Compare prices and buy ATX-304 from 5 research peptide vendors - also called suppliers or sources. Updated daily.
ATX-304 (CAS 1261289-04-6, formerly O304) is a small-molecule pan-activator of AMP-activated protein kinase (AMPK), not a peptide. Rather than binding AMPK allosterically, it shields the activating phosphate on threonine 172 from phosphatase removal, sustaining AMPK signaling without lowering cellular ATP. In diet-induced obese mice it increased skeletal muscle glucose uptake and reduced beta-cell stress, and it has been evaluated in an exploratory placebo-controlled trial in people with type 2 diabetes taking metformin. It is catalogued alongside the mitochondrial compounds by commercial overlap rather than chemical kinship, and it holds no FDA approval.
For research purposes only. Not medical advice.
ATX-304 is a small molecule, not a peptide. It is a thiadiazolone, 4-chloro-N-[2-[(4-chlorophenyl)methyl]-3-oxo-1,2,4-thiadiazol-5-yl]benzamide (C16H11Cl2N3O2S, CAS 1261289-04-6), catalogued here alongside the mitochondrial compounds because of commercial overlap rather than chemical kinship.
Its target is AMP-activated protein kinase (AMPK), a three-subunit enzyme that serves as the cell's energy sensor. It switches on when energy runs short, through phosphorylation of threonine 172 on its catalytic subunit by the upstream kinase LKB1, and once active suppresses anabolic pathways and promotes catabolic ones.
What separates it from most AMPK-directed molecules is where in that cycle it acts. Steneberg and colleagues reported that it does not activate the enzyme allosterically and does not lower cellular ATP, but instead suppresses phosphatase-mediated removal of the phosphate from threonine 172, without inhibiting the phosphatase itself. Which site on the enzyme it engages was left to later work.
That is a different lever from MOTS-c, a mitochondrially encoded peptide that also converges on AMPK, from 5-Amino-1MQ, which inhibits an enzyme in the NAD+ salvage route, and from SLU-PP-332 and SS-31, which act through nuclear-receptor transcription and inner-membrane lipid binding. The comparison is mechanistic and ranks nothing.
The compound was developed by Betagenon AB in Umea, Sweden. In obese mice, Steneberg and colleagues reported increased glucose uptake in skeletal muscle and reduced beta-cell stress. Norlin and colleagues, in Communications Biology in 2023, described the glycemic effect as dual, promoting muscle glucose effectiveness while preserving beta-cell function, and reported raised cellular respiration through mitochondrial uncoupling. Two 2021 papers reported preserved islet gene expression in obese mice and improved metabolic and cardiac function in aged mice.
Holm and colleagues, in JCI Insight in 2025, tested it in mice on a choline-deficient high-fat diet, a model of progressive fatty liver disease. Treatment reduced whole-body fat mass and blood cholesterol and lessened both liver steatosis and fibrosis, alongside a shift in the liver's metabolic program toward fatty-acid oxidation and away from lipid synthesis.
Steneberg and colleagues, in JCI Insight in 2018, reported an exploratory phase IIa trial named TELLUS, which randomized 65 patients with type 2 diabetes who were stably taking metformin to the compound or placebo over 28 days in Sweden.
The glycemic result comes from a subgroup defined after the fact by baseline fasting plasma glucose, comparing 25 treated with 24 placebo patients: mean fasting plasma glucose fell 0.60 mM by day 28 against 0.10 mM on placebo, a difference the authors reported as significant. In a blood-pressure analysis of 30 treated and 27 placebo patients, systolic pressure fell 5.8 mmHg and diastolic 3.8 mmHg by day 28, against small increases on placebo. Calf-muscle perfusion on MRI rose against placebo, in an analysis the authors call post hoc.
The authors set out the limits themselves, calling the study short, small, exploratory and confined to one dose level, and noting the placebo group averaged roughly 8 kg heavier and the arms were unbalanced at day 1. They reported the compound was well tolerated over the 28 days. Betagenon employees and shareholders are among the authors.
No regulator has approved the compound. Drugs@FDA lists no approved product containing it, and ClinicalTrials.gov returns no registered study under its name, its former name or its developer, both read on November 4, 2026, so the TELLUS trial was conducted outside that registry. Because it is a small molecule rather than a peptide, it also sits outside the compounding proceedings that shape much of this catalog: it appears on neither table of the FDA's Category 2 bulk drug substances page, on neither the 503A nor the 503B nomination category list, and in no FDA warning letter, all read on November 4, 2026, and it was absent from the July 2026 Pharmacy Compounding Advisory Committee agenda.
In sport it is covered by class rather than by name. The World Anti-Doping Agency's 2027 Prohibited List prohibits activators of AMP-activated protein kinase as a category of metabolic modulator, giving BAM15, AICAR and MOTS-c as examples rather than a closed list. Section S0 separately prohibits any substance holding no current approval by a governmental health authority.
Vendor titles use "ATX-304", the former developer code "O304" and the hyphenated "O-304" interchangeably, and all map to this page.
One title marks the salt form, which is chemistry rather than branding. The FDA's substance registry carries both the parent acid, the form this page's CAS number identifies, and a sodium salt of which the parent is roughly 94.5% by formula weight, so a milligram figure on a salt product refers to the salt unless the vendor states the free-acid mass.
The compound reaches this market in capsules rather than lyophilized vials, so its listings carry no per-milligram figure. PeptideScouter verifies identity against the molecular formula.
No. It is a small molecule, a thiadiazolone with the formula C16H11Cl2N3O2S and a formula weight of about 380. Peptides are chains of amino acids. It is catalogued on PeptideScouter because research vendors sell it beside mitochondrial and metabolic peptides, not because it is chemically related to them. One vendor title names a sodium salt of the compound, which carries its own registry number and a formula weight of about 402, of which the parent acid is roughly 94.5%, so a milligram figure on a salt product refers to the salt unless the vendor states the free-acid mass.
Yes. O304 was the developer code used by Betagenon AB in Umea, Sweden, and the compound was later renamed ATX-304. A 2025 JCI Insight paper states the change directly, describing the compound as ATX-304, formerly O304. CAS 1261289-04-6 covers both names, and PeptideScouter maps ATX-304, O304 and O-304 to one page so listings stay comparable.
Indirectly, by protecting the enzyme's activating phosphate rather than by binding it as an allosteric activator. AMPK becomes active when threonine 172 on its catalytic subunit is phosphorylated by the upstream kinase LKB1. Its developers reported that ATX-304 suppresses protein phosphatase 2C-mediated removal of that phosphate, without inhibiting the phosphatase itself and without lowering cellular ATP, and that the effect requires cells to express LKB1. They read the behaviour as mimicking the effect of ADP on AMPK rather than that of AMP. Which site on the enzyme the compound engages was not determined.
Yes, in one exploratory trial. Steneberg and colleagues reported a 28-day randomized, double-blind, placebo-controlled phase IIa study in Sweden, named TELLUS, in 65 patients with type 2 diabetes who were stably taking metformin, published in JCI Insight in 2018. It reported reductions in fasting plasma glucose and in HOMA-IR, an index of insulin resistance, lower systolic and diastolic blood pressure, and increased calf-muscle perfusion on MRI. The authors describe the study as short, small, exploratory and limited to a single dose level, note that the glucose analysis rested on a subgroup defined after the fact and that the treatment arms were unbalanced at baseline, and state the compound was well tolerated. No later-phase trial has been published, and ClinicalTrials.gov carried no registered study of the compound when read in November 2026.
Because a per-milligram price is computed only for vials sized in milligrams, where the listing is a single mass of material. ATX-304 is sold here as capsules, which are indexed with their prices but excluded from per-milligram comparisons, since a capsule listing is a count of units rather than one vial of material.
ATX-304 is sold by 5 research peptide vendors indexed on PeptideScouter, with 8 tracked listings compared per vendor in the table above. Pricing is normalized and refreshed daily.
All 5 indexed research peptide vendors currently have ATX-304 in stock. Stock state is refreshed daily from each vendor's catalog.
Discount codes are issued per vendor rather than per peptide, so any code applies across that vendor's whole catalog. All 5 vendors listing ATX-304 publish a PeptideScouter code, worth 10% to 15% off. These listings do not carry a comparable per-milligram price, so code availability is shown without a normalized effective price. Each vendor's code is shown beside its price in the table above.
5 research peptide vendors currently list ATX-304 on PeptideScouter. We track 8 listings across size and kit variants.
ATX-304's CAS Registry Number is 1261289-04-6. It is also sold as ATX-304 (Sodium Salt), O304, O-304.
