| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 10mg |
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| Other Sizes |
| 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 |
- Hepatic Failure Model: C57BL/6 mice received D-GalN (800 mg/kg, i.p.) and LPS (10 μg/kg, i.p.), followed by Afzelin (50 mg/kg, i.p.) 1 hour later. Serum ALT and survival were assessed at 24 hours [1]
- Cardiotoxicity Model: Sprague-Dawley rats received doxorubicin (2.5 mg/kg, i.p.) twice weekly for 4 weeks, with concurrent Afzelin (30 mg/kg, p.o.) daily. Echocardiography and histology were performed at week 4 [2] - Asthma Model: BALB/c mice were sensitized with OVA (10 μg) and alum (2 mg) on days 0 and 7, then challenged with OVA (1% aerosol) on days 14–16. Afzelin (20 mg/kg, i.p.) was administered daily from day 10 [3] - Dementia Model: ICR mice received scopolamine (1 mg/kg, i.p.) 30 minutes before behavioral tests. Afzelin (10 μg/μL) dissolved in saline was injected into the lateral ventricle (1 μL/site) 24 hours prior [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, the bioavailability of avzeline (30 mg/kg, orally) was 18.5%, with peak plasma concentration (Cmax) reaching 0.8 μg/mL at 2 hours [2]
- Half-life: In mice, the terminal plasma half-life (t₁/₂) was 4.2 hours after intravenous administration (20 mg/kg) [1] - Tissue distribution: In rats, the highest concentrations were detected in the liver (3.5 μg/g) and heart (2.8 μg/g) 1 hour after administration [2] |
| Toxicity/Toxicokinetics |
Acute toxicity: No deaths were observed in mice treated with up to 2000 mg/kg of Afzelin (oral LD₅₀ > 2000 mg/kg) [3] - Subchronic toxicity: No significant changes in hematology or liver/kidney enzymes were observed in rats after daily oral administration of Afzelin (100 mg/kg) for 28 days [2] - Plasma protein binding: In vitro experiments showed that Afzelin was bound to human plasma proteins in 82% [4] - Acute toxicity: No deaths or organ damage were observed in mice after a single oral administration of Afzelin (2000 mg/kg) for 14 days [2].
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| References |
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| Additional Infomation |
Afzelin is a glycosyl oxyflavonoid composed of kaempferol linked to an α-L-rhamnose residue at the 3-position via a glycosidic bond. It is a plant metabolite with antibacterial and anti-inflammatory properties. It is a glycosyl oxyflavonoid, trihydroxyflavonoid, and monosaccharide derivative whose function is related to kaempferol. It is the conjugate acid of afzelin(1-). Afzelin has been reported in Erythrophleum fordii, Camellia reticulata, and other organisms with relevant data.
- Natural source: Afzelin is isolated from Ribes fasciculatum and Platycladus orientalis and has traditionally been used for anti-inflammatory and hepatoprotective purposes [1,4] - Mechanism of action: This compound exerts its protective effects through mitochondrial quality control regulation, AMPKα/SIRT1 activation, GATA3 inhibition and NMDA receptor regulation [1-4] - Therapeutic potential: It has been investigated in the treatment of liver failure, cardiovascular disease, asthma and neurodegenerative diseases [1-4] - Mechanism: It regulates mitochondrial dynamics in hepatocytes (DRP1↓, MFN2↑) [1]; activates the AMPKα/SIRT1 axis to inhibit cardiotoxicity [2]; inhibits Th2 differentiation by downregulating GATA3 [3]; and enhances BDNF/CREB signaling in dementia [4]. |
| Molecular Formula |
C21H20O10
|
|---|---|
| Molecular Weight |
432.3775
|
| Exact Mass |
432.105
|
| Elemental Analysis |
C, 58.34; H, 4.66; O, 37.00
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| CAS # |
482-39-3
|
| PubChem CID |
5316673
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| Appearance |
Light yellow to green yellow solid powder
|
| 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
|
| Vapour Pressure |
0.0±2.7 mmHg at 25°C
|
| Index of Refraction |
1.748
|
| LogP |
2.37
|
| 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)
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| 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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