CJC-1295 DAC vs. CJC-1295 No DAC
CJC-1295 DAC and CJC-1295 (also known as Modified GRF 1-29) are both Growth Hormone Releasing Hormones (GHRH). Their action in the human body is identical but the difference between the two peptides are the span of the half-life. Modified GRF 1-29 and Sermorelin have a very short acting half-life of about 30 minutes, while CJC-1295 DAC has a half-life that can last up to approximately 8 days. Many a scientist have reported that the short half-life of Sermorelin and Modified GRF 1-29 is considered to be much more natural as they produce a short pulse of Human Growth Hormone.
Follistatin (FST) is a secreted glycoprotein that was first identified as a folliclestimulating hormone inhibiting substance in ovarian follicular fluid (1, 2). Human Follistatin cDNA encodes a 344 amino acid (aa) protein with a 29 aa signal sequence, an Nterminal atypical TGF binding domain, three Follistatin domains that contain EGFlike and kazallike motifs, and a highly acidic Cterminal tail. Follistatin is a secreted protein that binds to ligands of the TGF-Beta family and regulates their activity by inhibiting their access to signaling receptors. It was originally discovered as activin antagonists whose activity suppresses expression and secretion of the pituitary hormone FSH (follicle stimulating hormone). In addition to being a natural antagonist, follistatin can inhibit the activity of other TGF-Beta ligands including BMP-2,-4,-6,-7, Myostatin, GDF-11, and TGF-Beta1. Follistatin is expressed in the pituitary, ovaries, decidual cells of the endometrium, and in some other tissues. Recombinant human Follistatin 315 is a kDa protein containing amino acids 30-344 of the FST-344 protein.
The most serious complication of anabolic steroid use is the development of hepatic tumors, either adenoma or hepatocellular carcinoma. The hepatic tumors arise in patients on long term androgenic steroids, usually during therapy of aplastic anemia or hypogonadism, but occasionally in athletes or body builders using anabolic steroids illicitly. Tumors are typically found after 5 to 15 years of use, but onset within 2 years of starting therapy with testerosterone esters has been described. Many of the case reports have occurred in patients with other risk factors for cancer, such as Fanconi?s syndrome, iron overload or chronic hepatitis C (from blood transfusions). However, hepatic adenomas and hepatocellular carcinoma have also been described in patients taking androgenic steroids who have no other evidence of liver disease and normal histology in the nontumor parts of the liver. The pathology of the tumors is usually hepatic adenoma or ?well differentiated? hepatocellular carcinoma or hepatic adenoma with areas of malignant transformation. Rare instances of cholangiocarcinoma and angiosarcoma have also been described in patients on long term androgenic steroids. Clinical presentation is generally with right upper quadrant discomfort and a hepatic mass found clinically or on imaging studies. Routine liver tests are often normal unless there is extensive spread or rupture or an accompanying liver disease. Alphafetoprotein levels are usually normal. There is often (but not always) spontaneous regression in the tumor when the anabolic steroids are stopped. Hepatocellular carcinoma arising during anabolic steroid therapy is believed to have a better prognosis than that related to cirrhosis or chronic hepatitis B and C; however, deaths from hepatic rupture or tumor spread and metastasis have been reported in patients with anabolic steroid related hepatocellular carcinoma without cirrhosis.