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Human PPARd 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 Peroxisome Proliferator-Activated Receptor Delta. INDIGO’s Human PPAR delta reporter assay utilizes proprietary mammalian cells that have been engineered to provide constitutive expression of the Human PPAR delta. In addition to PPAR delta 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 PPAR delta. 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
  • PPARd Reporter Cells
  • Cell Recovery Medium (CRM)
  • Compound Screening Medium (CSM)
  • GW0742, (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 and Antagonist dose-response of the PPARδ receptor. PPARδ reference agonists and antagonists were analyzed. Average Relative Light Units (RLU) and their respective values of Standard Deviation (SD), Coefficient of Variation (CV), Fold-Activation and % Activity were calculated for each treatment concentration (n = 4). Z’ values were calculated as per Zhang, et al. (1999). Data plots were generated using GraphPad Prism software. Compound concentrations were Log transformed and RLU values were normalized to percent (%) activity of the receptor. Non-linear regression analyses were performed and EC50 & IC50 values determined. The large dynamic response and Z’ values confirm the robust performance of the PPARδ agonist and antagonist assays and demonstrate their suitability for use in HTS applications.

Target Background

Peroxisome proliferator-activated receptor delta (PPARδ or PPARβ), also known as NR1C2 is a nuclear receptor encoded by the PPARδ gene. This protein is a potential inhibitor of ligand-induced transcription activity of PPARα and PPARγ. It may function as an integrator of transcription repression and nuclear receptor signaling. The expression of PPARδ gene is found to be elevated in colorectal cancer cells. The elevated expression can be repressed by adenomatosis polyposis coli (APC), a tumor suppressor protein involved in the APC/beta-catenin signaling pathway. Knockout studies in mice suggested the role of PPARδ in myelination of the corpus callosum, epidermal cell proliferation, and glucose and lipid metabolism. PPARδ has been shown to be involved in differentiation, lipid accumulation, directional sensing, polarization, and migration in keratinocytes.

INDIGO’s PPARδ Reporter Assay Systems utilize proprietary mammalian cells engineered to express human PPARδ.

The principle application of this assay product is in the screening of test samples to quantify functional activities, either agonist or antagonist, that they may exert against the human peroxisome proliferator-activated receptor delta.


Retinol is widely used in topical skincare products to ameliorate skin aging and treat acne and wrinkles; however, retinol and its derivatives occasionally have adverse side effects, including the induction of irritant contact dermatitis. Previously, we reported that mead acid (5,8,11-eicosatrienoic acid), an oleic acid metabolite, ameliorated skin inflammation in dinitrofluorobenzene-induced allergic contact hypersensitivity by inhibiting neutrophil infiltration and leukotriene B4 production by neutrophils. Here, we showed that mead acid also suppresses retinol-induced irritant contact dermatitis. In a murine model, we revealed that mead acid inhibited keratinocyte abnormalities such as keratinocyte hyperproliferation. Consistently, mead acid inhibited p38 MAPK (mitogen-activated protein kinase) phosphorylation, which is an essential signaling pathway in the keratinocyte hyperplasia induced by retinol. These inhibitory effects of mead acid were associated with the prevention of both keratinocyte hyperproliferation and the gene expression of neutrophil chemoattractants, including Cxcl1 and Cxcl2, and they were mediated by a PPAR (peroxisome proliferator-activated receptor)-α pathway. Our findings identified the anti-inflammatory effects of mead acid, the use of which can be expected to minimize the risk of adverse side effects associated with topical retinoid application.
Multiple factors in addition to over consumption lead to obesity and non-alcoholic fatty liver disease (NAFLD) in the United States and worldwide. CYP2B6 is the only human detoxification CYP whose loss is associated with obesity, and Cyp2b-null mice show greater diet-induced obesity with increased steatosis than wildtype mice. However, a putative mechanism has not been determined. LC-MS/MS revealed that CYP2B6 metabolizes PUFAs, with a preference for metabolism of ALA to 9-HOTrE and to a lesser extent 13-HOTrE with a preference for metabolism of PUFAs at the 9- and 13-positions. To further study the role of CYP2B6 in vivo, humanized-CYP2B6-transgenic (hCYP2B6-Tg) and Cyp2b-null mice were fed a 60% high-fat diet for 16 weeks. Compared to Cyp2b-null mice, hCYP2B6-Tg mice showed reduced weight gain and metabolic disease as measured by glucose tolerance tests, however hCYP2B6-Tg male mice showed increased liver triglycerides. Serum and liver oxylipin metabolite concentrations increased in male hCYP2B6-Tg mice, while only serum oxylipins increased in female hCYP2B6-Tg mice with the greatest increases in LA oxylipins metabolized at the 9 and 13-positions. Several of these oxylipins, specifically 9-HODE, 9-HOTrE, and 13-oxoODE, are PPAR agonists. RNA-seq data also demonstrated sexually dimorphic changes in gene expression related to nuclear receptor signaling, especially CAR > PPAR with qPCR suggesting PPARγ signaling is more likely than PPARα signaling in male mice. Overall, our data indicates that CYP2B6 is an anti-obesity enzyme, but probably to a lesser extent than murine Cyp2b’s. Therefore, the inhibition of CYP2B6 by xenobiotics or dietary fats can exacerbate obesity and metabolic disease potentially through disrupted PUFA metabolism and the production of key lipid metabolites.

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Peroxisome Proliferator-Activated Receptor Delta (PPARd / PPARb, NR1C2)

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