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ACE-031 (1mg)

$180.00

Product Usage Disclaimer 

This material is supplied exclusively as a laboratory research chemical for in vitro scientific study. All descriptions and documentation are provided for informational and educational purposes only.

This compound is not approved for human or animal consumption, injection, ingestion, inhalation, topical use, or any other biological application. It must be handled only by qualified, trained personnel in a properly equipped laboratory.

This product is not a drug, supplement, food, cosmetic, or therapeutic agent, and it may not be rebranded, repackaged, or marketed as any such item. Misuse, mislabeling, or unauthorized application is strictly prohibited.

Nothing on this website constitutes medical advice, professional guidance, or a recommendation of use.

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Description

ACE-031 – Advanced Biochemical Mechanism & Signaling Profile

ACE-031 is a recombinant fusion protein consisting of the extracellular domain of the activin type IIB receptor (ActRIIB) linked to the Fc portion of human IgG. In research models, ACE-031 functions as a soluble decoy receptor that sequesters ligands involved in negative regulation of skeletal muscle growth, primarily myostatin (GDF-8) and related TGF-β superfamily members such as activins and GDF-11.


Receptor Kinetics & Ligand Binding

  • ActRIIB normally binds circulating myostatin and activins with high affinity

  • ACE-031 preserves the native ligand-binding region while lacking intracellular signaling domains

  • As a soluble receptor, ACE-031 sequesters ligands before they can bind to membrane-bound ActRIIB

  • This prevents the formation of the ActRIIB/ALK4 or ActRIIB/ALK5 receptor complexes required for canonical signaling

Researchers use ACE-031 to study ligand-receptor interactions, binding competition, and downstream suppression of inhibitory myokines in controlled models.


Smad Signaling Interference

Under normal conditions:

  1. Myostatin or activin binds ActRIIB

  2. Type I receptor (ALK4/ALK5) recruitment occurs

  3. Smad2/3 phosphorylation is triggered

  4. Smad2/3 form complexes with Smad4

  5. The complex translocates to the nucleus to regulate gene transcription

ACE-031 blocks Step 1 by binding circulating ligands, resulting in:

  • Reduced Smad2/3 phosphorylation

  • Lowered transcription of muscle-suppressive genes

  • Disinhibition of anabolic signaling pathways


Downstream Pathways & Gene Targets Studied

Suppression of Smad2/3 signaling allows researchers to examine changes in:

Muscle protein synthesis signaling

  • mTORC1 activation

  • Akt phosphorylation

  • Decreased expression of E3 ubiquitin ligases (e.g., MuRF1, MAFbx/Atrogin-1)

Satellite cell activity

  • Pax7, MyoD, Myf5 gene expression

  • Myoblast proliferation and myotube formation

  • Reduced expression of cell-cycle inhibitors involved in myostatin-mediated suppression

Extracellular matrix remodeling

  • Alterations in collagen-associated genes

  • Matrix signaling proteins involved in muscle fiber hypertrophy

This makes ACE-031 a frequent tool in studies of muscle atrophy, hypertrophy, and TGF-β–dependent transcriptional regulation.


Research Applications (In-Vitro / Laboratory Models Only)

ACE-031 is used to explore:

  • Myostatin ligand trapping and receptor competition

  • Disruption of TGF-β superfamily inhibitory signaling

  • Gene transcription changes resulting from decreased Smad2/3 activation

  • Cellular and molecular responses associated with skeletal muscle adaptation


Research-Only Classification

This material is supplied exclusively for in-vitro, laboratory research.
It is not a drug, supplement, therapy, or diagnostic agent, and is not approved for human or animal use.

Additional information

Weight N/A
Size

1 Mg