Follistatin vs ANP (Atrial Natriuretic Peptide)
A detailed comparison to help you understand the differences and choose the right peptide for your research goals.
Follistatin
Follistatin is a glycoprotein that inhibits myostatin, the protein responsible for limiting muscle growth. By blocking myostatin, follistatin can theoretically allow for increased muscle development beyond natural limits.
Full details →ANP (Atrial Natriuretic Peptide)
ANP is a cardiac hormone released by atrial myocytes in response to stretch. It promotes natriuresis, diuresis, and vasodilation, playing key roles in blood pressure and fluid regulation.
Full details →Side-by-Side Comparison
| Aspect | Follistatin | ANP (Atrial Natriuretic Peptide) |
|---|---|---|
| Mechanism | Binds to and neutralizes myostatin and activin, both of which are negative regulators of muscle mass. This removes the natural brake on muscle growth, allowing for enhanced hypertrophy. | Binds to natriuretic peptide receptors (NPR-A) to activate guanylyl cyclase, producing cGMP. This leads to vasodilation, increased kidney filtration, and inhibition of the renin-angiotensin-aldosterone system. |
| Typical Dosage | Research protocols typically use 100-300mcg daily, though optimal dosing is not well established. Gene therapy approaches have also been studied. | Clinical use: Carperitide (recombinant ANP) used in Japan for acute heart failure at 0.1mcg/kg/min IV infusion. |
| Administration | Subcutaneous injection. Different isoforms exist (FS344, FS315) with varying properties. Requires careful sourcing due to complexity. | Intravenous infusion only for clinical applications. Short half-life (~2 minutes) requires continuous administration. |
| Side Effects | Limited human data. Theoretical concerns about effects on other organs where activin signaling is important. | Hypotension (dose-limiting), headache, nausea, and potential arrhythmias at high doses. |
| Best For |