ATX-304 is an experimental small molecule compound studied for its effects on cellular energy regulation. It is not a peptide, although it appears alongside peptide products in search results and some online catalogs. The previous research designation O304 combines the current development program with studies of glucose metabolism, mitochondrial activity, and tissue damage. There are human studies, but the wide range of experimental results should not be equated with confirmation of broad clinical benefits.[1][2]
The article distinguishes the chemical identity of the compound, evidence from different experimental systems, and claims that remain unconfirmed. Its purpose is to explain the current state of research, not to present a treatment scheme.
What is ATX-304? Names, synonyms, and identity
ATX304 and ATX-304 are variants of the same development name. O304, sometimes written as O-304, is the earlier name used in published studies.
Searching for both names is important because restricting the search to ATX-304 results in the omission of important works published under the name O304, including a pilot study involving humans.
The letter O in the name O304 may also be confused with the zero digit in product descriptions and search results.[1][3]
The name identifies a specific experimental chemical substance, not a general category of metabolic supplements.
Its current development is associated with Amplifier Therapeutics as part of the Cambrian research portfolio.
Cambrian describes ATX-304 as an orally administered small molecule compound that acts on the AMPK signaling network.
The manufacturer's description defines the intended direction of development and classification, but in itself it does not constitute independent confirmation of clinical efficacy.[2]
When analyzing ATX-304, it is necessary to distinguish between three types of materials: the active substance used in the published experiment, the finished formulation used in an authorized clinical trial, and the material advertised by an independent vendor.
The common name does not confirm identical identity, pollutant profile, formulation, exposure, or suitability for human use.
Why is ATX-304 often confused with peptides?
The mistake stems primarily from the commercial classification of products, not from the chemistry.
Internet catalogs sometimes place experimental metabolic compounds alongside synthetic peptides, because both groups are discussed in studies of experimental physiology.
Such grouping does not indicate whether the compound contains peptide bonds or a specific amino acid sequence.
The classification of ATX-304 should therefore be based on its chemical identity, and not on the category of the website on which it was placed.
This is particularly important when comparing the relationship with metabolic peptides that act through different receptors or hormonal pathways.
The additional distinction concerns what the substance affects.
AMPK is an enzymatic complex composed of proteins, but the compound capable of changing its activity does not necessarily have to be of a protein nature itself.
Many chemically unrelated molecules influence the same signaling pathway.
Therefore, the term „AMPK activator” describes a functional observation, not a chemical family.
The scientific database should store separate information regarding the chemical class, molecular target or pathway, and the experimental result, rather than treating these categories as synonyms.
The name O304 also creates difficulties when searching for literature.
Publications from earlier stages of development may not include the current ATX-304 designation in the titles or summaries.
Meanwhile, more recent company materials can display the current name of the program, summarizing previous research.
Researchers should check whether both descriptions refer to the same active substance, and then verify the material and formulation used in a specific study.
The continuity of nomenclature helps to connect the research history, but it does not prove that all experiments used identical preparations or exposure conditions.
How is ATX-304 classified? Peptide, protein, mixture, or other substance?
ATX-304 is classified as a synthetic, low molecular weight compound.
It is not a peptide composed of an amino acid chain, a protein hormone, or a mixture of proteins.
Its association with AMPK does not change this classification. AMPK is a protein enzymatic system to which the substance acts, not a chemical class to which ATX-304 belongs.[2]
In published work, ATX-304 is often described as a pan-AMPK activator.
AMPK, or the protein kinase activated by AMP, is involved in detecting the energy status of cells and regulating metabolism.
The prefix „pan” refers to the activity towards the AMPK forms analyzed in experimental systems.
It should not be interpreted as evidence that all tissues respond identically or that any effect of further signal transmission is beneficial.[1]
More recent studies also describe activity associated with mitochondrial fission.
These terms relate to pharmacology, whereas the term „small molecule compound” refers to the chemical classification.
One substance can exhibit more than one experimental effect, without becoming a mixture.
On the other hand, the observation of AMPK activation does not itself establish a single direct binding site or explain all the effects.[4][5]
Terms such as „metabolic activator” and „physical effort mimicking substance” require special caution.
They summarize selected biological effects, but do not prove that the drug reproduces the cardiovascular, muscular-skeletal, neurological, and behavioral benefits resulting from physical activity.
The structure and composition of ATX-304 – what has been determined?
In the O304/ATX-304 studies, it is treated as a specific chemical compound, and not an undefined extract.
Unlike a peptide, it cannot be adequately characterized using an amino acid sequence.
The chemical identity, analytical characteristics, formulation, and material used in the study must be considered together. [1]
The credibility of an article is not increased by copying the summary format or the registration number from a commercial offer.
In this review, the unverified formula, molecular mass, and synthesis scheme derived from the vendor were not replicated.
The formulation may also contain ingredients other than the active substance.
They can affect dissolution and exposure without changing the identity of the active substance.
Documentation that includes accurate material identification, a method of assessing purity, batch information, formulation, and measured exposure is useful for comparing studies.
The nominal concentration alone does not confirm that cells, animals, and humans were subjected to comparable pharmacological conditions.
The behavior of the compound in the solvent used in cell culture cannot be automatically transferred to the oral clinical formulation.
Distinction is particularly important in mitochondrial experiments.
Concentrations reaching isolated mitochondria, intact cells, and tissues can vary significantly.
The structure identifies the molecule, while the experimental conditions determine how the observed effect can be interpreted.
Chemical identity, formulation, and reproducibility of results
A reliable comparison of the studies begins with the determination of the tested material.
The development code can identify the intended substance, but analytical confirmation requires appropriate characteristics.
Purity, contaminant profile, repeatability between batches, and stability are separate issues from the mere presence of the proper name on the label.
In the case of a formulated product, the carrier and the route of administration can also influence exposure.
This means that two preparations containing nominally the same active substance do not have to behave identically.
The analytical certificate should be interpreted in the context of the research that it actually documents.
The chromatographic purity value does not necessarily confirm the stereochemical identity, the toxicological significance of impurities, the correct content of the substance delivered, the microbiological quality, or the clinical usefulness.
Similarly, the summary pattern copied from the online catalog is not an independent verification of the material used in a specific study.
Therefore, the article does not intentionally present unconfirmed details regarding the design and synthesis as established facts.
These issues become even more important when comparing cell experiments with oral studies in humans.
In vitro concentrations describe the amount of substance used in the test system.
The clinical exposure, however, depends on absorption, distribution, metabolism and elimination.
Without appropriate measurements of exposure, the apparent consistency between the studies may be superficial.
Reproducibility requires as precise an adjustment as possible to the actual intervention and conditions, rather than simply using the same research name.
Studies on ATX-304 – evidence in humans, animals and in the laboratory
Human studies
A 2018 publication described a short proof-of-concept phase IIa study in people with type 2 diabetes receiving metformin.
Improvements in fasting glucose levels and the HOMA-IR index were reported, as well as results regarding peripheral microcirculation perfusion and blood pressure.
These are observations in humans, but they do not constitute evidence of reduced mortality, sustained remission of diabetes, or long-term prevention of cardiovascular complications.[1]
The current description of the manufacturer's development program also reports on the completed Phase Ib study in adults with obesity and pre-diabetes.
Changes in metabolic and body composition parameters have been reported, and subsequent Phase II studies have been presented as planned.
This information should be labeled as results reported by the manufacturer, and not be treated equally with a fully evaluated clinical publication.
A public description of the program is useful for tracking the development of the substance, but does not replace detailed methods, information about the course of participant involvement, estimates of uncertainties, and complete tables of adverse events.[2]
Animal studies
Literature on animals covers several distinct topics.
A 2023 study in mice analyzed the use of glucose and the functioning of the beta cells of the pancreas.
The 2025 study of fatty liver disease focused on the switching of metabolic pathways and pathological changes in the liver.
These studies justify further research, but none of them confirms the treatment of the corresponding disease in humans.[4][3]
In a separate study of renal damage, ATX-304 was tested in mice exposed to cisplatin and in cultured kidney tubular epithelial cells.
The protective results concerned a specific experimental model of damage and included an AMPK-dependent component.
They do not confirm that patients receiving chemotherapy should use ATX-304, nor that all types of kidney damage show a similar response.[6]
Laboratory studies and models of organisms
Experiments involving cells isolated from the arteries of rats and mice analyzed the function of mitochondria, vascular responses, and results related to lifespan.
Such systems can help identify mechanisms and potential threats.
However, they cannot confirm the prolongation of human life, the improvement of sports performance, or the safety of consumer anti-aging interventions.[5]
Each level of evidence answers a different question.
The cells help to investigate biological pathways.
Animals allow observations at the level of tissues and the entire organism.
Controlled studies in humans evaluate the results in a specific population.
Evidence does not become clinical just because several preclinical models indicate a similar direction of action.
What does AMPK activation actually tell researchers?
The AMP-activated protein kinase is often described as a cellular energy sensor because its signaling responds to changes in energy availability.
In experimental systems, researchers often assess the state of phosphorylation and markers of subsequent signaling steps to determine whether the pathway has been activated.
These measurements can indicate a change in metabolic signaling.
However, they do not in themselves prove that a person has lost weight, avoided complications of diabetes, or increased exercise performance.
Distinction is important because signaling pathways function in complex feedback systems.
The response of cultured muscle cells may differ from the response of hepatocytes or pancreatic beta cells.
The duration, availability of nutrients, and tissue status can influence the consequences of changes in AMPK signaling.
The compound can also affect mitochondrial processes, changing energy requirements.
This makes it difficult to assign all observations to a single pathway without carefully designed mechanistic experiments.
The term „pan-AMPK activator” is particularly prone to overinterpretation.
They should be understood as a characteristic of activity with respect to the analyzed AMPK configurations, and not as evidence that the substance reaches every organ to the same extent.
Biological activity also depends on tissue exposure, which cannot be inferred solely from a biochemical test.
Even when using the same substance, the concentrations in a laboratory experiment may differ from those achieved in a clinical study.
In the review of evidence, reporting the actual experimental measurement is most useful.
The increase in AMPK phosphorylation, the change in glucose utilization, and the change in fasting glucose levels are three different observations.
They can provide a coherent biological explanation, but each has a different level of significance for patients' health outcomes.
The clinical significance should be determined in appropriate human studies, and not assumed based on activation of the pathway.
Mechanism of action analyzed in the ATX-304 studies
Activation of AMPK is a major, recurring phenomenon.
The researchers analyzed the effect of O304 on AMPK phosphorylation and further metabolic processes, including glucose utilization and lipid metabolism.
Phosphorylation, however, is a mechanistic endpoint, not a clinical result.
It indicates a change in the signaling, but it does not itself confirm an improvement in health.[1]
The next analyzed action is mitochondrial fission.
In this context, researchers assess changes in respiration, membrane potential, and the relationship between energy expenditure and ATP production.
A 2023 study linked increased metabolic demand with glucose utilization, while later work analyzed crosstalk in additional experimental systems.
The effects depend on the concentration and the biological context.[4][5]
Changes consistent with increased fatty acid oxidation and reduced lipid synthesis were observed in studies of liver steatosis.
However, the liver's response was not uniform in all its areas.
This is important because the average tissue measurement may mask local differences, and a reduction in liver fat content is not automatically equivalent to an improvement in every aspect of the disease.[3]
Mechanistic explanations should therefore remain conditional.
The studies support several related metabolic actions, but do not justify describing ATX-304 as a universally beneficial switch or a guaranteed way to increase energy expenditure without adverse consequences.
Mitochondrial fusion – significance and limitations of interpretation
Mitochondria use electrochemical gradients to support ATP production.
The term „mitochondrial respiration” refers to the change in the relationship between respiration, the energy gradient, and ATP synthesis.
In experimental conditions, researchers can analyze oxygen consumption, membrane potential, and other parameters characterizing this phenomenon.
The presence of the binding signal does not confirm that the substance safely increases long-term energy expenditure in humans.
The size of the effect and the biological conditions are crucial.
A small change in one cellular model may not predict the consequences of prolonged exposure of the entire organism.
Tissues differ in their metabolic requirements and ability to compensate for changes in energy metabolism.
Laboratory results should therefore be interpreted in conjunction with the concentration, time of exposure, and specific model, rather than being transformed into a general statement regarding metabolic efficiency.
It is equally important not to equate increased energy consumption with improved health.
The expenditure of energy is only one element of metabolic regulation.
The clinical benefit would require confirmation using endpoints relevant to the population being studied and a systematic evaluation of adverse effects.
The cited mitochondrial studies help formulate hypotheses and analyze mechanisms.
However, they do not establish consumer intervention or a substitute for standard medical care.
Limitations of the scientific evidence regarding ATX-304
The main limitation remains the distance between broad preliminary results and confirmed clinical results.
Experiments involving glucose control, liver pathology, kidney damage, vascular tension, and lifespan should not be combined into a single list of benefits in humans.
The individual models use different exposure times, observation periods, and endpoints.
Short-term studies in humans also have limited ability to detect rare adverse reactions or to confirm results that have been developing over many years.
Changes in fasting glucose levels, a surrogate indicator of insulin resistance, or body composition parameters require interpretation taking into account absolute values, baseline levels, comparators, uncertainties, and discontinuation of treatment.
The producer's share is another important issue.
It does not invalidate the study, but funding, researcher affiliations, protocol registration, and completeness of reporting should be transparent.
Independent replication and detailed clinical reports would increase certainty.
The scientific publication cannot also confirm the authenticity of the product sold under the same name.
The evidence relates to the material under investigation and the conditions.
They do not confirm the safety, legality, or quality of unrelated commercial preparations.
Interpretation of evidence in humans – results, comparators and uncertainty
The published pilot study in people with type 2 diabetes provides a stronger link to clinical applications than experiments on isolated cells.
However, the reported changes in fasting glucose and HOMA-IR are indirect metabolic results.
They do not answer the question of whether the treatment prevents kidney disease, cardiovascular events, loss of vision, or death.
Such issues usually require larger studies, appropriate comparators, and longer observation periods than an early metabolic study.
HOMA-IR requires special interpretative caution because it is an estimation based on measurements taken on an empty stomach.
It does not constitute a direct clinical diagnosis of remission or a comprehensive measurement of the action of insulin in each tissue.
Changing this parameter may support the interpretation that metabolic regulation has changed under the tested conditions.
However, it does not confirm the resolution of the underlying disease, the maintenance of the result after discontinuation of the substance, or a similar response in other groups of patients.
The Phase Ib results reported by the manufacturer are relevant for tracking the development of the compound, but represent a different level of public documentation.
The summary of the program can describe the study population, general results, and development plans without disclosing the full protocol or detailed statistical analyses.
Such summaries should not be treated as independent confirmation of an earlier publication or as a supplement to missing information based on the magnitude of the effect or safety results.
When the full report of the study becomes available, it is necessary to analyze the number of people qualified and included in the analysis, the baseline characteristics, the treatment time, the control conditions, missing data, withdrawals due to adverse events, and the uncertainty of each effect.
These details determine whether the apparently beneficial result is reliable, clinically relevant, and applicable beyond the population being studied.
Distinguishing between exploratory and previously defined endpoints is also important when collecting many metabolic parameters.
What can and cannot be confirmed by animal models of diseases?
Experiments concerning fatty liver, pancreatic inflammation and kidney damage relate to various biological questions.
Their results should be evaluated separately, even if the same substance is present in each publication.
The mouse model of liver fat accumulation can provide information about lipid metabolism pathways, whereas the kidney damage model caused by cisplatin analyzes the response to a specific experimental factor.
None of them is a general model for all metabolic or kidney diseases in humans.
The 2025 liver study is particularly informative as an example of regional diversity.
When effects differ within a single organ, the average for the entire liver may conceal significant differences between tissue areas.
This limits the simplified claims that the substance uniformly switches the liver into a healthier metabolic state.
Researchers must understand both the distribution of the effect and its implications for clinically relevant outcomes.
In the cisplatin model, the research question concerns experimental protection in a specific damage protocol.
On this basis, it cannot be determined that ATX-304 can be safely combined with oncological treatment in patients.
The assessment of clinical significance would also have to take into account whether the intervention affects the intended anti-cancer activity of chemotherapy, as well as renal outcomes and overall safety.
The protective results in cultured canal cell lines do not resolve these competing issues.
The results regarding longevity at the whole-organism level require a similar limitation of interpretation.
Nicenes are useful models for studying preserved evolutionary responses to stress and metabolism, but their lifespan cannot be extrapolated to the expected human lifespan extension.
Even the reproducible survival effect in the model organism would leave unanswered questions regarding the mechanism, significance for mammals, exposure, and adverse effects.
Presenting such observations as evidence of anti-aging action in humans would inaccurately describe the population under study.
Practical guidelines for evaluating future publications on ATX-304
New publications should first be classified according to the type of study: biochemical test, cell experiment, animal model, early human study, or controlled clinical trial evaluating health outcomes.
Next, the studied population, the comparator, and the endpoint to be measured must be recorded.
The report on AMPK phosphorylation should not be considered the same category of evidence as studies measuring diabetes complications or functional health outcomes.
The next question is whether the study tested the ATX-304 itself, the earlier preparation known as O304, or a chemically modified derivative.
Authors should also distinguish between the direct experimental results and the explanations proposed by the researchers.
The observed relationship between mitochondrial changes and improved glucose utilization does not necessarily prove that one change caused the other, unless the experimental design allows for an assessment of such a causal relationship.
Finally, it is important to pay attention to the completeness and independence of reporting.
Registration, previously defined endpoints, appropriate controls, collection of data on adverse events, and access to full results strengthen interpretation.
Industrial funding does not automatically invalidate the results, but transparent methods and independent replication remain important.
As the program develops, the regulatory and clinical status should be updated based on the documentation appropriate for the given jurisdiction, rather than inferred from the project progress report.
Most frequently asked questions about the ATX-304
1. Does ATX304 mean one of the defined substances?
Yes. The development name refers to a specific experimental molecule with a small molecule structure. Earlier publications use the name O304, while newer works use ATX-304. However, this naming convention does not confirm the authenticity of every product labeled with any of these names.
The proper conclusion is that the investigational substance has been defined, whereas the identity of each individual preparation requires its own verification.[1][3]
2. What do the available studies on ATX304 confirm?
They confirm biological activity in several experimental systems and the existence of a limited body of clinical evidence in humans.
The published work justifies further metabolic research, but it does not confirm the broad benefits of disease prevention, the benefits associated with human longevity, or its suitability for routine treatment.
Results should be described by population and endpoint, rather than combined into a universal declaration of benefits.[1]
3. Is ATX-304 a peptide?
No. ATX-304 is a small molecule compound.
It affects protein signaling and mitochondrial processes, but affecting the protein does not make the substance a peptide.
The search result or the seller category does not constitute a chemical classification, therefore the term „ATX-304 peptide” is misleading. [2]
4. Are O304 and ATX-304 different research programs?
These are names used at different stages of the history of research on the same compound.
Searching for both is necessary to link previous studies on glucose metabolism with newer publications regarding ATX-304.
However, one should check the formulation and experimental conditions of each work, rather than assuming their identity.[1][3]
5. Does AMPK activation lead to weight loss?
No. Activation of the pathway does not clinically confirm a significant reduction in body weight.
Weight change is a result at the level of the entire organism, which is influenced by energy intake, energy expenditure, fluid balance, and other factors.
The measurement of AMPK supports the mechanistic argument, whereas the claim of weight reduction requires properly controlled data regarding the results in humans.
6. Is ATX-304 equivalent to physical activity?
No. Selected metabolic similarities do not make the substance equivalent to exercise.
Experiments may show overlapping pathways without replicating training adaptations, strength, coordination, or broader health effects.
The term „substance mimicking physical effort” is therefore a research description and should not be presented as a proven substitute for physical activity.
7. Does liver testing confirm the treatment of MASLD in humans?
No. The cited study on liver steatosis used a preclinical mouse model.
The metabolic and histological results justify studies in humans, but interspecies differences and regional variations in the liver response limit the possibility of extrapolation.
The declaration of treatment in humans requires clinical evidence in the appropriate patient population.[3]
8. Has the prolongation of human life been demonstrated?
The research discussed in the article does not lead to such a conclusion.
The results regarding the lifespan of nematodes and cellular measurements related to aging are useful experimental observations, but they do not measure human survival.
They should be presented as preclinical results, and not as proven anti-aging benefits in humans.[5]
9. Does mitochondrial fusion automatically mean an advantage?
No. The consequences depend on the magnitude of the effect, the exposure, the tissue, and the context.
Mitochondrial experiments may explain changes in energy metabolism, but the attractive mechanism does not specify a safe therapeutic range.
The benefits and risks must be evaluated together for the intended use in humans, and not inferred from the name of the mechanism.
10. Does kidney protection in mice justify clinical use?
No. The protection in the cisplatin-induced injury model does not constitute a basis for recommending treatment.
The time and conditions of experimental damage differ from the complexity of clinical chemotherapy.
Before justifying such an application in humans, they would have to assess the renal outcomes, overall safety, and possible impact on anti-cancer therapy.[6]
11. Does the improvement in HOMA-IR confirm remission of diabetes?
No. HOMA-IR is an alternative indicator calculated based on measurements taken on an empty stomach.
The change may indicate a metabolic response, but remission requires its own clinical definition and control observation.
Therefore, a short pilot study in humans should be described as showing measured metabolic changes, rather than sustained remission.[1]
12. Can the exposure in animals be converted into an individual dose?
No. Animal experiments do not provide a validated treatment regimen for a specific individual.
Absorption, metabolism, tissue distribution, and formulation vary between species and preparations.
The scientifically justified use of this data is to support the formal development and assessment of safety, rather than directly determining individual dosages.
13. Is the company's communication equivalent to a clinical publication?
No. The report usually presents a selected summary instead of a full set of evidence.
It can provide correct information about developmental progress, but detailed methods and complete results are needed to assess the uncertainties and the way the results are reported.
Therefore, the summary of Phase Ib presented by the manufacturer has been clearly separated from the scientific publications in this article.[2]
14. Does the „for research” designation confirm the product’s quality?
No. The label does not confirm the identity, content, impurities, or quality of the formulation.
Even a correct analytical result only measures the properties of the things actually subjected to testing.
Scientific literature cannot certify the non-related vial or capsule, therefore conclusions regarding a specific product require independent, appropriate documentation.
15. Can the results be generalized to all people with obesity?
No. The responses and risks may vary depending on the presence of diabetes, the medications used, age, organ function, and other factors.
The criteria for eligibility for the study define the population directly analyzed.
Wider application requires evidence, rather than assuming that common recognition means equivalence for all patients.
16. What additional evidence would increase certainty?
Larger controlled studies in humans with complete safety reporting and appropriate long-term follow-up would increase certainty.
Useful results include durability, clinical benefits, and effects in clearly defined groups of patients, rather than solely biomarkers of pathway activity.
Independent confirmation would also help assess the reproducibility of the reported effects.
17. What is the most accurate short description of ATX-304?
ATX-304 is an experimental non-peptide small molecule being studied for its metabolic activity related to AMPK and mitochondria.
This description conveys his identity without transforming the preliminary results into confirmed therapeutic claims.
The potential of the relationship should be evaluated based on specific studies in humans and their limitations. [2]
Applications
ATX-304 should be classified as a small molecule compound studied in the context of metabolic drugs, and not as a peptide.
Available evidence includes mechanistic studies, animal models of disease, and limited human studies.
These results justify further research, but broad claims regarding weight reduction, organ protection, performance, or longevity require stronger clinical evidence related to specific indications.
Educational, medical and regulatory reservations
The article is of an exclusively scientific and educational nature. It does not constitute medical advice, diagnosis, prescription, or recommendations for the acquisition, preparation, administration, or self-testing of ATX-304/O304. The compound is an experimental substance, and the studies presented do not confirm its suitability for routine treatment.
Preclinical results do not allow for determining a safe or effective dosing regimen in humans. Commercial products may differ from the preparations studied clinically in terms of identity, content, impurities, and stability. The safety and regulatory status depends on the specific product, indication, and jurisdiction, and requires verification in current official sources.
References
- Steneberg, P., Lindahl, E., Dahl, U., Lidh, E., Straseviciene, J., Backlund, F., Kjellkvist, E., Berggren, E., Lundberg, I., Bergqvist, I., Ericsson, M., Eriksson, B., Linde, K., Westman, J., Edlund, T., & Edlund, H. (2018). PAN-AMPK activator O304 improves glucose homeostasis and microvascular perfusion in mice and type 2 diabetes patients. JCI Insight, 3(12). https://doi.org/10.1172/jci.insight.99114
- Cambrian Bio. (n.d.). Pipeline: ATX-304. Retrieved October 26, 2026. https://www.cambrianbio.com/pipeline
- Holm, E., Vermeulen, I., Parween, S., López-Pérez, A., Cillero-Pastor, B., Vandenbosch, M., Remeseiro, S., & Hörnblad, A. (2025). AMPK activator ATX-304 reduces oxidative stress and improves MASLD via metabolic switching. JCI Insight, 10(7). https://doi.org/10.1172/jci.insight.179990
- Norlin, S., Axelsson, J., Ericsson, M., & Edlund, H. (2023). O304 ameliorates hyperglycemia in mice by simultaneously promoting muscle glucose efficiency and preserving β-cell function. Communications Biology, 6(1), 877. https://doi.org/10.1038/s42003-023-05255-6
- Li, W. F., Zeng, Y., Zhang, Y. D., Zhang, R., Lang, J., Bu, W. J., Zhao, M. K., Sun, Z. J., & Dong, D. L. (2025). O304 is a mitochondrial uncoupler that extends the lifespan of C. elegans and induces vasorelaxation of rat mesenteric arteries. Chemical-Biological Interactions, 421, 111788. https://doi.org/10.1016/j.cbi.2025.111788
- Katerelos, M., Gleich, K., Harley, G., Loh, K., Oakhill, J. S., Kemp, B. E., de Souza, D. P., Narayana, V. K., Coughlan, M. T., Laskowski, A., Ling, N. X. Y., Murray-Segal, L., Brink, R., Lee, M., Power, D. A., & Mount, P. F. (2024). The AMPK activator ATX-304 alters cellular metabolism to protect against cisplatin-induced acute kidney injury. Biomedicine & Pharmacotherapy, 175, 116730. https://doi.org/10.1016/j.biopha.2024.116730