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Antioxidant and chemopreventive
BML-EI345-0020 20 mg 84.00 USD
BML-EI345-0100 100 mg 336.00 USD
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Replaces Prod. #: ALX-385-008

Apigenin is an antioxidant flavonoid. Has chemopreventive and antitumor  properties. Induces apoptosis. Inhibits the proliferation of malignant tumor cells by G2/M arrest. Is a MAP-Kinase (MAPK/ERK) inhibitor. Inhibits hypoxia-inducible factor-1 (HIF-1) and vascular endothelial growth factor (VEGF) expression. Induces gastric relaxation in mouse stomach, mainly by suppressing Ca2+ influx through voltage-dependent calcium channels. Apigenin is a selective inhibitor of CK2. In WEHI 231 cells inhibition of CK2 by apigenin decreased the rate of IκBα turnover and nuclear levels of NF-κB (20 µM). It blocks proliferation of Wnt-1 transfected cells and abrogates phosphorylation of β-catenin. In a rat model of glomerulonephritis, inhibition of CK2 by apigenin ameliorates renal dysfunction.

Product Specification

Purity:≥97% (HPLC)
Appearance:light yellow to slightly brown powder
Solubility:Soluble in  diluted potassium hydroxyde or DMSO, slightly soluble in 100% ethanol (hot). Insoluble in water.
Long Term Storage:Ambient
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Product Literature References

Gastric relaxation induced by apigenin and quercetin: analysis of the mechanism of action: A. Rotondo et al.; Life. Sci. 85, 85 (2009), Abstract;
Apigenin and cancer chemoprevention: progress, potential and promise (review): D. Patel et al.; Int. J. Oncol. 30, 233 (2007), Abstract;
Apigenin blocks lipopolysaccharide-induced lethality in vivo and proinflammatory cytokines expression by inactivating NF-kappaB through the suppression of p65 phosphorylation: C. Nicholas et al.; J. Immunol. 179, 7121 (2007), Abstract;
Apigenin inhibits tumor angiogenesis through decreasing HIF-1alpha and VEGF expression: J. Fang et al.; Carcinogenesis 28, 858 (2007), Abstract;
Apigenin-induced cell cycle arrest is mediated by modulation of MAPK, PI3K-Akt, and loss of cyclin D1 associated retinoblastoma dephosphorylation in human prostate cancer cells: S. Shukla & S. Gupta; Cell Cycle 6, 1102 (2007), Abstract; R. Torkin et al.; Mol. Cancer. Ther. 4, 1 (2005), Abstract;
Inhibition of protein kinase CK2 prevents the progression of glomerulonephritis: M. Yamada et al.; PNAS 102, 7736 (2005), Abstract;
Phosphorylation by the protein kinase CK2 promotes calpain-mediated degradation of IkappaBalpha: J. Shen et al.; J. Immunol. 167, 4919 (2001), Abstract;
Apigenin inhibits endothelial-cell proliferation in G(2)/M phase whereas it stimulates smooth-muscle cells by inhibiting P21 and P27 expression: V. Trochon et al.; Int. J. Cancer. 85, 691 (2000), Abstract;
Endogenous protein kinase CK2 participates in Wnt signaling in mammary epithelial cells: D.H. Song et al.; J. Biol. Chem. 275, 23790 (2000), Abstract;
Structure-antioxidant activity relationships of flavonoids and phenolic acids: C. Rice-Evans et al.; Free Radic. Biol. Med. 20, 933 (1996), Abstract;
Reversion of v-H-ras-transformed NIH 3T3 cells by apigenin through inhibiting mitogen activated protein kinase and its downstream oncogenes: M. L. Kuo et al.; Biochem. Biophys. Res. Commun. 212, 767 (1995), Abstract;
Apigenin and tangeretin enhance gap junctional intercellular communication in rat liver epithelial cells: C. Chaumontet et al.; Carcinogenesis 15, 2325 (1994), Abstract;
Apigenin induces morphological differentiation and G2-M arrest in rat neuronal cells: F. Sato et al.; Biochem. Biophys. Res. Commun. 204, 578 (1994), Abstract;

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