PPAR Modulator

PPAR Modulators (38):

Cat. No.	Product Name	Effect	Purity

HY-101064

Fmoc-leucine	Modulator	99.91%
Fmoc-Leucine (N-FMOC-leucine) is an anti-inflammatory agent that not only promotes extracellular Ca²⁺ influx but also facilitates intracellular Ca²⁺ release. Fmoc-Leucine is a selective ligand for PPARγ (K_i = 15 μM), exhibiting insulin-sensitizing effects but with weak fatogenic activity. Fmoc-Leucine exhibits unique self-assembly properties and can form transient gels, stable gels, or crystals/2D sheets through different pathways. Fmoc-Leucine can be used in the research of diabetes, colitis, and bladder cancer.

HY-108022

Azemiglitazone	Modulator
Azemiglitazone (MSDC-0602) is an orally active thiazolidinedione (TZD) -like molecule, which binds to PPARγ with low binding and activating affinity. Azemiglitazone inhibits mitochondrial pyruvate carrier (MPC), which inhibits Alzheimer’s disease and diminishes nonalcoholic steatohepatitis (NASH) caused liver injury.

HY-100348

EPI-001	Modulator	99.34%
EPI-001, a selective inhibitor of Androgen Receptor (AR), targets transactivation unit 5 (Tau-5) of the AR. EPI-001 can inhibit transactivation of the AR amino-terminal domain (NTD), with an IC₅₀ of ~6 μM. EPI-001 is also a selective modulator of PPARγ. EPI-001 is active against castration-resistant prostate cancer.

HY-108022A

Azemiglitazone potassium	Modulator	98.94%
Azemiglitazone potassium (MSDC-0602K), a PPARγ-sparing thiazolidinedione (Ps-TZD), binds to PPARγ with the IC₅₀ of 18.25 μM. Azemiglitazone potassium modulates the mitochondrial pyruvate carrier (MPC). Azemiglitazone potassium can be used for the research of fatty liver including dysfunctional lipid metabolism, inflammation, and insulin resistance. Azemiglitazone potassium, an insulin sensitizer, improves insulinemia and fatty liver disease in mice, alone and in combination with Liraglutide.

HY-134377

Bocidelpar	Modulator	98.08%
Bocidelpar (ASP0367; MA-0211) is a selective, orally active PPARδ modulator. Bocidelpar activates the PPARδ downstream signaling pathway, upregulates the expression of target genes such as ABCA1 and ACAA2. Bocidelpar then promotes fatty acid oxidation (FAO) and mitochondrial biogenesis, and improves mitochondrial dysfunction. Bocidelpar can improve mitochondrial biogenesis and function in muscle cells. Bocidelpar is mainly used in the study of mitochondrial dysfunction diseases such as primary mitochondrial myopathy (PMM) and Duchenne muscular dystrophy (DMD).

HY-21197

Perfluoroenanthic acid	Modulator	98.0%
Perfluoroenanthic acid (Perfluoroheptanoic acid) is a kind of perfluoroalkyl carboxylic acid organic pollutant. Perfluoroenanthic acid has environmental persistence and bioaccumulation, and exposure can occur via oral, dermal and other routes. Perfluoroenanthic acid exhibits reproductive toxicity, neurotoxicity, hepatotoxicity, immunotoxicity and endocrine-disrupting effects. Perfluoroenanthic acid exerts definite adverse effects on development, spermatogenesis, neuronal activity and liver tissue.

HY-21193

Perfluoropentanoic acid	Modulator	98.0%
Perfluoropentanoic acid (PFPeA), a short-chain perfluorinated compound, serves as an important indicator of perfluorinated compound pollution in ecosystems. Perfluoropentanoic acid exhibits certain toxicity to mice.

HY-100428

Netoglitazone	Modulator	99.92%
Netoglitazone (MCC-555) is an orally active PPARγ ligand with an EC₅₀ of 8 μM. Netoglitazone mediates cell type-specific functional regulation, and modulates the transcriptional activity of PPARγ as a full agonist, partial agonist or antagonist. Netoglitazone induces adipogenesis, inhibits osteoblastogenesis, alters the weight of extramedullary fat depots and enhances insulin sensitivity. Netoglitazone reduces blood glucose levels. Netoglitazone can be used in research related to type 2 diabetes and non-insulin-dependent diabetes mellitus.

HY-111254

GQ-16	Modulator	98.12%
GQ-16 is an orally active PPARγ partial agonist with an IC₅₀ of 1.84 μM and a K_i of 160 nM against human PPARγ. GQ-16 inhibits Cdk5-mediated Ser-273 phosphorylation. GQ-16 improves insulin sensitivity and glucose tolerance in obese and diabetic mice. GQ-16 also exhibits certain cytotoxicity against tumor cells. GQ-16 can be used in research related to obesity, diabetes and cancer.

HY-101064S3

Fmoc-leucine-d₁₀	Modulator	99.40%
Fmoc-leucine-d₁₀ is the deuterium labeled Fmoc-leucine. Fmoc-leucine is a selective PPARγ modulator. Fmoc-leucine activates PPARγ with a lower potency but a similar maximal efficacy than rosiglitazone. Fmoc-leucine improves insulin sensitivity in normal, diet-induced glucose-intolerant, and in diabetic db/db mice. Fmoc-leucine has a lower adipogenic activity.

HY-101064S2

Fmoc-leucine-d₃	Modulator	99.25%
Fmoc-leucine-d₃ is the deuterium labeled Fmoc-leucine. Fmoc-leucine is a selective PPARγ modulator. Fmoc-leucine activates PPARγ with a lower potency but a similar maximal efficacy than rosiglitazone. Fmoc-leucine improves insulin sensitivity in normal, diet-induced glucose-intolerant, and in diabetic db/db mice. Fmoc-leucine has a lower adipogenic activity.

HY-114739

MA-0204	Modulator	99.31%
MA-0204 is a potent, highly selective and orally available peroxisome proliferator activated receptor δ (PPARδ) modulator with EC₅₀s of 0.4 nM, 7.9 nM and 10 nM for human, mouse and rat PPARδ, respectively. Potential treatment for Duchene Muscular Dystrophy (DMD).

HY-101064S1

Fmoc-leucine-¹³C₆,¹⁵N	Modulator	99.90%
Fmoc-leucine-¹³C₆,¹⁵N is a ¹⁵N-labeled and ¹³C-labled Fmoc-leucine. Fmoc-leucine is a selective PPARγ modulator. Fmoc-leucine activates PPARγ with a lower potency but a similar maximal efficacy than rosiglitazone. Fmoc-leucine improves insulin sensitivity

HY-172883

ABP/PPAR modulator 1	Modulator
ABP/PPAR modulator 1 is an orally active FABP and PPAR multiple modulator (IC₅₀s of 0.65  μM and 1.08  μM for FABP1 and FABP4, EC₅₀s of 9.19  μM, 2.20  μM and 1.58 μM for PPARα, PPARγ and PPARδ). ABP/PPAR modulator 1 has potent anti-metabolic dysfunction-associated steatohepatitis (MASH) activity. ABP/PPAR modulator 1 dose-dependently ameliorates multiple pathological characteristics of fatty liver in WD + Carbon tetrachloride-induced MASH mice model.

HY-W109107

GED 0507-34-Levo	Modulator
GED 0507-34-Levo is an orally active PPARγ modulator. GED 0507-34-Levo downregulates the expression of TGF-β, Smad3, IL-13, and CTGF in the colon. GED 0507-34-Levo improves DSS-induced chronic colitis and fibrosis.

HY-163432

YGL-12	Modulator
YGL-12 is a potent PPARγ modulator with good binding affinity and an IC₅₀ value of 0.85 μM. YGL-12 effectively blocks PPARγ Ser273 phosphorylation and can be used in diabetes research.

HY-170581

PPARγ/δ modulator 2	Modulator
PPARγ/δ modulator 2 (Compound 3h) is a PPARγ agonist and PPARδ antagonist. The K_i values for PPARγ and PPARδ are 2.8 μM and 43 nM, respectively. PPARγ/δ modulator 2 significantly enhances the production of Adiponectin and promotes adipogenic differentiation of human bone marrow mesenchymal stem cells (hBM-MSCs). PPARγ/δ modulator 2 can be used in the study of metabolic disorders associated with hypoadiponectinemia.

HY-180398

PA-082	Modulator
PA-082 is a selective PPAR-γ modulator that functions as a partial agonist. PA-082 causes partial recruitment of SRC1, TIF2, SRC3 and full recruitment of PGC1-α to PPAR-γ ligand-binding domain. PA-082 prevents triglyceride accumulation during de novo adipogenesis and antagonizes Rosiglitazone (HY-17386)-induced lipid accumulation. PA-082 potentiates insulin-stimulated glucose uptake in adipocytes and protects against TNFα-induced insulin resistance. PA-082 can be used for the research of type 2 diabetes.

HY-147757

PPARγ/δ modulator 1	Modulator
PPARγ/δ modulator 1 (compound 3e) is a potent PPAR modulator. PPARγ/δ modulator 1 is a PPARδ antagonist and a PPARγ partial agonist , with K_i values of 14.4 nM and 5.31 μM, respectively. PPARγ/δ modulator 1 has the EC₅₀ of 7.3 and 12.6 μM for PPARδ corepression and adiponectin production, respectively.

HY-160188

BAY-9683	Modulator
BAY-9683 is an orally active covalent PPARG inverse agonist. BAY-9683 can be used in the study of diseases with overactive PPARG, such as luminal bladder cancer.

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