Sequence: H-Ala-Trp-Arg-Gln-Asn-Thr-Arg-Tyr-Ser-Arg-Ile-Glu-Ala-Ile-Lys-Ile-Gln-Ile-Leu-Ser-Lys-Leu-Arg-Leu- NH2
Molecular Weight: 2956.5 g/mol
PubChem CID: 118732224
Peptide purity: greater than 98%
Other details: No TFA Salt, No Mannitol
Storage: Lyophilized peptide must be stored at -20°C and peptide solution at +4°C.
ACE-031 has low oral and excellent subcutaneous bioavailability.
The type IIB activin receptor (ACVR2B), that is a powerful regulator of muscle building in vivo, is available in soluble form as ACE-031. ACVR2B binds myostatin, a muscle development inhibitor, and then makes it inactive. Research carried out on mice models demonstrates that eliminating the activin receptor results in an increase in the mass of all of the muscle cells. Due of this relationship, ACE-031 has been studied in several clinical studies as a possible therapy for disorders that cause muscle wasting, such as Duchenne muscular dystrophy (DMD).
In a tiny placebo-controlled experiment, ACE-031 significantly increased lean body mass and the volume of the muscles in the thighs after only one dosage. After the injection, 29 days later, the results were seen. The research was especially exciting since it revealed a secondary, unsuspected result. Participants in trials who received ACE-031 saw improvements in their blood indicators of both fat and bone metabolism. This shows that ACE-031 likely limits fat storage and increases bone development in addition to being predominantly linked to muscle growth.
Research shows that a myostatin inhibitor like ACE-031 is the only way to achieve maximum skeletal muscle development. Furthermore, it seems that numerous pathways of myostatin blockage are most advantageous.
Myostatin may have a deleterious impact on the energy metabolism of muscles, according to research in mice. In other words, excessive myostatin causes severe muscular exhaustion. When the actions of the natural form of ACE-031 are blocked, it causes significant metabolic damage to the muscles and raised blood lactate levels in mice. Additionally, it causes a decrease in the number of blood vessels that supply muscle tissue. Adding ACE-031 not only encourages muscle development by inhibiting myostatin, but it also boosts your muscles' oxidative capacity, which guards against tiredness and the harmful consequences of free radical generation.
The potential of ACE-031 to enhance muscular function seems to be more complex than just myostatin inhibition. According to studies done on mice, ACE-031 may increase the muscle tissue's ability to generate force, in part by maintaining the energy supply and changing the muscle's thermodynamics to favour oxidative respiration. The mice's maximal and overall contractile forces were both increased by 40% and 25%, respectively, after receiving ACE-031. However, there was no overall difference in muscular exhaustion, showing that ACE-031 enhances muscle strength without changing energy dynamics.
In a recent clinical experiment, ACE-031 was subcutaneously injected once every two to four weeks. This caused a tendency toward maintenance of the 6-minute walk test, demonstrating the peptide's ability to maintain muscular function. Additionally, there was a tendency toward greater bone mineral density, decreased fat mass, and higher lean body mass.
Another mouse experiment in which mice were given either ACE-031, a stringent myostatin inhibitor, or a placebo demonstrated that ACE-031 had distinct effects on bone that are distinct from its effects on muscle. According to the findings, whereas both ACE-031 and the myostatin inhibitor increased muscle mass, only ACE-031 increased bone density. The femur, a bone susceptible to deterioration in senior people, had a 132% rise in bone density, while the density of the vertebrae increased by 27%. The findings were significant.
It is important to highlight that ACE-031 is a viable therapy for avoiding muscle atrophy in this situation since certain tumours manufacture myostatin on their own. Research in cell culture demonstrates that ACE-031 inhibits myostatin to stop muscle cell wasting. Inactivation of the normal form of ACE-031 and a decrease in the number of mitochondria (and hence a reduction in energy production) in muscle cells are two examples of the apparent direct impacts of cancer cells on muscle function.
Strength, lean body mass, and muscular composition are not the only factors that contribute to ACE-031's anti-cancer effects. It is obvious that preventing muscle loss during cancer therapy and in the presence of cancer significantly extends lifetime. Furthermore, myostatin inactivation in the presence of cancer enhances insulin sensitivity, decreases fat accumulation (lipodystrophy), lowers inflammation, and increases bone strength and rates of fracture repair.
F. Morvan et al., “Blockade of activin type II receptors with a dual anti-ActRIIA/IIB antibody is critical to promote maximal skeletal muscle hypertrophy” [PubMed]
H. Q. Han, X. Zhou, W. E. Mitch, and A. L. Goldberg, “Myostatin/activin pathway antagonism: molecular basis and therapeutic potential” [PubMed]
K. M. Attie et al., “A single ascending-dose study of muscle regulator ACE-031 in healthy volunteers” [PubMed]
N. Béchir et al., “ActRIIB blockade increases force-generating capacity and preserves energy supply in exercising mdx mouse muscle in vivo” [PubMed]
This product is intendend for lab research and development use only. These studies are performed outside of the body. This product is not medicines or drugs and has not been approved by the FDA or EMA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law. This product should only be handled by licensed, qualified professionals.
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