Peptides > Follistatin-344

Follistatin-344

Follistatin-344 stands as a synthetic counterpart to its natural counterpart. Its remarkable ability lies in its capacity to counteract the influence of myostatin, activin, and follicle stimulating hormone (FSH). In the realm of animal studies, this unique attribute translates into amplified muscle mass, encompassing both hypertrophy and hyperplasia, along with diminished scar formation and the suppression of specific inflammatory reactions. Additionally, it’s noteworthy that Follistatin-344 can undergo modifications within the body, giving rise to various Follistatin variants.

This PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. All product information available on this website is for educational purposes only. Bodily introduction of any kind into humans or animals is strictly forbidden by law. This product should only be handled by licensed, qualified professionals. This product is not a drug, food, or cosmetic and may not be misbranded, misused or mislabled as a drug, food or cosmetic.

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1. Introduction to Follistatin-344

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2. Molecular Structure of Follistatin-344

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3. Research on Follistatin-344

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4. Effects Of Follistatin-344

Introduction to Follistatin-344

Follistatin (FST) 344 is a synthetic version of the naturally occurring human follistatin protein. Follistatin is found in nearly all tissues of higher animals and comes in two separate isoforms as a result of alternative gene splicing. Its primary biological function is the neutralization of proteins in the TGF-beta superfamily. It has particularly potent neutralizing effects on activin, myostatin, and follicle-stimulating hormone.

Molecular Structure of Follistatin-344

Follistatin-315

Sequence: MVRARHQPGG LCLLLLLLCQ FMEDRSAQAG NCWLRQAKNG RCQVLYKTEL SKEECCSTGR LSTSWTEEDV NDNTLFKWMI FNGGAPNCIP CKETCENVDC GPGKKCRMNK KNKPRCVCAP DCSNITWKGP VCGLDGKTYR NECALLKARC KEQPELEVQY QGRCKKTCRD VFCPGSSTCV VDQTNNAYCV TCNRICPEPA SSEQYLCGND GVTYSSACHL RKATCLLGRS IGLAYEGKCI KAKSCEDIQC TGGKKCLWDF KVGRGRCSLC DELCPDSKSD EPVCASDNAT YASECAMKEA ACSSGVLLEV KHSGSCNSIS EDTEEEEEDE DQDYSFPISS ILEW
Molecular Weight: 3780 g/mol
PubChem CID: 178101631
Synonyms: Activin-Binding Protein, FSH-Suppressing Protein, FST

Future Research on Follistatin-344

Follistatin research encompasses a spectrum of human conditions, spanning from cancer and muscle disorders to hair growth and diabetes. This dynamic field remains highly active, with frequent publications and continual revelations into the intricate physiology of follistatin. The potential within follistatin research is immense, offering prospects for developing therapeutic solutions for various diseases and a deeper exploration of human physiology.

A. Comparison of Weight Loss: In the graph depicted above, we observe a distinct divergence in weight loss between the control group (represented by the blue line) and those administered with adipotide (illustrated in red). Notably, two varying doses of adipotide are represented in the red data points. This graphical representation underscores the significant impact of adipotide treatment on weight reduction, demonstrating a compelling difference in outcomes.

B. BMI Reduction Analysis: This graph portrays a compelling perspective on the impact of adipotide treatment on BMI reduction compared to the control group. The blue line represents the control group’s BMI, while the red line signifies the BMI of individuals who received adipotide treatment. The notable reduction in BMI within the treatment group serves as a compelling testament to the efficacy of adipotide in positively influencing body mass index, further substantiating its potential as a valuable tool in managing weight and related health parameters.

Effects Of Follistatin-344

Follistatin Research & Muscle Growth
Myostatin is a protein produced by muscle cells themselves that inhibits muscle cell growth and differentiation. It is a member of the TGF-beta protein family and therefore is susceptible to inhibition by follistatin. Previous research has shown that animals lacking myostatin have significantly more muscle mass and are stronger than normal. This led scientists to speculate that administration of follistatin could improve muscle growth and help to treat a number of medical conditions, like muscular dystrophy, that impact muscle growth and strength.

In mouse models, follistatin has been shown to increase lean muscle mass without the need for special dietary or exercise requirements. After just eight weeks of follistatin injections, mice in the treatment group had 10% more muscle mass than mice in the control group. This, again, is a result obtained without exercising the mice or subjecting them to special diets, indicating that gains could be even more substantial with appropriate training.

Research in everything from mice to monkeys has shown increased muscle size and strength when follistatin therapy is initiated. There is hope that the protein can be used to treat muscle disorders, such as inclusion body myositis, that have so far proved relatively resistant to pharmacologic intervention. Research in mouse models of Duchenne muscle dystrophy (DMD), for instance, show that follistatin treatment leads to hypertrophy of skeletal muscle while also reducing inflammation and fibrosis. The benefits are dose-dependent and lead to clinically relevant changes in strength in the setting of DMD. These are significant findings that could help doctors to reduce or eliminate the weakness associated with certain muscle disorders, thereby restoring quality of life and reducing morbidity in these conditions.

One interesting aspect of research into the effects of follistatin on muscle growth has found that gene administration of follistatin at any age 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 of the animal at the time of gene therapy.

Research indicates that follistatin boosts muscle growth by stimulating the insulin/IGF-1 pathway. Interestingly, the protein only requires that one of these signaling molecules be present for full anabolic effect. Follistatin actually causes a decrease in muscle expression of IGF-1, something that was initially counter-intuitive to scientists until they understood that its effects can also be mediated via insulin itself. Research indicates that follistatin influences the pancreas to produce more insulin, suggesting that the protein is intimately associated with insulin signaling.

Follistatin’s Potential to Enhance Breast Cancer Survival
A clinical investigation utilized reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry methods to examine the presence of follistatin in breast tumors. The study revealed that, for the most part, breast cancer tends to exhibit lower levels of follistatin expression. However, in a minority of cases, there is an overexpression of follistatin. In instances where follistatin is overexpressed, tumor growth is accelerated, yet invasiveness is reduced. The presence of follistatin demonstrates a strong correlation with improved survival rates and a decreased likelihood of breast cancer metastasis.

To validate follistatin’s potential to inhibit metastasis, researchers employed a mouse model of HER2-positive breast cancer. Their findings indicated that follistatin effectively impedes activin-induced migration of breast epithelial cells, a protein often lacking in typical breast tumors. Interestingly, reintroducing follistatin was observed to completely prevent the formation of lung metastases, even though it did not affect tumor growth.

Furthermore, follistatin is involved in benign proliferative disorders of the breast. Conditions like fibroadenoma, florid hyperplasia without atypia, and ductal carcinoma in situ are all characterized by elevated FST levels. Once again, the common trend is that follistatin promotes local growth while diminishing the likelihood of distant metastasis.

Follistatin in Esophageal Cancer 
Studies have identified bone morphogenic protein (BMP) as a contributing factor in the transformation of regular esophageal tissue into Barrett’s esophagus, a precursor to cancer. It seems that excessive BMP activity in the esophagus, triggered by acid reflux, plays a role in this transition. To potentially prevent the development of Barrett’s esophagus, researchers propose countering this excessive BMP activity through follistatin supplementation. Further research, especially in animal models, is needed to better understand how follistatin can be used to address BMP dysregulation.

 

Follistatin Research and Cancer Treatment
┬áResearchers have discovered that follistatin is active in various types of tumors, extending beyond breast cancer and liver carcinoma. With a deeper understanding of follistatin’s mechanisms, there is hope to develop clinical applications for this protein. Currently, follistatin expression has been linked to improved survival in breast cancer but reduced survival in lung, ovarian, and gastric cancers. This knowledge could lead to tailored treatment approaches for specific cancer types. Follistatin research might even pave the way for cancer prevention strategies or vaccines to slow metastasis and enhance long-term survival.

Follistatin’s Role in Cell Proliferation
Research on breast cancer has revealed an interesting paradox: follistatin promotes cell proliferation while restraining metastasis. This duality appears to be a common feature in most tissues. In the liver, for instance, hepatocytes require follistatin expression to proliferate. Studies in rats suggest that inhibiting activin through follistatin may be necessary for cell proliferation. This could explain why follistatin is associated with increased tumor growth but reduced tumor invasion and metastasis. During growth, it seems that a trade-off occurs, where a cell’s migratory functions are turned off to allocate energy towards growth and reproduction.

Follistatin Research and Liver Protection
Follistatin has demonstrated its ability to safeguard the liver against early-stage fibrosis, slowing the progression of liver disease. Rat studies have shown a 32% reduction in fibrosis after four weeks of follistatin treatment, attributed to an 87% decrease in hepatocyte death among treated groups. Dysregulation of follistatin has been linked to the progression from fibrosis to liver cancer.

Follistatin’s Insights into Congenital Blindness
The fusion of the optic nerve during early development is crucial for human vision. It has been known that TGF-beta signaling, particularly bone morphogenic protein (BMP), can hinder optic nerve fusion and potentially lead to blindness. Inhibiting these proteins can override their effects and promote fusion, thus reducing the risk of blindness. Basic research is exploring the benefits of supplementing with follistatin during critical stages of pregnancy to ensure proper optic nerve fusion.

Follistatin Research and Hair Growth
Human studies suggest that follistatin, especially when combined with other hair growth stimulants, can significantly enhance hair growth. A small trial involving 26 participants revealed a 20% increase in hair density and a nearly 13% increase in overall hair thickness. These improvements were sustained for at least one year following a single intradermal injection of a follistatin/Wnt-complex.

Follistatin Research and Insulin Deficiency and Diabetes
Mouse studies indicate that overexpression of follistatin can increase the mass of beta-islet cells responsible for insulin production. This results in improved insulin levels, reduced fasting glucose levels, and alleviation of diabetes symptoms. Most notably, mice treated with follistatin experienced a doubling of their lifespans as diabetes-related complications were virtually eliminated. There is optimism that follistatin may shed light on enhancing both type 1 and type 2 diabetes management by boosting the function of remaining functional islet cells in the pancreas. This approach, similar to using exogenous insulin, benefits from normal physiological controls that regulate insulin release, leading to improved diabetes outcomes through precise dosing.

Article Author

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.

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The product information featured on this website pertains exclusively to in-vitro studies. In-vitro studies, also known as ‘in glass’ studies, are conducted outside of living organisms. It’s important to emphasize that these products do not constitute medicines or drugs and have not received FDA approval for the prevention, treatment, or cure of any medical conditions, ailments, or diseases. It is crucial to note that the introduction of these products into the bodies of humans or animals is strictly prohibited by law.