8-Bromo-cGMP-sodium-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemE8-Bromo-cGMPsodiumCat.No.:HY-101379ACASNo.:51116-01-9分?式:C??H??BrN?NaO?P分?量:446.08作?靶點(diǎn):CalciumChannel作?通路:MembraneTransporter/IonChannel;NeuronalSignaling儲存?式:-20°C,sealedstorage,awayfrommoisture*Insolvent:-80°C,6months;-20°C,1month(sealed

storage,awayfrommoisture)溶解性數(shù)據(jù)體外實(shí)驗(yàn)H2O:100mg/mL(224.18mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲備液1mM2.2418mL11.2088mL22.4175mL5mM0.4484mL2.2418mL4.4835mL10mM0.2242mL1.1209mL2.2418mL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；?旦配成溶液，請分裝保存，避免反復(fù)凍融造成的產(chǎn)品失效。儲備液的保存?式和期限：-80°C,6months;-20°C,1month(sealedstorage,awayfrommoisture)。-80°C儲存時(shí)，請?jiān)?個(gè)?內(nèi)使?，-20°C儲存時(shí)，請?jiān)?個(gè)?內(nèi)使?。體內(nèi)實(shí)驗(yàn)請根據(jù)您的實(shí)驗(yàn)動物和給藥?式選擇適當(dāng)?shù)娜芙?案。以下溶解?案都請先按照InVitro?式配制澄的儲備液，再依次添加助溶劑：(為保證實(shí)驗(yàn)結(jié)果的可靠性，澄的儲備液可以根據(jù)儲存條件，適當(dāng)保存；體內(nèi)實(shí)驗(yàn)的?作液，建議您現(xiàn)?現(xiàn)配，當(dāng)天使?；以下溶劑前顯?的百分?指該溶劑在您配制終溶液中的體積占?；如在配制過程中出現(xiàn)沉淀、析出現(xiàn)象，可以通過加熱和/或超聲的?式助溶)1.請依序添加每種溶劑：PBSSolubility:100mg/mL(224.18mM);Clearsolution;Needultrasonic1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEBIOLOGICALACTIVITY?物活性8-Bromo-cGMPsodiumcGMP的膜滲透性類似物，?種PKG激活劑。8-Bromo-cGMPsodium可顯抑制Ca2+宏觀電流并損害?K+刺激的胰島素釋放。8-Bromo-cGMPsodium具有緩解疼痛和?管舒張作?。體外研究8-Bromo-cGMPsodium(1-100μM;8h)increasesresistanceofLLC-PK1cellstoCsAtoxicityconcentration-dependently[3].8-Bromo-cGMPsodium(1-100μM;16h)inducesthesynthesisofHO-1proteininaconcentration-dependentfashion[3].CellViabilityAssay[3]CellLine:LLC-PK1cells(ATCCCL101)Concentration:1-100μMIncubationTime:8hoursResult:IncreasedresistanceofLLC-PK1cellstoCyclosporinA(CsA)toxicityconcentration-dependentlyandaugmentedcellviabilitybyupto65%.WesternBlotAnalysis[3]CellLine:LLC-PK1cells(ATCCCL101)Concentration:1-100μMIncubationTime:16hoursResult:InducedthesynthesisofHO-1proteininaconcentration-dependentfashion.體內(nèi)研究8-Bromo-cGMPsodium(0.3,1,3.0nmol;intrathecaladministration;10minbeforetest)dose-dependentlyandsignificantlyincreasesthetail-flicklatencyinVincristine-treatedmicetothelevelobservedinvehicle-treatednaivemice(maleICRmice,4weeksofageandweighing20g).Vincristine(0.05mg/kg1dayafterthepre-drugtail-flicklatency,andthen0.125mg/kgtwiceaweekfor6weeks)caninducepainfulneuropathyinmice[4].8-Bromo-cGMPsodium(10mg/kg;iv;singledose)resultsinvasodilatorresponsesineNOS-TgmiceandWTlittermatesinC57BL/6background(19-35g)[5].REFERENCES[1].SarkarO,etal.NitricoxideattenuatesoverexpressionofGiαproteinsinvascularsmoothmusclecellsfromSHR:RoleofROSandROS-mediatedsignaling.PLoSOne.2017Jul10;12(7):e0179301.[2].TegederI,etal.Dualeffectsofspinallydelivered8-bromo-cyclicguanosinemono-phosphate(8-bromo-cGMP)informalin-inducednociceptioninrats.NeurosciLett.2002Oct31;332(2):146-50.[3].TobiasPolte,etal.Atrialnatriureticpeptidereducescyclosporintoxicityinrenalcells:roleofcGMPandhemeoxygenase-1.FreeRadicBiolMed.2002Jan1;32(1):56-63.2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE[4].JunzoKamei,etal.Possibleinvolvementofthespinalnitricoxide/cGMPpathwayinvincristine-inducedpainfulneuropathyinmice.Pain.2005Sep;117(1-2):112-20.[5].ElzaDvanDeel,etal.Vasomotorcontrolinmiceoverexpressinghumanendothelialnitricoxidesynthase.AmJPhysiolHeartCircPhysiol.2007Aug;293(2):H1144-53.McePdfHeightCaution:Producthasnot