DAC CJC 1295

DAC CJC 1295



DAC conjugated CJC 1295 (Receptor Grade) is an hGH secretogue that is unique by way of an additional lysine molecule that is added to facilitate the DAC complex. This conjugation makes for a much longer half-life. DAC CJC 1295 tends to have a very limited availability everywhere due to expense and difficulty to manufacture. CJC 1295 DAC is a exceptionally designed peptide and is known for being the finest of the hGH secretogues. Receptor grade: 98%+ pure 2000mcg / 2ml glass vial. THIS PRODUCT IS INTENDED FOR RESEARCH PURPOSES ONLY. CAN BE HARMFUL IF USED INAPPROPRIATELY.

In the healthy human body, large amounts of growth hormone are stored in the pituitary. The cells within the pituitary release growth hormone in response to signaling by GHRH (Growth Hormone Releasing Hormone), Ghrelin (of which GHRPs - Growth Hormone Releasing Peptides - are mimetics), and are inhibited from releasing these stores by Somatostatin. GHRH and Ghrelin act on different populations of somatotropes (GH releasing cells). GHRP/Ghrelin increases the number of somatotropes releasing GH but not the amount released by each cell;
GHRH affects both the number of secreting cells and - moreso - the amount they each secrete. [1] GHRH and Ghrelin are released in specific patterns that vary depending on event and environment: post-exercise, in response to slow wave sleep, in certain stages of life and physical development, and so on.

Most people (even the diseased) continue to possess the ability to make GH in the pituitary. The problem is in the signaling of the pituitary to release it (and make more). So yes CJC is meant to replace the external administration of GH in some (but not all) cases. Even most people with diseases that affect growth hormone secretion retain the ability to continue to make GH in their pituitaries. The disease states and symptoms result, most typically, in altered (dysfunctional) GH release signaling and this also affects the ability of the pituitary to continue to make more GH. [2]

GHRH, which has a forty-four amino acid long chain (and a specific shape - thus making it a peptide as well as a hormone), has been marketed for the longest as Sermorelin. However, Sermorelin has been demonstrated to be degraded rapidly in the body and is cost-inefficient. But because most patients in need of GH therapy doretain the ability to produce and secrete their own GH, treatment with a GHRH-type analog remained hypothetically preferable to exogenous GH treatment. GH itself when administered exogenously results not only in "unnatural" release patterns, it results universally in down regulation of endogenous GH production - as do many hormones when applied exogenously. [2]

Sermorelin's limitations naturally resulted in a variety of formulations of GHRH analogs for therapeutic. The most effective (in terms of minimal degradation in the body - which is different from half-life) analogs with the longest half-lives were those created with an attached 3-maleimidopropionic acid (MPA) unit, which results in binding to albumin after exogenous injection into blood plasma.
The research chemicals CJC-1293 and CJC-1295 are GHRH (the 44-amino acid long version) with 15 aminos removed, thus a total of 29 amino acids, and bound to MPA. [2] MPA is also called Drug Affinity Complex, and CJC-1295 is often referred to as GHRH with Drug Affinity Complex (DAC).

Based on measured GH release in rats over a two hour period, CJC-1295 released twice as much GH as CJC-1293, thus rendering it preferable based on immediate effectiveness; however, CJC-1293 has a 9% edge in stability (meaning less degradation) with in vitro stability tests.
CJC-1293, over a two-hour period, results in a rise-fall-rise-fall type pattern whereas CJC-1295 results in more of an inverted-U shape with a more gentle and longer peak. [2]

In a CJC-1295 pulsatility study performed on normal non-GH deficient people reported plasma levels were between 1 and 2 ng/ml or 1000-2000ng/L one week after injection of between 60 or 90 mcg/kg of CJC-1295. In a 100kg man that is a 6mg or 9mg per week dose.

"Knockout rats" are mice with genetically removed M3 muscarinic acetylcholine receptors. The scientists conducting the study [4] inhibited these genes and the mice became dwarves.. Those mice, labeled Br-M3-KO mice experienced short stature and a shrunken pituitary. Scientists treated Br-M3-KO mice and normal control mice with CJC-1295 for eight weeks, resulting in complete growth restoration in the knockout mice as well as - notably - a restored pituitary size. More specific data regarding CJC-1295 can be extrapolated by examining some of the control mice, which were not "knockout rats" but still received CJC-1295. The controls, male and female, experienced both accelerated & increased overall growth over the non-CJC-1295-dosed controls. Referring back to the notable finding that pituitary size was restored in knockout specimens dosed with CJC-1295, it is equally notable that the controls who did receive CJC-1295 did not have any pituitary hyperplasia or growth of the pituitary whatsoever. This supports the conclusion that CJC-1295 is a substantially less risky treatment for non-diseased subjects, and a substantially more beneficial therapy for subjects with pituitary disease, than conventional (synthetic) GH treatment. [4]

In conclusion, CJC-1295 is an exciting treatment from the standpoint of cost efficiency, safety, and ease of administration when compared with regular GHRH or synthetic Growth Hormone treatment. It has been demonstrated to be as effective as GH for most uses, and vastly preferable for safety reasons where feasible. GH will not be fully supplanted by GHRH analogs such as CJC-1295 for reasons alluded to above, but the vast majority of treatments in the types of applications mentioned in this article will probably begin to use CJC-1295 for safety, cost-efficiency, and the need to administer only one or two times per week instead of multiple times per day



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Raloxifen

Raloxifen


Raloxifen belongs to the class of compounds known as SERMs or selective estrogen receptor modulators. SERMs decrease activity of estrogen and are therefore considered an “anti-estrogen” treatment. However, SERMs do not act by decreasing serum estrogen or aromatase-mediated conversion, but rather through a blocking activity at the estrogen receptor on a cellular level. In other words, raloxifen and its metabolites are active at the estrogen receptor but not as an estrogen-like stimulus (agonist). Instead, they prevent estrogen from exerting its effects at the cellular level. This (as well as other means of blocking estrogenic activity or reducing estrogen levels) creates a rise in testosterone in men because testosterone production is modulated partially via serum estrogen levels.



Raloxifen and its sister drug tamoxifen are typically used in treating estrogen-receptor dependent breast cancer in women[1]. Raloxifen may prove to have more diverse uses than tamoxifen for several reasons:



Selective estrogen receptor modulators (SERMs) or estrogen agonists/antagonists have shown promise in osteoporosis in that they have the potential to reduce the risk of fracture, and also reduce the risk of breast cancer. SERMs maybe classified according to their core structure, which is typically a variation of the 17 beta-estradiol template and sub-classified according to the side chain at the helix 12 affector region. The best known are the triphenylethylenes such as tamoxifen, used in the management of breast cancer. However, the clinical application of this class of SERMs has been limited due to endometrial stimulation. A second class is the benzothiophenes such as raloxifene and arzoxifene, which have skeletal benefit with little, if any, uterine stimulation.[1]



In a study conducted by Christodoulakis et al, “raloxifene users did not exhibit any difference with respect to sex steroids and HOMA-IR levels.”[2]



Raloxifen increased serum testosterone but reduced serum IGF-1 in a study performed by Duschek et al:



In aging men serum levels of testosterone and insulin-like growth factor-1 (IGF-1) decline, potential factors in the reduced muscle strength, abdominal obesity, sexual dysfunction and impaired general well being of aging. The partial estrogen agonist and antagonist raloxifene increase serum testosterone levels in aging men, but the effect of raloxifene on serum IGF-1 levels in men is unknown. In this study the effects of raloxifene on IGF-1 levels and the associated increase in serum testosterone were compared to the effects of oral testosterone supplementation…. RESULTS: Compared to placebo raloxifene increased serum testosterone by 20% but it decreased serum IGF-1 levels by 24.5% (95% confidence interval (CI): -13.0 to -36.1%). No significant change in serum IGFBP-3 levels was found. The effect of raloxifene on serum IGF-1 has been observed with other oral estrogens, and, therefore, is likely to be ascribed to the partial estrogen agonist activity of raloxifene.[3]



According to Nordt et al, raloxifen may hold potential as an intervention in adolescent gynecomastia: “Newer treatment strategies, such as the antiestrogen raloxifene, have shown promising results; however, further studies are needed to determine long-term efficacy. As a result of the limited pharmaceutical treatment options, many more adolescents are seeking surgical intervention.[4]”



As the title of the study suggests, raloxifen is also a promising treatment for male osteoporosis:



Raloxifene has been shown to increase bone mineral density of the hip in men receiving androgen deprivation therapy for prostate cancer. Moreover, experimental data demonstrated dramatic increase in cell death in human prostate cancer cell lines after the treatment with raloxifene. All these observations suggest that SERMs may be useful for the prevention and treatment of osteoporosis not only in postmenopausal women but also in elderly men. However, our hypothesis should be tested in a proper designed clinical trial.[5]



Kastelan goes on to write that there are still issues of dose and duration to be assessed by further clinical study, as well as more markers of health and physical balance to be weighed against the benefits of raloxifen treatment.



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