ATX-304 (formerly O304)

an investigational oral AMPK activator with one small randomized diabetes trial, a newer obesity pilot, and an animal pharmacokinetic curve that cannot establish a human dosing interval.

tier B · weight loss · 65 participants in the published 28-day randomized trial

verdict

the AMPK pharmacology and early human signal are real, but the clinical file is too small and short to support the certainty implied by the current research-chemical market.

if you're asking whether ATX-304 and O304 are the same development program — yes. the molecule was published as O304 and is now developed as ATX-304. the free-parent chemical record is retained here, while the current clinical formulation may use a salt form that should not be silently treated as the same mass specification.

if you're asking whether it has human evidence — yes, but not an approval-grade record. a 65-person randomized placebo-controlled trial in metformin-treated type 2 diabetes lasted 28 days. a later 23-person obesity and prediabetes pilot was reported as a conference abstract, not a full peer-reviewed outcome paper.

if you're asking whether it is a proven weight-loss drug — no. the 2018 paper focused on fasting glucose, blood pressure, microvascular perfusion, and safety. the obesity pilot is small and preliminary. neither establishes durable weight loss or long-term risk.

if you're asking what its human half-life is — unknown. the page shows an explicitly animal-only mouse proxy derived from pooled concentrations in a supplemental graph. it is not a measured terminal half-life, not an allometric conversion, and not a basis for a human interval.

Every animal exposure remains attached to species, route, and study design. No human-equivalent dose is calculated.

why B-tier

B-tier reflects meaningful but limited human evidence. O304 produced metabolic and vascular signals in a randomized 65-person trial, and ATX-304 has a later small obesity pilot. It does not rise to A because the human program is short, small, investigational, and missing a published long-term outcome and safety package. The animal PK proxy cannot close the human pharmacokinetic gap.

the core tension

ATX-304 has more evidence than most compounds sold in the same market, including randomized human data. It still lacks an approval, a long-term safety record, a published human terminal half-life, and a mature obesity-outcomes program.

what it is

ATX-304 is the current name for O304, an orally developed small molecule that suppresses dephosphorylation of AMPK at Thr172. The free parent is reported as C16H11Cl2N3O2S, 380.25 g/mol, CAS 1261289-04-6. The current developer may formulate a salt, so a product specification must declare which form it actually contains.

what it does

By keeping AMPK in its activated phosphorylated state, O304 changed glucose handling, fatty-acid oxidation, lipolysis, and microvascular perfusion in preclinical work. The 28-day TELLUS trial reported a fasting-glucose signal, reduced systolic blood pressure, and improved microvascular perfusion in metformin-treated type 2 diabetes. Those are early metabolic and vascular findings, not proof of durable obesity treatment.

origin

O304 emerged from a Swedish AMPK drug-development program and entered human testing under the TELLUS study. The program later moved to Atrogi as ATX-304. The name change does not upgrade the evidence: the published clinical base remains one short randomized paper plus a small later conference report.

why researchers are interested

The appeal is mechanistically coherent. AMPK is a central energy-sensing pathway, the molecule is orally developed, and unlike many research chemicals it crossed into controlled human testing. The mistake is treating an early metabolic signal as if it settled chronic weight loss, safety, or pharmacokinetics.

does it work

It produced measurable metabolic and vascular effects in a small, short randomized human trial. That earns a B, not an approval-grade conclusion. Weight-loss efficacy, long-term safety, the current formulation's PK, and clinically meaningful outcomes remain open.

claims vs the data

• ATX-304 is a proven weight-loss drug — overreach — a small obesity pilot and animal work support research, while durable human weight-loss efficacy is not established.
• ATX-304 activates AMPK — supported — the published mechanism suppresses dephosphorylation of AMPK Thr172 and produced downstream metabolic effects.
• ATX-304 has an 11-hour human half-life — unsupported — the displayed 11-hour value is an explicitly mouse-only, graph-derived apparent decline. no human terminal half-life was located.
• short human testing establishes long-term safety — unsupported — the peer-reviewed randomized exposure lasted 28 days and cannot define chronic, reproductive, or interaction risk.

key facts

• molecular formula: C16H11Cl2N3O2S (free parent)
• molecular weight: 380.25 g/mol (free parent)
• amino acids: n/a (small molecule, not a peptide)
• half-life: human terminal half-life not published; approximately 11 hours shown only as a low-confidence mouse apparent-decline proxy
• type: investigational small-molecule indirect AMPK activator
• CAS: 1261289-04-6 (free parent)
• 65 participants in the published 28-day randomized trial
• 28 d duration of the peer-reviewed human trial
• 0 published human terminal half-life measurements
• ~11 h mouse apparent-decline proxy, not human PK

frequently asked questions

What is ATX-304?

ATX-304 is the current development name for O304, an investigational oral small-molecule AMPK activator. It is not a peptide and is not approved for human use.

Does ATX-304 cause weight loss?

Animal studies and a small 2026 obesity pilot support continued research. The published 2018 randomized trial was short and focused on diabetes, vascular, and safety measures. Durable human weight loss is not established.

What is the half-life of ATX-304?

No human terminal half-life was located. An approximately 11-hour mouse apparent decline is shown only as a low-confidence animal proxy and is not a measured or converted human value.

Is ATX-304 the same as O304?

It is the renamed development program. Chemical-form and formulation details still matter, because a current salt formulation should not inherit the free parent's mass specification without disclosure.

Is ATX-304 safe?

Long-term safety is unknown. Human exposure is small and short, while animal work includes blood-pressure changes at high dog exposures. AMPK's broad metabolic and cardiovascular reach makes interaction and chronic-safety questions material.

related peptides

• slu-pp-332 — a different preclinical metabolic small molecule with no human trial
• BAM15 — a mitochondrial uncoupler with animal-only evidence
• semaglutide — an approval-grade obesity comparator

reptides grades the research record and cites the literature behind every call. research reference only; not medical advice.