Muscle-growth booster peptide (AR2mini): blocks the muscle-growth brake
A small experimental cyclic peptide that blocks myostatin's receptor, freeing the body's muscle-building potential; experimental, not yet an approved drug.
A researcher, an agent, or an algorithm wrote down the sequence and picked a target to hit.
An AI model like OpenFold3 or AlphaFold built a 3D structure and scored how well it fits the binding site.
A second contributor repeated the computation on their own hardware and the scores matched.
A chemistry service or a researcher ordered the sequence, it was manufactured, and mass spectrometry confirmed the right molecule was produced.
A binding or activity measurement confirmed that it actually does what the computer predicted — or didn't.
Research directions for this peptide, selected from the current sources — hypotheses you can explore and model. None of it is proven yet; tap any one to see the full thinking.
Does the circular, locked shape of this peptide drive its ability to block the muscle-growth brake receptor, more than the specific amino acids it contains?
If true, scientists could redesign the ring geometry to make far more potent versions without needing to test every possible amino-acid combination. This could accelerate development of treatments for muscle-wasting diseases.
Does this peptide selectively block only activin-A, while leaving the related myostatin signal intact at the same receptor?
Drugs that block both signals at once can cause side effects in the heart and reproductive system. A more selective peptide could boost muscle in disease with fewer unwanted effects, making it safer for long-term use in patients with muscular dystrophy or cancer cachexia.
Could this peptide protect muscle mass in cancer patients by blocking a hormonal signal that tumors use to waste the body?
Cancer-related muscle loss kills patients faster and makes chemotherapy harder to tolerate. A peptide that blocks the wasting signal could help patients stay stronger and live longer, regardless of the cancer treatment they are receiving.
Could adding a second internal bridge to this peptide stop the body from breaking it down too quickly?
Most peptide drugs are destroyed within minutes in the blood. A longer-lasting version of AR2mini could be injected once a day or less, making it a realistic drug candidate for patients with muscle-wasting conditions who need ongoing treatment.
Could this muscle-focused peptide also help immune cells get into tumors that currently block them out?
Many cancers hide from the immune system by releasing signals that push immune cells away. If this peptide can cancel one of those signals, it could help immunotherapy drugs work in patients who currently do not respond to them.
Are the two arginine building blocks in this peptide the critical contact points that allow it to block the muscle-growth brake?
Knowing exactly which part of a peptide grabs its target allows chemists to build smaller, cheaper, more stable versions that keep only the essential grip. This could translate into lower-cost drug candidates for patients with muscular dystrophy or severe muscle loss.
▸full evidence table6 metrics
| metric | value | tool |
|---|---|---|
| Kd ActRIIB | 1.8 µM | SPR |
| Kd ActRIIA | 19 µM | SPR |
| IC50 Activin A | 5 µM | SMAD2/3 reporter assay (HEK293) |
| IC50 MSTN | 6 µM | SMAD2/3 reporter assay (HEK293) |
| IC50 GDF11 | 18 µM | SMAD2/3 reporter assay (HEK293) |
| IC50 BMP9 | 12 µM | SMAD2/3 reporter assay (HEK293) |
▸3-letter notation
▸citationbibtex
@peptide{pep10790,
sequence = {VCFGTSVRRICV},
target = {activin-a},
author = {peptidemodel},
year = {2026},
status = {bioassayed}
}