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ACE-031

IGF Axis & Muscle
ACVR2B-FcBimagrumab precursor

Overview

ACE-031, also known as ACVR2B-Fc or Bimagrumab precursor, is a recombinant fusion protein that combines the extracellular domain of the human activin receptor type IIB (ACVR2B) with the Fc portion of human IgG1. It is synthesized through recombinant DNA technology and is designed to act as a decoy receptor for myostatin and other ligands of the TGF-beta superfamily. This compound is primarily investigated for its potential to enhance muscle growth and strength by inhibiting signaling pathways that negatively regulate muscle mass. Researchers have explored ACE-031 in the context of muscle-wasting disorders, such as muscular dystrophy and cachexia, where it has shown promise in increasing muscle size and improving physical function in preclinical models. The mechanism of action of ACE-031 involves binding to myostatin and related ligands, preventing them from interacting with their natural receptors. This inhibition leads to an increase in muscle growth by promoting satellite cell activation and muscle protein synthesis. Pharmacokinetic studies of ACE-031 have shown that it has a relatively long half-life, allowing for less frequent dosing. Researchers have observed that the compound is stable and bioavailable when administered via injection, though specific half-life data by route is limited. As of the current research status, ACE-031 has been evaluated in early-phase clinical trials, but its development has faced regulatory challenges. It is not approved for therapeutic use, and further studies are needed to fully understand its safety and efficacy profile.

Mechanism of Action

ACE-031 functions by binding to myostatin and other ligands of the TGF-beta superfamily, such as activins, preventing their interaction with the activin receptor type IIB (ACVR2B). This blockade results in the promotion of muscle growth by enhancing satellite cell activation and muscle protein synthesis.

Half-Life

IntranasalNot applicable
OralNot applicable

The pharmacokinetic profile suggests a long half-life suitable for less frequent dosing, but specific data is limited.

Storage

Lyophilized

Stable for 2+ years at -20°C, 12 months at 4°C

Reconstituted

Use within 14 days when refrigerated at 4°C

Avoid

Avoid repeated freeze-thaw cycles, direct light

Solvent

Bacteriostatic water or sterile saline recommended

Solubility

Soluble in water and saline solutions, limited solubility in organic solvents.

Legal Status

🇩🇪DE

Not approved as a medicinal product. Not a controlled substance. Sale as research chemical is a legal grey area.

🇺🇸US

Not approved by the FDA as a medicinal product. Not scheduled by the DEA.

🇦🇺AU

Not listed in the Australian Register of Therapeutic Goods (ARTG).

🇬🇧UK

Not approved by the MHRA as a medicinal product.

Legal status information is provided for general reference only and may not reflect the most current regulatory changes. Always verify with official government sources before making any decisions.

10 Research Publications

Gel Electrophoretic Detection of Black Market ACE-031.

Human

Drug testing and analysis · 2025

Researchers studied black market products claiming to be ACE-031, a banned performance-enhancing substance. They found that most of these products contained a different protein instead of the intended compound, raising concerns about their safety and authenticity.

  • Of 14 tested black market products, 12 contained a protein that was not ACE-031 but rather the full-length human activin receptor IIB.
  • The study developed a detection method that successfully identified these products in rat serum for up to 48 hours after administration.
  • The presence of additional proteins in the black market products indicates potential risks associated with their use.
PubMed

Combined rapamycin and mesenchymal stem/stromal cells derived from induced pluripotent stem cells-mediated delivery of ACVR2B-Fc fusion protein reduces heterotopic ossification in a mouse model of fibrodysplasia ossificans progressiva.

Unknown

JBMR plus · 2025

Researchers studied a genetic condition called fibrodysplasia ossificans progressiva (FOP), which causes abnormal bone growth. They found that combining a specific protein treatment with stem cells from induced pluripotent stem cells significantly reduced this abnormal bone formation in a mouse model.

  • Researchers observed that the combination of rapamycin and stem cells effectively reduced heterotopic ossification in mice with FOP.
  • The study highlighted the role of the ACVR2B-Fc fusion protein in managing the effects of the disease.
  • Findings suggest a potential new approach for addressing abnormal bone growth associated with FOP.
PubMed

iMSC-mediated delivery of ACVR2B-Fc fusion protein reduces heterotopic ossification in a mouse model of fibrodysplasia ossificans progressiva.

In Vitro

Stem cell research & therapy · 2024

Researchers studied a rare genetic disease called fibrodysplasia ossificans progressiva (FOP), which causes abnormal bone growth. They found that using a specific type of stem cell, combined with a candidate drug, reduced this abnormal bone formation in a mouse model, suggesting a potential new approach for treatment.

  • Researchers observed that stem cells expressing ACVR2B-Fc reduced abnormal bone growth in a mouse model of FOP.
  • The study found that ACVR2B-Fc secreted by these stem cells decreased signaling pathways that lead to bone formation.
  • Local injections of these modified stem cells improved movement performance in the mice.
PubMed

Sex specificity of pancreatic cancer cachexia phenotypes, mechanisms, and treatment in mice and humans: role of Activin.

Human

Journal of cachexia, sarcopenia and muscle · 2022

Researchers studied the effects of pancreatic cancer cachexia, a severe muscle-wasting condition, in both mice and humans, focusing on how it differs between sexes. They found that male mice experienced more severe muscle loss compared to females, and this pattern was mirrored in human patients, where men showed greater muscle wasting than women. The hormone Activin was identified as a key factor driving this muscle loss, highlighting the need for sex-specific approaches in treatment development.

  • Male mice with pancreatic cancer exhibited earlier and more severe muscle loss compared to female mice.
  • In human patients, men experienced greater and faster muscle wasting than women during treatment for pancreatic cancer.
  • The hormone Activin plays a significant role in muscle loss, particularly in males, suggesting that sex differences are crucial for understanding and treating cachexia.
PubMed

ACVR2B antagonism as a countermeasure to multi-organ perturbations in metastatic colorectal cancer cachexia.

Animal

Journal of cachexia, sarcopenia and muscle · 2020

Researchers studied the effects of blocking a specific protein, ACVR2B, in mice with advanced colorectal cancer. They found that this intervention helped preserve muscle and fat mass, improved muscle strength, and maintained heart function, suggesting that targeting ACVR2B could be a promising approach to combat the muscle wasting and organ dysfunction associated with cancer cachexia.

  • Researchers observed significant loss of fat, bone, and skeletal muscle mass in mice with metastatic colorectal cancer.
  • The blockade of ACVR2B preserved fat and muscle mass, and improved muscle strength in these mice.
  • Heart function was fully maintained in mice treated with ACVR2B antagonism, despite the presence of cancer.
PubMed

Systemic blockade of ACVR2B ligands attenuates muscle wasting in ischemic heart failure without compromising cardiac function.

Animal

FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020

Researchers studied the effects of blocking ACVR2B ligands in mice with ischemic heart failure to see if it could help with muscle wasting without harming heart function. They found that while this treatment did not improve heart health, it effectively reduced muscle loss and preserved muscle size.

  • Blocking ACVR2B ligands did not improve heart function or prevent heart remodeling after ischemic injury.
  • The treatment reduced muscle wasting in chronic ischemic heart failure.
  • Muscle preservation was linked to changes in specific markers related to muscle growth and metabolism.
PubMed

Systemic Blockade of ACVR2B Ligands Protects Myocardium from Acute Ischemia-Reperfusion Injury.

Animal

Molecular therapy : the journal of the American Society of Gene Therapy · 2019

Researchers studied the effects of blocking specific proteins, known as ACVR2B ligands, on heart damage caused by restricted blood flow and subsequent restoration. They found that this blockade reduced heart injury and improved heart function in mice after such episodes.

  • Blocking ACVR2B ligands reduced heart tissue damage and improved heart function after ischemia-reperfusion injury.
  • The treatment also altered heart cell metabolism and reduced cell death under low-oxygen conditions.
  • Myostatin, a specific ACVR2B ligand, was found to worsen heart cell stress during low-oxygen situations.
PubMed

Prevention of chemotherapy-induced cachexia by ACVR2B ligand blocking has different effects on heart and skeletal muscle.

Animal

Journal of cachexia, sarcopenia and muscle · 2018

Researchers studied the effects of chemotherapy on heart and skeletal muscles in mice, focusing on a method to prevent muscle loss. They found that blocking certain proteins had a significant impact on skeletal muscle but only minor effects on the heart, suggesting different responses to chemotherapy in these tissues.

  • Chemotherapy caused similar muscle wasting in both skeletal and heart muscles, but the underlying mechanisms differed.
  • Blocking ACVR2B ligands significantly reduced muscle loss in skeletal muscle but had little effect on the heart.
  • The study identified specific genes that respond to blocking ACVR2B ligands, highlighting the unique responses of skeletal and cardiac muscles to chemotherapy.
PubMed

Antibody-based strategies for the detection of Luspatercept (ACE-536) in human serum.

Human

Drug testing and analysis · 2017

Researchers studied methods to detect Luspatercept, a protein that stimulates red blood cell production and may be misused in sports. They found two effective antibody-based techniques for identifying Luspatercept in human serum, which could be useful for anti-doping tests in the future.

  • One method, a commercial ELISA test, can quickly detect Luspatercept in small serum samples without cross-reacting with similar proteins.
  • Another method involves immunoprecipitation followed by specialized analysis, allowing for more precise detection of Luspatercept.
  • Both detection strategies are promising for future use in monitoring doping in sports due to Luspatercept's long-lasting presence in the body.
PubMed

ACVR2B/Fc counteracts chemotherapy-induced loss of muscle and bone mass.

Animal

Scientific reports · 2017

Researchers studied the effects of ACVR2B/Fc on muscle and bone loss caused by chemotherapy in mice. They found that ACVR2B/Fc effectively prevented the loss of muscle strength and bone density associated with the chemotherapy drug Folfiri, suggesting potential protective benefits against these side effects.

  • Folfiri chemotherapy led to significant muscle and bone loss in mice.
  • ACVR2B/Fc prevented the deterioration of muscle mass and strength during chemotherapy.
  • ACVR2B/Fc also preserved trabecular bone density in the femur and vertebrae affected by Folfiri.
PubMed

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This page is for informational and research purposes only. All information is based on published scientific literature. Nothing on this page constitutes medical advice or replaces consultation with a qualified healthcare professional.