BO-264-DataSheet-生命科學(xué)試劑-生命科學(xué)試劑-MedChemExpressVIP

Hotline:400-820-3792Inhibitors?Agonists?ScreeningLibrarieswww.MedChemEBO-264Cat.No.:HY-135960CASNo.:2408648-20-2分?式:C??H??N?O?分?量:353.38作?靶點:FGFR;Apoptosis作?通路:ProteinTyrosineKinase/RTK;Apoptosis儲存?式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性數(shù)據(jù)體外實驗DMSO:50mg/mL(141.49mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲備液1mM2.8298mL14.1491mL28.2981mL5mM0.5660mL2.8298mL5.6596mL10mM0.2830mL1.4149mL2.8298mL請根據(jù)產(chǎn)品在不同溶劑中的溶解度，選擇合適的溶劑配制儲備液，并請注意儲備液的保存?式和期限。體內(nèi)實驗請根據(jù)您的實驗動物和給藥?式選擇適當?shù)娜芙?案，配制前請先配制澄的儲備液，再依次添加助溶劑(為保證實驗結(jié)果的可靠性，體內(nèi)實驗的?作液，建議您現(xiàn)?現(xiàn)配，當天使?；澄的儲備液可以根據(jù)儲存條件，適當保存；以下溶劑前的百分?指該溶劑在您配制終溶液中的體積占?)：1.請依序添加每種溶劑：10%DMSO>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥2.08mg/mL(5.89mM);Clearsolution2.請依序添加每種溶劑：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:≥2.08mg/mL(5.89mM);Clearsolution3.請依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥2.08mg/mL(5.89mM);Clearsolution1/3MasterofSmallMolecules—您?邊的抑制劑?師www.MedChemEBIOLOGICALACTIVITY?物活性BO-264?種?效，?服活性的轉(zhuǎn)化酸性卷曲螺旋3(TACC3)抑制劑，IC50為188nM，Kd為1.5nM。BO-264特異性阻斷FGFR3-TACC3融合蛋?的功能。BO-264誘導(dǎo)紡錘體檢查點依賴的有絲分裂阻滯，DNA損傷和細胞凋亡(apoptosis)。BO-264具有?譜抗腫瘤活性。IC50&TargetIC50:188nM(Transformingacidiccoiled-coil3(TACC3))[1]Kd:1.5nM(TACC3)[1]體外研究BO-264(500nM;48hours;JIMT-1cells)treatmentinducesaprominentincrease(from4.1%to45.6%)inthefractionofapoptoticcellsasassessedbyAnnexinV/PIstaining[1].BO-264(500nM;24hours;RT112cells)treatmentdecreasesERK1/2phosphorylation,whichisamarkerforactivatedFGFRsignalingalongwithastrongmitoticarrest[1].BO-264inhibitscellviabilitywithIC50valuesof190nM,160nM,120nM,130nMand360nMforJIMT-1,HCC1954,MDA-MB-231,MDA-MB-436andCAL51,respectively.BO-264specificallytargetsbreastcancercellswhilesparingnormalcells.BO-264treatmentsignificantlyreducestheaveragecolonynumberofJIMT-1cells[1].BO-264inhibitstheviabilityofcancercellswithFGFR3-TACC3fusionwithIC50valuesof0.3μMand3.66μMforRT112andRT4,respectively[1].BO-264exhibitsaremarkableanti-canceractivityagainstmorethan90%oftheNCI26760humancancercelllinesrepresentingninedifferentsubpanelswithGI50valueslessthan1μM[1].BO-264inducesmitoticarrest(prominentinducesp-HistoneH3(Ser10)),apoptosis(cleavedPARP)andDNAdamage,causesaberrantspindleformationandreducescentrosomallocalizationofTACC3inJIMT-1cells[1].ApoptosisAnalysis[1]CellLine:JIMT-1cellsConcentration:500nMIncubationTime:48hoursResult:Inducedaprominentincrease(from4.1%to45.6%)inthefractionofapoptoticcellsasassessedbyAnnexinV/PIstaining.WesternBlotAnalysis[1]CellLine:RT112cellsConcentration:500nMIncubationTime:24hoursResult:DecreasedERK1/2phosphorylation.2/3MasterofSmallMolecules—您?邊的抑制劑?師www.MedChemE體內(nèi)研究BO-264(25mg/kg;oraladministration;daily;for3-4weeks;femalenudemice)treatmentshowsasignificantsuppressionoftumorgrowth.BO-264iswelltoleratedsincetreatmentdoesnotcausesasignificantbodyweightlossandorgantoxicity[1].AnimalModel:FemalenudemiceinjectedwithJIMT-1cells[1]Dosage:25mg/kgAdministration:Oraladministration;daily;for3-4weeksResult:Showedasignificantsuppressionoftumorgrowth.REFERENCES[1].AkbulutO,etal.AHighlyPotentTACC3InhibitorasaNovelAnti-cancerDrugCandidate.MolCancerTher.2020Mar26.pii:molcanther.0957.2019.McePdfHeightCaution:Producth