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ROR Retinoic Acid-related Orphan Receptor

Cat.No.  Name Information
M7321 SR 1001 SR 1001 is a RORα/γ inverse agonist with Ki values of 172 and 111 nM, respectively.
M25448 Dehydrolithocholic acid Dehydrolithocholic acid is a bile acid metabolite, which inhibits the diferentiation of TH17 cells by directly binding to the key transcription factor RORγt (Kd=1.13 μM).
M14531 Cintirorgon Cintirorgon (LYC-55716) is a first-in-class, selective and orally bioavailable RORγ agonist.
M11246 SR0987 SR0987, an analog of SR1078, is an agonist of RORγ T with an EC50 value of 800 nM. SR0987 up-regulated the expression of IL17 and inhibited the expression of PD-1.
M10929 Cedirogant Cedirogant (ABBV-157) is an orally active RORγt reverse agonist that can be used in the study of psoriasis.
M10170 S18-000003 S18-000003 is a potent, effective and orally active inhibitor of retinoic acid receptor-related orphan receptor-gamma-t (RORγt), with an IC50 of 29 nM.
M10106 Neoruscogenin Neoruscogenin is a bioavailable, potent, and high-affinity agonist of the nuclear receptor RORα (NR1F1).
M9265 Vimirogant Vimirogant (also known as AGN-242428 and VTP-43742) is a potent, selective and orally active RORγt inhibitor.
M9221 GSK805 GSK805 is a potent, orally bioavailable RORγγ Inhibitor, with pIC50 of 8.4 and >8.2 for RORγ FRET assay and Th17 assay.
M9220 SR2211 SR2211 is a synthetic RORγ-selective modulator, functions as an inverse agonist, with a Ki of 105 nM and an IC50 of ~320 nM.
M8943 GSK2981278 GSK2981278 is a highly potent and selective inverse agonist of retinoic acid receptor-related orphan receptor gamma (ROR gamma).
M5676 SR1078 SR1078 is an agonist of retinoic acid receptor-related orphan receptors (ROR) RORα/γ; increases transcription of RORα target genes; thought to increase p53 stability.
M5675 SR3335 SR3335 (ML-176) is a selective RORα synthetic ligand, directly binds to RORα, but not other RORs, and functions as a selective partial inverse agonist of RORα in cell-based assays.
M31061 Vimirogant hydrochloride Vimirogant (VTP-43742) hydrochloride is a potent, selective, and orally active RORγt inhibitor (Ki=3.5 nM; IC50=17 nM). Vimirogant hydrochloride exhibits >1000-fold selectivity versus the RORα and RORβ isotypes. Vimirogant hydrochloride inhibits Th17 differentiation and IL-17A secretion from mouse splenocytes (IC50=57 nM) without affecting Th1, Th2, or Treg cell differentiation.
M29661 BMS-986251  BMS-986251 is an orally active and selective RORγt inverse agonist with an EC50 of 12 nM for RORγt GAL4. BMS-986251 inhibits IL-17 with an EC50 of 24 nM in human whole blood assay. BMS-986251 demonstrates robust efficacy in mouse acanthosis and Imiquimod-induced models (preclinical models of psoriasis).
M29598 FM26  FM26 (compound 25) is a potent and allosteric retinoic acid receptor-related orphan receptor γt (RORγt) inverse agonists with an IC50 of 264 nM. FM26 has a distinct isoxazole chemotype and effectively reduces IL-17a mRNA production in EL4 cells.
M29487 Izumerogant Izumerogant (IMU-935) is an inverse agonist of retinoid-related orphan receptor-gamma (RORγ). Izumerogant (compound 123) also potently inhibits IL-17A, IL-17F and IFN-γ activity with IC50s <50 nM.
M29259 RORγt modulator 5  RORγt modulator 5 is a RORγt modulator with a Ki value of <100 nM. RORγt modulator 5 has the potential for inflammatory, metabolic, autoimmune and other diseases mediated by RORy study (WO2017132432A1; compound 2).
M29140 A-9758  A-9758 is a RORγ ligand and a potent, selective RORγt inverse agonist (IC50=5 nM), and exhibits robust potency against IL-17A release. A-9758 is effective in suppressing both Th17 differentiation and Th17 effector function. A-9758 significantly attenuates IL-23 driven psoriasiform dermatitis and is effective in blocking skin and joint inflammation.
M29048 CD12681  CD12681 (compound 14) is a potent and selective RORγ inverse agonist with IC50 of 19 nM and 10 nM for RORγ GAL4 and CD4-IL-17 cells, respectively. CD12681 decreases the IL-17 inflammatory cell recruitment. CD12681 has the potential for the research of psoriasis.

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