Butin
Based on 1 publication(s) in Google Scholar
Butin is a major biologically active flavonoid isolated from the heartwood of Dalbergia odorifera with oral activity, with strong antioxidant, antiplatelet and anti-inflammatory activities. Butin significantly alleviates myocardial infarction and improves heart function, together with prevents diabetes-induced cardiac oxidative damage in rat.
For research use only. We do not sell to patients.
- Purity : 99.31%
- CAS No.: 21913-99-5
- Formula: C15H12O5
- Molecular Weight:272.26
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Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
Publications Citing Use of MedChemExpress (MCE) Butin
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Biological Activity
Description
In Vitro
Butin (12.5-50 μM, 6 h) reduces cell apoptosis and death caused by I/R injury in H9c2 cells, and this effect is dose-dependent[1].
Butin (12.5-50 μM, 6 h) disrupts the interaction between Nrf2 and Keap1 in a dose-dependent manner[1].
Butin (12.5-50 μM, 6 h) increases the expression of antioxidant genes at both the mRNA and protein levels[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:H9c2
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Concentration:12.5, 25, 50 μM
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Incubation Time:6 h
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Result:Increased cell survival in a dose-dependent manner.
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Cell Line:H9c2
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Concentration:12.5, 25, 50 μM
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Incubation Time:6 h
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Result:Increased the expression of GSH-px, GSH, SOD, CAT and HO-1.
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Cell Line:H9c2
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Concentration:12.5, 25, 50 μM
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Incubation Time:6 h
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Result:Increased the levels of Nrf2 in the cytoplasm and nucleus in a dose-dependent manner and enhanced the expressions of GSH-px, GSH, SOD, CAT and HO-1.
In Vivo
Butin (25-50 mg/kg, intraperitoneal injection, single dose) can reduce behavioral changes and neuronal conditions in rats with cerebral hemorrhage by reducing apoptosis and inflammatory responses[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57/BL6J mice induced by STZ(HY-13753)[1]
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Dosage:10, 20, 40 mg/kg; twice a day; 15 days
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Administration:Oral
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Result:Improved cardiac function, significant increases in LVSP, +dP/dtmax and -dP/dtmin, reduced myocardial infarction area, reduced caspase-3 activity and Bax/Bcl-2 ratio, reduced GSH-px, GSH, SOD, CAT and GR activity.
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Animal Model:Intracerebral hemorrhage rats[2]
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Dosage:25, 50 mg/kg; single dose
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Administration:Intraperitoneal injection (i.p.)
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Result:Increased the neurological score, significantly reduced the volume of hemorrhagic lesions, significantly reduced the Bax/Bcl-2 ratio and caspase-3 protein expression, and significantly reduced brain tissue inflammatory mediators tumor necrosis factor-α (TNF-α) and interleukin. Reduced levels of 6 (IL-6).
Chemical Information
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CAS No. 21913-99-5
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Appearance Solid
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Molecular Weight 272.26
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Formula C15H12O5
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Color Light yellow to light brown
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SMILES
O=C1CC(C2=CC=C(O)C(O)=C2)OC3=CC(O)=CC=C13
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Publications (1)
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Journal Impact Factor
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Most Recent
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Autophagy
ESRRA-ATG5-Mediated mitophagy enhances arginine metabolism to alleviate diabetic kidney disease. [Abstract]2025 Dec 23:1-25. PMID: 41376268
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (367.30 mM; Need ultrasonic; 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.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.08 mg/mL (7.64 mM); Clear solution
This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.08 mg/mL (7.64 mM); Clear solution
This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
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.
Protocols
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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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 Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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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
Purity & Documentation
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Data Sheet (278 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]. Duan J, et al. Protective effect of butin against ischemia/reperfusion-induced myocardial injury in diabetic mice: involvement of the AMPK/GSK-3β/Nrf2 signaling pathway. Sci Rep. 2017 Jan 27;7:41491. [Content Brief]
[2]. Li P, et al. Butin Attenuates Brain Edema in a Rat Model of Intracerebral Hemorrhage by Anti Inflammatory Pathway. Transl Neurosci. 2018 May 8;9:7-12. [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 |
|---|---|---|---|---|---|
| DMSO | 1 mM | 3.6730 mL | 18.3648 mL | 36.7296 mL | 91.8240 mL |
| 5 mM | 0.7346 mL | 3.6730 mL | 7.3459 mL | 18.3648 mL | |
| 10 mM | 0.3673 mL | 1.8365 mL | 3.6730 mL | 9.1824 mL | |
| 15 mM | 0.2449 mL | 1.2243 mL | 2.4486 mL | 6.1216 mL | |
| 20 mM | 0.1836 mL | 0.9182 mL | 1.8365 mL | 4.5912 mL | |
| 25 mM | 0.1469 mL | 0.7346 mL | 1.4692 mL | 3.6730 mL | |
| 30 mM | 0.1224 mL | 0.6122 mL | 1.2243 mL | 3.0608 mL | |
| 40 mM | 0.0918 mL | 0.4591 mL | 0.9182 mL | 2.2956 mL | |
| 50 mM | 0.0735 mL | 0.3673 mL | 0.7346 mL | 1.8365 mL | |
| 60 mM | 0.0612 mL | 0.3061 mL | 0.6122 mL | 1.5304 mL | |
| 80 mM | 0.0459 mL | 0.2296 mL | 0.4591 mL | 1.1478 mL | |
| 100 mM | 0.0367 mL | 0.1836 mL | 0.3673 mL | 0.9182 mL |