Follistatin-344
also known as FST-344, Follistatin isoform 344
344-amino-acid isoform of follistatin, an endogenous glycoprotein that binds and neutralizes myostatin and activin A. Lacks the heparin-binding domain of FST-315, resulting in systemic circulation rather than tissue sequestration. Investigated as a myostatin antagonist for skeletal muscle hypertrophy and sarcopenia treatment. Mechanism centers on disruption of myostatin-ActRIIB signaling, relieving brake on muscle protein synthesis.
At a glance
Research · No approved protocol
Primary target — Myostatin (MSTN/GDF-8) and Activin A.
Pathway — FST-344 binds MSTN/Activin → prevents ActRIIB receptor engagement → disinhibits muscle anabolism.
Downstream effect — Elevated follistatin/myostatin ratio, increased muscle protein synthesis, attenuated muscle atrophy signaling [jeong-2026].
Origin — Endogenous glycoprotein, 344-AA isoform lacking heparin-binding domain (vs FST-315).
Feedback intact — Yes — indirect antagonist, preserves endogenous regulation.
| Parameter | Value |
|---|---|
| Clinical protocol | None — no approved dosing regimenFollistatin-344 measured as endogenous biomarker, not administered exogenously in cited trials. |
| Research context | Endogenous modulation via exercise + nutritionResistance training + EAA intake elevated FST/MSTN ratio by 15–25% in 12-week RCT (older women). |
| Evidence basis | Human observational / biomarker studies |
| Half-life | Not establishedCirculating isoform; lacks tissue-binding domain of FST-315. |
Reconstitution
A pure mass-to-volume utility. Enter what you have in the vial; the atlas computes the volume per dose. No prescription information.
No direct fat loss trials. Myostatin inhibitors focus on lean mass preservation; fat loss is indirect via muscle metabolic demand.
| Outcome | Finding |
|---|---|
| Primary target | Muscle mass preservation, not direct lipolysis |
| Indirect fat effect | Increased lean mass → elevated resting metabolic rateNot primary mechanism. Muscle-sparing during deficit. |
| Clinical evidence | Lorcaserin trial (6 mo) showed no MAFI axis changes during fat loss [ramirezcisneros-2026]Suggests follistatin not primary driver of fat loss in weight-reduction interventions. |
| GLP-1RA studies | Liraglutide (35 days) — no significant MAFI axis modulation despite fat/lean changes |
- — Active malignancy
- — No approved protocol — research use only
- — Insulin resistance / Type 2 diabetes (monitor glucose)
- — Pregnancy / lactation (unknown safety profile)
- 01Regulatory status
Follistatin-344 is not approved for human administration. All cited studies measure endogenous serum follistatin as a biomarker, not as an exogenous therapeutic agent.
- 02Endogenous modulation
Resistance exercise combined with essential amino acid (EAA) supplementation elevated the follistatin/myostatin ratio by 15–25% in 12-week randomized trials. Protein intake (1.2–1.5 g/kg/day) synergizes with training to upregulate endogenous follistatin.
- 03Measurement context
Serum follistatin and follistatin/myostatin ratio are used diagnostically in sarcopenia screening and as biomarkers of muscle anabolic balance in clinical trials.
- 04Research consideration
Gene therapy and recombinant follistatin delivery are under preclinical investigation for muscular dystrophy and sarcopenia. No human safety or efficacy data for exogenous FST-344 administration.
Follistatin-344 (myostatin antagonist) and BPC-157 (tissue repair peptide) address complementary pathways in muscle recovery. FST-344 promotes muscle protein synthesis by disinhibiting myostatin signaling, while BPC-157 accelerates healing of tendons, ligaments, and microtears via angiogenesis and collagen synthesis. Combined, they may support both hypertrophy and structural repair during high-volume training or injury recovery.
TB-500 (thymosin beta-4 fragment) promotes cell migration, angiogenesis, and anti-inflammatory signaling in muscle and connective tissue. Follistatin-344's anabolic signaling may synergize with TB-500's regenerative effects during muscle damage or overtraining, particularly in older adults where both myostatin inhibition and tissue repair are rate-limiting.
Sources
of 58 rendered claims carry a resolvable citation.
- [boonpiraks-2026]Boonpiraks 2026 — Diagnostic Performance of Serum Adiponectin and a Biomarker-Based Model for Sarcopenia in Compensated Cirrhosis.
journal, 2026 - [jeong-2026]Jeong 2026 — Effect of exercise on hormonal responses in adolescents with obesity and leptin resistance: a randomized trial.
journal, 2026 - [ramirezcisneros-2026]Ramirez-Cisneros 2026 — Lorcaserin induces abdominal fat loss with associated improvements of the circulating metabolome/lipidome and no changes in the myostatin-activin-follistatin-IGF-1 axes: A 6-month long randomized placebo-controlled clinical trial.
journal, 2026 - [samali-2025]Samali 2025 — Myostatin inhibitors in sarcopenia treatment: A comprehensive review of mechanisms, efficacy and future directions.
journal, 2025