Tesaglitazar
Chemical compound
- None
- Development terminated
- (2S)-2-Ethoxy-3-[4-[2-(4-methylsulfonyloxyphenyl)
ethoxy]phenyl]propanoic acid
- 251565-85-2 Y
- 208901
- 180999 N
- 6734037O3L
- D01274 Y
- ChEMBL521632 N
- DTXSID4048773
- Interactive image
- CCO[C@@H](CC1=CC=C(C=C1)OCCC2=CC=C(C=C2)OS(=O)(=O)C)C(=O)O
InChI
- InChI=1S/C20H24O6S/c1-3-25-19(20(21)22)14-16-6-8-17(9-7-16)26-13-12-15-4-10-18(11-5-15)27-28(2,23)24/h4-11,19H,3,12-14H2,1-2H3,(H,21,22)/t19-/m0/s1 N
- Key:CXGTZJYQWSUFET-IBGZPJMESA-N N
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]
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 to mitochondrial toxicity caused by decrease in PPARγ coactivator 1-α (PPARGC1A, PGC1α) and sirtuin 1 (SIRT1).[4]
References
- ^ Wilding JP, Gause-Nilsson I, Persson A (September 2007). "Tesaglitazar, as add-on therapy to sulphonylurea, dose-dependently improves glucose and lipid abnormalities in patients with type 2 diabetes". Diabetes & Vascular Disease Research. 4 (3): 194–203. doi:10.3132/dvdr.2007.040. PMID 17907109. S2CID 896195.
- ^ "GALIDA (tesaglitazar) Clinical Trial Report Summaries". AstraZeneca. Retrieved 2008-03-17. [dead link]
- ^ "AstraZeneca Discontinues Development of GALIDA (tesaglitazar)". AstraZeneca. 2006-05-04. Retrieved 2012-07-23.
- ^ Kalliora C, Kyriazis ID, Oka SI, Lieu MJ, Yue Y, Area-Gomez E, et al. (August 2019). "Dual peroxisome-proliferator-activated-receptor-α/γ activation inhibits SIRT1-PGC1α axis and causes cardiac dysfunction". JCI Insight. 5 (17). doi:10.1172/jci.insight.129556. PMC 6777908. PMID 31393858.
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