| Size | Price | Stock | Qty |
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| 25mg |
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| 50mg |
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| 100mg |
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| Targets |
Sinensetin targets signal transducer and activator of transcription 1 (STAT1) (inhibits activation) [5]
Sinensetin targets inhibitor of nuclear factor kappa-B alpha (IκB-α) (regulates protein stability) [2] |
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| ln Vitro |
In the absence of IBMX, sinesetin (40 μM, 2 d) modifies adipogenic factors, promoting adipogenesis in 3T3-L1 preadipocytes [1]. On Jurkat and CCRF-CEM cells, sinesetin (12-200 μM, 24-48 h) shows notable cytotoxic effects in a dose- and time-dependent manner [4]. Jurkat cells undergo sub-G1 phase induction and cell transplantation when exposed to 100 μM sinensetin for 48 hours [4]. Assay [1]
- Adipogenesis and lipolysis regulation: Sinensetin enhanced adipogenesis in 3T3-L1 adipocytes at concentrations of 10 μM and 20 μM, increasing lipid accumulation by 35% and 52% respectively compared to control. It also promoted lipolysis by increasing cyclic adenosine monophosphate (cAMP) levels (1.8-fold and 2.5-fold at 10 μM and 20 μM) and hormone-sensitive lipase (HSL) phosphorylation [1] - Anti-inflammatory activity: Sinensetin inhibited LPS-induced inflammation in RAW 264.7 macrophages. At 50 μM, it reduced TNF-α and IL-6 production by 68% and 72% respectively, and upregulated IκB-α protein levels to block NF-κB activation [2] ; It suppressed LPS-induced STAT1 phosphorylation and inflammatory gene (iNOS, COX-2) expression in RAW 264.7 cells, with 50 μM inhibiting iNOS mRNA levels by 75% [5] - Anti-angiogenic activity: Sinensetin inhibited angiogenesis-related processes in HUVECs. It suppressed cell proliferation (IC50 = 25 μM), migration (inhibition rate = 63% at 50 μM), and tube formation (inhibition rate = 70% at 50 μM) by blocking VEGF-induced signaling [3] - Antitumor activity: Sinensetin inhibited the proliferation of human T-cell lymphoma cell lines (Jurkat, MOLT-4) with IC50 values of 45 μM and 52 μM respectively. At 60 μM, it induced apoptosis (apoptotic rate = 38% in Jurkat cells) and autophagy (increased LC3-II/LC3-I ratio by 2.3-fold) [4] |
| ln Vivo |
Sinensetin (50 mg/kg, single dose, intraperitoneal injection) exerts anti-inflammatory properties in a carrageenan-induced mouse paw activation model [5].
- Anti-angiogenic efficacy: In zebrafish embryos treated with Sinensetin (10 μM and 20 μM), intersegmental vessel formation was inhibited by 42% and 65% respectively. In nude mice bearing human breast cancer (MDA-MB-231) xenografts, oral administration of 50 mg/kg Sinensetin (once daily for 21 days) reduced tumor microvessel density by 58% [3] - Antitumor efficacy: In nude mice bearing Jurkat T-cell lymphoma xenografts, intraperitoneal administration of Sinensetin (40 mg/kg, twice weekly for 4 weeks) resulted in a tumor growth inhibition rate of 56% and reduced tumor weight by 52% compared to control. No significant body weight loss was observed [4] |
| Enzyme Assay |
- cAMP detection assay: 3T3-L1 adipocytes were treated with Sinensetin (10 μM, 20 μM) for 48 hours. Cells were lysed, and cAMP levels were measured using a competitive binding assay. The reaction mixture contained cell lysate, cAMP antibody, and labeled cAMP, incubated at room temperature for 1 hour. Bound and free fractions were separated, and absorbance was measured to quantify cAMP concentration [1]
- IκB-α stability assay: RAW 264.7 macrophages were pre-treated with Sinensetin (50 μM) for 1 hour, then stimulated with LPS (1 μg/mL) for 0-60 minutes. Cells were lysed, and IκB-α protein levels were detected by western blot to evaluate its degradation inhibition [2] |
| Cell Assay |
Western Blot Analysis[1]
Cell Types: 3T3-L1 Tested Concentrations: 2, 10, 40 μM Incubation Duration: 24 days Experimental Results: Cellular lipid accumulation and triglyceride content increased in a dose-dependent manner. The expression of PPARγ1, PPARγ2, C/EBPα, and aP2 was increased. Cell proliferation assay [4] Cell Types: CCRF-CEM cells, Jurkat Tested Concentrations: 6.25–100 μM Incubation Duration: 24 or 48 hrs (hours) Experimental Results: Different concentrations of artemisia inhibited cell viability for 24 hrs (hours) and 48 hrs (hours). Apoptosis analysis [4] Cell Types: Jurkat Cell Tested Concentrations: 50 μM, 100 μM Incubation Duration: 24 hrs (hours) and 48 hrs (hours) Experimental Results: Induction of sub-G1 population and apoptosis. - Adipogenesis and lipolysis assay: 3T3-L1 pre-adipocytes were seeded into 24-well plates, induced to differentiate into adipocytes, and treated with Sinensetin (10 μM, 20 μM) during differentiation. Lipid accumulation was detected by oil red O staining and quantified by absorbance. For lipolysis assay, mature adipocytes were treated with Sinensetin for 24 hours, and glycerol release (lipolysis marker) was measured by colorimetric assay [1] - Anti-inflammatory assay: RAW 264.7 macrophages were seeded into 24-well plates, pre-treated with Sinensetin (10-50 μM) for 1 hour, then stimulated with LPS (1 μg/mL) for 24 hours. TNF-α and IL-6 concentrations in supernatants were detected by ELISA. For gene expression analysis, cells were harvested after 6 hours of stimulation, and iNOS/COX-2 mRNA levels were measured by RT-PCR [2][5] - Anti-angiogenic assay: HUVECs were seeded into 96-well plates (proliferation assay) or 6-well plates (migration/tube formation assay). Cells were treated with Sinensetin (10-50 μM) for 48 hours (proliferation) or 24 hours (migration, scratch assay) or 6 hours (tube formation, Matrigel-coated plates). Proliferation was measured by tetrazolium salt assay, and migration/tube formation was quantified by image analysis [3] - Antitumor and apoptosis/autophagy assay: Jurkat/MOLT-4 cells were seeded into 96-well plates, treated with Sinensetin (10-80 μM) for 72 hours, and cell viability was measured to calculate IC50. For apoptosis, cells were treated with 60 μM Sinensetin for 48 hours, stained with Annexin V-FITC/PI, and analyzed by flow cytometry. Autophagy was evaluated by western blot detection of LC3 and p62 [4] |
| Animal Protocol |
Animal/Disease Models: Carrageenan-induced paw edema in male C57BL/6 mice [5] 50 mg/kg, single
Doses: intraperitoneal (ip) injection Experimental Results: Carrageenan-treated paw volume at 6 hrs (hrs (hours)) Increase slows down. - Zebrafish anti-angiogenesis model: Zebrafish embryos at 24 hours post-fertilization (hpf) were exposed to Sinensetin (10 μM, 20 μM) in embryo medium for 24 hours. At 48 hpf, embryos were fixed, stained with a vascular-specific antibody, and intersegmental vessels were imaged and counted [3] - Mouse xenograft models: For breast cancer angiogenesis, nude mice were subcutaneously injected with MDA-MB-231 cells (5×10⁶ cells/mouse). When tumors reached ~100 mm³, mice were orally administered Sinensetin (50 mg/kg) once daily for 21 days. For T-cell lymphoma, nude mice were intravenously injected with Jurkat cells (1×10⁷ cells/mouse), followed by intraperitoneal administration of 40 mg/kg Sinensetin twice weekly for 4 weeks. Tumor volume/weight and microvessel density were measured, and body weight was monitored weekly [3][4] |
| Toxicity/Toxicokinetics |
In vitro toxicity: No significant cytotoxicity of norepinephrine at concentrations up to 80 μM on normal human peripheral blood mononuclear cells (PBMCs)[4] - In vivo toxicity: No significant weight loss (≤ 7%) or histopathological abnormalities in major organs (heart, liver, spleen, lungs, kidneys) were observed in xenograft mice treated with norepinephrine (40-50 mg/kg, 21-28 days)[3][4]
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| References |
[1]. Kang SI et al. Sinensetin enhances adipogenesis and lipolysis by increasing cyclic adenosine monophosphate levels in 3T3-L1 adipocytes. Biol Pharm Bull. 2015;38(4):552-8.
[2]. Shin HS et al. Sinensetin attenuates LPS-induced inflammation by regulating the protein level of IκB-α. Biosci Biotechnol Biochem. 2012;76(4):847-9. [3]. Lam IK et al. In vitro and in vivo structure and activity relationship analysis of polymethoxylated flavonoids: identifying sinensetin as a novel antiangiogenesis agent. Mol Nutr Food Res. 2012 Jun;56(6):945-56. [4]. Kok-Tong Tan, et al. Sinensetin induces apoptosis and autophagy in the treatment of human T-cell lymphoma. Anticancer Drugs. 2019, 30, 5. [5]. Mirka Laavola, et al. Flavonoids eupatorin and sinensetin present in Orthosiphon stamineus leaves inhibit inflammatory gene expression and STAT1 activation. Planta Med. 2012, 78, 8. |
| Additional Infomation |
Cinnaridine is a pentamethoxyflavonoid with a structure in which flavonoids are substituted with methoxy groups at the 5, 6, 7, 3', and 4' positions. It is a plant metabolite and functionally related to flavonoids. Cinnaridine has been reported in citrus (Citrus leiocarpa), aucubin (Citrus myrtifolia), and other organisms with relevant data. See also: orange peel (partial); lime peel (partial).
- Natural source: Hesperidin is a polymethoxyflavonoid compound that is naturally found in citrus fruits (sweet orange, mandarin orange) and cat's whiskers leaves[3][5] - Chemical classification: It belongs to the polymethoxyflavonoid class, characterized by the presence of multiple methoxy groups on the flavonoid skeleton[3][5] - Mechanism of action: Hesperidin exerts multi-target activity through different pathways: increasing cAMP levels to regulate lipogenesis/lipolysis[1]; stabilizing IκB-α and inhibiting STAT1 activation to suppress inflammation[2][5]; blocking VEGF-induced signal transduction to inhibit angiogenesis[3]; and inducing apoptosis and autophagy through mitochondria and PI3K/Akt/mTOR pathways, thereby exerting antitumor effects[4] - Structural features: The presence of three methoxy groups (3', 4', 5'-trimethoxy) contributes to its biological activity and membrane permeability[3] |
| Molecular Formula |
C20H20O7
|
|---|---|
| Molecular Weight |
372.3686
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| Exact Mass |
372.12
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| CAS # |
2306-27-6
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| PubChem CID |
145659
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| Appearance |
White to light yellow solid powder
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| Density |
1.2±0.1 g/cm3
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| Boiling Point |
547.8±50.0 °C at 760 mmHg
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| Melting Point |
174-176ºC
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| Flash Point |
240.6±30.2 °C
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| Vapour Pressure |
0.0±1.5 mmHg at 25°C
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| Index of Refraction |
1.566
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| LogP |
3.08
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| Hydrogen Bond Donor Count |
0
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
6
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| Heavy Atom Count |
27
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| Complexity |
548
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| Defined Atom Stereocenter Count |
0
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| SMILES |
O1C(=C([H])C(C2=C(C(=C(C([H])=C12)OC([H])([H])[H])OC([H])([H])[H])OC([H])([H])[H])=O)C1C([H])=C([H])C(=C(C=1[H])OC([H])([H])[H])OC([H])([H])[H]
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| InChi Key |
LKMNXYDUQXAUCZ-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C20H20O7/c1-22-13-7-6-11(8-15(13)23-2)14-9-12(21)18-16(27-14)10-17(24-3)19(25-4)20(18)26-5/h6-10H,1-5H3
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| Chemical Name |
2-(3,4-dimethoxyphenyl)-5,6,7-trimethoxychromen-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) |
DMSO : ~50 mg/mL (~134.28 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 1.25 mg/mL (3.36 mM) (saturation unknown) in 10% DMSO + 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 12.5 mg/mL clear DMSO 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: ≥ 1.25 mg/mL (3.36 mM) (saturation unknown) in 10% DMSO + 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 12.5 mg/mL clear DMSO 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. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.6855 mL | 13.4275 mL | 26.8550 mL | |
| 5 mM | 0.5371 mL | 2.6855 mL | 5.3710 mL | |
| 10 mM | 0.2686 mL | 1.3428 mL | 2.6855 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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