Delving into the Latest Updates on Rosiglitazone Sodium with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

太罗

Target

PPARγ

Action

agonists

Mechanism

PPARγ agonists(Peroxisome proliferator-activated receptor γ agonists), Insulin sensitizers

Therapeutic Areas

Endocrinology and Metabolic Disease

Active Indication

Diabetes Mellitus, Type 2

Inactive Indication-

Originator Organization

Taiji Group Co. Ltd.

Active Organization

Taiji Group Co. Ltd.

Inactive Organization-

Drug Highest PhaseApproved

First Approval Date

China (14 Sep 2004),

Diabetes Mellitus, Type 2

Regulation-

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Structure/Sequence

Molecular FormulaC18H19N3NaO3S

InChIKeyMIXMIJXAFUYUNO-UHFFFAOYSA-N

CAS Registry316371-83-2

View All Structures (2)

A novel series of thiazolidinedione derivatives (D1-D30) were designed, synthesized, and characterized for potential anti-diabetic activity.Compounds D6, D8, and D24 emerged as promising candidates based on their structural attributes.These compounds were characterized using spectroscopic techniques.Mol. docking studies demonstrated their interactions with the Peroxisome Proliferator-Activated Receptor Gamma (PPAR-γ), a target for anti-diabetic drugs.Mol. dynamics simulations validated the stability of these ligand-PPAR-γ complexes.Addnl., the cytotoxicity of the compounds was evaluated using the MTT assay in L6 myoblast cell lines, a standard method to assess cell viability.The synthesized compounds were also tested for their in vitro glucose-uptake activity, revealing that D6, D8, and D24 exhibited significant glucose-uptake activity compared to the reference drug Pioglitazone.These findings suggest that these compounds have potential as effective anti-diabetic agents.

01 Apr 2025·Molecular and Cellular Endocrinology

Vitamin D augments insulin secretion via calcium influx and upregulation of voltage calcium channels: Findings from INS-1 cells and human islets

Article

Author: El-Huneidi, Waseem ; Al Shehadat, Ola Saed ; Taneera, Jalal ; Youssef, Mona ; Yaseen, Deema ; Madkour, Mohamed I ; Khalique, Anila ; Bustanji, Yasser ; Mohammed, Abdul Khader

Vitamin D (VD) has been implicated in regulating insulin secretion and pancreatic β-cell function. Yet, the underlying molecular mechanism of VD in glucose homeostasis is not fully understood. This study investigates the effect of VD in regulating insulin secretion and pancreatic β-cell function. INS-1 β-cells were treated with VD to assess cell viability, reactive oxygen species production (ROS), insulin secretion, glucose uptake, proliferation, gene expression alterations, mitochondria metabolism, calcium influx, as well as the effects of antidiabetic drugs on VDR expression. Additionally, RNA sequencing from human pancreatic islets were utilized to examine VDR expression in relation to clinical parameters such as HbA1c, BMI, age, and gender. VD treatment enhanced glucose-stimulated insulin secretion and elevated intracellular calcium levels without affecting insulin content, glucose uptake, ROS production, proliferation, or mitochondrial metabolism. Expression levels of key β-cell function genes, including Ins, Pdx1, and Glut2, remained unchanged with VD treatment. However, genes associated with calcium channels were upregulated. Cell exposure to rosiglitazone and dexamethasone elevated VDR expression in INS-1 cells, while metformin and insulin had no effect. RNA-seq analysis in human islets showed that VDR expression levels in human islets were significantly higher than in other metabolic tissues and were notably reduced in hyperglycemic donors compared to normoglycemic individuals. Furthermore, VDR expression positively correlated with several genes regulating voltage-gated calcium channels. In conclusion, the study indicates that VD plays a significant role in enhancing insulin secretion through modulation of intracellular calcium dynamics, highlighting its potential therapeutic implications for managing type 2 diabetes.

01 Mar 2025·Theriogenology

Regulation of PPARγ in the development of early sheep embryos in vitro

Article

Author: Pi, Wenhui ; Zhang, Yue ; Yu, Hengbin ; Li, Zhenghang ; Hu, Guangdong ; Liu, Chang

Lipid metabolism plays an important role in the regulation of early embryonic development in mammals. However, the effect of lipid metabolism mediated by peroxisome proliferator-activated receptor γ (PPARγ) on the early embryonic development of sheep remains unclear. In this study, rosiglitazone (RSG), a PPARγ activator, was added to the in vitro embryo culture (IVC) medium to regulate the continuous expression of PPARγ. This study aimed to evaluate PPARγ expression during early embryonic development in sheep as well as its effects on lipid deposition, reactive oxygen species (ROS) and glutathione (GSH) levels, apoptosis and lipid metabolism-related gene expression, and embryonic development. PPARγ was not detected at 2-cell, 4-cell, 8-cell, and morula stage, while widely expressed with obvious nuclear expression features in blastocysts. Notably, treatment with 5 μM RSG in sheep parthenogenetic activated (PA) embryos significantly increased the blastocyst rate, lipid content, and GSH levels, while decreasing ROS levels. Further analysis revealed that RSG treatment upregulated the expression levels of antioxidant genes (SOD2 and CAT), anti-apoptotic gene (BCL2), and lipid metabolism-related genes (SCD-1, CD36, PLIN2, FABP3, and FABP4). Taken together, these results suggest that PPARγ plays a vital role in promoting embryonic development by enhancing lipid metabolism and reducing oxidative stress.

100 Deals associated with Rosiglitazone Sodium

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External Link

KEGG	Wiki	ATC	Drug Bank
-	-	A10BG02	-

R&D Status

10 top approved records.

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Indication	Country/Location	Organization	Date
Diabetes Mellitus, Type 2	China	Taiji Group Co. Ltd.	14 Sep 2004

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT00577590 (T2DM, CTgov)	Not Applicable	Diabetes Mellitus, Type 2	78	Lovaza+Metformin (Metformin and Lovaza)	zncrywuxlm(cjgvppqfyc) = udgzenikla uyettnffxl (pkdfxmzyqu, axbfxoqfrc - edzafrfkxa) View more	-	31 Aug 2018
				Rosiglitazone+Metformin (Metformin and Rosiglitazone)	zncrywuxlm(cjgvppqfyc) = enmlsoyoyr uyettnffxl (pkdfxmzyqu, zpbdoamoxo - ekzkbhabpw) View more
NCT00186537 (CTgov)	Not Applicable	Hypertriglyceridemia \| Insulin Resistance	47	fenofibrate (Fenofibrate)	jduuxqghrh(joxpzvnopw) = lxbstjnmpq fqbznzxocn (izndtjakkr, uucaoiprlg - fzxnbexbrj) View more	-	05 May 2016
				Rosiglitazone (Rosiglitazone)	jduuxqghrh(joxpzvnopw) = oyniakcbzm fqbznzxocn (izndtjakkr, wnolofrtjv - vrkuyxwcea) View more
NCT00785213 (CTgov)	Phase 1	-	23	Rosiglitazone 4 mg Tablets	pmokjlngng(iizwfsylzt) = jxbfvjtrte usoqinhzeu (yxsmnzmivm, vhplyvaecz - kgqqkadaze) View more	-	26 Nov 2009
NCT00095654 (DREAM, Pubmed \| Diabetes Care)	Phase 3	Glucose Intolerance	-	Ramipril	(esrxigisfm) = Rosiglitazone increased heart failure (0.53 vs. 0.08%) agefzhwycm (orlpfisivj )	-	01 May 2008
				Rosiglitazone
NCT00095654 (Pubmed \| Lancet)	Phase 3	Glucose Intolerance	5,269	Rosiglitazone	fhkzvuvllh(cvxrrayyxn): hazard ratio = 0.4 (95% CI, 0.35 - 0.46), P-Value = <0.0001 View more	Positive	23 Sep 2006
				Placebo