Yellow crystalline powder
5,6-Dihydroxy-4-oxo-2-phenyl-4H-chromen-7-yl 6-O-β-D-glucopyranosyl-β-D-glucopyranoside/Baicalin-7-diglucoside/Oroxin B/4H-1-Benzopyran-4-one, 7-[(6-O-β-D-glucopyranosyl-β-D-glucopyranosyl)oxy]-5,6-dihydroxy-2-phenyl-
Methanol; Ethanol; Water
957.5±65.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:114482-86-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
This study aims to investigate the anticancer effect of Oroxin B (OB) both in vitro and in vivo, and the molecular mechanism involved in microRNA-221 and the PI3K/Akt/PTEN pathway through modulation of apoptosis in Hepatocellular carcinoma (HCC). DEN-induced rats and HepG2 cells based on the microfluidic chip were employed, while the mRNA and protein expression of microRNA-221, PI3K, p-Akt and PTEN were evaluated by RT-PCR and Western blot analysis. Based on Microfluidic Chip and DEN-induced rat model, OB effectively exerts anti-liver cancer effect both in vitro and in vivo, and the expression of miR-221 in OB treated groups was significantly lower than that in the control group (** p < 0.01). The RT-PCR and Western blot results suggested the PI3K mRNA and protein in OB treated groups were both lower than those in control group and indicated the overexpression of PTEN. Therefore, OB effectively exerts anticancer effects by positively regulating the PTEN gene and then inactivating the PI3K/Akt signaling pathway through down-regulating the expression of the microRNA-221, thereby inducing apoptosis of liver cancer cells. This study offers a theoretical evidence for further development and clinical guidance of OB as an anti-tumor agent.
DEN-induced rats model; Microfluidic Chip; Oroxin B; PI3K/Akt/PTEN pathway; liver cancer; microRNA-221.
Oroxin B Induces Apoptosis by Down-Regulating MicroRNA-221 Resulting in the Inactivation of the PTEN/PI3K/AKT Pathway in Liver Cancer
Nannan Li 1 , Wenxiao Men 1 , Yibo Zheng 1 , Hechen Wang 1 , Xiansheng Meng 1 2 3 4
2019 Nov 30
A highly sensitive LC-MS/MS method was developed to measure oroxin B in rat plasma and tissue homogenates. The analyte and IS were isolated from biological matrices by a simple protein precipitation followed by centrifugation. Detection was conducted by electrospray negative-ionization mass spectrometry in selected-reaction monitoring mode. The assay was linear in the concentration range 4.52-904 ng/mL with intra- and inter-day precision of <14.41%. It was successfully applied to the pharmacokinetics and tissue distribution studies of oroxin B after an intravenous dose of 1.0 mg/kg in rats. The results would be useful for further development of oroxin B.
LC-MS/MS; oroxin B; pharmacokinetic study; tissue distribution.
Pharmacokinetics and Tissue Distribution of Oroxin B in Rats Using a Validated LC-MS/MS Assay
Kai Niu 1 , Huiyu Yan 2 , Chunjie Guo 3 , Sixi Zhang 2 , Wei Zhu 1 , Shiyong Teng 4
Cancer cells have both tumor-adaptive and -suppressive endoplasmic reticulum (ER) stress machineries that determine cell fate. In malignant tumors including lymphoma, constant activation of tumor-adaptive ER stress and concurrent reduction of tumor-suppressive ER stress favors cancer cell proliferation and tumor growth. Current ER stress-based anti-tumor drugs typically activate both tumor-adaptive and -suppressive ER stresses, resulting in low anti-cancer efficacy; hence, selective induction of tumor-suppressive ER stress and inhibition of tumor-adaptive ER stress are new strategies for novel anti-cancer drug discovery. Thus far, specific tumor-suppressive ER stress therapeutics have remained absent in clinical settings. In this study, we explored unique tumor-suppressive ER stress agents from the traditional Chinese medicinal herb Oroxylum indicum, and found that a small molecule oroxin B selectively induced tumor-suppressive ER stress in malignant lymphoma cells, but not in normal cells, effectively inhibited lymphoma growth in vivo, and significantly prolonged overall survival of lymphoma-xenografted mice without obvious toxicity. Mechanistic studies have revealed that the expression of key tumor-adaptive ER-stress gene GRP78 was notably suppressed by oroxin B via down-regulation of up-stream key signaling protein ATF6, while tumor-suppressive ER stress master gene DDIT3 was strikingly activated through activating the MKK3-p38 signaling pathway, correcting the imbalance between tumor-suppressive DDIT3 and tumor-adaptive GRP78 in lymphoma. Together, selective induction of unique tumor-suppressive ER stress and concurrent inhibition of tumor-adaptive ER stress in malignant lymphoma are new and feasible approaches for novel anti-lymphoma drug discovery and anti-lymphoma therapy.
Apoptosis; Cancer therapy; DDIT3; ER stress; GRP78; Lymphoma; Oroxin B.
Oroxin B Selectively Induces Tumor-Suppressive ER Stress and Concurrently Inhibits Tumor-Adaptive ER Stress in B-lymphoma Cells for Effective Anti-Lymphoma Therapy
Ping Yang 1 , Shilong Fu 1 , Zhifei Cao 1 , Huaidong Liao 1 , Zihe Huo 1 , Yanyan Pan 1 , Gaochuan Zhang 1 , Aidi Gao 1 , Quansheng Zhou 2
2015 Oct 15
Oroxin B (OB) is a flavonoid isolated from traditional Chinese herbal medicine Oroxylum indicum (L.) Vent. Oroxin B (OB) possesses obvious inhibitory effect and induces early apoptosis rather than late apoptosis on liver cancer cells through upregulation of PTEN, down regulation of COX-2, VEGF, PI3K, and p-AKT.Oroxin B (OB) selectively induces tumor-suppressive ER stress in malignant lymphoma cells.