Tesaglitazar

Tesaglitazar (also known as AZ 242) is a dual peroxisome proliferator-activated receptor agonist with affinity to PPARα and PPARγ, proposed for the management of type 2 diabetes.[1]

Tesaglitazar
Clinical data
ATC code
  • None
Legal status
Legal status
  • Development terminated
Identifiers
CAS Number
PubChem CID
ChemSpider
UNII
KEGG
ChEMBL
ECHA InfoCard100.201.079
Chemical and physical data
FormulaC20H24O6S
Molar mass392,47 g/mol g·mol−1
3D model (JSmol)
 NY (what is this?)  (verify)

The drug had completed several phase III clinical trials,[2] however in May, 2006 AstraZeneca announced that it had discontinued further development.[3]

Cardiac toxicity of tesaglitazar is related mitochondrial toxicity caused by decrease in PPARγ coactivator 1-α (PPARGC1A, PGC1α) and sirtuin 1 (SIRT1).[4]

References
  1. Wilding JP, Gause-Nilsson I, Persson A (2007). "Tesaglitazar, as add-on therapy to sulphonylurea, dose-dependently improves glucose and lipid abnormalities in patients with type 2 diabetes". Diab Vasc Dis Res. 4 (3): 194–203. doi:10.3132/dvdr.2007.040. PMID 17907109.
  2. "GALIDA (tesaglitazar) Clinical Trial Report Summaries". AstraZeneca. Retrieved 2008-03-17.
  3. "AstraZeneca Discontinues Development of GALIDA (tesaglitazar)". AstraZeneca. 2006-05-04. Retrieved 2012-07-23.
  4. Kalliora, Charikleia; Kyriazis, Ioannis D.; Oka, Shin-ichi; Lieu, Melissa J.; Yue, Yujia; Area-Gomez, Estela; Pol, Christine J.; Tian, Ying; Mizushima, Wataru; Chin, Adave; Scerbo, Diego; Schulze, P. Christian; Civelek, Mete; Sadoshima, Junichi; Madesh, Muniswamy; Goldberg, Ira J.; Drosatos, Konstantinos (2019). "Dual PPARα/γ activation inhibits SIRT1-PGC1α axis and causes cardiac dysfunction". JCI Insight. 4 (17). doi:10.1172/jci.insight.129556. ISSN 2379-3708.
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