of peroxides, the downregulation of IGF-1 receptor, and the commitment of apoptosis.46

The authorities have branded it as a banned substance in the competitive athletics and bodybuilding to prevent the unfair advantage users are likely to gain from this drug. But many athletes and bodybuilders continue to pursue the drug actively. Then there are those people who are ready to try just about anything to lose all of their extra weight. There is always heavy demand for fat cutters and the demand for GHRP-6 is no exception. A majority of the demand groups don't have prescriptions for this drug and are likely to procure this from the black market or the internet. This is where the authorities need to step in.


There is no “one right way”, to use Ipamorelin. For example, if you are using 500 to 1000 mcg doses daily, twice a day, your cycle might run for an 8 week period. If on the other hand, you are an athlete training for a competition, you might be on 3 injections per day, at 300-500 mcg, and will stay on for a 12 week period. For new users, you might find a 300 mcg injection is too high, and you will cut back to 200 mcg until your body gets used to it, for an 8-week cycle.

Consistent with these data, our group observed a transient inotropic effect of about 15 minutes in both healthy and infarcted rabbits following a single GHRP-6 intravenous bolus (400 µg/kg). Echocardiography recordings indicated a 15%–20% elevation of the ejection fraction as an increase in shortening fraction (Juan Valiente Mustelier and Jorge Berlanga Acosta, unpublished observations, 2007). More recent studies based on isolated murine hearts that underwent periods of ischemia and reperfusion (I/R) confirm that pre- or posttreatments with hexarelin for instance prevented the intracellular disturbances in Ca+2 transients through recovery of p-PLB after the I/R insult.43 Other studies involving adult Wistar rat ventricular myocytes have confirmed the positive inotropic response induced by hexarelin and other secretagogue peptides that bind the GHS-R1a, which activates protein kinase C signaling cascade.44

From the standpoint of protein synthesis and muscle repair, IGF-1 injections have also been shown to enhance the anticatabolic effects of insulin and to increase the protein synthesis normally induced by growth hormone. This is because, like insulin, IGF-1 encourages amino acid uptake into muscle cells, stimulates peripheral tissue uptake of glucose (which lowers blood glucose levels), and suppresses liver glucose production. That last fact is important and is actually why IGF-1 is even being considered as a diabetes-prevention drug. Insulin resistance can cause the liver to produce excess glucose, which then causes even more insulin insensitivity and can eventually result in type II diabetes, and IGF-1 can decrease the need for this type excessive insulin release.

In 1984, a synthetic hexapeptide, His-d-Trp-Ala-Trp-d-Phe-Lys-NH2 (GHRP-6), was identified by Bowers and colleagues. This hexapeptide was shown to potently stimulate GH release in vitro and in vivo by an unknown mechanism. Because of its poor oral bioavailability (0.3%) and short half-life (20 min) in human serum, GHRP-6 was selected only as a structural model to design a nonpeptide mimetic. Based on the structure–activity relationships (SARs) of GHRP-6, the nonpeptidyl growth hormone secretagogue (GHS) L-692,429 was identified by Smith et al. in 1993. This nonpeptidyl GHS synergizes with GHRP-6 to stimulate GH release and cAMP production, accompanied by a significant increase in intracellular calcium concentration ([Ca2 +]i), indicating that this nonpeptidyl GHS acts through a distinct signal transduction pathway. In 1995, a potent oral GHS L-163,191 (MK-0677) was reported by Patchett et al. This agent was found to have excellent oral bioavailability and specificity in its release of GH, without significant effect on plasma levels of other hormones such as aldosterone, luteinizing hormone, thyroxine, and prolactin.
It has been previously explained that some individuals will elect to administer GHRP-6 doses twice daily, and some more than three times daily. Twice daily administration of at least 100mcg (typically upon awaking and before sleeping) will yield anti-aging and general health benefits. 3 times daily administration should yield general health benefits, fat loss, and muscle gain. 4 times daily or greater administration should provide more pronounced muscle gains and fat loss.

ADV Research ADV-17 Post Cycle Therapy PRODUCT STRENGTH (CONCENTRATION): 30MG/ML KEY BENEFITS Raises testosterone levels Lowers estrogen levels Raises luteinizing hormone (LH) levels Lowers cortisol levels Enhances recovery speed Promotes vascularity (hardening and drying out) Increases libido Inhibits gynecomastia (male breast enlargement) Promotes fat loss Not liver toxic GENDER SUITABILITY ADV-17 is suitable for use by males. Females should not…
Abbreviations: AKT1, RAC-alpha serine/threonine-protein kinase; AMI, acute myocardial infarction; CTGF, connective tissue growth factor; DCM, dilated cardiomyopathy; dP/dt, the rate of left ventricle maximal pressure rise in early systole; DX, doxorubicin; ECM, extracellular matrix; EGF, epidermal growth factor; ERK1/2, extracellular signal-regulated kinase 1/2; GH, growth hormone; GHRH, growth hormone-releasing hormone; GHRPs, growth hormone-releasing peptides; GHS, growth hormone secretagogues; GHS-R, growth hormone secretagogue receptor; GHS-R1a, growth hormone secretagogue receptor type 1a; HIF-1α, hypoxia-inducible factor-1 alpha; I/R, ischemia and reperfusion; IGF-1, insulin-like growth factor-1; IL-1β, interleukin-1 beta; IL-6, interleukin 6; LPS, lipopolysaccharide; LV, left ventricle; LVEF, left ventricular ejection fraction; MBP, mean blood pressure; MIF, macrophage migration inhibitory factor; MCP-1, monocyte chemoattractant protein-1; MMP, matrix metalloproteinase; MOD, Multiple Organs Damage; NEP, nitrosylation end products; NIH, National Institute of Health; PDGF, platelet-derived growth factor; PGC1α, peroxisome proliferator-activated receptor gamma coactivator 1 alpha; PI-3K, phosphatidylinositol-4,5-bisphosphate 3-kinase; PPARγ, peroxisome proliferator-activated receptor gamma; RAS, rennin–angiotensin system; rhGH, recombinant human growth hormone; ROS, reactive oxygen species; TGF-β, transforming growth factor beta; TIMP, tissue inhibitor of metalloproteinase; TNF-α, tumor necrosis factor alpha.
As a athlete, incorporating a growth hormone-like Ipamorelin is extremely beneficial. Not only in the development of lean muscle tissue and muscle mass, but also in the decreased recovery time you are going to experience after each workout. You can workout more, you can workout and lift harder, and you can increase your level of exertion at the gym to experience the greatest gains, as your body is going to heal much faster than it would without the growth hormone.
This peptide is a modified fragment of hGH which contains the portion of the molecule that is believed to be responsible for hGH’s anti-obesity effects. The peptide has been shown to increase fat burning without the increase in blood sugar and growth rate that has been seen with hGH itself. AOD 9604 has been deemed safe for chronic use by the FDA, receiving Human GRAS status in 2014. In addition to its utility as an anti-obesity peptide, AOD 9604 has been shown to have very favorable cartilage repair and regenerative properties, especially when paired with peptide BPC 157.
The mechanisms supporting the GHRP-6-mediated HTS prevention may be related to a potential modulation of the fibrogenic response, especially by TGF-β1 transcriptional deactivation and its downstream effector CTGF, as has been previously described [30]. Nevertheless, we have not elucidated the pathways involved in the GHRP-6-mediated TGFB1 gene expression reduction. Under these circumstances, we have reproducibly observed [7] that GHRP-6 increases PPARG expression which may have counteracted TGF-β1-associated fibrogenic input. The fact that CD36 occupation by GHRP-6 upregulates PPARG gene expression is noteworthy in this context and represents an additional pharmacologic property for this peptide. Although the molecular pathways underlying the antifibrotic effects of PPARγ remain elusive, an antagonistic relationship is proposed between PPARγ and TGF-β1 signaling in fibrosis. For more than a decade ago, PPARγ has been reputed as a fibrosis-response regulating factor and its activation represents an innovative pathway to control fibrotic diseases [31, 32].
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 a substance; b) the purposes for which a substance is to be used and the extent of use of a substance; c) the toxicity of a substance; d) the dosage, formulation, labelling, packaging and presentation of a substance; e) the potential for abuse of a substance; f) any other matters that the Secretary considers necessary to protect the public health.
Application would result in all current OTC paracetamol/ phenylephrine products being up-scheduled to S3. Applicant’s justification for changing current combination products from exempt or S2 to S3 is on theoretical basis only, and no evidence provided of clinical risk. Pharmacokinetic study found that co-administration of paracetamol with phenylephrine increased plasma phenylephrine levels – applicant says this has potential for cardiac safety risk in susceptible patients.
Superior SARMS products are manufactured to be a safe and effective steroid and peptide alternative. Unlike androgenic drugs such as traditional anabolic steroids, Superior SARMS are  much more selective in their action as they directly target androgen receptors in muscle, bone, body fat and connective tissues in the body.  Our products increase the metabolic rate within the body without disturbing its natural hormones, which in turn greatly assist in achieving maximum results such as lean muscle gain and enhanced muscle recovery along with the added benefits of anti-aging effects, further with regenerating overall connective tissue and repair. All Superior SARMS products are also orally administered with no intravenous injections. It must be noted that Superior SARMS are for “Research Purposes Only”.
The most important initial historical time points in the development of the enlarging ghrelin system were 1973, 1976, 1982, 1984, 1990, 1996, 1998, and 1999 during which the following sequentially occurred: isolation of somatostatin; discovery of unnatural growth-hormone-releasing peptides (GHRPs); isolation of growth-hormone-releasing hormone (GHRH); hypothesis of a new natural GHRP different from GHRH; GHRP+GHRH synergism in humans; discovery of the growth hormone secretagogue GHS/GHRP receptor; cloning of the receptor; isolation; and identification of the new natural endogenous GHRP ghrelin.1

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Experimental studies in 1997 proved that hexarelin could reverse the cardiac dysfunction in GH-deficient animals immunized by the administration of an anti-GHRH serum. Ex vivo and in vivo systems converged to document that hexarelin progressively and globally improved LV function even under postischemic scenarios. These experiments showed that the synthetic secretagogue protective activity was independent from any further stimulation derived from the somatotropic function.26 In 1998, this group demonstrated that hexarelin protected against postischemic ventricular dysfunction in senescent hearts of aged male rats. Both ex vivo and in vivo, GHRPs offered a striking heart protection against reperfusion stunning, improved ventricular pressures and volumes, and reduced CK concentration in perfusate. Again, they sustained the concept that the protection afforded by the peptide is likely due to a direct cardiotropic action that appeared far greater than that induced by GH administration in a concurrent control group.27 A more defining protocol was assumed in 1999 as the study included hypophysectomized rats, to ascertain whether hexarelin had non-GH-mediated protective effects on the heart. The authors showed that hexarelin attenuated the ischemia/reperfusion damage and prevented elevation of LV end-diastolic pressure, coronary perfusion pressure, reactivity of the coronary vasculature to angiotensin II, and the release of creatine kinase in hypophysectomized animals.28 These three experiments were pivotal to define GHRP intrinsic cardioprotective ability.
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