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    InvivoChem Cat #: V1577
    CAS #: 173529-46-9Purity ≥98%

    Description: HMN-214 (HMN 214; HMN214), stilbene derivative, is a potent and orally bioactive prodrug of HMN-176, which alters the cellular spatial orientation of Plk1 (polo-like kinase-1). HMN-214 interferes with the subcellular spatial location of PLK1 (polo-like kinase-1), a serine/threonine kinase that regulates critical mitotic events. HMN-176 showed potent cytotoxicity, with a mean IC50 of 118 nM. In addition, judging by its low resistance indices, HMN-176 was more cytotoxic toward the drug-resistant phenotypes of tumor cells than were the other agents tested.         

    References: Invest New Drugs. 2003 Nov;21(4):387-99; Cancer Res. 2003 Oct 15;63(20):6942-7.

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    Molecular Weight (MW)424.47
    CAS No.173529-46-9
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 12 mg/mL (28.3 mM)
    Water:<1 mg/mL
    Ethanol: <1 mg/mL
    Solubility (In vivo)0.5% methylcellulose: 30 mg/mL
    SynonymsHMN214; HMN 214; HMN-214

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    In Vitro

    In vitro activity: HMN-214 is an oral prodrug that is rapidly converted to HMN-176. The in vitro data of HMN-214 are scarce. However, HMN-176, active metabolite of HMN-214, shows potent and broad-spectrumanti-tumor activity against various cancer cells, including HeLa, PC-3, DU-145, MIAPaCa-2, U937, MCF-7, A549, and WiDr, with a mean IC50 value of 118 nM. HMN-176 is also cytotoxic to drug-resistant human and murine cell lines, including P388/CDDP, P388/VCR, K2/CDDP, and K2/VP-16, with IC50 values ranging from 143 nM–265 nM. In HeLa cells, HMN-176 (3 μM) blocks cell cycle at G2/M phase. In Doxorubicin-resistant K2/ARS cells, HMN-176 inhibits cell growth with an IC50 value of 2 μM. HMN-176 (3 μM) down-regulates the expression of the multidrug resistance gene (MDR1), due to the disturbance of NF-Y transcription factor binding to the MDR1 promoter. In human RPE1 and CFPAC-1 cells, HMN-176 (2.5 μM) delays satisfaction of the spindle assembly checkpoint. HMN-176 (250 nM–2.5 μM) inhibits meiotic spindle assembly and aster formationin Spisula oocytes. HMN-176 (2.5 μM) also inhibits aster microtubule formation from human centrosomes. These results indicate that the anti-tumor activity of HMN-176 is at least partially via disrupting centrosome-mediated MT assembly during mitosis.  

    Kinase Assay: HMN-214 is a potent and orally active prodrug of HMN-176, which alters the cellular spatial orientation of Plk1. 

    Cell Assay: Cells are seeded into a 96-well microplate at a density of 3 × 103–1 × 104 cells/well. Dilutions of HMN-214 or HMN-176 are added the next day and the plate is incubated for 72 hours. The inhibition of growth is measured by the MTT assay and IC50 values are then obtained.

    In VivoHMN-214 is an oral pro-drug of HMN-176 with improved oral absorption. HMN-214 (30 mg/kg) triggers no obvious neurotoxicity in mice. In mouse xenograft model of PC-3, A549, and WiDr cells, HMN-214 (10 mg/kg–20 mg/kg) inhibits tumor growth. In nude mice model bearing multidrug-resistant KB-A.1 cells, HMN-214 (10 mg/kg–20 mg/kg) significantly suppresses MDR1 mRNA expression.
    Animal modelMale BALB/c nude mice bearing xenografts of PC-3, A549, and WiDr cells
    Formulation & DosageDissolved in 0.5% methylcellulose; 10, 20 mg/kg; Oral gavage 

    Invest New Drugs. 2003 Nov;21(4):387-99; Cancer Res. 2003 Oct 15;63(20):6942-7.

    These protocols are for reference only. InvivoChem does not independently validate these methods.


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