316371-84-3

316371-84-3 structure

Name: UNII:2V3E7D3089
Chemical Name: potassium,5-[[4-[2-[methyl(pyridin-2-yl)amino]ethoxy]phenyl]methyl]-1,3-thiazolidin-3-ide-2,4-dione
CAS Number: 316371-84-3
Molecular Formula: C₁₈H₁₈KN₃O₃S
Molecular Weight: 395.517
Catalog: Signaling Pathways Apoptosis Apoptosis
Create Date: 2017-02-12 06:45:01
Modify Date: 2024-01-03 19:52:42
Rosiglitazone (BRL 49653) potassium is an orally active selective PPARγ agonist (EC50: 60 nM, Kd: 40 nM). Rosiglitazone potassium is a TRPC5 activator (EC50: 30 μM) and TRPM3 inhibitor. Rosiglitazone potassium can be used in the research of obesity and diabetes, senescence, ovarian cancer[1][2][4][7].

Name	potassium,5-[[4-[2-[methyl(pyridin-2-yl)amino]ethoxy]phenyl]methyl]-1,3-thiazolidin-3-ide-2,4-dione
Synonyms	UNII:2V3E7D3089 Potassium 5-(4-{2-[methyl(2-pyridinyl)amino]ethoxy}benzyl)-4-oxo-4,5-dihydro-1,3-thiazol-2-olate 2,4-Thiazolidinedione, 5-[[4-[2-(methyl-2-pyridinylamino)ethoxy]phenyl]methyl]-, potassium salt (1:1)

Description	Rosiglitazone (BRL 49653) potassium is an orally active selective PPARγ agonist (EC50: 60 nM, Kd: 40 nM). Rosiglitazone potassium is a TRPC5 activator (EC50: 30 μM) and TRPM3 inhibitor. Rosiglitazone potassium can be used in the research of obesity and diabetes, senescence, ovarian cancer[1][2][4][7].
Related Catalog	Signaling Pathways >> Membrane Transporter/Ion Channel >> TRP Channel Signaling Pathways >> Apoptosis >> Apoptosis Research Areas >> Cancer Signaling Pathways >> Apoptosis >> Ferroptosis Signaling Pathways >> Autophagy >> Autophagy Signaling Pathways >> Cell Cycle/DNA Damage >> PPAR Research Areas >> Inflammation/Immunology Research Areas >> Metabolic Disease Research Areas >> Neurological Disease
Target	PPARγ:40 nM (Kd) PPARγ:60 nM (EC50) TRPC5:30 μM (EC50) TRPM3
In Vitro	Rosiglitazone potassium (0.1-10 μM, 72 h) results in pluripotent C3H10T1/2 stem cell differentiation to adipocytes[1]. Rosiglitazone potassium (1 μM, 24 h) activates PPARγ, which binds to NF-α1 promoter to activate gene transcription in neurons[3]. Rosiglitazone potassium (1 μM, 24 h) protects Neuro2A cells and hippocampal neurons against oxidative stress, and up-regulates BCL-2 expression in an NF-α1-dependent manner[3]. Rosiglitazone potassium (0.01-100 μM, 15 min) inhibits TRPM3 with IC50 values of 9.5 and 4.6 μM against nifedipine- and PregS-evoked activity respectively[4]. Rosiglitazone potassium (0.5-50 μM, 7 days) inhibits ovarian cancer cell proliferation[7]. Rosiglitazone potassium (5 μM, 7 days) suppresses Olaparib (HY-10162)‑induced alterations of cellular senescence and promotes apoptosis in A2780 and SKOV3 cells[7]. Cell Proliferation Assay[7] Cell Line: A2780 and SKOV3 cells Concentration: 0.5-50 μM Incubation Time: 1-7 days Result: Inhibited cell proliferation in a time‑dependent and concentration‑dependent manner. Western Blot Analysis[3] Cell Line: Hippocampal neurons Concentration: 1 μM Incubation Time: 24 h Result: Increased NF-α1 and BCL-2 protein level.
In Vivo	Rosiglitazone potassium (oral administration, 5 mg/kg, daily for 8 weeks) decreases the serum glucose in diabetic rats[5]. Rosiglitazone potassium (intraperitoneal injection, 3 mg/kg/day) ameliorates airway inflammation induced by cigarette smoke via inhibiting the M1 macrophage polarization by activating PPARγ and RXRα in male Wistar rats[6]. Rosiglitazone potassium (intraperitoneal injection, 10 mg/kg, once every 2 days) inhibits subcutaneous ovarian cancer growth in A2780 and SKOV3 mouse subcutaneous xenograft models[7]. Animal Model: Streptozotocin (STZ)-induced diabetic rats[5] Dosage: 5 mg/kg Administration: Oral administration, daily for 8 weeks. Result: Decreased IL-6, TNF-α, and VCAM-1 levels in diabetic group. Displayed lower levels of lipid peroxidation and NOx with an increase in aortic GSH and SOD levels compared to diabetic groups. Animal Model: Male Wistar rats[6] Dosage: 3 mg/kg/day Administration: Intraperitoneal injection, twice a day, 6 days per week for 12 consecutive weeks Result: Ameliorated emphysema, elevated PEF, and higher level of total cells, neutrophils and cytokines (TNF-α and IL-1β) induced by cigarette smoke (CS). Inhibited CS-induced M1 macrophage polarization and decreased the ratio of M1/M2.
References	[1]. Lehmann JM, et al. An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferator-activated receptor gamma (PPAR gamma). J Biol Chem. 1995 Jun 2;270(22):12953-6. [2]. Willson TM, et al. The structure-activity relationship between peroxisome proliferator-activated receptor gamma agonism and the antihyperglycemic activity of thiazolidinediones. J Med Chem. 1996 Feb 2;39(3):665-8. [3]. Thouennon E, et al. Rosiglitazone-activated PPARγ induces neurotrophic factor-α1 transcription contributing to neuroprotection. J Neurochem. 2015 Aug;134(3):463-70. [4]. Majeed Y, et al. Rapid and contrasting effects of rosiglitazone on transient receptor potential TRPM3 and TRPC5 channels. Mol Pharmacol. 2011 Jun;79(6):1023-30. [5]. Ateyya H, et al. Beneficial effects of rosiglitazone and losartan combination in diabetic rats. Can J Physiol Pharmacol. 2018 Mar;96(3):215-220. [6]. Haoshen Feng, et al. Rosiglitazone ameliorated airway inflammation induced by cigarette smoke via inhibiting the M1 macrophage polarization by activating PPARγ and RXRα. Int Immunopharmacol. 2021 Aug;97:107809. [7]. Zehua Wang, et al. Rosiglitazone ameliorates senescence and promotes apoptosis in ovarian cancer induced by olaparib. Cancer Chemother Pharmacol. 2020 Feb;85(2):273-284.

Molecular Formula	C₁₈H₁₈KN₃O₃S
Molecular Weight	395.517
Exact Mass	395.070587
PSA	88.04000
LogP	2.60550

Hazard Codes	Xi

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