MyoMed 205
Based on 1 Customer Validation
MyoMed 205 is an orally active muscle ring finger protein 1 (MuRF1) inhibitor. MyoMed-205 reduces ubiquitination and subsequent proteasomal degradation of muscle proteins by inhibiting MuRF1 activity. MyoMed 205 augments muscle performance, attenuates muscle weight loss and alleviates disease-induced weight loss. MyoMed 205 can be used for the research of cancer cachexia, type 2 diabetes mellitus, and heart failure with preserved ejection fraction.
연구목적의 판매만을 진행합니다. 환자를 대상으로 한 판매는 하지 않습니다.
- Purity : 98.10%
- CAS No.: 2614161-13-4
- 화학식: C26H25N3O5S
- 분자량:491.56
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보관:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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용액&용해도
- Protocol
- 순도&문서
- References
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Help & FAQs
Biological Activity
제품 설명
In Vivo
MyoMed 205 (1 g/kg; p.o.; continuously; 24 days) increases body weight, lean mass, fat content, and muscle strength in healthy C57BL/6N mice without altering food intake[1].
MyoMed 205 (1 g/kg; p.o.; diet supplementation; continuously; 28 days) significantly attenuates muscle holding impulse loss in diet-induced obese type 2 diabetic mice and normalizes their lymphocyte-granulocyte blood counts, with no significant impact on serum glucose[2].
MyoMed 205 (0.1% w/w in rat chow; p.o.; daily; 12 weeks) improves myocardial diastolic function, attenuates skeletal muscle atrophy, and restores skeletal muscle force in obese ZSF1 rats with HFpEF, while reducing pathological molecular alterations in both tissues[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6N (male, 8 months old, initial bodyweight 25.1 g, inoculated subcutaneously with B16F10 melanoma cells)[1]
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Dosage:0.1% (w/w) in mouse chow Tu-205
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Administration:p.o.; continuously; day 3 to day 24 post-tumor inoculation
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Result:Attenuated tumor-induced bodyweight loss to 2% at day 12 vs. 5% in untreated tumor-bearing mice.
Preserved muscle strength as measured by wire hang test holding impulses at days 9, 16, and 23.
Attenuated wasting of soleus, tibialis anterior, and extensor digitorum longus (EDL) muscles, with the greatest effect on EDL muscle mass preservation.
Attenuated epididymal fat tissue loss, protected against thymus atrophy, and reduced splenomegaly.
Restored mitochondrial citrate synthase activity in EDL muscle.
Rescued mitochondrial complex I activity in EDL muscle.
Normalized tumor-induced elevated MuRF1 protein levels in EDL muscle to control levels.
Normalized tumor-induced elevated ubiquitin K48-modified protein levels in EDL muscle to control levels.
Partially normalized tumor-induced elevated Nox2 and nitro-tyrosine (ROS stress markers) in EDL muscle.
Normalized tumor-induced depleted LC3 I/II ratio in EDL muscle to control levels.
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Animal Model:C57/Bl6 (male, diet-induced obese type 2 diabetic model)[2]
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Dosage:1 g/kg
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Administration:diet supplementation; continuously; 28 days
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Result:Attenuated progressive loss of muscle holding impulse, with significantly improved latency time at day 28 compared to untreated mice.
Normalized lymphocyte-granulocyte ratios and absolute counts in sera, reversing diabetic stress-induced lymphopenia.
Showed no significant effects on basal serum glucose or glucose tolerance.
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Animal Model:ZSF1 rats (20-week-old female, obese)[3]
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Dosage:0.1% w/w in rat chow
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Administration:p.o.; daily; 12 weeks
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Result:Increased EDL muscle weight normalized to tibia length compared.
Attenuated TA muscle weight loss and myofibre cross-sectional area loss.
Restored maximal absolute muscle force in EDL and soleus to levels not significantly different from lean controls.
Improved maximal specific force in EDL.
Reduced MuRF1 and Trim72 protein expression, and reduced total muscle protein ubiquitination in TA muscle.
Increased mitochondrial complex I activity, and up-regulated protein synthesis of mitochondrial complexes I-V and citrate synthase enzyme activity in TA muscle.
Down-regulated uncoupling protein 3 (UCP3) expression in TA muscle.
Improved diastolic function, including reduced E/e' ratio, left ventricular end-diastolic pressure (LVEDP), and left ventricular stiffness constant beta.
Restored left ventricular ejection fraction (LVEF) to lean control levels.
Reduced perivascular fibrosis and matrix metalloproteinase-2 (MMP2) activity.
Normalized titin phosphorylation status.
Increased left ventricular cGMP levels.
Reduced advanced glycation end-products (AGEs).
Reduced mRNA expression of ANP, collagen-1 (Col1a1), and collagen-3 (Col3a1) to levels not significantly different from lean controls.
Slightly but significantly reduced heart weight normalized to tibia length.
Produced significantly greater body weight gain over 12 weeks.
Chemical Information
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CAS No. 2614161-13-4
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Appearance Solid
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분자량 491.56
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화학식 C26H25N3O5S
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Color White to off-white
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SMILES
O=C1OC2=C(C(C)=C1)C=CC(OCC3=CC=C(C(NCCNC(NCC4=CC=CS4)=O)=O)C=C3)=C2
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
용액&용해도
In Vitro:
DMSO : 25 mg/mL (50.86 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocol
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
순도&문서
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Data Sheet (276 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
[1]. Adams V, et al. Small-Molecule Chemical Knockdown of MuRF1 in Melanoma Bearing Mice Attenuates Tumor Cachexia Associated Myopathy. Cells. 2020;9(10):2272. Published 2020 Oct 11. [Content Brief]
[2]. Labeit S, et al. Regulation of Glucose Metabolism by MuRF1 and Treatment of Myopathy in Diabetic Mice with Small Molecules Targeting MuRF1. Int J Mol Sci. 2021;22(4):2225. Published 2021 Feb 23. [Content Brief]
[3]. Adams V, et al. Targeting MuRF1 by small molecules in a HFpEF rat model improves myocardial diastolic function and skeletal muscle contractility. J Cachexia Sarcopenia Muscle. 2022;13(3):1565-1581. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
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| DMSO | 1 mM | 2.0343 mL | 10.1717 mL | 20.3434 mL | 50.8585 mL |
| 5 mM | 0.4069 mL | 2.0343 mL | 4.0687 mL | 10.1717 mL | |
| 10 mM | 0.2034 mL | 1.0172 mL | 2.0343 mL | 5.0858 mL | |
| 15 mM | 0.1356 mL | 0.6781 mL | 1.3562 mL | 3.3906 mL | |
| 20 mM | 0.1017 mL | 0.5086 mL | 1.0172 mL | 2.5429 mL | |
| 25 mM | 0.0814 mL | 0.4069 mL | 0.8137 mL | 2.0343 mL | |
| 30 mM | 0.0678 mL | 0.3391 mL | 0.6781 mL | 1.6953 mL | |
| 40 mM | 0.0509 mL | 0.2543 mL | 0.5086 mL | 1.2715 mL | |
| 50 mM | 0.0407 mL | 0.2034 mL | 0.4069 mL | 1.0172 mL |
MyoMed 205 Related Classifications
HY-164027 Related Classifications
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