drtbear1967
Musclechemistry Board Certified Member
Follistatin Alley is a sterile, non-pyrogenic, white lyophilized powder intended for subcutaneous or intramuscular injection, after reconstitution with steriie Water for Injection (0,3% m-Cresol).
FST-344 is a secreted glycoprotein that was first identified as a follicle*stimulating 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 N*terminal atypical TGF binding domain, three Follistatin domains that contain EGF*like and kazal*like motifs, and a highly acidic C*terminal tail.
Folli 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. FST-344 is expressed in the pituitary, ovaries, decidual cells of the endometrium, and in some other tissues.
Follistatin mechanism of action
FST 344 secreted as a glycoprotein, was originally identified in porcine ovarian follicular fluid and received its name because it suppresses synthesis and secretion of follicle-stimulating hormone (FSH) from the pituitary gland.
The Follistatin gene localizes to chromosome 5q11.2. It is composed of a relatively small 6-kb genomic DNA consisting of six exons. There is an alternative splice site that generates two major species, a full-length version that encodes a 344- amino acid pre-protein differing by a 27-amino acid sequence from its carboxy- shortened version of the 317-amino acid form missing exon 6.
The Follistatin gene consists of six exons. Alternative splicing generates two iso forms, FS317 and FS344.
At the time FST-344 was first isolated, little was known of its mechanism of action. In a major breakthrough, Follistatin was found to be an activin-binding protein. An important function of Follistatin is its collaborative role in reproductive physiology with other TGF-(3 superfamily members, activin and inhibins. These TGF-(3 family peptides have overlapping autocrine/paracrine functions. All three were initially purified from gonadal fluids and characterized based on their ability to modulate FSH.
In addition to gonadal sites of production (ovary/testes), these peptides are all pro duced by cells in the hypothalamic-pituitary axis (gonadatropes and folliculostellate cells). Follistatin binds activin and attenuates the release of FSH. Activin is secreted by the follicle of the ovary and serves to enhance FSH secretion, inhibins, which are secreted in two forms (A and B), inhibit the release of FSH at the hypothalamic—pituitary level. In addition, it is well documented that FST can abrogate the effects of GnRH in stimulating FSH secretion. This is also due in part to the block ing of transcriptional activation of the GnRH receptor gene by activing.
Follistatin is produced locally in the pituitary gland and in gonads, ovaries, and testes. Overall, measurements of FST during the menstrual cycle show few changes. However, a notable exception is during pregnancy, when FST concentrations rise toward term in parallel with activin. Follistatin is widely distributed throughout multiple organs, and the majority of FST found in the circulation is likely secreted from the walls of blood vessels.
In conclusion, Follistatin seems to operate by binding to Myostatin and inhibiting Myostatin binding to the activin IIB receptor. However, in a study done by creating mice without genes for this receptor the results were unexpected. The results show that knockout mice for the activin receptor IIB were much more muscular than nor mal control mice but the Follistatin group were significantly more muscular than either the control or activin knockout group. This shows that FST does more than just inhibit the activin receptor IIB. In one example the muscle mass was increased 194%-327% with 66% increase in muscle cell count and 28% increase in muscle cell size. This shows that although Follistatin is a Myostatin inhibitor it may be the best non-steroidal mass builder for other reasons. One hypothesis this, was that Myostatin is a member of the TGF Beta superfamily. In this family there are cross receptor activations. Perhaps the Follistatin inhibited the binding of other TGF family members to their respective receptors.
Follistatin Adverse reactions
It has been determined through scientific study based on animal test subjects that there are no negative side effects that have been linked to the presence of Follistatin 344. Despite the fact that there are still ongoing studies that are being conducted in order to determine if there is any correlation that could conceivably link a mutation of the peptide with polycystic ovary syndrome, it should be reiterated that such studies do not involve instances of FST 344 that are considered to be non- mutated in its form. As of now, there has been no negative association linked to Follistatin 344's non-mutated iteration.
Follistatin Dosage
The recommended dose for Follistatin-344 is 50-100 mcg daily, for a period between 10-30 days. It hasn't prove that dosage of 100+mcg daily gives better results.
There is also another way that significant number of users prefer: to inject FST-344 locally, into a specific muscle that you want to bring up.
In that case it is recommended to split it bilaterally into the muscle.
FST-344 is a secreted glycoprotein that was first identified as a follicle*stimulating 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 N*terminal atypical TGF binding domain, three Follistatin domains that contain EGF*like and kazal*like motifs, and a highly acidic C*terminal tail.
Folli 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. FST-344 is expressed in the pituitary, ovaries, decidual cells of the endometrium, and in some other tissues.
Follistatin mechanism of action
FST 344 secreted as a glycoprotein, was originally identified in porcine ovarian follicular fluid and received its name because it suppresses synthesis and secretion of follicle-stimulating hormone (FSH) from the pituitary gland.
The Follistatin gene localizes to chromosome 5q11.2. It is composed of a relatively small 6-kb genomic DNA consisting of six exons. There is an alternative splice site that generates two major species, a full-length version that encodes a 344- amino acid pre-protein differing by a 27-amino acid sequence from its carboxy- shortened version of the 317-amino acid form missing exon 6.
The Follistatin gene consists of six exons. Alternative splicing generates two iso forms, FS317 and FS344.
At the time FST-344 was first isolated, little was known of its mechanism of action. In a major breakthrough, Follistatin was found to be an activin-binding protein. An important function of Follistatin is its collaborative role in reproductive physiology with other TGF-(3 superfamily members, activin and inhibins. These TGF-(3 family peptides have overlapping autocrine/paracrine functions. All three were initially purified from gonadal fluids and characterized based on their ability to modulate FSH.
In addition to gonadal sites of production (ovary/testes), these peptides are all pro duced by cells in the hypothalamic-pituitary axis (gonadatropes and folliculostellate cells). Follistatin binds activin and attenuates the release of FSH. Activin is secreted by the follicle of the ovary and serves to enhance FSH secretion, inhibins, which are secreted in two forms (A and B), inhibit the release of FSH at the hypothalamic—pituitary level. In addition, it is well documented that FST can abrogate the effects of GnRH in stimulating FSH secretion. This is also due in part to the block ing of transcriptional activation of the GnRH receptor gene by activing.
Follistatin is produced locally in the pituitary gland and in gonads, ovaries, and testes. Overall, measurements of FST during the menstrual cycle show few changes. However, a notable exception is during pregnancy, when FST concentrations rise toward term in parallel with activin. Follistatin is widely distributed throughout multiple organs, and the majority of FST found in the circulation is likely secreted from the walls of blood vessels.
In conclusion, Follistatin seems to operate by binding to Myostatin and inhibiting Myostatin binding to the activin IIB receptor. However, in a study done by creating mice without genes for this receptor the results were unexpected. The results show that knockout mice for the activin receptor IIB were much more muscular than nor mal control mice but the Follistatin group were significantly more muscular than either the control or activin knockout group. This shows that FST does more than just inhibit the activin receptor IIB. In one example the muscle mass was increased 194%-327% with 66% increase in muscle cell count and 28% increase in muscle cell size. This shows that although Follistatin is a Myostatin inhibitor it may be the best non-steroidal mass builder for other reasons. One hypothesis this, was that Myostatin is a member of the TGF Beta superfamily. In this family there are cross receptor activations. Perhaps the Follistatin inhibited the binding of other TGF family members to their respective receptors.
Follistatin Adverse reactions
It has been determined through scientific study based on animal test subjects that there are no negative side effects that have been linked to the presence of Follistatin 344. Despite the fact that there are still ongoing studies that are being conducted in order to determine if there is any correlation that could conceivably link a mutation of the peptide with polycystic ovary syndrome, it should be reiterated that such studies do not involve instances of FST 344 that are considered to be non- mutated in its form. As of now, there has been no negative association linked to Follistatin 344's non-mutated iteration.
Follistatin Dosage
The recommended dose for Follistatin-344 is 50-100 mcg daily, for a period between 10-30 days. It hasn't prove that dosage of 100+mcg daily gives better results.
There is also another way that significant number of users prefer: to inject FST-344 locally, into a specific muscle that you want to bring up.
In that case it is recommended to split it bilaterally into the muscle.
