View the slide viewer

Have questions about this assay kit?

Human LXRβ Reporter Assay Kit

1 x-96 well format assays
3 x-32 assays in-96 well format
1 x-384 well format assays
1 x-96 well format assays
3 x-32 assays in-96 well format
1 x-384 well format assays

Product Description and Product Data

This is an all-inclusive cell-based luciferase reporter assay kit targeting the Human Liver X Receptor Beta (LXR). INDIGO’s LXR Beta reporter assay utilizes proprietary mammalian cells that have been engineered to provide constitutive expression of the LXR Beta. In addition to LXR Beta Reporter Cells, this kit provides two optimized media for use during cell culture and in diluting the user’s test samples, a reference agonist, Luciferase Detection Reagent, and a cell culture-ready assay plate. The principal application of this assay is in the screening of test samples to quantify any functional activity, either agonist or antagonist, that they may exert against human LXR Beta. This kit provides researchers with clear, reproducible results, exceptional cell viability post-thaw, and consistent results lot to lot. Kits must be stored at -80C. Do not store in liquid nitrogen. Note: reporter cells cannot be refrozen or maintained in extended culture.


  • Ready to Use Upon Receipt

  • Includes All Needed Components
  • Contains Transfected Reporter Cells
  • Eliminates Cell Licensing Fees
  • Clear, Reproducible Results
  • Consistent Results Lot to Lot

Product Specifications

Target TypeNuclear Hormone Receptor
Receptor FormHybrid
Assay ModeAgonist, Antagonist
Kit Components
  • LXRb Reporter Cells
  • Cell Recovery Medium (CRM)
  • Compound Screening Medium (CSM)
  • TO901317, (ref. agonist; in DMSO)
  • Detection Substrate
  • Detection Buffer
  • White, sterile, cell-culture ready assay plate
Shelf Life6 months
Orthologs AvailableYes
Shipping RequirementsDry Ice
Storage temperature-80C


Agonist dose-response analyses. LXRβ Reporter Cells were treated with a dilutions series of the reference agonists T0901317 (provided), APD (Cayman Chem.) or GW3965 (Tocris).
Antagonist dose-response analyses performed by co-treating reporter cells with a fixed (EC80) concentration or TO901317 and varying concentrations of the reference antagonists GSK 2033 or SR 9243 (Tocris). Luminescence was quantified and average relative light units (RLU) and corresponding values of standard deviation (SD) were determined for each treatment concentration (n = 3). Fold-Activation and Z’ values were calculated as described by Zhang, et al. (1999). Non-linear regression and EC50 / IC50 analyses were performed using GraphPad Prism software.

Target Background

Liver X receptor β (LXRβ) is a member of the nuclear receptor family of transcription factors. LXRβ is encoded by the NR1H2 gene (nuclear receptor subfamily 1, group H, member 2). The Liver X receptors (LXRs) were originally identified as orphan members of the nuclear receptor superfamily because their ligands were unknown. Like other receptors in the family, LXRs heterodimerize with the Retinoid X Receptor and bind to specific response elements (LXREs) characterized by direct repeats separated by 4 nucleotides.

These LXRβ Reporter Assay Systems utilize proprietary mammalian cells engineered to express human NR1H2 protein, commonly referred to as LXRβ.

The principle application of this LXRβ assay product is in the screening of test samples to quantify functional activities, either agonist or antagonist, that they may exert against the human liver x receptor beta.


Tris(1,3-dichloro-2-propyl) phosphate (TDCPP) is an organophosphate flame retardant. The primary TDCPP metabolite, bis(1,3-dichloro-2-propyl) phosphate (BDCPP), is detectable in the urine of over 90 % of Americans. Epidemiological studies show sex-specific associations between urinary BDCPP levels and metabolic syndrome, which is an established risk factor for type 2 diabetes, heart disease, and stroke. We used a mouse model to determine whether TDCPP exposure disrupts glucose homeostasis. Six-week old male and female C57BL/6J mice were given ad libitum access to diets containing vehicle (0.1 % DMSO) and TDCPP resulting in the following treatment groups: 0 mg/kg/day, 0.02 mg/kg/day, 1 mg/kg/day, or 100 mg/kg/day. After being on the experimental diet for five weeks without interruption, body composition was analyzed, glucose and insulin tolerance tests were performed, and fasting glucose and insulin levels were quantified. TDCPP at 100 mg/kg/day caused male sex-specific adiposity, fasting hyperglycemia, and insulin resistance. TDCPP-induced modulation of nuclear receptor activation was investigated using an in vitro screen to identify potential mechanisms of metabolic disruption. TDCPP activated farnesoid X receptor (FXR) and pregnane X receptor (PXR), and inhibited the androgen receptor (AR). PXR target genes, but not FXR target genes, were upregulated in livers from mice exposed to 100 mg TDCPP/kg/day. Interestingly, PXR target genes were differentially expressed in livers from both males and females. It remains to be determined whether TDCPP-induced metabolic disruption occurs via modulation of nuclear receptor activity. Taken together, these studies build upon the association of TDCPP exposure and metabolic syndrome in humans by identifying sex-specific effects of TDCPP on glucose homeostasis in mice.
Selective liver X receptor (LXR) agonists have been extensively pursued as therapeutics for Alzheimer’s disease and related dementia (ADRD) and, for comorbidities such as type 2 diabetes (T2D) and cerebrovascular disease (CVD), disorders with underlying impaired insulin signaling, glucose metabolism, and cholesterol mobilization. The failure of the LXR-focused approach led us to pursue a novel strategy to discover nonlipogenic ATP-binding cassette transporter A1 (ABCA1) inducers (NLAIs): screening for ABCA1-luciferase activation in astrocytoma cells and counterscreening against lipogenic gene upregulation in hepatocarcinoma cells. Beneficial effects of LXRβ agonists mediated by ABCA1 include the following: control of cholesterol and phospholipid efflux to lipid-poor apolipoproteins forming beneficial peripheral HDL and HDL-like particles in the brain and attenuation of inflammation. While rare, ABCA1 variants reduce plasma HDL and correlate with an increased risk of ADRD and CVD. In secondary assays, NLAI hits enhanced cholesterol mobilization and positively impacted in vitro biomarkers associated with insulin signaling, inflammatory response, and biogenic properties. In vivo target engagement was demonstrated after oral administration of NLAIs in (i) mice fed a high-fat diet, a model for obesity-linked T2D, (ii) mice administered LPS, and (iii) mice with accelerated oxidative stress. The lack of adverse effects on lipogenesis and positive effects on multiple biomarkers associated with T2D and ADRD supports this novel phenotypic approach to NLAIs as a platform for T2D and ADRD drug discovery.

Also available as a service

Liver X Receptor Beta (LXRb, NR1H2)

Have questions about this assay kit?