We use analytics and advertising cookies, which you can accept or reject; see our privacy policy.

Current choice:

Fig. 1 · Structure
Cat. No.
A11981
CAS No.
97322-87-7
Formula
C24H27NO5S
Mol. Weight
441.54

Documents & Downloads

Troglitazone

Cat. No. A11981 CAS 97322-87-7

PPARγ agonist

Troglitazone is a selective PPARγ receptor agonist (EC50 values are 780 and 555 nM at murine and human PPARγ receptors respectively).

In Stock

Publications for Troglitazone

2 publications citing this product

  1. Gede Ngurah Rsi Suwardana, .et al. , Antiviral Res, 2025, Aug 30:243:106267 PMID: 40889532
  2. Julien Allard, .et al. , Cell Biol Toxicol, 2020, Jun 14 PMID: 32535746
Notify me when the price drops

For laboratory research use only. We do not sell to patients.

Free Aliquoting for Your Order

Tell us your preferred amount per vial. We’ll confirm the options.

Biological Activity

Bioactivity / Mechanism

Troglitazone activated a PPARγ-responsive transcriptional reporter in PC-3 cells. The response was inhibited by GW9662, supporting its use as a PPARγ agonist in this assay. This functional readout does not establish a receptor-binding affinity. [1]

At 40 μM, troglitazone increased ERK1/2 phosphorylation in PC-3 cells. GW9662 did not prevent this response, whereas U0126 attenuated it, supporting a PPARγ-independent, MEK-associated component under these conditions. Troglitazone responses should therefore be interpreted with pathway and model controls. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
PPARγ 550 nM (EC50, Human PPARγ)

Cellular Effect

Cell Line Activity Value Description Reference
A549 GI50 15 μM Inhibition of human lung cancer cell line (A549) by 50% in sulforhodamine B assay [PMID: 15454234]
CHO EC50 0.44 μM Agonist activity at human recombinant PPARgamma expressed in CHO cells cotransfected with pGL3-PPRE3-TK-luc reporter assessed as beta-galactosidase activity at after 24 hrs by luciferase based transactivation assay [PMID: 22424300]
CHO EC50 0.44 μM Agonist activity at human PPARgamma expressed in CHO cells co-transfected with pGL3-PPRE3-TK-luc assessed as transactivation after 24 hrs by firefly luciferase reporter gene assay [PMID: 22342624]
CV-1 EC50 0.4 μM Transactivation of human PPARgamma expressed in african green monkey CV1 cells by luciferase reporter gene assay [PMID: 22579420]
HCT-15 IC50 > 100 μM Antitumor activity against human HCT15 cells assessed as inhibition of cell proliferation after 1 day by MTT assay [PMID: 22081932]
HCT-15 IC50 50.9 μM Antitumor activity against human HCT15 cells assessed as inhibition of cell proliferation after 2 days by MTT assay [PMID: 22081932]
HEK293 EC50 0.4 μM Activation of PPARgamma transfected in HEK293 cells after 18 hrs by firefly luciferase reporter gene-based luminescence assay relative to control [PMID: 21800856]
HEK-293T IC50 4.5 μM Inhibition of mouse Ido2 transfected in HEK293T cells using L-tryptophan as substrate assessed as kynurenine formation after 45 mins by spectrophotometric analysis [PMID: 23122865]
HEK-293T IC50 61 μM Inhibition of mouse Ido1 transfected in HEK293T cells using L-tryptophan as substrate assessed as kynurenine formation after 45 mins by spectrophotometric analysis [PMID: 23122865]
HepG2 EC50 0.72 μM Transactivation of GAL4-fused PPARgamma ligand binding domain transfected in human HepG2 cells after 20 hrs by luciferase reporter gene assay [PMID: 23031596]
HepG2 EC50 0.73 μM Transactivation of GAL4-fused PPARgamma LBD expressed in HepG2 cells after 20 hrs by luminescence assay [PMID: 22381047]
HepG2 EC50 31.6 μM Activation of human PXR expressed in human HepG2 (DPX-2) cells after 24 hrs by luciferase reporter gene based luminescent analysis [PMID: 20966043]
HepG2 EC50 6.9 μM Activation of human PXR expressed in human HepG2 (DPX-2) cells assessed as induction of CYP3A4 after 24 hrs by luminescent analysis [PMID: 20966043]
Hs-578T IC50 > 100 μM Antiproliferative activity against human Hs578T cells in 10% FCS by crystal violet staining based assay [PMID: 31838327]
HT-29 IC50 > 100 μM Antitumor activity against human HT-29 cells assessed as inhibition of cell proliferation after 1 day by MTT assay [PMID: 22081932]
HT-29 IC50 50 μM Antitumor activity against human HT-29 cells assessed as inhibition of cell proliferation after 2 days by MTT assay [PMID: 22081932]
LNCaP IC50 22 μM Cytotoxicity against human LNCAP cells after 24 hrs by MTT assay [PMID: 22546208]
LoVo IC50 > 100 μM Antitumor activity against human LoVo cells assessed as inhibition of cell proliferation after 1 day by MTT assay [PMID: 22081932]
LoVo IC50 65 μM Antitumor activity against human LoVo cells assessed as inhibition of cell proliferation after 2 days by MTT assay [PMID: 22081932]

19 records · Scroll to view more

In Vitro Studies

Troglitazone reduced PC-3 cell accumulation and DNA synthesis. MEK inhibition with U0126 did not rescue these effects; the 10 μM troglitazone combination reduced both readouts more than either agent alone. These results do not establish formal drug synergy or clinical antitumor efficacy. [1]

In differentiated HepaRG cells, Adooq-sourced troglitazone (A11981) increased neutral lipid accumulation at 47.5 μM after four days. ApoB secretion and de novo lipogenesis decreased, while mitochondrial fatty-acid oxidation increased at 40 and 45 μM. These findings support model-specific hepatic liability and limit an explanation based solely on inhibition of fatty-acid oxidation. [2]

PPARγ reporter activation and pharmacologic dissection of ERK signaling

Cell-based study · Human PC-3 prostate cancer cells [1]

Troglitazone increased PPRE-reporter activity and ERK1/2 phosphorylation. GW9662 suppressed the reporter response but did not prevent ERK phosphorylation; U0126 attenuated phosphorylation without significantly changing the troglitazone reporter response. These pharmacologic results support distinct signaling components in this model.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
PPRE-driven transcriptionreported response Increased by troglitazone; GW9662 inhibited the response. U0126 did not significantly alter the response at each troglitazone concentration tested.[1]
ERK1/2 phosphorylationreported response Induction most pronounced at 40 μM and 2 h; attenuated by U0126 but not prevented by GW9662.[1]

Literature-Reported Treatment Conditions

Treatment concentration
Reporter: 2.5, 10 and 40 μM; ERK time course: 40 μM; ERK concentration series: 1, 5, 10 and 40 μM
Exposure duration
Reporter: 24 h; ERK: 15 min, 30 min and 2 h; inhibitor pretreatment: 1 h
Method
PPRE-luciferase normalized to CMV β-galactosidase; Western blots for phospho-ERK, total ERK and actin
Vehicle
DMSO control; final DMSO percentage not specified
Co-treatment
Separate arms with GW9662 (10 μM) or U0126 (10 μM); comparator TZDs in Figure 3A
Reported limits
No direct receptor-binding affinity measured in this experiment; reported representative results do not provide pooled effect-size estimates.
Methods and source locations

Compound reported in the paper: Troglitazone; Compound label in the paper: troglitazone

Results apply to the reported troglitazone material and model; stereochemical equivalence and current Adooq lot performance were not established.

Sections 2.2, 2.4, 2.5, 2.7, 3.1–3.3; Figures 2, 3 and 4 with captions

PPRE-driven transcription: Luciferase/β-galactosidase; representative experiment, mean ± SD of three wells; experiments performed at least three times. — Figure 3B; Figure 4 and captions; sections 2.5, 3.2–3.3

ERK1/2 phosphorylation: Western blot; total ERK and actin controls. No curve-derived values extracted. — Figures 2 and 3C; sections 2.4, 3.1–3.3

MEK inhibition does not rescue troglitazone-associated growth suppression

Cell-based study · Human PC-3 prostate cancer cells [1]

Troglitazone reduced cell accumulation and thymidine incorporation. U0126 did not rescue these responses; at 10 μM troglitazone, the combination produced a larger reduction than either agent alone in the reported assays.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cell number and DNA synthesisreported response U0126 did not block reductions induced by troglitazone; 10 μM troglitazone plus U0126 reduced both readouts more than either alone (P < 0.05).[1]

Literature-Reported Treatment Conditions

Treatment concentration
Troglitazone 2.5–40 μM in cell-count design; 10 and 40 μM in Figure 6 combination comparisons
Exposure duration
Cell counts: 6 days; fresh medium/drug every 3 days. Figure 6A thymidine exposure duration is not specified in its caption; general method spans 2–6 days. U0126 added 1 h before troglitazone.
Method
Coulter cell counting; [3H]-thymidine incorporation
Vehicle
DMSO control; final percentage not specified
Co-treatment
Separate single-agent controls and cotreatment with U0126 (10 μM)
Reported limits
Precise Figure 6A exposure duration is not reported in the figure caption; no numerical IC50 supplied.
Methods and source locations

Compound reported in the paper: Troglitazone; Compound label in the paper: troglitazone

Results apply to the reported troglitazone material and model; stereochemical equivalence and current Adooq lot performance were not established.

Sections 2.2, 2.6, 2.7 and 3.4; Figure 6 and caption

Cell number and DNA synthesis: Representative experiment; mean ± SD of three wells; experiments performed at least three times; one-way ANOVA. — Figure 6A/B and caption; section 3.4

Neutral lipid accumulation and metabolic flux responses in HepaRG cells

Cell-based study · Differentiated human HepaRG cells [2]

A four-day concentration-response design showed neutral lipid accumulation at the highest selected troglitazone concentration, together with reduced apoB secretion and de novo lipogenesis. Fatty-acid oxidation increased at 40 and 45 μM, rather than showing the inhibition that would be required for a simple mtFAO-inhibition explanation of steatosis.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Neutral lipid accumulationreported response Significantly increased at 47.5 μM versus control (P < 0.05).[2]
Mitochondrial fatty-acid oxidation, de novo lipogenesis and apoB secretionreported response mtFAO significantly increased at 40 and 45 μM; DNL and apoB secretion decreased across 40–47.5 μM. ApoB secretion was less than 10% of control at 45 and 47.5 μM, as stated in Results.[2]

Literature-Reported Treatment Conditions

Treatment concentration
40, 45 and 47.5 μM troglitazone
Exposure duration
4 consecutive daily treatments; assessments at 96 h (24 h after fourth treatment)
Method
Nile red neutral lipid imaging normalized per nuclei; radiolabeled substrate assays for mtFAO and DNL; supernatant apoB ELISA normalized to cellular protein
Vehicle
1% DMSO fixed in all control and treated conditions; 2% FBS
Co-treatment
None for troglitazone; amiodarone used as steatogenic positive-control drug in parallel
Reported limits
Salt, stereochemical composition and lot-level analytical characterization not specified.
Methods and source locations

Compound reported in the paper: Troglitazone; Compound label in the paper: TRO

Results apply to the reported troglitazone material and model; stereochemical equivalence and current Adooq lot performance were not established.

Chemicals and reagents; Cell culture and treatments; Selection of drug concentrations; Figures 1 and 3D and captions; Results: Mechanisms of drug-induced steatosis

Neutral lipid accumulation: Nile red normalized by nuclei; mean ± SD, 5–9 independent cultures; one-way ANOVA. — Figure 1, troglitazone panel and caption

Mitochondrial fatty-acid oxidation, de novo lipogenesis and apoB secretion: mtFAO: [U-14C]palmitic acid; DNL: [2-14C]acetic acid; apoB: ELISA. Means ± SD; mtFAO/DNL 5–9 independent cultures; apoB 5 independent cultures; one-way ANOVA, P < 0.05 markers. — Figure 3D and caption; Results paragraph beginning “In addition to AMIO”

In Vivo Studies

Troglitazone responses differed between lipoatrophic mouse models. Five weeks of dietary treatment lowered fasting glucose and insulin in aged aP2/DTA mice. In younger A-ZIP/F-1 mice, two weeks of oral-gavage treatment did not significantly lower fed-state glucose or insulin, although serum triglycerides decreased. Different models, regimens and sampling conditions prevent a direct efficacy comparison or a general claim that the glycemic response is independent of adipose tissue. [3,4]

Five-week dietary troglitazone in aged lipoatrophic and wild-type mice

Animal study · Wild-type and aP2/DTA mice with marked lipoatrophy at 8–9 months of age [3]

In the aP2/DTA model, dietary troglitazone lowered fasting serum glucose and insulin, with lower circulating triglycerides and cholesterol. Insulin did not normalize to wild-type values. This result is restricted to the reported model and regimen.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Fasting serum glucose and insulinreported response aP2/DTA fasting glucose and insulin decreased significantly; insulin reduction described as fivefold, with levels remaining above wild-type.[3]
Fasting serum triglycerides and cholesterolreported response Fasting serum triglycerides and cholesterol decreased significantly in treated aP2/DTA mice.[3]

Conditions shared by the study groups

Route
Oral, dietary admixture
Frequency
Dietary access; not a fixed once-daily bolus
Treatment course
5 weeks
Vehicle
Ground standard chow
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Wild-type mice receiving troglitazone
16.6 mg troglitazone per gram of chow		Genotype-matched ground chow without troglitazone; wild-type n=6, aP2/DTA n=7Lower fasting glucose and circulating lipids relative to matched chow controls; basal insulin was not significantly changed.[3]
aP2/DTA mice receiving troglitazone
16.6 mg troglitazone per gram of chow		Genotype-matched ground chow without troglitazone; wild-type n=6, aP2/DTA n=7Fasting glucose and insulin decreased, with insulin remaining above wild-type levels; serum triglycerides and cholesterol decreased.[3]
Wild-type mice receiving troglitazone
Model: Wild-type mice, 8–9 months; n=6 (2 male/4 female), Table I
Reported limits: Consumed dose varied with food intake; no mg/kg dose assumed. Salt/stereoisomer not specified.
aP2/DTA mice receiving troglitazone
Model: aP2/DTA lipoatrophic mice, 8–9 months; n=7 (2 male/5 female), Table I
Reported limits: Consumed dose varied with food intake; no mg/kg dose assumed. Salt/stereoisomer not specified.
Methods and source locations

Compound reported in the paper: Troglitazone; Compound label in the paper: troglitazone

Results apply to the reported troglitazone material and model; stereochemical equivalence and current Adooq lot performance were not established.

PDF p. 2901 Diet and troglitazone treatment / Serum chemistries; Table I p. 2902; Figure 3A/B p. 2903; Figure 4 p. 2904; Results pp. 2902–2904

Fasting serum glucose and insulin: Serum glucose analyzer and insulin RIA; n=5–7 determinations per point. No decimal values inferred from bars. — Figure 3A/B and caption p. 2903; Results p. 2904

Fasting serum triglycerides and cholesterol: Commercial enzymatic assays; n=5–7 determinations per point. No bar-derived effect size adopted. — Figure 4A/B and caption p. 2904

Wild-type mice receiving troglitazone · PDF p. 2901 Diet and troglitazone treatment / Serum chemistries; Table I p. 2902; Figure 3A/B p. 2903; Figure 4 p. 2904; Results pp. 2902–2904

aP2/DTA mice receiving troglitazone · PDF p. 2901 Diet and troglitazone treatment / Serum chemistries; Table I p. 2902; Figure 3A/B p. 2903; Figure 4 p. 2904; Results pp. 2902–2904

Troglitazone has limited glycemic effects in severely lipoatrophic A-ZIP/F-1 mice

Animal study · Female FVB/N wild-type and hemizygous A-ZIP/F-1 mice, 6–8 weeks old before treatment; fed-state endpoints; n=6 per group [4]

Two weeks of troglitazone did not significantly lower glucose or insulin in A-ZIP/F-1 mice, while serum triglycerides decreased. Liver triglyceride concentrations were unchanged in this model but decreased in wild-type mice.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Fed-state glucose, A-ZIP/F-1 control versus troglitazonereported response 929 ± 90 versus 859 ± 58 mg/dl; mean ± SEM, n=6; no significant treatment effect reported.[4]
Fed-state insulin, A-ZIP/F-1 control versus troglitazonereported response 113 ± 24 versus 99 ± 31 ng/ml; mean ± SEM, n=6; no significant treatment effect reported.[4]
Fed-state serum triglycerides, A-ZIP/F-1 control versus troglitazonereported response 919 ± 83 versus 595 ± 58 mg/dl; mean ± SEM, n=6; P < 0.05.[4]
Liver triglyceride concentration, control versus troglitazonereported response A-ZIP/F-1: 279 ± 34 versus 281 ± 21 μmol/g (not significant); wild type: 50 ± 6 versus 24 ± 5 μmol/g (P < 0.05); mean ± SEM, n=6.[4]

Conditions shared by the study groups

Route
Oral gavage
Frequency
Daily
Treatment course
2 weeks
Vehicle
H2O for drug administration
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Wild-type mice receiving troglitazone
10 mg in 100 μl H2O per administration		Genotype-matched control group; n=6 per group; Table 1 does not specify a sham-gavage control procedureLiver triglyceride decreased; no significant glucose or insulin decrease is marked in Table 1.[4]
A-ZIP/F-1 mice receiving troglitazone
10 mg in 100 μl H2O per administration		Genotype-matched control group; n=6 per group; Table 1 does not specify a sham-gavage control procedureGlucose and insulin did not significantly decrease; circulating triglycerides decreased, while liver triglyceride was unchanged.[4]
Wild-type mice receiving troglitazone
Model: Female FVB/N wild-type mice, 6–8 weeks old at treatment start
Reported limits: Control gavage handling not specified; no mg/kg conversion.
A-ZIP/F-1 mice receiving troglitazone
Model: Female hemizygous A-ZIP/F-1 mice on FVB/N background, 6–8 weeks old at start
Reported limits: Control gavage handling not specified; no mg/kg conversion.
Methods and source locations

Compound reported in the paper: Troglitazone; Compound label in the paper: troglitazone

Results apply to the reported troglitazone material and model; stereochemical equivalence and current Adooq lot performance were not established.

Methods p. 1222 Mice and Biochemical assays; Table 1 and footnote p. 1223; Results pp. 1222–1223

Fed-state glucose, A-ZIP/F-1 control versus troglitazone: Blood glucose measurement; reported group means, not an IC50. — Table 1 glucose row and footnote; Results p. 1222

Fed-state insulin, A-ZIP/F-1 control versus troglitazone: Serum insulin assay referenced to prior methods by the authors; not pooled with fasting values from Burant. — Table 1 insulin row and footnote; Results p. 1222

Fed-state serum triglycerides, A-ZIP/F-1 control versus troglitazone: Serum triglyceride assay; within-genotype control-versus-treatment comparison. — Table 1 triglyceride row and footnote

Liver triglyceride concentration, control versus troglitazone: Ethanolic KOH hydrolysis and glycerol assay. — Table 1 liver triglyceride (μmol/g) row and footnote

Wild-type mice receiving troglitazone · Methods p. 1222 Mice and Biochemical assays; Table 1 and footnote p. 1223; Results pp. 1222–1223

A-ZIP/F-1 mice receiving troglitazone · Methods p. 1222 Mice and Biochemical assays; Table 1 and footnote p. 1223; Results pp. 1222–1223

Specifications

Manufacturer Adooq Bioscience
Actions Agonist
CAS Number 97322-87-7
Applications PPARγ agonist
Formula C24H27NO5S
Molecular Weight 441.54
Synonyms Rezulin
SMILES
CC1=C(C(=C2CCC(OC2=C1C)(C)COC3=CC=C(C=C3)CC4C(=O)NC(=O)S4)C)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO Warmed: 85 mg/mL (192.51 mM)
Water Insoluble
Ethanol Warmed: 15 mg/mL (33.97 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
28 mg/mL
Vehicle
1% CMC Na

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Bolden A, Bernard L, Jones D, et al. The PPAR Gamma Agonist Troglitazone Regulates Erk 1/2 Phosphorylation via a PPARγ-Independent, MEK-Dependent Pathway in Human Prostate Cancer Cells. PPAR research (2012). PMID: 22448169 DOI: 10.1155/2012/929052 Source material
  2. [2] Allard J, Bucher S, Massart J, et al. Drug-induced hepatic steatosis in absence of severe mitochondrial dysfunction in HepaRG cells: proof of multiple mechanism-based toxicity. Cell biology and toxicology (2021). PMID: 32535746 DOI: 10.1007/s10565-020-09537-1 Source material
  3. [3] Burant CF, Sreenan S, Hirano K, et al. Troglitazone action is independent of adipose tissue. The Journal of clinical investigation (1997). PMID: 9389757 DOI: 10.1172/jci119839 Source material
  4. [4] Chao L, Marcus-Samuels B, Mason MM, et al. Adipose tissue is required for the antidiabetic, but not for the hypolipidemic, effect of thiazolidinediones. The Journal of clinical investigation (2000). PMID: 11086023 DOI: 10.1172/jci11245 Source material

Publications

2 publications citing this product

  1. Gede Ngurah Rsi Suwardana, .et al. , Antiviral Res, 2025, Aug 30:243:106267 PMID: 40889532
  2. Julien Allard, .et al. , Cell Biol Toxicol, 2020, Jun 14 PMID: 32535746

Added to your cart

View Cart Checkout
Loading...