product name Troglitazone (CS-045)
Description: Troglitazone is a PPARγ agonist with anti-inflammatory and anti-tumor activity. Troglitazone significantly inhibits cell growth by cell cycle arrest and apoptotic cell death. Troglitazone also downregulates surface expression of CD97, a novel dedifferentiation marker, in FTC-133 cells and upregulated sodium iodide symporter (NIS) mRNA in TPC-1 and FTC-133 cells. Troglitazone also induces antiproliferation and redifferentiation in thyroid cancer cell lines.
References: Thyroid. 2005 Mar;15(3):222-31; PPAR Res. 2012;2012:929052; J Biol Chem. 2003 Feb 21;278(8):5845-53.
441.54
Formula
C24H27NO5S
CAS No.
97322-87-7
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 88 mg/mL (199.3 mM)
Water: <1 mg/mL
Ethanol: 15 mg/mL (34 mM)
Solubility (In vivo)
Synonyms
Rezulin, Romglizone, Romozin, Prelay, CS-045, CS045
other peoduct :
| In Vitro |
In vitro activity: Troglitazone significantly inhibits cell growth by cell cycle arrest and apoptotic cell death. Troglitazone also downregulates surface expression of CD97, a novel dedifferentiation marker, in FTC-133 cells and upregulated sodium iodide symporter (NIS) mRNA in TPC-1 and FTC-133 cells. Troglitazone, a PPARγ agonist, induces antiproliferation and redifferentiation in thyroid cancer cell lines. Troglitazone induces Erk phosphorylation in human prostate cancer cells via a PPARγ-independent signaling pathway. TGZ(Troglitazone) up-regulates nitric oxide synthesis, induces the p53 pathway, inhibits cholesterol biosynthesis, induces p21 cyclin-dependent kinase inhibitor, has antioxidant function, and activates extracellular signal-regulated protein kinase (ERK) in a PPARγ-independent manner. TGZ induces Egr-1 expression by transcriptional and post-transcriptional regulation. Egr-1 induction by TGZ results in the increase of binding affinity and transactivation of the promoter containing Egr-1 consensus sequences, thereby possibly inducing other anti-tumorigenic proteins. Kinase Assay: Standard incubation mixtures (final volume of 0.20 mL) containe recombinant P450 (0.010 μM) in 50 mM potassium phosphate buåer (pH 7.4) containing an NADPH-generating system (0.5 mm NADP+, 5 mM glucose 6-phosphate, 0.5 unit glucose 6-phosphate dehydrogenase/mL) and substrates (1±100 lM). For determination of CYP1A2, CYP2B6, CYP2E1 and CYP3A4 activities, 100 mM potassium phosphate buffer (pH 7.4) is used. When human liver microsomes are used as the enzyme source, 500, 25, 100 and 25 pmol totalP450 per mL are used for paclitaxel 6a-hydroxylation, S-warfarin 7-hydroxylation,S-mephenytoin 4´-hydroxylation and testosterone 6b-hydroxylation respectively. Cell Assay: Growth experiments are done in a 96-well plate in hexaplicate. Cells at 85%-100% confluency are harvested with 1×Trypsin/EDTA solution and seeded into a 96-well plate at 3-5×10<sup>3</sup> cells per well depending upon growth rate and maintained in 200 μL H5 medium in a humidified incubator. After 24 hours, cells are incubated with different concentrations of troglitazone and the media was changed daily. Colorometric dimethyl-thiazol-diphenyltetrazolium bromide (MTT) proliferation assays are performed at 0, 2, 4, and 6 days after treatment. MTT (400 μg/mL) is added to each well and incubated for 3 hours. It is solubilized with 0.04 N HCl/iso-propanol/3% SDS and incubated for 1 hour. The optical densities in the 96-well plates are determined using an enzyme-linked immunosorbent assay (ELISA) microplate reader at 595 nm/620 nm. |
|---|---|
| In Vivo | Troglitazone is an effective antidiabetic drug with a fundamentally new mechanism of action. However, within a year after its widespread use, individual cases of liver injury and failure are reported. TGZ significantly inhibits tumor growth of human colorectal cancer cells (HCT-116), human breast cancer cells (MCF-7), and human prostate cancer cells (PC-3) in immunodeficient mice. Troglitazone attenuates pancreatic damage and inflammation in experimental chronic pancreatitis. |
| Animal model | C57BL/6 mice |
| Formulation & Dosage | Supplemented chow diet (0.2%); oral |
| References | Thyroid. 2005 Mar;15(3):222-31; PPAR Res. 2012;2012:929052; J Biol Chem. 2003 Feb 21;278(8):5845-53. |
