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| Targets |
Fustin targets multiple pathways and molecular entities involved in neurodegeneration and oxidative stress. It has been shown to increase muscarinic M1 receptor gene expression and binding activity. Fustin also modulates amyloid-β (Aβ)-induced toxicity, increases acetylcholine levels and choline acetyltransferase (ChAT) activity, while decreasing acetylcholinesterase (AChE) activity induced by Aβ(1-42). The compound protects against 6-hydroxydopamine-induced neuronal cell death, indicating activity against oxidative stress pathways. Fustin may also modulate the activity of antioxidant enzymes such as superoxide dismutase (SOD) and catalase, enhancing their ability to neutralize reactive oxygen species. In neuronal cells, fustin has been shown to modulate the levels of neurotransmitters and brain-derived neurotrophic factor (BDNF).
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| ln Vitro |
In vitro, fustin demonstrates significant antioxidant activity by scavenging free radicals and reducing oxidative stress markers. It has been shown to inhibit oxidative free radicals and inflammatory cytokines in cerebral cortex and hippocampus in cell-based models. Fustin modulates the activity of endogenous antioxidant enzymes, enhancing the cellular defense against reactive oxygen species. In neuronal cell models, fustin protects against 6-hydroxydopamine-induced cell death, a classic model of dopaminergic neurotoxicity. The compound also shows protective effects against Aβ-induced neurotoxicity, suggesting potential activity against Alzheimer's disease-related pathology. Fustin induces apoptosis in various cancer cell lines and modulates genes critical for cell cycle control and proliferation, showing promising anticancer activity.
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| ln Vivo |
Fustinis ((±)-Fustin; 3,7,3',4'-tetrahydroxyflavanone) (50-100 mg/kg; oral; daily for 11 days; Aβ-treated C57BL/6 mice) attenuated Aβ (1-42) - induced impairment of conditioned fear learning and passive avoidance behavior [1]. Fustinis ((±)-Fustin; 3,7,3',4'-tetrahydroxyflavanone) (50-100 mg/kg; oral; daily for 11 days; Aβ-treated C57BL/6 mice) alters Aβ (1-42) - causes changes in ACh levels, AChE and ChAT activity, and gene expression [1]. Increased fustinis ((±)-Fustin; 3,7,3',4'-tetrahydroxyflavanone) (50-100 mg/kg; oral; daily for 11 days; Aβ-treated C57BL/6 mice) Aβ(1-42)-induced reduction in M1 receptor mRNA and protein expression in Aβ-treated C57BL/6 mice. Fustin increases the expression of p-ERK and p-CREB in Aβ-treated C57BL/6 mice [1].
In vivo, fustin demonstrates neuroprotective effects, protecting against oxidative stress and neurodegeneration in animal models. Studies have shown that fustin inhibits oxidative free radicals and inflammatory cytokines in the cerebral cortex and hippocampus, and protects against cognitive impairment in streptozotocin-induced diabetic rats. Fustin modulates genes critical for cell cycle control and proliferation, showing promising anticancer activity in preclinical models. The compound's antioxidant and anti-inflammatory properties contribute to its neuroprotective effects in vivo. Fustin has been shown to improve cognitive function in animal models of diabetes-induced cognitive impairment, suggesting potential therapeutic applications for cognitive disorders. |
| Enzyme Assay |
Fustin's binding to muscarinic M1 receptor is assessed using radioligand binding assays. In these assays, membrane preparations from cells expressing the M1 receptor are incubated with a radiolabeled ligand (e.g., [3H]-ligand) and varying concentrations of fustin. Bound radioactivity is measured by scintillation counting to determine the binding affinity (Ki) of fustin for the receptor. Competition binding curves are generated to calculate IC50 values, which are then converted to Ki values using the Cheng-Prusoff equation. These assays provide quantitative information on the direct interaction between fustin and its target receptors.
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| Cell Assay |
Fustin is evaluated in cell-based models of neurotoxicity, including Aβ-induced neurotoxicity and 6-hydroxydopamine-induced neurotoxicity. SH-SY5Y or PC12 neuronal cells are pre-treated with fustin (1-100 µM) for various time periods, then exposed to neurotoxic insults such as Aβ(1-42) or 6-hydroxydopamine. Cell viability is measured by MTT or LDH release assays; oxidative stress markers (ROS, MDA, GSH) are quantified using fluorescent probes or colorimetric assays; apoptosis is assessed by flow cytometry or caspase activity assays. Inflammatory cytokine levels are measured by ELISA. These cell-based assays provide mechanistic insights into the neuroprotective effects of fustin.
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| Animal Protocol |
Animal/Disease Models: Aβ-treated C57BL/6 mice [1]
Doses: 50 and 100 mg/kg Route of Administration: po (po (oral gavage)) one time/day for 11 days Experimental Results: Ach, ChAT gene expression and ChAT activity increased. Reduce AChE gene expression and AChE activity. Animal/Disease Models: Aβ-treated C57BL/6 mice [1] Doses: 50 and 100 mg/kg Route of Administration: Oral; one time/day for 11 days Experimental Results: M2-, M3-, M4-, M5-, α4β , α7-receptor, p-ERK and p-CREB. Fustin is evaluated in animal models of neurodegeneration and cognitive impairment. In streptozotocin-induced diabetic rats, fustin is administered orally or intraperitoneally, and cognitive function is assessed using behavioral tests such as the Morris water maze or novel object recognition test. Oxidative stress markers and inflammatory cytokine levels are measured in brain tissues (cerebral cortex and hippocampus) following treatment. Neurodegeneration is assessed by histological staining and immunohistochemistry for markers of neuronal damage. These in vivo studies provide evidence for the neuroprotective and cognitive-enhancing effects of fustin. |
| ADME/Pharmacokinetics |
Dedicated pharmacokinetic studies for fustin are limited in the available literature. As a flavonoid compound, fustin is expected to be absorbed from the gastrointestinal tract following oral administration, undergo extensive first-pass metabolism, and be distributed to various tissues including the brain. Flavonoids generally have moderate oral bioavailability due to poor aqueous solubility and extensive metabolism. Fustin is likely metabolized by phase I and phase II enzymes in the liver and intestine, with metabolites excreted in urine and bile. The compound's ability to cross the blood-brain barrier is suggested by its neuroprotective effects observed in vivo.
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| Toxicity/Toxicokinetics |
The toxicity profile of fustin is not extensively characterized in the available literature. As a naturally occurring flavonoid from Rhus verniciflua Stokes, fustin is generally considered to have low toxicity. Flavonoids are generally well-tolerated at moderate doses, though high doses may cause gastrointestinal disturbances or interact with drug-metabolizing enzymes. Fustin's antioxidant properties suggest it may have a protective effect against oxidative damage rather than causing toxicity. However, comprehensive toxicological studies including acute, subchronic, and chronic toxicity assessments have not been reported in the available literature.
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| References | |
| Additional Infomation |
(+)-trans-fustin is the (2R,3R)-stereoisomer of fustin. Fustin has been reported in Virgilia oroboides, Capsicum annuum, and other organisms for which data are available. See also: whole (partial) Toxicodendron succedaneum.
Fustin is a research compound derived from the plant Rhus verniciflua Stokes, a traditional medicinal plant used in East Asian medicine. The compound is primarily used in preclinical research for its neuroprotective, antioxidant, and anti-inflammatory properties. Fustin is not approved as a therapeutic agent by any regulatory authority. The compound is of interest for the study of neurodegenerative diseases including Parkinson's disease, Alzheimer's disease, and diabetes-associated cognitive impairment. Fustin is also being investigated for its potential anticancer activity. The compound's mechanism of action involves modulation of multiple pathways including oxidative stress, inflammation, and neurotransmitter systems. |
| Molecular Formula |
C15H12O6
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|---|---|
| Molecular Weight |
288.25218
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| Exact Mass |
288.063
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| CAS # |
20725-03-5
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| PubChem CID |
5317435
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| Appearance |
White to off-white solid powder
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| Density |
1.6±0.1 g/cm3
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| Boiling Point |
644.2±55.0 °C at 760 mmHg
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| Melting Point |
216-217ºC
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| Flash Point |
249.2±25.0 °C
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| Vapour Pressure |
0.0±2.0 mmHg at 25°C
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| Index of Refraction |
1.729
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| LogP |
1.38
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| Hydrogen Bond Donor Count |
4
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
1
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| Heavy Atom Count |
21
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| Complexity |
400
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| Defined Atom Stereocenter Count |
2
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| SMILES |
C1=CC(=C(C=C1[C@@H]2[C@H](C(=O)C3=C(O2)C=C(C=C3)O)O)O)O
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| InChi Key |
FNUPUYFWZXZMIE-LSDHHAIUSA-N
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| InChi Code |
InChI=1S/C15H12O6/c16-8-2-3-9-12(6-8)21-15(14(20)13(9)19)7-1-4-10(17)11(18)5-7/h1-6,14-18,20H/t14-,15+/m0/s1
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| Chemical Name |
(2R,3R)-2-(3,4-dihydroxyphenyl)-3,7-dihydroxy-2,3-dihydrochromen-4-one
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.4692 mL | 17.3461 mL | 34.6921 mL | |
| 5 mM | 0.6938 mL | 3.4692 mL | 6.9384 mL | |
| 10 mM | 0.3469 mL | 1.7346 mL | 3.4692 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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