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Neobavaisoflavone Sale

(Synonyms: 新补骨脂异黄酮) 目录号 : GC30085

A natural isoflavone

Neobavaisoflavone Chemical Structure

Cas No.:41060-15-5

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10mM (in 1mL DMSO)
¥540.00
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5mg
¥491.00
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10mg
¥732.00
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产品描述

Neobavaisoflavone is a natural isoflavone that was first isolated from seeds of P. corylifolia, which are used in traditional herbal medicine to treat various skin diseases. Neobavaisoflavone has been found to have diverse effects in isolated mammalian cells, including inhibiting DNA polymerase and carboxylesterase 1 (Ki = 5.3 ?M).1,2 It also displays antibiotic activity against Gram-negative multidrug resistant bacteria.3

1.Sun, N.J., Woo, S.H., Cassady, J.M., et al.DNA polymerase and topoisomerase II inhibitors from Psoralea corylifoliaJ. Nat. Prod.61(3)362-366(1998) 2.Sun, D.X., Ge, G.B., Dong, P.P., et al.Inhibition behavior of fructus psoraleae's ingredients towards human carboxylesterase 1 (hCES1)Xenobiotica46(6)503-510(2016) 3.Mbaveng, A.T., Sandjo, L.P., Tankeo, S.B., et al.Antibacterial activity of nineteen selected natural products against multi-drug resistant Gram-negative phenotypesSpringerPlus4:823(2015)

Chemical Properties

Cas No. 41060-15-5 SDF
别名 新补骨脂异黄酮
Canonical SMILES O=C1C(C2=CC=C(O)C(C/C=C(C)\C)=C2)=COC3=CC(O)=CC=C13
分子式 C20H18O4 分子量 322.35
溶解度 DMSO : ≥ 31 mg/mL (96.17 mM) 储存条件 Store at -20°C
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1 mM 3.1022 mL 15.5111 mL 31.0222 mL
5 mM 0.6204 mL 3.1022 mL 6.2044 mL
10 mM 0.3102 mL 1.5511 mL 3.1022 mL
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Research Update

Neobavaisoflavone inhibits antitumor immunosuppression via myeloid-derived suppressor cells

Int Immunopharmacol 2022 Oct;111:109103.35944461 10.1016/j.intimp.2022.109103

Neobavaisoflavone (Neo), as a traditional Chinese medicine, is the active ingredient in the herb Psoralea corylifolial and has antitumor activity. Myeloid-derived suppressor cells (MDSCs), which are a heterogeneous population of haematopoietic cells of the myeloid lineage, have been reported to be closely related to the pathogenesis of tumour progression, but whether Neo can regulate MDSC expansion and function remains unclear. Here, we found that Neo could inhibit the expansion and suppressive function of MDSCs by targeting STAT3. Importantly, Neo inhibited the growth of 4T1 and LLC tumours in vivo, as well as lung metastasis of 4T1 tumours in vivo. Furthermore, we identified MDSCs as the direct targets by which Neo attenuated tumour progression. In addition, Neo notably enhanced anti-PD-1 efficacy in anti-PD-1-insensitive 4T1 tumours. Therefore, our study sheds light on the development of Neobased therapeutic strategies against cancer.

Neobavaisoflavone-mediated TH9 cell differentiation ameliorates bowel inflammation

Int Immunopharmacol 2021 Dec;101(Pt A):108191.34601328 10.1016/j.intimp.2021.108191

Neobavaisoflavone (Neo), is the active constituent of the herb Psoralea corylifolial, used in the traditional Chinese medicine, and has anti-inflammatory activity, but whether Neo could regulate colitis remains unclear. T helper 9 (TH9) cells, a subset of CD4+ T helper cells characterized by secretion of IL-9, have been reported to be involved in the pathogenesis of many autoimmune and inflammatory diseases, but whether Neo could control TH9 cell differentiation also remains unclear. Here, we found that Neo could decrease IL-9 production of CD4+ T cells by targeting PU.1 in vitro. Importantly, Neo had therapeutic effects on DSS-induced colitis. Furthermore, we identified TH9 cells as the direct target of Neo for attenuating bowel inflammation. Therefore, Neo could serve as a lead for developing new therapeutics against inflammatory bowel disease.

Neobavaisoflavone inhibits allergic inflammatory responses by suppressing mast cell activation

Int Immunopharmacol 2022 Sep;110:108953.35724607 10.1016/j.intimp.2022.108953

Neobavaisoflavone (NBIF), a monomolecular compound extracted from Psoralea corylifolia (Leguminosae), is commonly used in traditional Chinese medicine for multiple purposes. NBIF is known to exert anti-fungal and anti-tumor effects, and promote bone formation. Whether NBIF exhibits anti-allergic effects by regulating mast cell activation remains unclear. Therefore, we designed this study to investigate the anti-allergic effects of NBIF on IgE/Ag-induced mouse bone marrow-derived mast cells and ovalbumin-induced asthma, and the passive systemic anaphylaxis (PSA) reaction in mice. Our results showed that NBIF suppresses the production of leukotriene C4, prostaglandin D2 and inflammatory cytokines, and decreases the degranulation of BMMCs stimulated by IgE/Ag. A thorough investigation ascertained that NBIF suppresses the phosphorylation of mitogen-activated protein kinases, and represses the nuclear factor-κB-related signaling pathway. In addition, the oral administration of NBIF in mice inhibited the IgE-induced PSA reaction in a dose-dependent manner. Overall, we provide new insights into how NBIF regulates the IgE/Ag-mediated signaling pathways. Moreover, our investigation promotes the potential use of NBIF in treating allergy and asthma.

Neobavaisoflavone Induces Bilirubin Metabolizing Enzyme UGT1A1 via PPARα and PPARγ

Front Pharmacol 2021 Feb 8;11:628314.33628187 PMC7897654

UDP-glucuronosyltransferase 1A1 (UGT1A1) is an essential enzyme in mammals that is responsible for detoxification and metabolic clearance of the endogenous toxin bilirubin and a variety of xenobiotics, including some crucial therapeutic drugs. Discovery of potent and safe UGT1A1 inducers will provide an alternative therapy for ameliorating hyperbilirubinaemia and drug-induced hepatoxicity. This study aims to find efficacious UGT1A1 inducer(s) from natural flavonoids, and to reveal the mechanism involved in up-regulating of this key conjugative enzyme by the flavonoid(s) with strong UGT1A1 induction activity. Among all the tested flavonoids, Neobavaisoflavone (NBIF) displayed the most potent UGT1A1 induction activity, while its inductive effects were confirmed by both western blot and glucuronidation activity assays. A panel of nuclear receptor reporter assays demonstrated that NBIF activated PPARα and PPARγ in a dose-dependent manner. Meanwhile, we also found that NBIF could up-regulate the expression of PPARα and PPARγ in hepatic cells, suggesting that the induction of UGT1A1 by NBIF was mainly mediated by PPARs. In silico simulations showed that NBIF could stably bind on pocket II of PPARα and PPARγ. Collectively, our results demonstrated that NBIF is a natural inducer of UGT1A1, while this agent induced UGT1A1 mainly via activating and up-regulating PPARα and PPARγ. These findings suggested that NBIF can be used as a promising lead compound for the development of more efficacious UGT1A1 inducers to treat hyperbilirubinaemia and UGT1A1-associated drug toxicities.

Neobavaisoflavone Demonstrates Valid Anti-tumor Effects in Non-Small- Cell Lung Cancer by Inhibiting STAT3

Comb Chem High Throughput Screen 2022;25(1):29-37.33280587 10.2174/1386207323666201204135941

Aim and objective: Lung cancer is the most commonly occurring cancer, which contributes to the majority of death caused by cancer, where non-small-cell lung cancer (NSCLC) accounts for approximately 85% of lung cancer. To treat NSCLC, STAT3 has been identified as a target with therapeutic potential. The Neobavaisoflavone (NBIF) is one of the flavonoids of traditional Chinese medicine Psoralea corylifolial. Materials and methods: Human NSCLC cell lines, PC-9, H460, and A549, were applied to determine NBIF's anti-proliferative effects through cell viability and colony formation detection. The effect of NBIF on cell apoptosis was determined through flow cytometry-based assay. Western blotting was used in this study to confirm the levels of P-STAT3, Bcl-2, and Bax, which are apoptotic proteins. Results: It was observed that NBIF could decrease the cell viability and its migration and induce apoptosis in human NSCLC cell lines dose-dependently. Levels of P-STAT3, as well as the downstream signals of the STAT3 pathway, were downregulated, suggesting that the tumorsuppression effects of NBIF might be related to the inhibition of STAT3 signaling. Furthermore, NBIF could contribute to the upregulation of BAX and downregulation of BCL2. Conclusion: NBIF might perform the anti-NSCLC efficacy as a result of the inhibition of the STAT3 pathway. Besides, our work suggests that NBIF could provide therapeutic alternatives for NSCLC.