| Stereochemistry | RACEMIC |
| Molecular Formula | C21H16FNO3S |
| Molecular Weight | 381.42 |
| Optical Activity | ( + / - ) |
| Defined Stereocenters | 0 / 1 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
FC1=CC=CC=C1COC2=CC3=C(C=C2)C=C(CC4SC(=O)NC4=O)C=C3
InChI
InChIKey=PKWDZWYVIHVNKS-UHFFFAOYSA-N
InChI=1S/C21H16FNO3S/c22-18-4-2-1-3-16(18)12-26-17-8-7-14-9-13(5-6-15(14)11-17)10-19-20(24)23-21(25)27-19/h1-9,11,19H,10,12H2,(H,23,24,25)
| Molecular Formula | C21H16FNO3S |
| Molecular Weight | 381.42 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | RACEMIC |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 1 |
| E/Z Centers | 0 |
| Optical Activity | ( + / - ) |
Netoglitazone (also called MCC-555) is a hypoglycemic agent belonging to the thiazolidinedione group that exerts both peroxisome proliferator-activated receptor (PPAR) alpha and gamma agonist activity. It was developed by Mitsubishi-Tokyo (formerly Mitsubishi Chemical) as a potential treatment for type 2 diabetes due to the enhancement of insulin sensitivity. This drug was in clinical trial phase II but then was discontinued. In addition, was also investigated the behaviour of MCC-555 on colorectal cancer (CRC) cells and was revealed, that the drug had an effect on the early events of colon carcinogenesis and could be a potential preventive compound for CRC.
Originator
Approval Year
Sourcing
PubMed
Patents
Sample Use Guides
in mice: MCC-555 (NETOGLITAZONE) was suspended in 1.5% carboxymethylcellulose (CMC) with 0.2% Tween 20. The control group was orally gavaged with CMC alone, and the second and third groups received 30 and 60 mg/kg MCC-555 suspended in CMC for 4 weeks, respectively. Starting at 7 weeks of age, mice in all the 3 groups were injected i.p. once a week for a total of 4 weeks
Route of Administration:
Intraperitoneal
It was examined the effects of a novel TZD MCC-555 on vascular cell adhesion molecule-1 (VCAM-1) expression in vascular endothelial cells (ECs). Human aortic ECs were treated with MCC-555, followed by stimulation with tumor necrosis factor (TNF)-alpha. Cell surface VCAM-1 protein expression and human monocytoid U937 cell adhesion to these cells were determined. MCC-555 efficiently inhibited TNF-alpha-stimulated VCAM-11expression and U937 cell adhesion. Transient transfection of bovine aortic ECs with a VCAM-1 promoter construct revealed that MCC-555 inhibited TNF-alpha-induced VCAM-1 promoter activity. Electrophoretic mobility-shift assay demonstrated that MCC-555 reduced the amount of nuclear factor-kappaB (NF-kappaB) bound to its recognition site on the VCAM-1 promoter. These results indicated that MCC-555 was a strong TZD agent to inhibit the cytokine-induced VCAM-1 expression in vascular ECs. The effect was exerted probably through activation of PPARalpha and/or PPARdelta, rather than PPARgamma, mediating down-regulation of NF-kappaB activity.
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