Mitochondrial
ATX-304
Also known as O304
Investigational drug; not approved
In simple words: An experimental drug (formerly called O304) that turns on AMPK, the body's “low fuel” sensor that exercise also switches on.
How it works
It is a small-molecule activator of AMPK, not a peptide. Activating AMPK pushes cells to burn fuel and improves how muscle uses glucose; research also shows it acts as a mild mitochondrial uncoupler.
Targets: AMPK, Mitochondrial uncoupling (reported) · Class: Small-molecule pan-AMPK activator (not a peptide)
Uses, latest studies & pairings
Typically used for
- Obesity and metabolism (investigational oral drug).
- Being explored as a partner to GLP-1 medicines to keep muscle and limit weight regain.
Commonly paired with
- Semaglutide, in mouse studies only. No human combination results have been published.
Latest studies & news
- 2025
Mouse data (ENDO 2025, from the developer): with semaglutide, weight loss came mostly from fat, with lean mass kept, and less regain after stopping semaglutide. Not yet shown in people.
- 2025
JCI Insight: reduced fatty liver in mice.
What the research shows
Human clinical evidence
Human- A small 2018 phase IIa trial in people with type 2 diabetes, published alongside mouse data, reported lower fasting glucose and better small-vessel blood flow (JCI Insight 2018).
- The developer describes it as an oral drug in clinical development for obesity; larger human trials, and the human results with semaglutide, have not been published. It is not an approved medicine.
Animal research
Animal- In mice it lowered blood sugar by improving muscle glucose use and protecting insulin-making cells (2023).
- In aged mice it improved metabolic and heart function and exercise capacity (2021).
- In mouse models it reduced fatty liver (MASLD) and oxidative stress (2025) and protected the kidneys.
- With semaglutide, in obese mice (ENDO 2025 conference abstract OR22-05 by the developer, Amplifier Therapeutics): weight loss with ATX-304 alone or combined with semaglutide came mostly from fat, with lean mass preserved, and after semaglutide was stopped ATX-304 reduced weight regain in a dose-dependent way. This is a company conference abstract, not a peer-reviewed paper, and mouse doses (mg per kg) don't translate into human milligram doses.
Animal and lab results suggest what might happen; they don't prove an effect in people.
Safety & what to watch
- Human safety profile is not established.
- Investigational; not available as an approved treatment.
Amounts
No dose is given for unapproved substances. If you are considering it, discuss it with a licensed clinician who knows your history and bloodwork.
📦 My peptide supply kit
The supplies I use, in one Amazon list. Only use them for medicines your clinician prescribes. Never share or reuse needles, and put used ones in a sharps container.
Studies & references
- PAN-AMPK activator O304 improves glucose homeostasis and microvascular perfusion in mice and type 2 diabetes patients. JCI Insight 2018PMID 29925691
- AMPK activator ATX-304 reduces oxidative stress and improves MASLD via metabolic switching. JCI Insight 2025PMID 40197369
- AMPK activator O304 improves metabolic and cardiac function, and exercise capacity in aged mice. Commun Biol 2021PMID 34795407
- O304 ameliorates hyperglycemia in mice by dually promoting muscle glucose effectiveness and preserving β-cell function. Commun Biol 2023PMID 37626210
- O304 is a mitochondrial uncoupler which extends C. elegans lifespan. Chem Biol Interact 2025PMID 41130350
- ENDO 2025 abstract OR22-05: ATX-304 alone, with semaglutide and after semaglutide withdrawal in obese mice (developer announcement)
Draft profile pending editorial review. Educational only, not medical advice. Never start, stop or change a medicine without your prescriber.