Follistatin 344

Combined RE+EAA significantly increased muscle mass and senior fitness test scores.; The follistatin/myostatin ratio increased most in the RE+EAA group, significantly versus control and EAA groups.; IL-6 and IL-1β were reduced in both RE and RE+EAA groups; TNF-α decreased only in the RE+EAA group.; Combined intervention was superior to either alone for enhancing myokine profiles and reducing inflammation.

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All resistance training types increased skeletal muscle mass, strength, power, follistatin, adiponectin, and irisin.; All training groups reduced fat mass, body fat percentage, myostatin, CRP, and TNF-α.; Combined upper- and lower-body training produced the largest increases in follistatin and adiponectin and decreases in myostatin and CRP.; Changes in myostatin and CRP showed strong positive correlations with fat mass, while follistatin and adiponectin had strong negative correlations.

Both Cr-HCl and CrM groups showed significant increases in strength, arm and thigh muscle cross-sectional area, and skeletal muscle mass, along with decreased body fat.; Supplementation groups had significant increases in growth hormone, IGF-1, follistatin/myostatin ratio, and testosterone/cortisol ratio, and decreases in cortisol and ACTH.; Cr-HCl did not provide any additional benefit over CrM for any measured outcome.

Median serum myostatin was significantly lower in spinal muscular atrophy patients (98 pg/mL) versus controls (412 pg/mL).; Lower myostatin levels correlated with greater disease severity based on clinician-rated outcomes.; Myostatin levels further decreased after 12 months in spinal muscular atrophy cases.; Follistatin levels did not differ between groups, but the follistatin:myostatin ratio was increased and inversely correlated with motor severity.

All IRT intensities increased decorin and follistatin, and decreased myostatin, TGF-β1, total cholesterol, triglycerides, and LDL.; Moderate- and high-intensity IRT produced greater improvements in activin A, follistatin, and TGF-β1 than low-intensity IRT.; Low-intensity IRT did not significantly change fat mass, VO2peak, HDL, triglycerides, glucose, activin A, or decorin compared to control.

What is Follistatin 344?

**Mechanism of Action** Follistatin 344 (FST-344) is a 344-amino acid splice variant of the follistatin gene, functioning as an activin-binding glycoprotein. It neutralizes myostatin (GDF-8) and other TGF-β superfamily ligands (e.g., activin A, GDF-11) by directly binding to them, preventing their interaction with cell

How does Follistatin 344 work?

Activin-binding glycoprotein that antagonizes myostatin (GDF-8) to release the brake on skeletal muscle growth.

What is the research status of Follistatin 344?

Follistatin 344 is currently classified as preclinical, with 28 research references on record. This is for research purposes only and is not medical advice.