2. Signaling Pathways
  3. Cell Cycle/DNA Damage
    Metabolic Enzyme/Protease
    Vitamin D Related/Nuclear Receptor
  4. PPAR
  5. PPAR Antagonist

PPAR Antagonist

PPAR Isoform Comparison

PPAR Antagonists (17):

Cat. No. Product Name Effect Purity
  • HY-16578
    GW9662
    		Antagonist 99.87%
    GW9662 is a potent and selective PPARγ antagonist with an IC50 of 3.3 nM, showing 10 and 1000-fold selectivity over PPARα and PPARδ, respectively.
  • HY-15372
    GW6471
    		Antagonist 98.81%
    GW6471 is a potent PPARα antagonist.
  • HY-13202
    T0070907
    		Antagonist 99.98%
    T0070907 is a potent PPARγ antagonist with a Ki of 1 nM.
  • HY-14166
    MK-886
    		Antagonist 99.77%
    MK-886 (L 663536) is a potent, cell-permeable and orally active FLAP (IC50 of 30 nM) and leukotriene biosynthesis (IC50s of 3 nM and 1.1 μM in intact leukocytes and human whole blood, respectively) inhibitor. MK-886 is also a non-competitive PPARα antagonist and can induce apoptosis.
  • HY-12377
    GSK0660
    		Antagonist 99.19%
    GSK0660 is a potent antagonist of PPARβ and PPARδ, with IC50s of 155 nM for both isoforms.
  • HY-15577
    GSK3787
    		Antagonist 98.03%
    GSK3787 is a selective and irreversible peroxisome proliferator-activated receptor δ (PPARδ) antagonist with pIC50 of 6.6.
  • HY-19737A
    DG172 dihydrochloride
    		Antagonist 99.03%
    DG172 dihydrochloride is a selective PPARβ/δ antagonist, with an IC50 of 27 nM.
  • HY-114263
    NXT629
    		Antagonist 99.20%
    NXT629 is a potent, selective, and competitive PPAR-α antagonist, with an IC50 of 77 nM for human PPARα, shows high selectivity over other nuclear hormone receptor, such as PPARδ, PPARγ, ERβ, GR and TRβ, IC50s are 6.0, 15, 15.2, 32.5 and >100 μM, respectively. NXT629 has potent anti-tumor activity and inhibits experimental metastasis of cancer cell in animal models.
  • HY-148352
    BAY-4931
    		Antagonist 98.83%
    BAY-4931 is a potent, covalent and selective PPARγ inverse-agonist with an IC50 of 0.17 nM.
  • HY-148351
    BAY-0069
    		Antagonist 98.07%
    BAY-0069 is a potent and selective PPARγ inverse agonist with an IC50 value of 6.3 nM and 24 nM for human PPARγ and mouse PPARγ. BAY-0069 can be used to research cancer.
  • HY-117727
    Leriglitazone
    		Antagonist
    Leriglitazone (MIN-102; Hydroxypioglitazone), a metabolite of pioglitazone. Leriglitazone PioOH is a PPARγ agonist, stabilizes the PPARγ activation function-2 (AF-2) co-activator binding surface and enhances co-activator binding, affording slightly better transcriptional efficacy. Leriglitazone binds to the PPARγ C-terminal ligand-binding domain (LBD) with a Ki of 1.2 μM，Leriglitazone induces transcriptional efficacy of the PPARγ (LBD) with an EC50 of 680 nM.
  • HY-160162
    SR 11023
    		Antagonist
    SR 11023 is an orally active antagonist of PPARγ, with the IC50 value of 109 nM that plays an important role in diabetic research.
  • HY-14166A
    MK-886 sodium salt
    		Antagonist
    MK-886 (L 663536) sodium salt is a potent, cell-permeable and orally active FLAP (IC50 of 30 nM) and leukotriene biosynthesis (IC50s of 3 nM and 1.1 μM in intact leukocytes and human whole blood, respectively) inhibitor. MK-886 sodium salt is also a non-competitive PPARα antagonist and can induce apoptosis.
  • HY-120188
    CC618
    		Antagonist
    CC618 is a selective peroxisome proliferator-activated receptor (PPARβ/δ) antagonist that exhibits antagonism by covalently binding to PPARβ/δ receptors.
  • HY-16578S
    GW9662-d5
    		Antagonist
    GW9662-d5 is the deuterium labeled GW9662. GW9662 is a potent and selective PPARγ antagonist with an IC50 of 3.3 nM, showing 10 and 1000-fold selectivity over PPARα and PPARδ, respectively[1][2].
  • HY-117727S
    Leriglitazone-d4
    		Antagonist
    Leriglitazone-d4 (MIN-102-d4; Hydroxypioglitazone-d4) is deuterium labeled Leriglitazone. Leriglitazone (Hydroxypioglitazone), a metabolite of pioglitazone.Leriglitazone (Hydroxypioglitazone) PioOH is a PPARγ agonist, stabilizes the PPARγ activation function-2 (AF-2) co-activator binding surface and enhances co-activator binding, affording slightly better transcriptional efficacy.Leriglitazone (Hydroxypioglitazone) binds to the PPARγ C-terminal ligand-binding domain (LBD) with Ki of 1.2 μM，induces transcriptional efficacy of the PPARγ (LBD) with EC50 of 680 nM.
  • HY-128487
    H-​Trp-​Glu-​OH
    		Antagonist
    H-​Trp-​Glu-​OH is a selective, reversible and cell-permeable PPARγ with a Kd of ~8 µM. H-​Trp-​Glu-​OH might be developed as a possible lead compound in diabetes research.