Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEFGFR1/VEGFR2-IN-2Cat.No.:HY-161995分?式:C??H??ClF?NO?S分?量:469.86作?靶點:Apoptosis;Necroptosis;FGFR;VEGFR;PDGFR作?通路:Apoptosis;ProteinTyrosineKinase/RTK儲存?式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY?物活性FGFR1/VEGFR2-IN-2(compound6)?種VEGFR2/FGFR1雙重抑制劑，對VEGFR2和FGFR1的IC50值分別為0.025μM和0.026μM，對EGFR和PDGFR-β的IC50值為0.106μM和0.077μM。FGFR1/VEGFR2-IN-2對NCI-60細胞系表現出顯著抗癌活性(GI=60.38%)，在T-47D細胞株中IC50為8.51μM，具有抗遷移作?，使細胞停滯于G1期并促進凋亡和壞死;對MCF-7細胞株IC50超過100μM，對MDA-MB-231的IC50為69.17μM，對正常細胞?毒性[1]。IC50&TargetFGFR1VEGFR2PDGFRβFGFR0.026μM(IC50)0.025μM(IC50)0.077μM(IC50)0.106μM(IC50)體外研究FGFR1/VEGFR2-IN-2(10μM)hasanti-tumorproliferationactivitywithanaverageGIof60.38%[1].FGFR1/VEGFR2-IN-2hasgoodcytotoxicityagainstbreastcancercelllinesT-47D,MCF-7andMDA-MB-231,andhasnoeffectonnormalcellsVero[1].FGFR1/VEGFR2-IN-2(10,20μM)blocksT-47DcellsintheG1phase[1].FGFR1/VEGFR2-IN-2(2.12,4.25μM)promotesearlyandlateapoptosisofT-47Dcellsandpromotescellnecrosis[1].FGFR1/VEGFR2-IN-2(3.7-4.8μM)promotescellnecrosis,increasestheexpressionofBAXandCaspase-3,anddecreasestheexpressionofBCL-2[1].FGFR1/VEGFR2-IN-2(6μM;24,48h)hasananti-migratoryeffectinT-47D[1].CellCytotoxicityAssay[1]CellLine:T-47D,MCF-7,MDA-MB-231,VeroConcentration:10μM1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEIncubationTime:Result:HadnocytotoxicitytoVerocellsandtheIC50forT-47Dwas8.51μM,theIC50forMCF-7wasgreaterthan100μM,andtheIC50forMDA-MB-231was69.17μM.CellProliferationAssay[1]CellLine:NCI-60Concentration:10μMIncubationTime:Result:Inhibitedlungcancer(NCI-H460),coloncancer(HCC-2998),centralnervoussystemcancer(SF-295),melanoma(UACC-62),ovariancancer(OVCAR-5),kidneycancer(UO-31),andbreastcancer(MDA-MB-231),GIwere89.11%,81.73%,82.33%,97.59%,81.63%,87.08%and82.85%.CellCycleAnalysis[1]CellLine:T-47DConcentration:10,20μMIncubationTime:Result:IncreasedthenumberofT-47DcellsintheG1phasefrom60.81%to72.62%.CellMigrationAssay[1]CellLine:T-47DConcentration:6.0μMIncubationTime:0,24,48hResult:Increasedthewoundhealingratefrom25.2%to19.8%after24hoursandfrom42.2%to31.2%after48hours.ApoptosisAnalysis[1]CellLine:T-47DConcentration:2.12,4.25μMIncubationTime:Result:IncreasedtheearlyapoptosisrateofT-47Dcellsby25%and20%at2.12and4.25μM,andthelateapoptosisrateby10%and16%.At2.12μM,theapoptosisrateincreasedby2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE8%,andat4.25μM,theapoptosisrateincreasedby16%.At2.12and4.25μM,thenecroticcellsincreasedfrom5%to12%.RT-PCR[1]CellLine:T-47DConcentration:1/2×IC50(T-47D),IC50=8.5μMIncubationTime:Result:IncreasedtheexpressionlevelofBAXby5.82times,decreasedtheexpressionlevelofBCL-2by0.243times,andincreasedtheexpressionlevelofCaspase-3by8.2times.REFERENCES[1].RashaMHassan,etal.NovelbenzenesulfonamidesasdualVEGFR2/FGFR1inhibitorstargetingbreastcancer:Design,synthesis,anticanceractivityandinsilicostudies.BioorgChem.2024Aug17:152:107728.McePdfHeightCaution:Producthasnotbeen