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Millepachine Sale

目录号 : GC61065

Millepachine是来自中草药MillettiapachycarpaBenth的生物活性天然查尔酮,在体内外对多种人类癌细胞均显示出强大的抗肿瘤作用。

Millepachine Chemical Structure

Cas No.:1393922-01-4

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5mg
¥2,250.00
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10mg
¥3,600.00
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产品描述

Millepachine is a bioactive natural chalcone from Chinese herbal medicine Millettia pachycarpa Benth, exhibits strong antitumor effects against numerous human cancer cells both in vitro and in vivo[1].

Millepachine (1.25-20 μM; 48 h) remarkably inhibits the proliferation of cisplatin-resistant A2780CP cells[1].Millepachine (2-8 μM; 24 or 48 h) induces G2/M arrest and apoptosis cisplatin-sensitive A2780S and cisplatin-resistant A2780CP cells[1].Millepachine (2-8 μM; 24 h) decreases topoisomerase II levels in A2780S and A2780CP cells[1].Millepachine (2-8 μM; 24 h) inhibits ATP-binding cassette transporter activity in A2780CP cells[1]. Cell Proliferation Assay[1] Cell Line: A2780CP cells

Millepachine (20 mg/kg; i.v. every two days for 14 day) inhibits tumor growth in mice[1].Millepachine (20 mg/kg; i.v. every two days for 14 day) does not induce acquired drug resistance in an excised A2780S xenograft model[1]. Animal Model: Female BALB/c nude mice (6 weeks) are injected A2780S or A2780CP cells[1]

[1]. Wu W, et, al. Millepachine showed novel antitumor effects in cisplatin-resistant human ovarian cancer through inhibiting drug efflux function of ATP-binding cassette transporters. Phytother Res. 2018 Dec; 32(12):2428-2435.

Chemical Properties

Cas No. 1393922-01-4 SDF
Canonical SMILES O=C(C1=C2C(C=CC(C)(C)O2)=C(OC)C=C1)/C=C/C3=CC=C(OC)C=C3
分子式 C22H22O4 分子量 350.41
溶解度 储存条件 Store at -20°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.8538 mL 14.269 mL 28.538 mL
5 mM 0.5708 mL 2.8538 mL 5.7076 mL
10 mM 0.2854 mL 1.4269 mL 2.8538 mL
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Research Update

Millepachine, a potential topoisomerase II inhibitor induces apoptosis via activation of NF-κB pathway in ovarian cancer

Oncotarget 2016 Aug 9;7(32):52281-52293.PMID:27447570DOI:10.18632/oncotarget.10739.

Millepachine (MIL) was a novel chalcone that was separated from Millettia pachycarpa Benth (Leguminosae). We found MIL induced apoptosis through activating NF-κB pathway both in SK-OV-3 and A2780S cells. Western blot showed that MIL increased the levels of IKKα, p-IKKα/β, p-IκBα and NF-κB (p65) proteins, and decreased the expression of IκBα protein. Immunohistochemistry analysis indicated that translocation of NF-κB into the nucleus increased in both ovarian cancer cells. EMSA assay proved MIL enhanced NF-κB DNA-binding activity in the nuclear. That specific NF-κB inhibitors alleviated MIL-induced apoptosis suggested NF-κB activation showed a pro-apoptotic function in SK-OV-3 and A2780S cells. Since NF-κB could be activated by double strand breaks and showed a pro-apoptotic function in the DNA damage response, SCGE assay and western blot revealed that MIL caused DNA strand breaks and significantly increased the level of p-ATM protein and further increased the levels of p-IKKα/β and NF-κB (p65) protein in SK-OV-3 and A2780S cells, while a specific ATM inhibitor could alleviated these effects. Moreover, Topoisomerase II drug screening kit and computer modeling assay were used to prove that MIL induced the production of linear DNA and inhibited the activity of topoisomerase II through binding with Topoisomerase II-Cleaved DNA complex to stabilize the complex. Taken together, our results identified that MIL exhibited anti-tumor activity through inhibiting topoisomerase II activity to induce tumor cells DNA damage, and MIL-activated NF-κB pathway showed a pro-apoptotic function in response to DNA damage.

Millepachine showed novel antitumor effects in cisplatin-resistant human ovarian cancer through inhibiting drug efflux function of ATP-binding cassette transporters

Phytother Res 2018 Dec;32(12):2428-2435.PMID:30123958DOI:10.1002/ptr.6180.

Millepachine (MIL), a bioactive natural chalcone from Chinese herbal medicine Millettia pachycarpa Benth, exhibits strong antitumor effects against many human cancer cells both in vitro and in vivo. In this study, we found that MIL significantly inhibited the proliferation of cisplatin-resistant A2780CP cells via inducing obvious G2/M arrest and apoptosis and down-regulating the activity of topoisomerase II protein. We further found that the mechanism by which MIL showed good antitumor effects in cisplatin-resistant human ovarian cancer was associated with inhibiting the expression of ATP-binding cassette transporters in cisplatin-resistant A2780CP cells. Importantly, MIL did not only significantly inhibit the tumor growth in cisplatin-sensitive A2780S xenograft model, with an inhibitory rate of 73.21%, but also inhibited the tumor growth in the cisplatin-resistant A2780CP xenograft model, with an inhibitory rate of 65.68% (p < 0.001 vs. control; p < 0.001 vs. DDP). In addition, MIL did not induce acquired drug resistance in A2780S tumor-bearing mice with an inhibitory rate of 60.03%. The promising in vitro and in vivo performance indicated that MIL exhibited potential significance for drug research and development.

The effect and mechanism of millepachine-disrupted spindle assembly in tumor cells

Anticancer Drugs 2018 Jun;29(5):449-456.PMID:29649038DOI:10.1097/CAD.0000000000000618.

Millepachine (MIL) is a bioactive natural product that shows great potential for cancer treatment. Previous studies showed that MIL was a novel cancer drug candidate with a special structure. To provide reference for the research and development of MIL, we further investigated the mechanism of MIL inducing G2/M arrest and found MIL disrupted spindle assembly in tumor cells. In this study, we investigated the disrupting spindle assembly effects of MIL with a focus on its potential mechanism of action. First, we indicated that MIL did not inhibit microtubule polymerization from the results of in-vivo microtubule nucleation assay and microtubule polymerization in-vitro assay but delayed this process by inhibiting the production of ATP in tumor cells. Thereafter, we investigated the effect of MIL on the mitotic spindle. We found that MIL induced multipolar spindles by inhibiting the activity of Eg5 and inhibited mitotic spindle formation and chromatin condensation by the activation of the spindle assembly checkpoint (SAC) in tumor cells. These results established a novel function of MIL in regulating the assembly of mitotic spindle. As Eg5 and SAC are antitumor targets, effect of MIL on the Eg5 protein and SAC activation hinted that MIL has novel application in the development of antitumor drugs.

Dual-targeting antitumor hybrids derived from Pt(IV) species and Millepachine analogues

Eur J Med Chem 2018 Mar 25;148:1-25.PMID:29448138DOI:10.1016/j.ejmech.2018.02.012.

Many strategies have been developed to circumvent the shortcomings of Pt(II)-based chemotherapy, but the inherent problems still have not been effectively resolved. Here we report a new series of dual-targeting Pt(IV) prodrugs, conjugates of Millepachine analogues with the related Pt(IV) complexes derived from cisplatin or oxaliplatin, respectively, which can inhibit tubulin polymerization and induce DNA damage. Among them, compound 19 possessed excellent antitumor activities against the tested human cancer cell lines, and arrested the cell cycle at the G2/M phases and ultimately induced cell apoptosis. Interestingly, its low cytotoxicity toward two human normal cells and sensitivity toward two cisplatin-resistant cells revealed the possibility for cancer therapy. More importantly, 19 displayed excellent antitumor efficacy in the SK-OV-3 xenograft model better than cisplatin and the corresponding Millepachine analogue. Our research provided an efficient strategy for multi-targeting antitumor drug development.

Synthesis and biological evaluation of novel Millepachine derivative containing aminophosphonate ester species as novel anti-tubulin agents

Bioorg Chem 2020 Jan;94:103486.PMID:31818482DOI:10.1016/j.bioorg.2019.103486.

A new series of Millepachine derivative containing aminophosphonate ester moieties were designed and synthesized, and evaluated for their anticancer activities using MTT assay. Among all the compounds, compound 9m exhibited the most potent cytotoxic activity against all tested human cancer cell lines including multidrug resistant phenotype, which inhibited cancer cell growth with IC50 values ranging from 0.85 to 3.09 μM, respectively. In addition, its low cytotoxicity toward human normal liver cells HL-7702 and sensitivity toward to doxorubicin or cisplatin-resistant cells indicated the possibility for cancer therapy. Furthermore, 9m significantly induced cell apoptosis and cell cycle arrest in G2/M phase and dramatically disrupted the microtubule organization. Moreover, a decrease in MMP, an increase in reactive oxygen species (ROS) generation and Bax/Bcl-2 ratio, accompanied by activated caspase-3 and -9, were observed in HepG-2 cells after incubation with 9m, indicating that the mitochondrial pathway was involved in the 9m-mediated apoptosis.