ATX-304 Capsules
ATX-304 Capsules USA — Capsules
Pan-AMPK Activator
ATX-304 is a small-molecule direct activator of AMP-activated protein kinase (AMPK) supplied for laboratory research. It is not a peptide, and it is studied in controlled experimental systems rather than applied settings.
This product is intended strictly for laboratory research use within the United States. It is not approved by the FDA for the diagnosis, treatment, cure, or prevention of any disease. Not for human or veterinary use.
By purchasing, you confirm the material will be used solely for lawful research purposes in accordance with applicable U.S. federal, state, and local regulations.
ATX-304 is a small-molecule direct activator of AMP-activated protein kinase (AMPK) supplied for laboratory research. It is not a peptide, and it is studied in controlled experimental systems rather than applied settings.
The published record on ATX-304 is limited. The available literature consists of a small number of rodent and cell-based studies examining AMPK activation and the associated shift in cellular fuel handling, in models of metabolic dysfunction-associated steatotic liver disease and of cisplatin-induced acute kidney injury.
Third-party tested for purity, ID, quantity.
Coming Soon
The certificate of analysis for this lot is being finalised and will be published here as soon as the lab returns it.
ATX-304 is described in the literature as a direct, broad-spectrum AMPK activator. AMPK is a heterotrimeric kinase that responds to cellular energy state and, when activated, is associated with suppression of anabolic lipid synthesis and increased reliance on fatty acid oxidation. In the reported studies, ATX-304 treatment was accompanied by phosphorylation of canonical AMPK substrates, including acetyl-CoA carboxylase, consistent with engagement of this pathway.
Research endpoints evaluated to date include hepatic lipid accumulation, markers of oxidative stress, and transcriptional and metabolomic signatures of substrate switching in a dietary mouse model of MASLD, and renal injury markers, tubular metabolism, and fatty acid oxidation readouts in a mouse model of cisplatin-induced acute kidney injury. Both reports frame the compound as a tool for interrogating what sustained AMPK activation does to tissue metabolism under stress, rather than as a characterised clinical agent.
ATX-304 appears in the published literature as a direct AMPK-activating small molecule developed in the course of work on pharmacological AMPK agonists. The detailed discovery history, medicinal chemistry lineage, and originating programme are not well documented in the references available here, and no account of its synthesis or structural optimisation can be given on the present record.
The research record is recent and narrow. Published work has concentrated on two organ systems, liver and kidney, in rodent and cell-based models. No broader body of independent replication, pharmacokinetic characterisation, or human study is represented in the available literature.
Laboratory investigations into ATX-304 have centred on direct AMPK activation and the downstream reorganisation of cellular metabolism that accompanies it. Reported frameworks include a dietary mouse model of metabolic dysfunction-associated steatotic liver disease, in which hepatic lipid handling and oxidative stress markers were assessed, and a mouse model of cisplatin-induced acute kidney injury, in which renal tubular metabolism and injury markers were examined. Across both, the stated endpoints involve a shift from lipid synthesis toward fatty acid oxidation, evaluated by biochemical, transcriptional and histological readouts under controlled preclinical conditions.
5 of the 5 areas below are addressed directly by a paper cited on this page.
AMPK activation signalling models
Addressed on this page by Holm 2025, Katerelos 2024. Each is linked to its source record in the references below, so what was measured — and in what system — can be read rather than taken on trust.
- Holm, E. et al. (2025) — AMPK activator ATX-304 reduces oxidative stress and improves MASLD via metabolic switching
- Katerelos, M. et al. (2024) — The AMPK activator ATX-304 alters cellular metabolism to protect against cisplatin-induced acute kidney injury
Hepatic lipid metabolism and MASLD models
Addressed on this page by Holm 2025, Katerelos 2024. Each is linked to its source record in the references below, so what was measured — and in what system — can be read rather than taken on trust.
- Holm, E. et al. (2025) — AMPK activator ATX-304 reduces oxidative stress and improves MASLD via metabolic switching
- Katerelos, M. et al. (2024) — The AMPK activator ATX-304 alters cellular metabolism to protect against cisplatin-induced acute kidney injury
Renal tubular injury models
Addressed on this page by Katerelos 2024. Each is linked to its source record in the references below, so what was measured — and in what system — can be read rather than taken on trust.
- Katerelos, M. et al. (2024) — The AMPK activator ATX-304 alters cellular metabolism to protect against cisplatin-induced acute kidney injury
Oxidative stress marker studies
Addressed on this page by Holm 2025. Each is linked to its source record in the references below, so what was measured — and in what system — can be read rather than taken on trust.
- Holm, E. et al. (2025) — AMPK activator ATX-304 reduces oxidative stress and improves MASLD via metabolic switching
Cellular fuel-switching research
Addressed on this page by Holm 2025, Katerelos 2024. Each is linked to its source record in the references below, so what was measured — and in what system — can be read rather than taken on trust.
- Holm, E. et al. (2025) — AMPK activator ATX-304 reduces oxidative stress and improves MASLD via metabolic switching
- Katerelos, M. et al. (2024) — The AMPK activator ATX-304 alters cellular metabolism to protect against cisplatin-induced acute kidney injury
The references section of this page cites 2 primary papers published between 2024 and 2025 — a thin record. Every citation is linked to its PubMed or DOI record so it can be read rather than taken on trust, and the summaries above describe what those papers report rather than what the compound is claimed to do.
ATX-304 Capsules is frequently listed as a peptide by suppliers in this market. It is not one. The structure published on this page is the compound's actual chemistry, and research on it should be read against its own class rather than against peptide literature.
Research compounds attract claims that outrun their evidence. Below are the ones most often encountered for ATX-304 Capsules, set against what the papers cited on this page actually report. Where the record is thin or contested, that is stated rather than smoothed over.
ATX-304 Capsules is commonly described online in connection with weight loss, appetite suppression and fat reduction. In the research literature the same compound is filed under AMPK activation signalling models, hepatic lipid metabolism and MASLD models and renal tubular injury models.
The 2 papers cited on this page, published between 2024 and 2025 describe laboratory and animal work. None reports a controlled trial in humans. Findings in cell culture or in a rodent model describe what happened in that system; they do not establish that the same occurs in humans, and this compound is not approved for human use.
Presented alongside compounds with decades of published research, as though the evidence base is comparable.
It is not. ATX-304 Capsules rests on 2 cited papers (between 2024 and 2025). A record that thin cannot support conclusions about mechanism, effect or safety, and the honest reading is that this compound has been studied very little rather than studied and validated.
Nothing above is a statement of what this material does. It is a summary of what has been published and what has not. Eppix Labs supplies research materials only and provides no dosing, administration or protocol guidance.
Every lot of ATX-304 Capsules is independently assayed before it is released, and the certificate for the lot shipped is published rather than summarised. Where a certificate for a current lot is not yet posted, the lot has not yet been released against it.
Researchers who buy ATX-304 Capsules in the United States through Eppix Labs receive a batch-labelled vial whose certificate is published against that lot code, so the material can be matched to its analysis rather than to a generic specification.
- Storage
- Cool, dry, away from direct light
- Humidity
- Keep sealed; capsule shells are hygroscopic
- Reconstitution
- Not applicable — supplied pre-measured
- Format
- Oral capsule
ATX-304 Capsules is supplied in capsule form, which removes the reconstitution step entirely: there is no vehicle to add, no reconstitution volume to record and no post-reconstitution stability window to track. What that leaves a laboratory to control is storage — capsule shells draw moisture from the air, so the container should be kept sealed and dry rather than decanted into an open vessel.
Because the material is already at its labelled quantity per capsule, batch verification carries more weight in this format than it does for powder: there is no point at which the researcher independently confirms mass by weighing. The measured content published for each lot is the figure that answers that question.
- 1 × sealed capsule bottle (100mg per capsule / Single Bottle - Pack of 60), batch-labelled
- Batch documentation for the lot shipped, once its certificate is published
- Discreet outer packaging with no product names on the exterior
- FedEx, tracked, typically 1–3 business days domestically
- Laboratory consumables of any kind
- Dosing, administration or protocol guidance of any kind
No. Eppix Labs products are supplied exclusively for laboratory research. We do not provide dosing, administration, or usage guidance.
Each capsule contains the labeled quantity of ATX-304. Independent third-party analysis verifies purity, identity, and net content per batch.
The container holds only the encapsulated compound. Any laboratory materials required for extraction, preparation, or experimental procedures must be sourced separately.
Duration depends entirely on research design, storage conditions, and laboratory protocol.
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