Follistatin-344

1mg Vial

2 September 2026Updated 2 September 2026

Follistatin-344

Overview Research0 Mechanism Protocols Safety

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Full range of benefits for Follistatin-344

Neutralises myostatin signalling, relieving inhibition of muscle growth

Supports muscle hypertrophy in preclinical and early clinical studies

Enhances satellite cell activation and muscle regeneration after injury

Attenuates muscle wasting in animal models of cachexia and disuse

Modulates activin pathways, potentially reducing muscle fibrosis

Investigated for improving muscle strength in muscular dystrophy models

Shown to improve age-related muscle decline in preclinical studies

Modulates activin-mediated FSH regulation in reproductive tissues

This peptide's combination-safety and interaction data below always stays visible, regardless of membership.

Warning

Important information. The data compiled from scientific literature is provided for educational purposes. Dosage ranges reflect what is reported in studies and do not constitute a recommendation, prescription, or usage guidance. Health decisions should always be made with a qualified professional.

Peptide Interactions

// 15 known interactions

Synergistic(4)Compatible(3)Monitor(4)Avoid(4)

Use with professional oversight

Insulin and oral hypoglycaemic agents (e.g., insulin, sulfonylureas)

Increases in muscle mass and changes in insulin sensitivity from follistatin may alter glucose disposal, requiring blood glucose monitoring and possible dose adjustments of antidiabetic drugs.

Androgens/anabolic steroids

Concomitant anabolic therapy can have additive effects on erythrocytosis, liver enzymes and lipids, necessitating monitoring of hematocrit, LFTs and lipid profile.

Immunomodulatory biologics or immunosuppressants (e.g., TNF inhibitors, calcineurin inhibitors)

Because follistatin modulates activin/TGF-β pathways involved in immune regulation, co-administration with immune-modifying agents may alter immune responses and warrants monitoring for infections and immune function.

Reproductive hormone therapies and gonadotropins (e.g., FSH, hCG)

Follistatin binds activin and can influence FSH regulation and gonadal function, so reproductive hormone levels and fertility treatment responses should be monitored when therapies are combined.

All interaction categories

Synergistic (4)

Insulin-like growth factor 1 (IGF-1 / mecasermin): IGF-1 stimulates AKT/mTOR-mediated muscle protein synthesis and when combined with follistatin's myostatin/activin inhibition can produce additive anabolic effects on skeletal muscle.
Growth hormone (somatropin): Growth hormone increases endogenous IGF-1 and anabolism, which can amplify follistatin-driven muscle hypertrophy and lean mass gains.
Testosterone (or testosterone replacement/anabolic androgens): Androgens promote muscle protein synthesis and together with follistatin's blockade of myostatin/activin signaling can produce enhanced hypertrophic responses.
Insulin: Insulin is an anabolic, anti-catabolic hormone that increases amino acid uptake and glycogen storage in muscle and may potentiate follistatin-mediated increases in muscle mass.

Compatible (3)

Vitamin D (cholecalciferol): Vitamin D supports bone and muscle health and has no known direct pharmacokinetic or pharmacodynamic antagonism with follistatin therapy.
Creatine monohydrate (supplement): Creatine is a commonly used ergogenic aid that is pharmacologically neutral with follistatin and may support strength gains without known adverse interactions.
Statins (HMG-CoA reductase inhibitors): Statins used for lipid lowering do not have a direct interaction with follistatin, though routine clinical monitoring for muscle symptoms is reasonable when used concurrently.

Monitor (4)

Insulin and oral hypoglycaemic agents (e.g., insulin, sulfonylureas): Increases in muscle mass and changes in insulin sensitivity from follistatin may alter glucose disposal, requiring blood glucose monitoring and possible dose adjustments of antidiabetic drugs.
Androgens/anabolic steroids: Concomitant anabolic therapy can have additive effects on erythrocytosis, liver enzymes and lipids, necessitating monitoring of hematocrit, LFTs and lipid profile.
Immunomodulatory biologics or immunosuppressants (e.g., TNF inhibitors, calcineurin inhibitors): Because follistatin modulates activin/TGF-β pathways involved in immune regulation, co-administration with immune-modifying agents may alter immune responses and warrants monitoring for infections and immune function.
Reproductive hormone therapies and gonadotropins (e.g., FSH, hCG): Follistatin binds activin and can influence FSH regulation and gonadal function, so reproductive hormone levels and fertility treatment responses should be monitored when therapies are combined.

Avoid (4)

Other myostatin/activin pathway inhibitors (e.g., ACE-031, anti-myostatin antibodies, ActRII decoys): Combining multiple agents that block myostatin/activin signaling can excessively amplify on-target effects and increase risks such as disproportionate tissue growth, tendon injury, or off-target toxicities.
Systemic corticosteroids: Chronic corticosteroid therapy causes catabolism and immunosuppression and may counteract therapeutic goals or increase infection/metabolic risks when used with follistatin, so risks and benefits should be carefully evaluated.
Anthracycline chemotherapeutics (e.g., doxorubicin): Given potential effects of myostatin/activin modulation on cardiac and skeletal muscle, co-administration with cardiotoxic chemotherapies warrants cautious evaluation and cardiac monitoring.
Pregnancy-related hormonal therapies and agents affecting fertility (e.g., estrogen-containing contraceptives, assisted reproduction protocols): Because follistatin alters activin/FSH signaling and may affect reproductive function and fetal development, use in women planning pregnancy or on pregnancy-related hormonal regimens should be approached with caution and specialist advice.