| Size | Price | Stock | Qty |
|---|---|---|---|
| 1mg |
|
||
| 5mg |
|
||
| 100mg | |||
| Other Sizes |
| Targets |
Ankaflavin primarily targets PPARγ (Peroxisome Proliferator-Activated Receptor Gamma), functioning as an orally active agonist. By activating PPARγ, it exerts anti-inflammatory, anti-cancer, anti-atherosclerotic, and hypolipidemic effects. The compound shows selective cytotoxicity towards cancer cells while sparing normal cells. Its anti-inflammatory activity involves modulation of inflammatory mediators. Ankaflavin induces apoptosis in cancer cells through PPARγ-mediated pathways.
|
|---|---|
| ln Vitro |
Ankaflavin (0-50 µg/mL, 48 h) exhibits cytotoxicity towards cancer cells, but normal cells are not significantly harmed [1]. Ankaflavin (0-30 µg/mL, 0-48 hours) in a dose- and time-dependent way stops the Hep G2 cell cycle in the sub-G1 phase [1]. In Hep G2 cells, ankaflavin (25 µg/mL, 48 h) causes apoptosis[1].
In vitro, Ankaflavin (0-50 µg/mL, 48 h) exhibits cytotoxicity towards cancer cells, while normal cells are not significantly harmed. The compound shows selective cytotoxic effects and induces cell death through apoptosis in cancer cells. Ankaflavin has anti-inflammatory, anti-cancer, anti-atherosclerotic, and hypolipidemic effects. Its PPARγ agonist activity has been confirmed in cell-based assays. The compound's anti-inflammatory activity is assessed by measuring inhibition of pro-inflammatory cytokine production. |
| ln Vivo |
Ankaflavin (10 mg/kg; oral; given once daily for 28 days) may enhance pancreatic and liver function in addition to its antidiabetic and anti-inflammatory properties [2].
In vivo, Ankaflavin (10 mg/kg; p.o.; daily for 28 days) shows antidiabetic and anti-inflammatory activity, improves liver function and pancreatic function. The compound is orally active and has been studied in animal models for its anti-inflammatory, anti-cancer, anti-atherosclerotic, and hypolipidemic effects. It shows selective cytotoxic effects towards cancer cells. Ankaflavin has potential therapeutic applications in treating inflammatory diseases and cancer. Further in vivo studies are ongoing to fully characterize its therapeutic potential. |
| Enzyme Assay |
Ankaflavin PPARγ binding assays involve measuring agonist activity at PPARγ. PPARγ activation is assessed using reporter gene assays or coactivator recruitment assays in cell-free systems. The compound's EC50 for PPARγ activation is determined through dose-response curves. Anti-inflammatory activity is assessed by measuring inhibition of pro-inflammatory cytokine production (e.g., TNF-α, IL-6) in cell-free systems. Anti-cancer activity is evaluated by assessing inhibition of cancer cell proliferation or induction of apoptosis. Assays are performed in appropriate buffer systems with positive controls such as known PPARγ agonists (e.g., rosiglitazone).
|
| Cell Assay |
Cytotoxicity assay[1]
Cell Types: A549, Hep G2, MRC-5 and WI-38 Tested Concentrations: 1, 10, 25 and 50 µg/mL Incubation Duration: 48 hrs (hours) Experimental Results: Shows cytotoxicity against A549 and Hep G2 cells No significant toxicity to normal cells (MRC-5 and WI-38) in a dose-dependent manner. Cell cycle analysis[1] Cell Types: Hep G2 Cell Tested Concentrations: 15, 20, 25 and 30 µg/mL Incubation Duration: 12, 24, 36 and 48 hrs (hours) Experimental Results: Induction of clear sub-G1 peak in Hep G2 cells at dose and time-dependent manner. Apoptosis analysis[1] Cell Types: Hep G2 Cell Tested Concentrations: 25 µg/mL Incubation Duration: 48 hrs (hours) Experimental Results: Hoechst staining shows significant chromatin condensation (fluorescent spots). Ankaflavin cell-based assays are conducted in cancer cell lines and normal cells. Cells are cultured in appropriate media at 37°C with 5% CO2 and treated with Ankaflavin at varying concentrations (0-50 µg/mL, 48 h). Cell viability is assessed by MTT or CCK-8 assays. Apoptosis is evaluated by Annexin V/PI staining and caspase activity assays. PPARγ activation is assessed by measuring target gene expression. Inflammatory markers are measured by ELISA. Selectivity is confirmed by comparing effects on cancer cells versus normal cells. Experiments are performed in triplicate with appropriate positive and negative controls. |
| Animal Protocol |
Animal/Disease Models: Wistar rats (4 weeks old), treated with methylglyoxal (MG) (600 mg/kg; oral) for 4 weeks to induce diabetes [2]
Doses: 10 mg/kg Route of Administration: Oral administration 28-day Experimental Results: PPARγ agonist activity exerted. Effectively reduces AGE (advanced glycation end products) levels in serum, liver and pancreas of MG-induced rats. Ankaflavin in vivo studies are conducted in rodent models of inflammation, cancer, diabetes, and atherosclerosis. Animals are treated with Ankaflavin via oral administration (e.g., 10 mg/kg; p.o.; daily for 28 days). Disease progression is monitored by appropriate endpoints. For anti-diabetic studies, blood glucose and insulin levels are measured. For anti-inflammatory studies, cytokine levels are measured. For anti-cancer studies, tumor growth is monitored. For anti-atherosclerotic studies, lipid profiles and atherosclerotic plaque formation are assessed. Animals are monitored for clinical signs. Tissues and blood samples are collected for histopathological and biomarker analysis. |
| ADME/Pharmacokinetics |
Ankaflavin (MW 386.48 g/mol, C23H30O5) is a natural azaphilone yellow pigment. It is soluble in DMSO and other organic solvents. The compound is stable under recommended storage conditions. Ankaflavin is orally active and has been studied for its pharmacokinetic properties in preclinical studies. Pharmacokinetic parameters such as half-life, bioavailability, and tissue distribution have been characterized. The compound is isolated from Monascus-fermented red rice.
|
| Toxicity/Toxicokinetics |
Ankaflavin is generally well-tolerated in preclinical studies at therapeutic doses. The compound is a natural pigment from Monascus-fermented products with established safety profiles. Its anti-inflammatory, anti-cancer, anti-atherosclerotic, and hypolipidemic effects have been demonstrated with acceptable safety profiles. No significant adverse effects have been reported in the available literature at research-use concentrations. The compound is intended for research use only. Standard safety precautions should be followed when handling. Comprehensive toxicological evaluation would be required for therapeutic development.
|
| References |
|
| Additional Infomation |
Reports indicate that Monascus purpureus and Monascus purpureus contain anoflavin, and relevant data is available for reference.
Ankaflavin is a natural azaphilone yellow pigment from Monascus-fermented red yeast rice and an orally active PPARγ agonist. It shows selective cytotoxic effects and induces apoptosis in cancer cells while sparing normal cells. Ankaflavin has anti-inflammatory, anti-cancer, anti-atherosclerotic, and hypolipidemic effects. It shows antidiabetic and anti-inflammatory activity, improving liver and pancreatic function in vivo. All applications are limited to non-human research use. |
| Molecular Formula |
C23H30O5
|
|---|---|
| Molecular Weight |
386.4813
|
| Exact Mass |
386.209
|
| CAS # |
50980-32-0
|
| PubChem CID |
15294091
|
| Appearance |
Light yellow to yellow solid powder
|
| Density |
1.15±0.1 g/cm3(Predicted)
|
| Boiling Point |
590.7±50.0 °C(Predicted)
|
| LogP |
4.223
|
| Hydrogen Bond Donor Count |
0
|
| Hydrogen Bond Acceptor Count |
5
|
| Rotatable Bond Count |
8
|
| Heavy Atom Count |
28
|
| Complexity |
757
|
| Defined Atom Stereocenter Count |
3
|
| SMILES |
CCCCCCCC(=O)[C@@H]1[C@H]2CC3=C(COC(=C3)/C=C/C)C(=O)[C@@]2(OC1=O)C
|
| InChi Key |
AQTJNEHGKRUSLT-ODTNPMSZSA-N
|
| InChi Code |
InChI=1S/C23H30O5/c1-4-6-7-8-9-11-19(24)20-18-13-15-12-16(10-5-2)27-14-17(15)21(25)23(18,3)28-22(20)26/h5,10,12,18,20H,4,6-9,11,13-14H2,1-3H3/b10-5+/t18-,20+,23-/m1/s1
|
| Chemical Name |
(3S,3aR,9aR)-9a-methyl-3-octanoyl-6-[(E)-prop-1-enyl]-3,3a,4,8-tetrahydrofuro[3,2-g]isochromene-2,9-dione
|
| HS Tariff Code |
2934.99.9001
|
| 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) |
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
|
|---|---|
| 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 | 2.5875 mL | 12.9373 mL | 25.8746 mL | |
| 5 mM | 0.5175 mL | 2.5875 mL | 5.1749 mL | |
| 10 mM | 0.2587 mL | 1.2937 mL | 2.5875 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.
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
