ACE-031, also known as ramatercept, is an experimental fusion protein developed to act on signaling pathways regulating skeletal muscle development. In scientific publications, this substance is described as a soluble receptor trap that binds selected signaling molecules outside cells.
In online search engines, ACE-031 is sometimes referred to as „ACE-031 peptide”. However, this is a simplification that does not reflect its actual structure.
ACE-031 is not a short synthetic peptide. It is a recombinant fusion protein composed of the extracellular part of the ActRIIB type IIB receptor (ActRIIB) linked to the Fc fragment of IgG1 immunoglobulins [1].
Preclinical studies and early clinical trials have shown that ACE-031 can affect selected parameters related to muscle mass and structure.
However, it has not been confirmed that the substance provides sustained improvement in strength, physical performance, or a beneficial balance of efficacy and safety in humans.
The results of studies involving boys with Duchenne muscular dystrophy are particularly important; in these studies, adverse effects were reported that contributed to the discontinuation of the study program [3].
The article discusses the identity of ACE-031, its structure, the mechanism of its interaction with myostatin and other ligands, the results of studies in humans and animals, and the limitations of the current scientific evidence.
What is ACE-031 (ramatercept)? Name and identity of the substance
ACE-031 is the developmental designation of a substance also known as ramatercept.
Both names refer to the same intended fusion protein.
In the FDA’s substance identification registry, ACE-031 is associated with the UNII number 42HQC6QLEK [1].
This number helps determine the identity of the substance, but it does not mean that it can be placed on the market as a medicinal product.
What other names are used for ACE-031?
In publications and online inquiries, you can encounter several variants:
- ACE-031;
- ACE031;
- ACE 031;
- ramatercept;
- ActRIIB–Fc;
- ActRIIB–IgG1;
- ACE-031 peptide.
The first three terms are variants of the notation for developmental marking.
The name ramatercept identifies the same substance in the scientific nomenclature.
By contrast, the terms ActRIIB–Fc and ActRIIB–IgG1 describe the molecular architecture, i.e., the combination of the receptor fragment with the Fc region of the antibody.
However, this does not mean that every experimental ActRIIB–Fc protein is identical to ACE-031.
Different constructs can contain different receptor fragments, sequence modifications, linkers, or variants of the Fc region [4,5].
Why does the substance's name not confirm the content of the sample?
The chemical identity of a substance must be distinguished from the composition of a particular laboratory material.
| Question | The appropriate type of evidence | What doesn’t it confirm on its own? |
|---|---|---|
| What substance does the name ACE-031 mean? | Records of substances and scientific documentation | The contents of a specific vial |
| What material was used in the study? | Methodology, production data and analytical characteristics | Comparability with another commercial product |
| What does the supplied sample contain? | Appropriate analytical studies and reference material | Clinical efficacy or usefulness for human use |
The correct name on the label alone does not replace the analysis of the composition.
Similarly, confirmation of the identity of the research material does not mean that the substance is an approved drug.
Is ACE-031 a peptide, a protein, or some other substance?
ACE-031 should be classified as an experimental recombinant receptor-Fc fusion protein.
It is not a typical short synthetic peptide.
All proteins contain amino acids linked by peptide bonds, but this does not mean that the term „peptide” adequately describes their structure and properties.
In the case of ACE-031, its multi-domain structure and ability to bind specific biological ligands are of significant importance.
Why ACE-031 is not just a normal peptide?
A short synthetic peptide can consist of several dozen or hundreds of amino acids that form a single chain.
ACE-031 is a much more complex structure.
It contains a fragment of the receptor responsible for recognizing ligands and an Fc region derived from immunoglobulin.
Its properties depend on the correct combination of domains, spatial organization, and characteristics specific to recombinant proteins.
Therefore, assumptions regarding synthesis, stability, or analysis of typical short peptides should not be transferred to ACE-031.
Is ACE-031 a steroid or a SARM?
No.
ACE-031 is not an anabolic steroid or a small molecule selective androgen receptor modulator.
Its mechanism does not involve the direct activation of the androgen receptor.
It is also not a full-length monoclonal antibody with a classic antigen-recognizing structure.
The Fc region is derived from the antibody, but the part responsible for ligand binding is a fragment of the ActRIIB receptor [3].
What does the term „receptor trap” mean?
The receptor trap is a soluble structure capable of binding specific signaling molecules outside the cells.
A ligand is a substance that can interact with a receptor.
If the soluble receptor fragment captures the ligand, it can limit its availability to receptors located on the cell surface.
It is on this principle that ACE-031 was developed [4].
This is not a mechanism that involves delivering amino acids to the muscles or directly stimulating androgen receptors.
Molecular structure of ACE-031 – ActRIIB, Fc fragment and protein identification
ACE-031 contains the extracellular domain of the human type IIB receptor coupled to a linker with the Fc region of human immunoglobulin IgG1.
The resulting protein has a dimeric structure and is glycosylated [1,5].
This means that its characteristics require evaluation not only of the amino acid sequence, but also of the organization of the entire molecule and of selected posttranslational modifications.
Why is the receptor fragment not the same as the full ActRIIB receptor?
The full receptor ActRIIB is a membrane protein.
It contains the extracellular region, a part passing through the membrane, and the intracellular domain involved in signal transmission.
ACE-031 does not contain a complete receptor in this form.
It uses a fragment of the ligand binding domain that has been linked to the Fc region.
Therefore, it acts as a soluble structure that captures specific signaling molecules, rather than as a full receptor anchored in the cell membrane [4].
What did the study of products labeled ACE-031 from 2025 reveal?
In an analytical study published in 2025, 14 products sold under the name ACE-031 were evaluated [5].
No expected fusion protein was detected in any of them.
In 12 samples, a full-length human type IIB receptor was identified, while the other two contained other substances.
This result does not mean that all products offered by all suppliers have an incorrect composition.
However, it shows that the label itself is not sufficient evidence of molecular identity.
The study also showed why detecting a fragment related to the ActRIIB receptor is not sufficient to confirm the complete fusion structure.
What information is needed to identify ACE-031?
The evaluation of the research material should take into account the presence of appropriate regions of the sequence, the confirmation of the domain junction, and the characterization of the entire protein.
Contaminants, the presence of other proteins, and properties related to the manufacturing process also play a role.
A single percentage cleanliness result does not answer all of these questions.
It is necessary to distinguish:
- molecular identity;
- sample composition;
- analytical purity;
- biological activity;
- safety and clinical effectiveness.
These are separate areas of assessment.
Studies on ACE-031 in humans and animals – what has been shown?
The studies of ACE-031 included laboratory experiments, animal models, and early clinical trials.
Various endpoints were analyzed, including lean body mass, muscle volume, strength in experimental models, and motor performance.
The results of these cannot be considered as repeated evidence of a single, confirmed clinical effect.
Study in healthy postmenopausal women
In a randomized, double-blind, placebo-controlled study, 48 healthy postmenopausal women participated [2].
The researchers analyzed the body's response after a single administration of ACE-031.
On the 29th day of observation, an increase in the measured lean body mass and thigh muscle volume was observed in the group with the highest exposure.
The results indicated early biological activity related to muscle mass regulation.
However, they did not confirm improvements in strength, sports performance, or long-term functional benefits.
The change in muscle volume in an imaging study is not equivalent to an improvement in their function.
The study is associated with registration NCT00755638 [6].
Second study in healthy participants
The ClinicalTrials.gov registry also contains the completed multicenter trial of ACE-031, designated NCT00952887.
70 participants were registered in it [7].
Information about the completion of the study and the number of participants helps reconstruct the course of the development program.
However, it is not synonymous with the publication of positive results.
The record analyzed did not include the results that would allow a full assessment of efficacy and safety.
Therefore, it should not be assumed that this study yielded beneficial results solely based on the status of „completed”.
ACE-031 in studies on Duchenne muscular dystrophy
Duchenne muscular dystrophy (DMD) is a genetic disease that leads to progressive damage and weakening of the muscles.
ACE-031 was studied in this population due to its effect on pathways that limit muscle growth.
What did the NCT01099761 study show?
The study included 24 boys with DMD who retained the ability to walk independently [3,8].
The main objective was to assess safety.
Selected parameters related to muscle function were also analyzed, including the distance covered during the six-minute walking test.
The results indicated a favorable direction of changes in this parameter, but the difference between the groups did not reach statistical significance.
Therefore, this result cannot be considered as confirmation of improvement in walking ability.
What adverse reactions have been reported?
The study included, among other things, nosebleeds and telangiectasias, which are visible enlargements of small blood vessels [3].
The safety observations contributed to the conclusion of the study.
This is of crucial importance for interpreting the results.
Even if a change in a specific body structure parameter is observed in the study, adverse events cannot be ignored.
The benefits and risks must be evaluated together.
What is known about the extended study?
The study extended NCT01239758 included 11 participants and was also terminated due to preliminary safety concerns [9].
It is not necessary to automatically add participants to the extended study to the number of participants in the primary study as if they were a completely independent group.
An early conclusion also limits the ability to assess long-term results.
Therefore, the results of the DMD program do not confirm the favorable balance of efficacy and safety of ACE-031.
Animal studies on ACE-031 and the ActRIIB pathway
Animal studies help to understand the biological mechanisms involved in the regulation of muscle development.
However, they do not replace clinical studies in humans.
Studies on mice from 2010
A study published in 2010 analyzed the effect of the soluble receptor ActRIIB on the skeletal muscles of mice [10].
An increase in muscle size was observed involving different types of fibers.
This result supports the hypothesis that the capture of specific ligands can influence the development of muscle tissue.
However, this does not mean that every increase in muscle size leads to a proportional increase in strength.
It also does not confirm the efficacy of ACE-031 in humans.
Study ACE-031 in marmosets from 2026
In a 2026 publication, ACE-031 was evaluated in marmosets in an 14-week experiment [11].
Eight animals receiving the substance and four control animals participated in the study.
The authors described the increase in muscle fiber size and the increase in intrinsic strength in isolated muscle studies.
At the same time, detailed results indicated that differences regarding the absolute strength of a single contraction and the contraction of the diaphragm were not statistically significant.
This distinction matters.
Intrinsic strength and absolute strength of the muscle are not the same parameter.
The interpretation should be based on specific endpoints, and not solely on the general formulations contained in the publication's summary.
The small number of animals also limits the scope of the applications.
The study does not confirm the efficacy of ACE-031 in humans nor constitutes evidence of the resumption of the clinical program.
How does ACE-031 affect myostatine and actinine?
ACE-031 was developed to capture selected signaling molecules involved in the regulation of muscle growth.
One of them is myostatin, also known as GDF-8.
Myostatin belongs to a signaling network that limits the development of skeletal muscles.
However, ACE-031 is not a substance that exclusively blocks myostatin.
Why is ACE-031 not a selective inhibitor of myostatine itself?
Part of the binding ligands comes from the ActRIIB receptor.
This receptor is involved in the recognition of more than one signaling factor.
Therefore, ACE-031 may also affect other ligands associated with this system [2,3].
Basic studies in mice showed that the soluble type II receptor activator can affect muscle growth even in the absence of myostatin, although the effect was smaller [4].
This suggests the involvement of additional ligands.
However, this experience should not be considered as a direct clinical study of ACE-031.
How does the proposed mechanism of action work?
The mechanism can be described in three stages.
First, the soluble fusion protein binds to specific ligands outside the cells.
Then it reduces their availability to receptors present on the surface of the cells.
Consequently, there may be changes in the transmission of signals affecting the development of muscle tissue.
This mechanism helps explain why researchers observed parameters related to muscle growth.
However, it does not allow the patient to independently determine the magnitude of the clinical benefit or the overall risk.
Why is a wide range of ligand binding important for safety?
Signal molecules associated with the ActRIIB receptor can participate in biological processes that also occur outside skeletal muscles.
Therefore, the effect of ACE-031 on other tissues is an important research issue.
Adverse events observed in the DMD program should not be overlooked simply because the main objective of developing the substance was to regulate muscle mass [3].
At the same time, the occurrence of a specific event itself does not yet identify its exact molecular mechanism.
This would require additional research.
It cannot also be assumed that every substance that acts on a similar pathway will have an identical risk profile.
The selectivity of a particular molecule is important.
What are the limitations of the scientific studies on ACE-031?
ACE-031 has a documented history of research.
The most important limitation is therefore not the complete lack of data, but the difference between the reported biological activity and the confirmed clinical benefit.
Increasing muscle mass is not synonymous with increasing strength
Lean body mass, magnetic resonance muscle volume, the strength of the isolated muscle, and motor fitness are different endpoints.
Changing one parameter does not automatically mean that the other parameters will improve.
In a clinical study, it is necessary to demonstrate an effect that is significant for the population being studied.
This may include motor function, independence, or other appropriately defined outcomes.
The populations studied do not represent all potential users
The main clinical studies included healthy postmenopausal women and boys with DMD.
These results cannot be directly transferred to young adults, athletes, strength-training individuals, or patients after injuries.
Differences between populations can affect the biological response and safety.
Preclinical studies do not replace clinical trials
Experiments on mice and marmosets may support hypotheses regarding the mechanism of action.
However, they do not confirm that ACE-031 improves human physical performance.
Differences between species, the size of groups, the method of measurement, and the time of observation limit the possibility of directly transferring the results.
Publication and registration of a study are different sources of evidence
The research register allows determining its purpose, project, number of participants and status.
However, it does not always include full results.
Similarly, a conference abstract, a preprint, and a peer-reviewed publication are not equivalent in terms of the scope of the available documentation.
The 2025 preprint and the 2026 publication on marmosets represent the same research line and should not be counted as two independent confirmations [11,12].
The date of publication itself does not also prove that clinical trials have resumed.
ACE-031 remains an experimental substance
Registration of a substance in the FDA database does not mean its approval as a drug.
The FDA clearly distinguishes the UNII identifier from the regulatory assessment and product approval [1].
The 2025 analytical publication also indicated that at that time an approved medicinal product containing ACE-031 was not available [5].
The presence of products with this name in online sales does not change the status of clinical evidence.
The absence of reported incidents does not mean that there is no risk
Small and short-term studies have limited ability to detect rare or delayed adverse effects.
Some events may not be observed during the study.
Others may not be subject to detailed monitoring.
Therefore, the statement that a specific problem has not been described should not be taken to mean that it cannot occur.
Frequently asked questions about ACE-031
1. Does ACE-031 mean a specific substance?
Yes. In the scientific nomenclature, ACE-031 stands for ramatercept, which is a specific recombinant receptor-Fc fusion protein. However, this identity does not guarantee that every product labeled with this name contains the correct molecule. The substance registry helps determine the intended structure, while the composition of a specific sample requires analytical confirmation. Differentiation is particularly important in the case of materials sourced from different suppliers [1].
2. What do the available studies on ACE-031 confirm?
The studies confirm the biological activity of ACE-031 and the occurrence of certain changes related to mass and muscle structure. However, they do not unequivocally demonstrate a lasting improvement in functional performance or a beneficial balance of efficacy and safety. Body composition results are not equivalent to improved fitness, and animal studies do not replace clinical trials. Therefore, ACE-031 should be presented as an experimental substance with a documented history of research [2,3].
3. Is the term „ACE-031 peptide” correct?
This is an imprecise term. ACE-031 contains polypeptide chains, but its proper classification is recombinant receptor-Fc fusion protein. The general term „peptide” does not adequately describe the multi-domain structure, glycosylation, and the way ligands bind. In scientific papers, it is worth explaining the popular search phrase and then using more precise terminology [1].
4. Is ramatercept the same as ACE-031?
Yes. Ramatercept and ACE-031 are names associated with the same substance in the FDA’s identification registry. The naming consistency facilitates publication search and comparison, but does not automatically confirm the equivalence of different commercial samples. Analytical documentation is still needed to determine whether a particular material corresponds to the intended fusion protein structure [1].
5. Is ACE-031 the same as the full-length receptor ActRIIB?
No. ACE-031 contains the extracellular domain of the ActRIIB receptor combined with the Fc region of the immunoglobulin. The full-length receptor contains additional structural elements and functions as a membrane protein. These are different molecules, even if a specific test recognizes the common sequence fragment. Confirmation of the complete architecture of the fusion protein is necessary for proper identification [4].
6. Does ACE-031 block only myostatine?
No. ACE-031 was designed as a receptor trap that acts on more than one ligand associated with the ActRIIB pathway. Myostatin is one of the important components of this system, but not the only one. Basic research indicates that other ligands also participate in muscle growth regulation. A broader range of effects may be relevant both for the observed biological activity and for safety [4].
7. Was ACE-031 studied in humans?
Yes. ACE-031 has been evaluated in studies involving healthy participants and boys with Duchenne muscular dystrophy. However, the existence of such studies does not imply confirmed efficacy or the approval of the substance for clinical use. Interpretation requires consideration of the purpose of each study, the number of participants, the results obtained, and safety information [6–8].
8. Did the DMD study prove that ACE-031 improves walking ability?
No. The study described a favorable direction of distance change in the six-minute walking test, but the difference between the groups was not statistically significant. Therefore, it cannot be considered as confirmation of efficacy. Additionally, the study had a small number of participants and was completed in the context of safety issues. The exploratory result should be interpreted in conjunction with these limitations [3].
9. Does increasing lean body mass mean greater strength?
No. Lean body mass and muscle strength are separate parameters. Increasing muscle volume does not automatically confirm improved mobility, endurance, or daily functioning. In ACE-031 studies, it is necessary to clearly specify what is being measured. Claims regarding strength require direct strength tests, not just body composition measurements or imaging studies [2].
10. Does the study on marmosets from 2026 confirm the efficacy of ACE-031 in humans?
No. The study provides preclinical data regarding the structure and selected muscle strength parameters in an animal model. It does not confirm efficacy or clinical safety in humans. Additionally, it included a small number of animals, and not all strength measurements showed statistically significant differences. The results may support further hypotheses, but they do not replace clinical studies [11].
11. Can the results of other substances that affect ActRIIB be attributed to ACE-031?
No. The common biological pathway does not imply identical binding profile, pharmacokinetics, formulation, or safety. Different receptor constructs, antibodies, and fusion proteins may exhibit different properties. Studies of other substances can provide mechanistic context, but conclusions regarding ACE-031 should be based on data specific to this molecule or clearly labeled as an extrapolation [4].
12. Is the registration of a clinical trial evidence of effectiveness?
No. Registration documents the study plan, its characteristics and status, but the number of participants or information on completion does not confirm a favorable outcome. For example, in a completed study of multiple dosing with ACE-031, the results were not made available in the analyzed record. Registries help identify studies and evidence gaps, but they do not allow for the completion of missing results through hypothesis [7].
13. Does the laboratory confirmation of the identity of ACE-031 mean that it is suitable for use in humans?
No. The correct molecular identity is only one element of the evaluation of a substance. Purity, impurities, formulation, production control, and clinical evidence address other questions. Even reliable confirmation of the presence of the appropriate fusion protein does not prove safety or efficacy. The analytical result should be interpreted only within the scope that actually encompasses the method used.
14. Does the product labeled as ACE-031 always contain the tested substance?
No. An analytical study from 2025 showed a discrepancy between the labeling and the composition of all 14 evaluated products. This result does not allow calculating the percentage of incorrectly labeled products across the market, but it shows that consistency cannot be assumed based on the labeling. Proper analytical characterization is needed to determine the identity of a specific material [5].
15. Does the lack of severe adverse reactions in a small study prove the safety of ACE-031?
No. Small and short-term studies have limited ability to detect rare or delayed adverse reactions. The safety assessment requires consideration of all reported events, exposure time, monitoring methods, and reasons for discontinuing the study. In the case of ACE-031, observations from the DMD program, whose course was limited due to safety concerns [8], are of particular importance.
16. Does the FDA identification number mean that ACE-031 is approved?
No. The UNII number serves to identify the substance and does not constitute a confirmation of the product's marketing authorization. The FDA clearly distinguishes the registration of the substance's identity from the process of evaluating and approving the drug. Therefore, the presence of ACE-031 in the identification database cannot be presented as evidence of its approved clinical use [1].
17. What studies would be needed to confirm the efficacy of ACE-031?
Appropriately controlled clinical trials using validated material and assessing functionally relevant endpoints would be needed. Sufficiently long follow-up observations, systematic safety assessment, and independent replication of the results would also be necessary. Changes in muscle mass, activity of the signaling pathway, or animal test results do not substitute for direct confirmation of clinical benefits.
Applications
ACE-031, ramatercept, is an experimental ActRIIB–Fc fusion protein developed to capture specific growth-regulating ligands associated with muscle growth.
The studies showed the biological activity of the substance and changes in selected parameters related to muscle mass and structure.
However, no sustained, clinically significant improvement in muscle function or a favorable balance of efficacy and safety were confirmed in humans.
Safety issues arose in the studies concerning Duchenne muscular dystrophy, which led to the termination of the program.
More recent animal studies provide additional mechanistic information, but they do not automatically change the conclusions from clinical studies.
The identity of the products labeled with the ACE-031 name also remains an important issue, because a 2025 analysis showed that the composition of all 14 evaluated samples did not match the expected fusion protein.
The most substantiated conclusion is that ACE-031 remains an experimental substance with documented biological activity, but without proven general use as a safe and effective agent to increase muscle mass or strength.
Educational reservation
The article is educational and scientifically informative in nature. It does not constitute medical advice, therapeutic recommendations, or instructions for the use, preparation, purchase, or administration of ACE-031.
Laboratory and animal studies do not confirm the safety or efficacy of products labeled ACE-031 in humans. Any potential clinical application requires appropriate research and regulatory assessment.
References
- U.S. Food and Drug Administration. (n.d.). Ramatercept (UNII: 42HQC6QLEK). UNII Search Service. Retrieved October 23, 2026, from https://precision.fda.gov/uniisearch/srs/unii/42hqc6qlek
- Attie, K. M., Borgstein, N. G., Yang, Y., Condon, C. H., Wilson, D. M., Pearsall, A. E., Kumar, R., Willins, D. A., Seehra, J. S., & Sherman, M. L. (2013). A single ascending-dose study of muscle regulator ACE-031 in healthy volunteers. Muscle & Nerve, 47(3), 416–423. https://doi.org/10.1002/mus.23539
- Campbell, C., McMillan, H. J., Mah, J. K., Tarnopolsky, M., Selby, K., McClure, T., Wilson, D. M., Sherman, M. L., Escolar, D., & Attie, K. M. (2017). Myostatin inhibitor ACE-031 treatment of ambulatory boys with Duchenne muscular dystrophy: Results of a randomized, placebo-controlled clinical trial. Muscle & Nerve, 55(4), 458–464. https://doi.org/10.1002/mus.25268
- Lee, S. J., Reed, L. A., Davies, M. V., Girgenrath, S., Goad, M. E., Tomkinson, K. N., Wright, J. F., Barker, C., Ehrmantraut, G., Holmstrom, J., Trowell, B., Gertz, B., Jiang, M. S., Sebald, S. M., Matzuk, M., Li, E., Liang, L. F., Quattlebaum, E., Stotish, R. L., & Wolfman, N. M. (2005). Regulation of muscle growth by multiple ligands signaling through activin type II receptors. Proceedings of the National Academy of Sciences of the United States of America, 102(50), 18117–18122. https://doi.org/10.1073/pnas.0505996102
- Reichel, C., Filip, T., Gmeiner, G., & Thevis, M. (2025). Gel electrophoretic detection of black market ACE-031. Drug Testing and Analysis, 17(10), 1934–1946. https://doi.org/10.1002/dta.3898
- Acceleron Pharma, Inc. (n.d.). A Safety, Tolerability, Pharmacokinetic and Pharmacodynamic Study of ACE-031 (ActRIIB-IgG1) in Healthy Postmenopausal Volunteers (NCT00755638) [Clinical trial registration]. ClinicalTrials.gov. Retrieved October 23, 2026, from https://clinicaltrials.gov/study/NCT00755638
- Acceleron Pharma, Inc. (n.d.). A Safety, Tolerability, Pharmacokinetic and Pharmacodynamic Study of ACE-031 in Healthy Postmenopausal Women (NCT00952887) [Clinical trial registration]. ClinicalTrials.gov. Retrieved October 23, 2026, from https://clinicaltrials.gov/study/NCT00952887
- Acceleron Pharma, Inc. (n.d.). Study of ACE-031 in Subjects With Duchenne Muscular Dystrophy (NCT01099761) [Clinical trial registration]. ClinicalTrials.gov. Retrieved October 23, 2026, from https://clinicaltrials.gov/study/NCT01099761
- Acceleron Pharma, Inc. (n.d.). Extension Study of ACE-031 in Subjects With Duchenne Muscular Dystrophy (NCT01239758) [Clinical trial registration]. ClinicalTrials.gov. Retrieved October 23, 2026, from https://clinicaltrials.gov/study/NCT01239758
- Cadena, S. M., Tomkinson, K. N., Monnell, T. E., Spaits, M. S., Kumar, R., Underwood, K. W., Pearsall, R. S., & Lachey, J. L. (2010). Administration of a soluble activin type IIB receptor promotes skeletal muscle growth independent of fiber type. Journal of Applied Physiology, 109(3), 635–642. https://doi.org/10.1152/japplphysiol.00866.2009
- Cadena, S. M., Bogdanovich, S., Khurana, T. S., Pullen, A., Pearsall, R. S., Curran, E., Faucette, R., Lane, J., Seehra, J., Lachey, J. L., Mizener, A. D., & Pistilli, E. E. (2026). ACE-031, a soluble activin type IIB receptor, increases muscle mass and strength in the common marmoset (Callithrix jacchus). PLOS ONE, 21(2), Article e0342666. https://doi.org/10.1371/journal.pone.0342666
- Cadena, S. M., Bogdanovich, S., Khurana, T. S., Pullen, A., Pearsall, R. S., Curran, E., Faucette, R., Lane, J., Seehra, J., Lachey, J. L., Mizener, A. D., & Pistilli, E. E. (2025). ACE-031, a soluble activin type IIB receptor, increases muscle mass and strength in the common marmoset (Callithrix jacchus) [Preprint]. bioRxiv. https://doi.org/10.1101/2025.10.01.679778