
SR 2211inverse agonist of RORγ, potent and selective |
Sample solution is provided at 25 µL, 10mM.
































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- Purity = 98.00%
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Cas No. | 1359164-11-6 | SDF | Download SDF |
Chemical Name | 1,1,1,3,3,3-hexafluoro-2-(2-fluoro-4"-((4-(pyridin-4-ylmethyl)piperazin-1-yl)methyl)-[1,1"-biphenyl]-4-yl)propan-2-ol | ||
Canonical SMILES | FC1=CC(C(C(F)(F)F)(C(F)(F)F)O)=CC=C1C2=CC=C(C=C2)CN3CCN(CC4=CC=NC=C4)CC3 | ||
Formula | C26H24F7N3O | M.Wt | 527.48 |
Solubility | Soluble in DMSO | Storage | Store at -20°C |
Physical Appearance | A crystalline solid | Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size:ship with RT , or blue ice upon request |
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. |
SR 2211 is a potent and selective inverse agonist of RORγ with IC50 value of 320 nM [1].
RAR-related orphan receptor gamma (RORγ) is a nuclear receptor and a DNA-binding transcription factor. RORγ plays an important role in the regulation of circadian rhythms and Th17 cell differentiation [2].
SR 2211 is a potent and selective RORγ inverse agonist. SR2211 bound to RORγ with Ki value of 105 nM. SR2211 (10 μM) inhibited RORγ activity by 90% but didn’t affect the transcriptional activity of RORα and farnesoid X receptors (FXR). SR2211 showed weak activation of liver X receptor α (LXRα). In EL-4 murine T lymphocyte cell line, SR2211 (5 μM) followed by PMA/ionomycin significantly inhibited the expression of IL-17 and IL-23 receptor in a dose-dependent way [1]. Enriched naive CD4+ T cells under Th17 polarizing conditions, SR2211 significantly inhibited the production of IL-17, which suggested that SR2211 inhibited Th17 cell differentiation. In LPS-stimulated RAW 264.7 cells, SR2211 (5 μM) inhibited the expression of TNFα, IL-1β and IL-6, the proinflammatory cytokines that played an important role in the pathogenesis of RA [2].
Of the CIA mouse model, SR2211 (20 mg/kg) inhibited the development of arthritis in a dose-dependent way [2].
References:[1]. Kumar N, Lyda B, Chang MR, et al. Identification of SR2211: a potent synthetic RORγ-selective modulator. ACS Chem Biol, 2012, 7(4): 672-677. [2]. Chang MR, Lyda B, Kamenecka TM, et al. Pharmacologic Repression of Retinoic Acid Receptor-Related Orphan Nuclear Receptor γ Is Therapeutic in the Collagen-Induced Arthritis Experimental Model. Arthritis Rheumatol, 2014, 66(3): 579-588.
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NaturalProteinStopsDeadlyHumanBrainCancerInMice
ScientistsfromJohnsHopkinsandfromtheUniversityofMilanhaveeffectivelyproventhattheycaninhibitlethalhumanbraincancersinmiceusingaproteinthatselectivelyinducespositivechangesintheactivityofcellsthatbehavelikecancerstemcells.ThereportispublishedinNature.
Themostcommontypeofbraincancer-glioblastoma-ismarkedbythepresenceofthesestem-cell-likebraincells,which,insteadoftriggeringthereplacementofdamagedcells,formcancertissue.Stemcells,unlikeallothercellsinthebody,arecapableofformingalmostanykindofcellwhentheright"signals"triggertheirdevelopment.
Fortheirtreatmentexperiment,theresearchersreliedonaclassofproteins,bonemorphogenicproteins,thatcauseneuralstem-cell-likeclusterstolosetheirstemcellproperties,whichinturnstopstheirABIlitytodivide.
Firsttheypretreatedhumanglioblastomacellswithbonemorphogenicprotein4(BMP4),theninjectedthesetreatedcellsintomousebrains.Inmiceinjectedwithcellsthatwerenotpretreated,large,invasivecancersgrew.InthemicewithBMP4-treatedcells,nocancersgrewatall.Threetofourmonthsafterinjection,allmicethatgotuntreatedcellsdied,andnearlyallmicewithBMP4-treatedcellswerealive.
Next,thescientistsdeliveredslow-releaseBMP4-containing"beads"directlyintomousebrainswithimplantedglioblastomacells.Micethatgotemptybeadsdevelopedlargemalignanttumorsanddied.MicewithBMP4beadssurvivedmuchlonger,and80percentsurvivedfourmonthsaftercancercellimplants.
"OurideaistotreatpatientswithBMP4orsomethinglikeitrightaftersurgerytoremoveglioblastomainhopesofpreventingtheregrowthofthecancerandimprovingsurvivaltime,"saysAlessandroOlivi,M.D.,directoroftheDivisionofNeurosurgicalOncologyatHopkinsandacontributortothestudy.
OlivisaysclinicalstudiesusingBMP4couldbeginwithinayearand,ifsuccessful,drugtherapiescouldbeavailabletothepublicwithinthreetofouryears.
"ThiswasproofoftheideathatBMPscouldstopglioblastomabydepletingthestem-cell-likepopulationthatfeedsit,"saysHenryBrem,M.D.,chairmanoftheDepartmentofNeurosurgeryatHopkinsandacollaboratorinthestudy."Thisopensexcitingdoorstofutureresearchintotreatmentsandtherapiesforsuchadevastatingdisease."

