SR3335 | RORα partial inverse agonist

SR3335 Supplier | CAS 293753-05-6 | Focus Biomolecules

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SR3335 (293753-05-6) is a selective RORα partial inverse agonist (IC50 = 480 nM) – displays no activity at RORß, RORγ, or FXR.1 It was able to suppress gluconeogenesis in diet-induced obese mice.  SR3335 was able to upregulate uncoupling protein 1 (UCP1), a unique mitochondrial protein devoted to thermogenesis, in wild type mice leading to decreased body weight and fat mass.2,3 It inhibited the development of mouse and human TH17 cells in vitro and in vivo leaving thymic T cells intact.4  SR3335’s ability to block pathogenic, but not protective TH17 cell function makes it an important new tool in the study of TH17-mediated inflammatory and autoimmune diseases.
References/Citations:

  1. Kumar et al. (2011), Identification of SR3335 (ML176): a synthetic RORα selective inverse agonist; ACS Chem. Biol. 6 218
  2. Monnier et al. (2018), The nuclear retinoid-related orphan receptor RORα controls circadian thermogenic programming in white fat depots; Physiol. Rep. 6 e13678
  3. Auclair et al. (2021), Pharmacological modulation of ROR α controls fat browning, adaptive thermogenesis, and body weight in mice; Am. J. Physiol. Endocrinol. 320 E219
  4. Wang et al. (2021), Genetic and pharmacological inhibition of the nuclear receptor RORα regulates TH17 driven inflammatory disorders; Nat. Commun. 12 76
293753-05-6, ML-176, ML176, ML176 supplier, RORα inverse agonist, RORα partial inverse agonist, SR 3335, SR3335, SR3335 supplier
Alternate Name:
ML176

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Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee

SR3335 (293753-05-6) is a selective RORα partial inverse agonist (IC50 = 480 nM) – displays no activity at RORß, RORγ, or FXR.1 It was able to suppress gluconeogenesis in diet-induced obese mice.  SR3335 was able to upregulate uncoupling protein 1 (UCP1), a unique mitochondrial protein devoted to thermogenesis, in wild type mice leading to decreased body weight and fat mass.2,3 It inhibited the development of mouse and human TH17 cells in vitro and in vivo leaving thymic T cells intact.4  SR3335’s ability to block pathogenic, but not protective TH17 cell function makes it an important new tool in the study of TH17-mediated inflammatory and autoimmune diseases.
References/Citations:

  1. Kumar et al. (2011), Identification of SR3335 (ML176): a synthetic RORα selective inverse agonist; ACS Chem. Biol. 6 218
  2. Monnier et al. (2018), The nuclear retinoid-related orphan receptor RORα controls circadian thermogenic programming in white fat depots; Physiol. Rep. 6 e13678
  3. Auclair et al. (2021), Pharmacological modulation of ROR α controls fat browning, adaptive thermogenesis, and body weight in mice; Am. J. Physiol. Endocrinol. 320 E219
  4. Wang et al. (2021), Genetic and pharmacological inhibition of the nuclear receptor RORα regulates TH17 driven inflammatory disorders; Nat. Commun. 12 76

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