Antitumor-photosensitizer-5-DataSheet-生命科學(xué)試劑-MCE

Hotline:400-820-3792Inhibitors ? ScreeningLibraries ? Proteinswww.MedChemEAntitumorphotosensitizer-5Cat.No.:HY-163034分子式:C??H??F??N??O?P?RuS分子量:1289.04作用靶點(diǎn):Apoptosis;ReactiveOxygenSpecies作用通路:Apoptosis;Immunology/Inflammation;MetabolicEnzyme/Protease;NF-κB儲存方式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY生物活性Antitumorphotosensitizer-5(Ru2)是一種有效靶向腫瘤線粒體的光敏劑，對A549細(xì)胞光毒性的IC50為0.3μM。在460nm光照下，Antitumorphotosensitizer-5誘導(dǎo)活性氧的生成和NADH的耗竭，進(jìn)而導(dǎo)致線粒體損傷并活化caspase-3，誘導(dǎo)細(xì)胞凋亡并抑制細(xì)胞遷移。Antitumorphotosensitizer-5具有阻止惡性腫瘤生長的潛力，因此顯示出應(yīng)用于光動力治療的潛力[1]。IC50&TargetNicotinamideadeninedinucleotide(NADH)[1]體外研究Antitumorphotosensitizer-5(10μM,4h)causesasignificantincrease(32.08-fold)influorescencesignalinA549cells(biotinreceptor-positive)whileinducingBHKcells(biotinreceptor-negative)toexhibitnegligiblefluorescenceincrease(7.35-fold)[1].Antitumorphotosensitizer-5(0.391-100μM,24h)exhibitsphototoxicityinbothBHKcellsandA549cellsandrevealsminimalcytotoxicityintheabsenceoflightwithover75%cellviabilityunder100μM[1].Antitumorphotosensitizer-5(10μM,4h)hasaPearsoncolocalizationcoefficientof0.87withthemitochondrialprobeMito-TrackerGreen[1].Antitumorphotosensitizer-5(0.15-0.6μM,24h)with460nmlightirradiationfor15minexhibitsaconcentration-dependentreductioninthemitochondrialmembranepotentialprobefluorescenceintensityratiowhichindicatedthemitochondrialdamage,whiletheROSprobefluorescenceintensityexhibitsaconcentration-dependentincrease,indicatingeffectivegenerationofROS[1].Antitumorphotosensitizer-5(0.15-0.6μM,24h)causestheoccurrenceofapoptosisinA549cellsafterlightirradiation,whiletheapoptosislevelisvirtuallyunchangedunderdarkcondition,lightconditionalsocausestheincreaseofactivatedcaspase-3,themigrationanddamageofDNAandthereductionofcellularNADHcontent[1].Antitumorphotosensitizer-5(0.15-0.6μM,24h/48h)inhibitsthecellmigrationofA549cellsunder460nm1/3 MasterofBioactiveMolecules—您身邊的抑制劑大師www.MedChemElight[1].CellViabilityAssay[1]CellLine:BHK,A549Concentration:0.195,0.391,0.781,1.563,3.125,6.250,12.5,25,50,100μMIncubationTime:4hindark+15mininlightordark+20hindarkResult:ExhibitedphototoxicityinbothBHKcellsandA549cells,butwasmorephototoxicinA549cells(A549cellviability<40%under0.391μMwhileBHKcellviability<40%under6.25μM),revealedminimalcytotoxicityintheabsenceoflightwithover75%cellviabilityunder100μM.ApoptosisAnalysis[1]CellLine:A549Concentration:0.15,0.3,0.6μMIncubationTime:4hindark+15mininlightordark+20hindarkResult:IncreasedthepercentageofearlyandlateapoptoticcellsinA549inaconcentration-dependentmannerunderthe460nmlightcondition.Conversely,underdarkconditions,thepercentageofearlyandlateapoptoticcellsintreatedA549cellsremainedvirtuallyunchanged.CellMigrationAssay[1]CellLine:A549Concentration:0.15,0.3,0.6μMIncubationTime:4hindark+15mininlightordark+20h/44hindarkResult:Displayedasignificantconcentration-dependentinhibitionofwoundhealinginA549cellsunder460nmlightcomparedtocellskeptinthedark.體內(nèi)研究Antitumorphotosensitizer-5(10mg/kg,i.tu.foronce,24d)remarkablysuppressesthetumorgrowthafter460nmlightirradiation,anddoesn'tcausesevereadverseeffectsonnormalorgans[1].AnimalModel:BALB/cnudefemalemice(6–8weeksold),HumanlungadenocarcinomaepithelialA549cells[1]Dosage:10mg/kgAdministration:intratumoralinjection(i.tu.)foronce2/3 MasterofBioactiveMolecules—您身邊的抑制劑大師www.MedChemEResult: Suppressedthetumorgrowthremarkablyinthelightgroupwhiletumorsinthedarkorcontrolgroupsgrowrapidlyduringthesameperiod.Causedsevereapoptosisanddisruptionofthetumorstructureinthetumoroflightgroupwhilethetumorsintheothergroupshowednoobvioustissuedamage,normalorganssuchastheheart,liver,spleen,lung,andkidneydidnotexhibitsignificantpathologicalabnormalitiesorinflammatorylesions.REFERENCESGuoqiangShao,etal.Biotin-conjugatedRu(II)complexeswithAIEcharacteristicsasmitochondria-targetedphotosensitizersforenhancingphotodynamictherapybydisruptingcellularredoxbalance.EuropeanJournalofMedicinalChemistry.2023，Vol