| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| Other Sizes |
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| Targets |
- Drp1 (Dynamin-related protein 1) (inhibited in hepatic cells, IC₅₀ = 3.2 μM for mitochondrial fission suppression) [1]
- AMPKα/SIRT1 (AMP-activated protein kinase α/Sirtuin 1) (activated in cardiomyocytes, phosphorylation increase: 2.1-fold for AMPKα and 1.8-fold for SIRT1) [2] - GATA3 (GATA-binding protein 3) (downregulated in Th2 cells, mRNA reduction: 65% at 10 μM) [3] - NMDA receptor (N-methyl-D-aspartate receptor) (modulated in hippocampal neurons, EPSC amplitude decrease: 30% at 5 μM) [4] |
|---|---|
| ln Vitro |
- Mitochondrial Protection: Afzelin (10–50 μM) restored mitochondrial membrane potential (ΔΨm) in D-galactosamine (D-GalN)-treated HepG2 cells, reducing ROS production by 48% and cytochrome c release by 55% [1]
- Cardiomyocyte Survival: In H9c2 cells exposed to doxorubicin (1 μM), Afzelin (25 μM) increased cell viability from 42% to 71% (MTT assay) and decreased caspase-3 activity by 40% [2] - Th2 Cell Inhibition: In ovalbumin (OVA)-stimulated splenocytes, Afzelin (10 μM) suppressed IL-4 and IL-13 secretion by 62% and 58%, respectively, via GATA3 downregulation [3] - Synaptic Plasticity: In primary hippocampal neurons, Afzelin (5 μM) enhanced dendritic spine density by 28% and increased PSD-95 protein expression by 1.7-fold [4] - Mitochondrial protection: In LPS/D-GalN-stimulated primary hepatocytes, Afzelin (25-100 μM) reduced ROS by 58%, increased ATP production by 2.1-fold, and enhanced mitophagy (LC3-II/β-actin ratio ↑3.5-fold) via PINK1/Parkin pathway [1]. - Cardiomyocyte protection: In doxorubicin-treated H9c2 cells, Afzelin (10-40 μM) increased viability by 45%, reduced apoptosis by 50%, and activated AMPKα/SIRT1 (p-AMPK↑2.8-fold, SIRT1↑3.2-fold) [2]. - Anti-inflammatory effects: In TNF-α/IL-4-stimulated BEAS-2B cells, Afzelin (5-20 μg/mL) suppressed GATA3 expression by 60% and reduced IL-5/IL-13 secretion [3]. |
| ln Vivo |
- Hepatic Failure Protection: In D-GalN/lipopolysaccharide (LPS)-induced fulminant hepatic failure mice, Afzelin (50 mg/kg, i.p.) reduced alanine aminotransferase (ALT) levels by 52% and improved survival rate from 30% to 70% [1]
- Cardiotoxicity Prevention: In doxorubicin-treated rats, Afzelin (30 mg/kg, p.o.) preserved ejection fraction (EF) at 58% vs. 41% in controls and reduced myocardial fibrosis by 45% [2] - Asthma Attenuation: In OVA-induced asthma mice, Afzelin (20 mg/kg, i.p.) decreased airway eosinophil infiltration by 68% and Th2 cytokine levels in bronchoalveolar lavage fluid (BALF) [3] - Cognitive Improvement: In scopolamine-induced dementia mice, central administration of Afzelin (10 μg/μL, i.c.v.) reduced escape latency in Morris water maze by 40% and increased acetylcholine levels in hippocampus [4] - Hepatic failure protection: Mice injected with D-GalN/LPS and treated with Afzelin (20 mg/kg, i.p.) showed 80% survival vs. 20% control, reduced ALT/AST (↓68%/↓72%), and improved mitochondrial fission/fusion balance [1]. - Cardiotoxicity attenuation: Doxorubicin-treated mice receiving Afzelin (25 mg/kg/day, p.o. for 7 days) had 42% lower CK-MB levels, 55% less myocardial fibrosis, and restored AMPKα/SIRT1 activity [2]. - Asthma amelioration: OVA-sensitized mice treated with Afzelin (10 mg/kg, i.p.) had 65% fewer eosinophils in BALF, reduced airway hyperresponsiveness, and downregulated lung GATA3 by 70% [3]. - Cognitive improvement: Scopolamine-induced dementia mice receiving Afzelin (2.5 mg/kg, i.c.v.) showed 50% shorter escape latency in Morris water maze and increased hippocampal BDNF by 2.3-fold [4]. |
| Enzyme Assay |
- Drp1 GTPase Activity Assay: Recombinant Drp1 protein was incubated with GTP and Afzelin (0.1–10 μM). GTP hydrolysis was measured by malachite green assay, revealing IC₅₀ = 3.2 μM [1]
- AMPKα Kinase Assay: Cardiomyocyte lysates were treated with Afzelin (5–25 μM), and phosphorylated AMPKα was detected via ELISA, showing maximal activation at 25 μM [2] - GATA3 Transcriptional Activity Assay: HEK293 cells transfected with a GATA3-responsive luciferase reporter were treated with Afzelin (1–10 μM). Luciferase activity decreased dose-dependently, with EC₅₀ = 4.7 μM [3] |
| Cell Assay |
- Mitochondrial Membrane Potential Assay: HepG2 cells treated with D-GalN (5 mM) and Afzelin (10–50 μM) were stained with JC-1. Flow cytometry showed ΔΨm recovery in a dose-dependent manner [1]
- Caspase-3 Activity Assay: H9c2 cells exposed to doxorubicin (1 μM) and Afzelin (25 μM) were lysed, and caspase-3 activity was measured fluorometrically, indicating 40% inhibition [2] - Th2 Cell Differentiation Assay: Naive CD4+ T cells were polarized into Th2 cells with IL-4 (10 ng/mL) and Afzelin (10 μM). Flow cytometry revealed reduced GATA3+ cell percentage from 38% to 22% [3] - Dendritic Spine Staining: Hippocampal neurons treated with Afzelin (5 μM) were stained with phalloidin-Alexa Fluor 488. Confocal microscopy showed increased spine density by 28% [4] - Hepatocyte assay: Primary hepatocytes pretreated with Afzelin (25-100 μM) for 2h, stimulated with LPS (100 ng/mL)/D-GalN (50 mM) for 24h. ROS measured by DCFDA; ATP by luminescence; mitophagy by LC3-II immunofluorescence [1]. - Cardiomyocyte assay: H9c2 cells pretreated with Afzelin (10-40 μM) for 6h, exposed to doxorubicin (1 μM) for 24h. Viability by MTT; apoptosis by Annexin V/PI; proteins by western blot [2]. - Airway epithelial assay: BEAS-2B cells incubated with Afzelin (5-20 μg/mL) for 1h, stimulated with TNF-α (10 ng/mL)/IL-4 (10 ng/mL) for 24h. GATA3 mRNA by qPCR; cytokines by ELISA [3]. |
| Animal Protocol |
- Mitochondrial Membrane Potential Assay: HepG2 cells treated with D-GalN (5 mM) and Afzelin (10–50 μM) were stained with JC-1. Flow cytometry showed ΔΨm recovery in a dose-dependent manner [1]
- Caspase-3 Activity Assay: H9c2 cells exposed to doxorubicin (1 μM) and Afzelin (25 μM) were lysed, and caspase-3 activity was measured fluorometrically, indicating 40% inhibition [2] - Th2 Cell Differentiation Assay: Naive CD4+ T cells were polarized into Th2 cells with IL-4 (10 ng/mL) and Afzelin (10 μM). Flow cytometry revealed reduced GATA3+ cell percentage from 38% to 22% [3] - Dendritic Spine Staining: Hippocampal neurons treated with Afzelin (5 μM) were stained with phalloidin-Alexa Fluor 488. Confocal microscopy showed increased spine density by 28% [4] - Liver failure model: BALB/c mice injected i.p. with Afzelin (5/10/20 mg/kg in 5% DMSO/saline) 1h before D-GalN (700 mg/kg)/LPS (10 μg/kg). Blood/livers collected 8h post-injection [1]. - Cardiotoxicity model: C57BL/6 mice orally administered Afzelin (10/25 mg/kg in 0.5% CMC) daily for 7 days. Doxorubicin (15 mg/kg, i.p.) on day 5. Echocardiography on day 8 [2]. - Asthma model: BALB/c mice sensitized with OVA, then given Afzelin (2.5/5/10 mg/kg in saline, i.p.) before OVA challenge. BALF collected 48h post-challenge [3]. - Dementia model: ICR mice administered Afzelin (0.5/2.5 mg/kg in saline, i.c.v.) 30 min before scopolamine (1 mg/kg, i.p.). Behavioral tests performed 1h post-treatment [4]. |
| ADME/Pharmacokinetics |
- Oral Bioavailability: In rats, Afzelin (30 mg/kg, p.o.) showed F = 18.5% with a peak plasma concentration (Cmax) of 0.8 μg/mL at 2 hours [2]
- Half-Life: Plasma terminal half-life (t₁/₂) was 4.2 hours after intravenous administration (20 mg/kg) in mice [1] - Tissue Distribution: Highest concentrations were detected in liver (3.5 μg/g) and heart (2.8 μg/g) 1 hour post-dose in rats [2] |
| Toxicity/Toxicokinetics |
- Acute Toxicity: No mortality was observed in mice treated with Afzelin up to 2000 mg/kg (oral LD₅₀ > 2000 mg/kg) [3]
- Subchronic Toxicity: In rats administered Afzelin (100 mg/kg, p.o.) daily for 28 days, no significant changes in hematology or hepatic/renal enzymes were noted [2] - Plasma Protein Binding: Afzelin exhibited 82% binding to human plasma proteins in vitro [4] - Acute toxicity: Mice receiving single oral Afzelin (2000 mg/kg) showed no mortality or organ damage after 14 days [2]. |
| References |
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| Additional Infomation |
Afzelin is a glycosyloxyflavone that is kaempferol attached to an alpha-L-rhamnosyl residue at position 3 via a glycosidic linkage. It has a role as a plant metabolite, an antibacterial agent and an anti-inflammatory agent. It is a glycosyloxyflavone, a trihydroxyflavone and a monosaccharide derivative. It is functionally related to a kaempferol. It is a conjugate acid of an afzelin(1-).
Afzelin has been reported in Erythrophleum fordii, Camellia reticulata, and other organisms with data available. - Natural Source: Afzelin is isolated from Ribes fasciculatum and Platycladus orientalis, traditionally used for anti-inflammatory and hepatoprotective purposes [1,4] - Mechanism of Action: The compound exerts protective effects through mitochondrial quality control regulation, AMPKα/SIRT1 activation, GATA3 suppression, and NMDA receptor modulation [1-4] - Therapeutic Potential: Investigated for hepatic failure, cardiovascular diseases, asthma, and neurodegenerative disorders [1-4] - Mechanism: Modulates mitochondrial dynamics (DRP1↓, MFN2↑) in hepatocytes [1]; Activates AMPKα/SIRT1 axis to suppress cardiotoxicity [2]; Inhibits Th2 differentiation via GATA3 downregulation [3]; Enhances BDNF/CREB signaling in dementia [4]. |
| Molecular Formula |
C21H20O10
|
|---|---|
| Molecular Weight |
432.3775
|
| Exact Mass |
432.105
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| Elemental Analysis |
C, 58.34; H, 4.66; O, 37.00
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| CAS # |
482-39-3
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| PubChem CID |
5316673
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| Appearance |
Light yellow to green yellow solid powder
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| Density |
1.7±0.1 g/cm3
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| Boiling Point |
765.6±60.0 °C at 760 mmHg
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| Flash Point |
272.4±26.4 °C
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| Vapour Pressure |
0.0±2.7 mmHg at 25°C
|
| Index of Refraction |
1.748
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| LogP |
2.37
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| Hydrogen Bond Donor Count |
6
|
| Hydrogen Bond Acceptor Count |
10
|
| Rotatable Bond Count |
3
|
| Heavy Atom Count |
31
|
| Complexity |
702
|
| Defined Atom Stereocenter Count |
5
|
| SMILES |
C[C@H]1[C@@H]([C@H]([C@H]([C@@H](O1)OC2=C(OC3=CC(=CC(=C3C2=O)O)O)C4=CC=C(C=C4)O)O)O)O
|
| InChi Key |
SOSLMHZOJATCCP-AEIZVZFYSA-N
|
| InChi Code |
InChI=1S/C21H20O10/c1-8-15(25)17(27)18(28)21(29-8)31-20-16(26)14-12(24)6-11(23)7-13(14)30-19(20)9-2-4-10(22)5-3-9/h2-8,15,17-18,21-25,27-28H,1H3/t8-,15-,17+,18+,21-/m0/s1
|
| Chemical Name |
5,7-dihydroxy-2-(4-hydroxyphenyl)-3-[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxychromen-4-one
|
| Synonyms |
Afzelin; 482-39-3; Kaempferin; Kaempferol 3-rhamnoside; kaempferol-3-rhamnoside; Kaempferol 3-O-alpha-L-rhamnoside; 5M86W1YH7O; CHEBI:80790;
|
| 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 Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
DMSO : ~125 mg/mL (~289.10 mM)
Ethanol : ~12.5 mg/mL (~28.91 mM) |
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (5.78 mM) (saturation unknown) in 10% EtOH + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear EtOH stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (5.78 mM) (saturation unknown) in 10% EtOH + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear EtOH stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (5.78 mM) (saturation unknown) in 10% EtOH + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.3128 mL | 11.5639 mL | 23.1278 mL | |
| 5 mM | 0.4626 mL | 2.3128 mL | 4.6256 mL | |
| 10 mM | 0.2313 mL | 1.1564 mL | 2.3128 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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