Follistatin 344 Effects
Follistatin Research and Muscle Growth
Myostatin can be explained as a type of protein and it is produced by cells that prohibit the growth and differentiation of muscle cells. It is also recognized as a member of the TGF-beta protein family and hence is susceptible to prohibition by follistatin. There is some evidence too on the basis of previous research that myostatin genes can cause muscle waste in various diseases, like muscular dystrophy. Animal test subjects with a lack of myostatin usually have more muscle mass and are stronger than normal. Scientists think that activating follistatin proteins through genetic manipulation could be a way to treat diseases like muscular dystrophy.
In mouse models, follistatin has been depicted to addition of lean muscle mass without any requirement for special diet regime or physical exercise. In only eight weeks of follistatin injections, mice used in the treatment group had nearly 10% more muscle mass than mice in the control group. With that said, again, this is a result that has been obtained in the absence of any special diets. Hence, it indicates that muscle gain could be even more significant with appropriate training.
Chronic muscle disorders have been notoriously hard to treat with pharmacologic interventions. The follistatin therapy has been shown to be a promising therapy for chronic muscle disorders, such as muscular dystrophy. Animal models in mice have shown that follistatin initiates hypertrophy of muscle tissue and reduces inflammation and fibrosis when administered at a high dose. Giving the protein on a regular basis has also shown to improve strength in mouse models of Duchenne muscular dystrophy (DMD). These findings are significant and could help doctors give their patients more quality of life by reducing or eliminating the weakness associated with certain chronic muscle disorders.  
One interesting aspect of research into the effects of follistatin on muscle growth is that it can lead to long-term benefits on muscle hypertrophy. In mouse models, one-time administration of follistatin via gene therapy has led to more than two years of enhanced mass and strength in both normal and dystrophic animals. These benefits were observed regardless of the age at which the animal was administered the gene; follistatin is effective at any age.
Research suggests that follistatin is relevant to muscle growth. This protein only requires one molecule of either insulin or IGF-1 to have an anabolic effect, and it actually decreases expression of IGF-1. Moreover, follistatin also stimulates the pancreas to produce more insulin, which suggests that the protein has a direct association with insulin signaling. 
Changes in strength as a result of follistatin (FS) treatment.
Follistatin May Improve the chances to Survival in Breast Cancer
The presence of follistatin in breast tumors was examined in a clinical study using reverse transcription polymerase chain reaction (RT-PCR) as well as immune-histochemistry techniques. It was found that follistatin is under-expressed in breast cancer for the most part, but is over-expressed in a small proportion of cases. In the cases where follistatin is over-expressed, tumors grow faster but are less invasive. The presence of follistatin correlates strongly with survival and reduce breast cancer metastasis.
Follistatin has been found to suppress metastasis in a mouse model of HER2-positive breast cancer. Using these mice, researchers found that the protein blocks activin-induced migration of breast epithelial cells, but it is usually absent from the average tumor. Restoring follistatin had an impact on lung metastases and tumor growth.
Follistatin is also very important in benign breast conditions, such as fibroadenoma. In this condition, the cells grow rapidly and form benign tumors. The role of follistatin is to boost cell growth while inhibiting the that of fat cells, which encourages them to differentiate into more mature cells. These tumors are often characterized by high levels of FST. Again, this points to a trend that follistatin enhances localized growth while reducing the probability of metastasis.
Probability of breast cancer recurrence in the brain or lung in low versus high follistatin (FST) environments.
Follistatin in Esophageal Cancer
Research has identified bone morphogenic protein (BMP) as a causative agent in the transition of normal esophageal tissue to Barrett’s esophagus, a precursor to cancer. It appears that acid reflux over-activates BMP in the esophagus and that counteracting this over-activation, such as through follistatin supplementation, could prevent the development of Barrett’s esophagus in the first place.
When researchers studied breast cancer, they found that the protein BMP misregulation is actually present in colon cancer. For example, impaired BMP signaling is important in the progression of colon cancer. It’s crucial that more research is done on animals, to better quantify how follistatin can be used in fighting against BMP misregulation.
Follistatin Research and Cancer Treatment
Researchers have found that follistatin is active in a number of different cancers, including breast cancer and liver carcinoma. It is hoped that research into the workings of this protein will lead to the development of more cancer treatments. Currently, there is evidence to suggest that when expressed at high levels, follistatin improves survival rates in breast cancer patients, but shortens life in lung, ovarian and gastric cancer patients. By understanding these differences between various types of cancers and studying the impact it may have on their treatment or prognosis, we could learn how to design new treatments or vaccinations that slow or prevent metastasis or help patients survive longer. 
Follistatin Associated with Cell Proliferation
Researchers have recently uncovered a dichotomy in the way follistatin works. When located in certain cells, follistatin promotes cell proliferation but restricts metastasis. As it turns out, this is true for most of the body, including the liver. Rat models show that when activin is suppressed by follistatin, proliferation seems to increase. This may explain why follistatin appears to be associated with increased tumor growth without any effect on migration or invasion; energy is being redirected from migration and changed into reproduction instead. 
Follistatin Research and Liver Protection
Follistatin has been studied extensively for its potential in the prevention of liver diseases. Studies show that it can be helpful to slow the progression of hepatopathy as a result of early fibrosis, a trait that occur due to the 87% reduction of hepatocellular death in treatment groups. Dysregulation of follistatin has also been linked to the cancerous progression of liver disease.  
Follistatin Provides Insight into Congenital Blindness
Research suggests that high levels of TGF-beta proteins, such as BMP (bone morphogenic protein), can suppress optic fusion. By inhibiting these proteins during important developmental periods of pregnancy, optic nerve fusion is made more likely and blindness is reduced. There is basic research into the benefits of follistatin supplementation to ensure that optic nerve fusion takes place during important phase of pregnancy. 
Follistatin Research and Hair Growth
Human researches shows that follistatin, specifically when used with other hair-growth stimulants, can improve hair growth significantly. Measurements in a trial of 26 individuals depicted a 20% increase in hair density and a nearly 13% increase in overall thickness. These results remained similar for at least one year following treatment with a single intradermal injection of a follistatin/Wnt- complex.
Follistatin Research and Insulin Deficiency and Diabetes
Long-term therapy with follistatin can lead to nearly total prevention of the complications associated with type 1 and type 2 diabetes. By treating diabetic patients, researchers have increased their longevity. The compound works by helping islet cells produce insulin and as a result, blood glucose levels are greatly improved. A form of this treatment may work for both type 1 and type 2 diabetics. This study can lead to long-term improvements with the hopes of preventing or curing diabetes altogether. 
The Future of Follistatin Research
Follistatin 344 is a protein with many medical uses. It has low oral and excellent subcutaneous bioavailability in mice. Healthwise, the side effects are moderate but it can be used to treat many diseases. It yields good information about human physiology and may someday yield treatments for several different diseases. Large doses have not yet been tested in humans, and for that reason, Follistatin 344 is sold strictly for research purposes only. If you are looking for follistatin 344 1mg peptide for sale, you will find that this caution is accomplished by adding an extra warning label on our product pages.
The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.
Scientific Journal Author
Ruth A. Keri, PhD. Professor and Vice Chair at Department of Pharmacology in Case Western University School of Medicine. Dr. Keri is an Associate Director for Basic Research, Case Comprehensive Cancer Center. For more than 17 years, her research has been tend to focused on the genomic and signaling mechanisms that control the development of mammary gland and cancer. This has involved generating and using data from cell lines and genetically manipulated mouse models of breast cancer as well as evaluation of publicly available human breast cancer array data. She has designed and used mouse models of disease throughout her research career, including assessing the efficacy of therapeutic agents such as vitamin D analogs, rapamycin, and dasatinib in mammary cancer models. Most specifically, she studied Follistatin’s effect of suppressing metastatis in a mouse model of HER2-positive breast cancer. She also has significant experience assessing drug synergy, in vitro and in vivo. Her laboratory extensively uses xenograft models of breast cancer. They also have expertise in the analysis of proliferation and apoptosis, migration and invasion, centrosome defects and genomic instability, and gene-specific chromatin immunoprecipitation as well as immunohistochemistry of mouse and human tissues. Underscoring this ability, she was the co-leader of the Breast Cancer Program-in-Development in the Case Comprehensive Cancer Center (Case CCC) before becoming its Associate Director for Basic Research. Moreover, she has significant expertise in Pharmacology, having earned my doctoral in this field. She was recently awarded the Garvin and Frackelton Professor of Cancer Research at CWRU.
Ruth A. Keri, PhD. is being referenced as one of the leading scientists involved in the research and development of Follistatin 344. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between peptidesforsale.com and this doctor. The purpose of citing the doctor is to acknowledge, recognize, and credit the exhaustive research and development efforts conducted by the scientists studying this peptide. Dr. Keri is listed in  under the referenced citations.
-  C. Schumann et al., “Increasing lean muscle mass in mice via nanoparticle-mediated hepatic delivery of follistatin mRNA,” Theranostics, vol. 8, no. 19, pp. 5276–5288, Oct. 2018.
-  L. R. Rodino-Klapac, A. M. Haidet, J. Kota, C. Handy, B. K. Kaspar, and J. R. Mendell, “Inhibition of myostatin with emphasis on follistatin as a therapy for muscle disease,” Muscle Nerve, vol. 39, no. 3, pp. 283–296, Mar. 2009.
-  A. Iskenderian et al., “Myostatin and activin blockade by engineered follistatin results in hypertrophy and improves dystrophic pathology in mdx mouse more than myostatin blockade alone,” Skelet. Muscle, vol. 8, Oct. 2018.
-  A. M. Haidet et al., “Long-term enhancement of skeletal muscle mass and strength by single gene administration of myostatin inhibitors,” Proc. Natl. Acad. Sci. U. S. A., vol. 105, no. 11, pp. 4318–4322, Mar. 2008.
-  C. Barbé et al., “Role of IGF-I in follistatin-induced skeletal muscle hypertrophy,” Am. J. Physiol. – Endocrinol. Metab., vol. 309, no. 6, pp. E557–E567, Sep. 2015.
-  C. Zabkiewicz, J. Resaul, R. Hargest, W. G. Jiang, and L. Ye, “Increased Expression of Follistatin in Breast Cancer Reduces Invasiveness and Clinically Correlates with Better Survival,” Cancer Genomics Proteomics, vol. 14, no. 4, pp. 241–251, Aug. 2017.
-  D. D. Seachrist, S. T. Sizemore, E. Johnson, F. W. Abdul-Karim, K. L. Weber Bonk, and R. A. Keri, “Follistatin is a metastasis suppressor in a mouse model of HER2-positive breast cancer,” Breast Cancer Res. BCR, vol. 19, no. 1, p. 66, 05 2017.
-  E. Bloise et al., “Differential expression of follistatin and FLRG in human breast proliferative disorders,” BMC Cancer, vol. 9, p. 320, Sep. 2009.
-  L. SHI, J. RESAUL, S. OWEN, L. YE, and W. G. JIANG, “Clinical and Therapeutic Implications of Follistatin in Solid Tumours,” Cancer Genomics Proteomics, vol. 13, no. 6, pp. 425–436, Oct. 2016.
-  H. Ooe et al., “Proliferation of rat small hepatocytes requires follistatin expression,” J. Cell. Physiol., vol. 227, no. 6, pp. 2363–2370, Jun. 2012.
-  S. Patella, D. J. Phillips, J. Tchongue, D. M. de Kretser, and W. Sievert, “Follistatin attenuates early liver fibrosis: effects on hepatic stellate cell activation and hepatocyte apoptosis,” Am. J. Physiol. Gastrointest. Liver Physiol., vol. 290, no. 1, pp. G137-144, Jan. 2006.
-  M. Grusch et al., “Deregulation of the activin/follistatin system in hepatocarcinogenesis,” J. Hepatol., vol. 45, no. 5, pp. 673–680, Nov. 2006.
-  M. D. Knickmeyer et al., “TGFβ-facilitated optic fissure fusion and the role of bone morphogenetic protein antagonism,” Open Biol., vol. 8, no. 3, 2018.
-  M. P. Zimber et al., “Hair regrowth following a Wnt- and follistatin containing treatment: safety and efficacy in a first-in-man phase 1 clinical trial,” J. Drugs Dermatol. JDD, vol. 10, no. 11, pp. 1308–1312, Nov. 2011.
-  C. Zhao et al., “Overcoming Insulin Insufficiency by Forced Follistatin Expression in β-cells of db/db Mice,” Mol. Ther., vol. 23, no. 5, pp. 866–874, May 2015.
Kevin Levrone –