| Cas No.: | 35354-74-6 |
| Chemical Name: | NSC 293100; NSC293100; NSC-293100 |
| Synonyms: | NSC 293100; NSC293100; NSC-293100 |
| SMILES: | OC1=C(CC=C)C=C(C2=CC(CC=C)=CC=C2O)C=C1 |
| Formula: | C18H18O2 |
| M.Wt: | 266.33 |
| Sotrage: | 4°C for 1 year, -20°C for more than 2 years |
| Description: | Honokiol is a bioactive, biphenolic phytochemical that possesses potent antioxidative, anti-inflammatory, antiangiogenic, and anticancer activities by targeting a variety of signaling molecules. It inhibits the activation of Akt and enhances the phosphorylation of ERK1/ERK2. |
| In Vivo: | Honokiol-NM (40 mg/kg, p.o.) produces superior anticancer effects, and the PCNA, Cyclin D1 and cleaved caspase 3 expressions are 2.12, 1.92 and 1.68-fold significantly altered in this treated group[2]. |
| In Vitro: | Honokiol (0, 12.5, 25 and 50 μM) inhibits the growth of GBM cells and induces apoptosis, with IC50 of appr against 30 μM DBTRG-05MG cell. Honokiol-induced apoptosis of GBM cells is associated with the downregulation of the Rb protein and cleavage of PARP and Bcl-x (S/L). Honokiol (50 μM) increases the level of autophagy markers in GBM cells[1]. Honokiol has anticancer effect, and the IC50 values with MDA-MB-231, MDA-MB-468, and MDA-MB-453 cell lines is 16.99 ± 1.28 μM, 15.94 ± 2.35 μM and 20.11 ±3.13 μM respectively. Honokiol (3, 10 μM) produces significant inhibition on the spheroid number and spheroid sizes in the clonogenic assay[2]. Honokiol (0.1-1.0 μM) specifically inhibits washed human platelet aggregation stimulated by collagen, but not by other agonists. honokiol (0.6 and 1.0 μM) can concentration-dependently inhibit the collagen-induced ATP-release reaction in washed human platelets. Honokiol specifically inhibits platelet aggregation and the phosphorylation of Lyn, PLCγ2, and PKC stimulated with convulxin. Honokiol (5, 10 μM) significantly inhibits convulxin-stimulated MAPKs and Akt activation[3]. Honokiol (10, 20 μM) increases ERK1/2 phosphorylation in a dose-dependent manner depending on CaMK II activation[4]. |

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