ACE-031 – 1mg

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ACE-031 – 1mg

Original price was: $89.99.Current price is: $69.99.

1 mg

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EXCELLENT SERVICE

Properties

Molecular Formula

C133H227N43O33

Molecular Weight 2956.5 g/mol
Monoisotopic Mass
Polar Area
Complexity6600
XLogP -8.1
Heavy Atom Count
Hydrogen Bond Donor Count 48
Hydrogen Bond Acceptor Count 40
Rotatable Bond Count 107
Physical Appearance Fine White Lyophilized Powder
Stability
PubChem LCSS

PubChem LCSS

Identifiers

CID118732224
CAS1621169-52-5
InChIInChI=1S/C133H227N43O33/c1-18-68(11)101(125(205)160-81(35-25-27-51-135)115(195)173-102(69(12)19-2)126(206)162-87(45-48-98(138)182)117(197)175-104(71(14)21-4)128(208)169-91(58-67(9)10)119(199)170-95(63-177)123(203)157-80(34-24-26-50-134)112(192)166-90(57-66(7)8)118(198)155-83(37-29-53-150-131(143)144)111(191)164-89(106(140)186)56-65(5)6)172-108(188)73(16)154-109(189)88(46-49-100(184)185)163-127(207)103(70(13)20-3)174-116(196)85(39-31-55-152-133(147)148)158-124(204)96(64-178)171-120(200)92(59-75-40-42-77(180)43-41-75)167-113(193)84(38-30-54-151-132(145)146)161-129(209)105(74(17)179)176-122(202)94(61-99(139)183)168-114(194)86(44-47-97(137)181)159-110(190)82(36-28-52-149-130(141)142)156-121(201)93(165-107(187)72(15)136)60-76-62-153-79-33-23-22-32-78(76)79/h22-23,32-33,40-43,62,65-74,80-96,101-105,153,177-180H,18-21,24-31,34-39,44-61,63-64,134-136H2,1-17H3,(H2,137,181)(H2,138,182)(H2,139,183)(H2,140,186)(H,154,189)(H,155,198)(H,156,201)(H,157,203)(H,158,204)(H,159,190)(H,160,205)(H,161,209)(H,162,206)(H,163,207)(H,164,191)(H,165,187)(H,166,192)(H,167,193)(H,168,194)(H,169,208)(H,170,199)(H,171,200)(H,172,188)(H,173,195)(H,174,196)(H,175,197)(H,176,202)(H,184,185)(H4,141,142,149)(H4,143,144,150)(H4,145,146,151)(H4,147,148,152)/t68-,69-,70-,71-,72-,73-,74+,80-,81-,82-,83-,84-,85-,86-,87-,88-,89-,90-,91-,92-,93-,94-,95-,96-,101-,102-,103-,104-,105-/m0/s1
InChIKeyHXWLNPUQPASIHW-OOXKGWPCSA-N
Isomeric SMILES
Canonical SMILES CC[C@H](C)[C@@H](C(=O)N[C@@H](CCCCN)C(=O)N[C@@H]([C@@H](C)CC)C(=O)N[C@@H](CCC(=O)N)C(=O)N[C@@H]([C@@H](C)CC)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CO)C(=O)N[C@@H](CCCCN)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](CCCNC(=N)N)C(=O)N[C@@H](CC(C)C)C(=O)N)NC(=O)[C@H](C)NC(=O)[C@H](CCC(=O)O)NC(=O)[C@H]([C@@H](C)CC)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](CO)NC(=O)[C@H](CC1=CC=C(C=C1)O)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H]([C@@H](C)O)NC(=O)[C@H](CC(=O)N)NC(=O)[C@H](CCC(=O)N)NC(=O)[C@H](CCCNC(=N)N)NC(=O)[C@H](CC2=CNC3=CC=CC=C32)NC(=O)[C@H](C)N
IUPAC Name (4S)-5-[[(2S)-1-[[(2S,3S)-1-[[(2S)-6-amino-1-[[(2S,3S)-1-[[(2S)-5-amino-1-[[(2S,3S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-amino-4-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-4-[[(2S,3S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-4-amino-2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-aminopropanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-5-carbamimidamidopentanoyl]amino]-5-oxopentanoyl]amino]-4-oxobutanoyl]amino]-3-hydroxybutanoyl]amino]-5-carbamimidamidopentanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-hydroxypropanoyl]amino]-5-carbamimidamidopentanoyl]amino]-3-methylpentanoyl]amino]-5-oxopentanoic acid

Description

ACE-031

Product is sold for prescriber purposes only. Please handle with care and follow all safety guidelines for the specific chemicals involved.

ACE-031, a recombinant fusion protein designed to inhibit myostatin and related ligands, has garnered attention for its potential to enhance muscle mass and strength. Myostatin, a member of the transforming growth factor-beta (TGF-β) superfamily, negatively regulates muscle growth. By binding to activin type II receptors, myostatin initiates signaling pathways that suppress muscle differentiation and growth. Inhibiting this pathway with ACE-031 can, therefore, promote muscle hypertrophy.(Wikipedia)

In a study examining the effects of ACE-031 on suboccipital musculature in rats, a 16-week administration of the inhibitor led to significant muscle hyperplasia. This muscular activation was associated with increased intracranial pressure, suggesting a functional role of the myodural bridge in cerebrospinal fluid dynamics. The findings underscore the systemic effects of localized muscle growth and the importance of understanding the broader physiological implications of myostatin inhibition. (PubMed)

Further research into myostatin and its inhibitors has demonstrated that blocking this pathway can lead to substantial increases in muscle mass. For instance, a study involving mice treated with a soluble activin type IIB receptor, which functions similarly to ACE-031, showed muscle mass increases of up to 60%. These results highlight the potent anabolic effects of myostatin inhibition and its potential therapeutic applications. (Wikipedia)

The therapeutic potential of ACE-031 extends beyond muscle hypertrophy. By promoting muscle growth, ACE-031 may offer benefits in conditions characterized by muscle wasting, such as muscular dystrophy or age-related sarcopenia. However, the systemic effects observed in studies, such as alterations in intracranial pressure, emphasize the need for comprehensive evaluations of safety and efficacy in long-term applications.

In conclusion, ACE-031 represents a promising avenue for enhancing muscle mass through myostatin inhibition. While preclinical studies in rats have demonstrated significant muscle growth, further research is essential to fully understand the systemic effects and therapeutic potential of this intervention.(Wikipedia)

References

  1. Zhang, Y., et al. “The relationship between myodural bridges, hyperplasia of suboccipital musculature, and cerebrospinal fluid dynamics.” PubMed, 2022. https://pubmed.ncbi.nlm.nih.gov/36054096/(PubMed)
  2. “Myostatin.” Wikipedia, 2025. https://en.wikipedia.org/wiki/Myostatin(Wikipedia)
  3. Nakamura, R., et al. “Adrenomedullin administration immediately after myocardial infarction ameliorates progression of heart failure in rats.” Circulation, 2004. https://pubmed.ncbi.nlm.nih.gov/15262849/(PubMed)
  4. Zimmermann, R., et al. “Effect of long-term ACE inhibition on myocardial tissue in hypertensive stroke-prone rats.” Journal of Molecular and Cellular Cardiology, 1999. https://pubmed.ncbi.nlm.nih.gov/10423343/(PubMed)
  5. Lavrentyev, E. N., & Malik, K. U. “High glucose-induced Nox1-derived superoxides downregulate PKC-betaII, which subsequently decreases ACE2 expression and ANG(1-7) formation in rat VSMCs.” American Journal of Physiology-Heart and Circulatory Physiology, 2009. https://pubmed.ncbi.nlm.nih.gov/18978194/(PubMed)

ALL LITERATURE, INFORMATION, AND DATA, PROVIDED ON THIS WEBSITE ARE FOR INFORMATIONAL AND EDUCATIONAL PURPOSES ONLY.

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