Apigenin

N° de catalogueS2262 Lot :S226206

Imprimer

Données techniques

Formule

C15H10O5

Poids moléculaire 270.24 Numéro CAS 520-36-5
Solubilité (25°C)* In vitro DMSO 54 mg/mL (199.82 mM)
Water Insoluble
Ethanol Insoluble
In vivo (Ajouter les solvants au produit individuellement et dans l'ordre.)
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
* <1 mg/ml signifie légèrement soluble ou insoluble.
* Veuillez noter que Selleck teste la solubilité de tous les composés en interne, et la solubilité réelle peut différer légèrement des valeurs publiées. Ceci est normal et est dû à de légères variations d'un lot à l'autre.
* Expédition à température ambiante (les tests de stabilité montrent que ce produit peut être expédié sans aucune mesure de refroidissement.)

Préparation des solutions mères

Activité biologique

Description Apigenin est un puissant inhibiteur de P450 pour le CYP2C9 avec un Ki de 2 μM.
Cibles
CYP2C9
2 μM(Ki)
In vitro Apigenin inhibits PKC by competing with adenosine triphosphate (ATP). This compound also reduces the level of TPA-stimulated phosphorylation of cellular proteins and inhibits TPA-induced c-jun and c-fos expression. It exhibits the reverting effect on the transformed morphology of v-H-ras transformed NIH3T3 cells. It has been shown to possess anti-mutagenic properties in a setting of nitropyrene-induced genotoxicity in Chinese hamster ovary cells. This chemical suppresses of LPS-induced cyclooxygenase-2 and nitric oxide synthase-2 activity and expression in mouse macrophages. It has been reported to inhibit protein kinase C activity, mitogen-activated protein kinase (MAPK), transformation of C3HI mouse embryonic fibroblasts and downstream oncogenes in v-Ha-ras-transformed NIH3T3 cells. This compound blocks peroxisome proliferation-regulated kinase (ERK), a MAPK in isolated hepatocytes. It has further been shown to down-regulate the expression of the Na+/Ca2+-exchanger, a protein important for calcium extrusion in neonatal rat cardiac myocytes. It induces a reversible G2/M and G0/G1 arrest by inhibiting p34 (cdc2) kinase activity, accompanied by increased p53 protein stability in epidermal cells and fibroblasts. It is also effective in inhibiting TNFα-induced intracellular adhesion molecule-1 upregulation in cultured human endothelial cells. It inhibits the expression of HIF-1α and VEGF via the PI3K/Akt/p70S6K1 and HDM2/p53 pathways in human ovarian cancer cells. It inhibits differentiation by suppressing MAPK signal transduction and reducing API transcription factor level in human keratinocytes. This compound also inhibits proliferating of human keratinocytes.
In vivo Apigenin down-regulates production of IL-4 in ovalbumin-immunized BALB/C mice. This compound inhibits melanoma lung metastases by impairing interaction of tumor cells with endothelium. It is shown to cause a significant increase in uterine weight and overall uterine concentration of estrogen receptor (ER)-α in female mice (64) and also suppresses prostate and breast cancer cell growth through estrogen receptor β1. This chemical suppresses the levels of IGF-I in prostate tumor xenografts and increases levels of IGFBP-3, a binding protein that sequesters IGF-I in vascular circulation. This compound (12.5 mg/kg) increases cell proliferation in the dentate gyrus of hippocampus of adult mice.
Caractéristiques Beaucoup plus puissant que le kaempférol et la myricétine dans l'inhibition de la CT-L.

Protocole (de référence)

Test cellulaire :

[5]
  • Lignées cellulaires

    WI-38, T-24, HT-1376 and PC-3 cells

  • Concentrations

    0, 1, 5, 10, 20, 30, 40, and 50 μg/ml

  • Temps d'incubation

    24 h

  • Méthode

    To measure the effect of apigenin on cell viability, the WI-38, T-24, HT-1376 and PC-3 cells were seeded in 24-well plates (1 × 105 cells/well) for 16-18 h. The cells were then treated with or without various concentrations (0, 1, 5, 10, 20, 30, 40, and 50 μg/ml) of this compound for 24 h. Each treatment was repeated 3 times. After the exposure period, the medium was removed and followed by washing the cells with PBS. The medium was then changed and incubated with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) solution (5 mg/ml)/well for 4 h. The medium was removed, and formazan was solubilised in isopropanol and measured spectrophotometrically at 563 nm. The percentage of viable cells was estimated by comparing them with the untreated control cells.
Étude animale :

[6]
  • Modèles animaux

    heterozygous C57BL/TGN TRAMP mice

  • Posologies

    20 and 50 μg/mouse/day

  • Administration

    p.o.

Références

  • https://pubmed.ncbi.nlm.nih.gov/9589348/
  • https://pubmed.ncbi.nlm.nih.gov/20306120/
  • https://pubmed.ncbi.nlm.nih.gov/17493651/
  • https://pubmed.ncbi.nlm.nih.gov/19441930/
  • https://pubmed.ncbi.nlm.nih.gov/25859163/
  • https://pubmed.ncbi.nlm.nih.gov/24067903/

Validation du produit par le client

<p>Western blotting confirmed that both GLUT-1 (A) and p-Akt (B) were expressed in Hep-2 cells in different apigenin and cisplatin concentration.</p>

, , Int J Clin Exp Pathol, 2014, 7(7):3938-3.

SKH-1 mice were subjected to UVB radiation (1000 J/m2 daily, 5 days), or topical apigenin (Api, 5 μmol, in 200 μl vehicle, DMSO: acetone 1:9) was applied 1 h prior to each UVB exposure. Mice were also sham-irradiated and treated with apigenin, and the control group of mice was subjected to sham irradiation and vehicle. 24 h after the final UVB exposure, the mice were euthanized, dorsal skin was harvested, fixed in formalin and paraffin-embedded. (A) Representative Hematoxylin and Eosin (H&E) staining of skin sections (scale bar, 100 μm). (B) Quantitation of epidermal thickness (mean ± SD), *, P < 0.001; **, P< 0.0001. Three sections per mouse and 3 mice per group were evaluated.

Données de [ , , Cell Signal, 2016, 28(5):460-468 ]

The effects of apigenin and GLUT-1 AS-ODNs on xenograft apoptosis (the second experiment), observed an under optical microscope (magnification, ×400), and the percentage of apoptotic cells in 100 cells per field was counted and used to calculate the mean apoptosis index (AI). AI, apoptotic index.

Données de [ , , Oncol Rep, 2015, 34(4):1805-14 ]

GLUT-1 mRNA expression levels were significantly reduced in the ACC-2 human adenoid cystic carcinoma cells following treatment with increasing doses of apigenin (P<0.05), as determined by reverse transcription-quantitative polymerase chain reaction. Following treatment with 10 µM apigenin, the expression levels of GLUT-1 mRNA did not vary significantly with increasing treatment duration (P>0.05). Following treatment with 40 and 160 µM apigenin, the expression levels of GLUT-1 mRNA were significantly reduced with increasing treatment duration. *P<0.05 vs. control. GLUT-1, glucose transporter-1.

Données de [ , , Mol Med Rep, 2015, 12(5):6461-6 ]

Selleck's Apigenin A été cité par 39 Publications

Apigenin promotes remodeling of peripheral and skeletal adipocytes in response to β3-AR and TLR4 activation [ Frontiers in Endocrinology, October 17, 2025, 1633584] PubMed: 41180186
Apigenin inhibits proliferation of human chondrosarcoma cells via cell cycle arrest and mitochondrial apoptosis induced by ROS generation-an in vitro and in vivo study [ International Journal of Clinical and Experimental Medicine, March 30, 2018, 1615-1631]
Synergism Antiproliferative Effects of Apigenin and Naringenin in NSCLC Cells [ Molecules, June 23, 2023, 4947] PubMed: 37446609
Apigenin induces apoptosis and counteracts cisplatin-induced chemoresistance via Mcl-1 in ovarian cancer cells [ Experimental and Therapeutic Medicine, June 11, 2020, 1329-1336] PubMed: 32742367
Apigenin inhibits lipid metabolism of hepatocellular carcinoma cells by targeting the histone demethylase KDM1A [ Phytomedicine, 2024, 135:156024] PubMed: 39341125
The Effects of Resveratrol and Apigenin on Jejunal Oxidative Injury in Ducks and on Immortalized Duck Intestinal Epithelial Cells Exposed to H2O2 [ Antioxidants (Basel), 2024, 13(5)611] PubMed: 38790716
Viscoelastic high-molecular-weight hyaluronic acid hydrogels support rapid glioblastoma cell invasion with leader-follower dynamics [ bioRxiv, 2024, 2024.04.04.588167] PubMed: 38617333
Connexin43 is associated with the progression of clear cell renal carcinoma and is regulated by tangeretin to sygergize with tyrosine kinase inhibitors [ Transl Oncol, 2023, 35:101712] PubMed: 37354638
Synergism Antiproliferative Effects of Apigenin and Naringenin in NSCLC Cells [ Molecules, 2023, 28(13)4947] PubMed: 37446609
Nao Tan Qing ameliorates Alzheimer's disease-like pathology by regulating glycolipid metabolism and neuroinflammation: A network pharmacology analysis and biological validation [ Pharmacol Res, 2022, 185:106489] PubMed: 36228869

POLITIQUE DE RETOUR
La politique de retour inconditionnelle de Selleck Chemical garantit une expérience d'achat en ligne fluide à nos clients. Si vous n'êtes en aucun cas satisfait de votre achat, vous pouvez retourner tout article dans les 7 jours suivant sa réception. En cas de problèmes de qualité du produit, qu'il s'agisse de problèmes liés au protocole ou au produit, vous pouvez retourner tout article dans les 365 jours suivant la date d'achat initiale. Veuillez suivre les instructions ci-dessous lors du retour des produits.

EXPÉDITION ET STOCKAGE
Les produits Selleck sont transportés à température ambiante. Si vous recevez le produit à température ambiante, soyez assuré que le service d'inspection de la qualité de Selleck a mené des expériences pour vérifier que le placement à température normale pendant un mois n'affectera pas l'activité biologique des produits en poudre. Après réception, veuillez stocker le produit conformément aux exigences décrites dans la fiche technique. La plupart des produits Selleck sont stables dans les conditions recommandées.

NON DESTINÉ À UN USAGE HUMAIN, VÉTÉRINAIRE DIAGNOSTIQUE OU THÉRAPEUTIQUE.