molecular formula C18H19N3O3S B1679542 Rosiglitazone CAS No. 122320-73-4

Rosiglitazone

Cat. No.: B1679542
CAS No.: 122320-73-4
M. Wt: 357.4 g/mol
InChI Key: YASAKCUCGLMORW-UHFFFAOYSA-N
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Description

Rosiglitazone is a thiazolidinedione (TZD) class drug and a potent peroxisome proliferator-activated receptor gamma (PPARγ) agonist. It is primarily used to improve glycemic control in type 2 diabetes by enhancing insulin sensitivity. This compound activates PPARγ, a nuclear receptor regulating adipogenesis, lipid metabolism, and glucose homeostasis . Its mechanism involves binding to the PPARγ ligand-binding domain (LBD), inducing conformational changes that recruit coactivators to modulate gene expression . Despite its efficacy, this compound has been scrutinized for cardiovascular risks, prompting comparisons with structurally and functionally similar compounds .

Preparation Methods

Synthetic Routes and Reaction Conditions

The synthesis of rosiglitazone involves several key steps:

    Reaction of 2-chloropyridine with 2-methylaminoethanol: This reaction is catalyzed by trityl sodium to produce 2-[N-methyl-N-(2-pyridine)amino]ethanol.

    Williamson Synthesis Reaction: The N-substituted benzaldehyde and 4-fluorobenzaldehyde undergo a Williamson synthesis reaction catalyzed by bis(trimethylsilyl)amino potassium to form 4-[2-[N-methyl-N-(2-pyridine)amino]ethoxy]benzaldehyde.

    Condensation Reaction: The resulting compound is then condensed with thiazoline-2,4-diketone to yield 5-{4-[2-[N-methyl-N-(2-pyridine)amino]ethoxy]benzylidene}thiazoline-2,4-diketone.

    Reduction Reaction: Finally, the compound undergoes a reduction reaction catalyzed by an organic manganese reagent to produce this compound.

Industrial Production Methods

For industrial production, the synthesis of this compound is optimized for scalability and efficiency. The process involves a five-step synthetic route with commercially available starting materials, including 2-chloropyridine, N-methylethanolamine, 4-fluorobenzaldehyde, and 1,3-thiazolidine-2,4-dione. The steps include cyclization, alkylation, etherification, condensation, and reduction, with an overall yield of approximately 40% .

Chemical Reactions Analysis

Types of Reactions

Rosiglitazone undergoes various chemical reactions, including:

Common Reagents and Conditions

    Sodium Borohydride: Used in the reduction step.

    Cobalt Chloride Hexahydrate and Dimethylglyoxime: Catalysts for the reduction reaction.

    Trityl Sodium: Catalyst for the reaction of 2-chloropyridine with 2-methylaminoethanol.

    Bis(trimethylsilyl)amino Potassium: Catalyst for the Williamson synthesis reaction.

Major Products Formed

The major product formed from these reactions is this compound itself, with intermediate compounds such as 2-[N-methyl-N-(2-pyridine)amino]ethanol and 4-[2-[N-methyl-N-(2-pyridine)amino]ethoxy]benzaldehyde .

Scientific Research Applications

Diabetes Management

Efficacy in Glycemic Control
Rosiglitazone has been shown to effectively lower blood glucose levels in patients with type 2 diabetes. In clinical trials, it significantly reduced hemoglobin A1c levels by approximately 1.2 to 1.5 percentage points compared to placebo . The drug's mechanism involves activating the peroxisome proliferator-activated receptor gamma (PPAR-γ), which enhances insulin sensitivity in muscle and adipose tissues .

Monotherapy and Combination Therapy
this compound can be used as a monotherapy or in combination with other antidiabetic agents such as metformin or sulfonylureas. Studies indicate that it can reduce insulin resistance by 16% to 24% and improve pancreatic beta-cell function . This dual action makes it a valuable option for patients who do not achieve adequate glycemic control with lifestyle modifications alone.

Cardiovascular Implications

Risk Assessment
The cardiovascular safety of this compound has been a subject of extensive research. A meta-analysis indicated that this compound therapy was associated with an increased risk of myocardial infarction but not cardiovascular mortality . Specifically, the odds ratio for myocardial infarction was found to be 1.28, suggesting a significant risk factor that healthcare providers must consider when prescribing this medication .

Long-term Outcomes
In the RECORD trial, which evaluated cardiovascular outcomes in patients treated with this compound, findings suggested that while there may be risks associated with heart failure, the drug did not significantly increase overall cardiovascular mortality compared to other treatments .

Additional Therapeutic Benefits

Anti-inflammatory and Anti-cancer Properties
Emerging research highlights potential anti-inflammatory and anti-cancer effects of this compound. Studies have shown that it may exert protective effects against ischemia-reperfusion injury and reduce inflammatory markers in diabetic models . This suggests that this compound could have broader applications beyond glycemic control.

Impact on Diabetic Retinopathy
Preclinical studies indicate that this compound may help mitigate the progression of diabetic retinopathy by improving vascular health and reducing inflammatory responses within the retina . These findings warrant further exploration in clinical settings.

Case Study 1: Monotherapy Efficacy

A randomized controlled trial involving 493 patients demonstrated that this compound monotherapy effectively reduced fasting plasma glucose levels and improved insulin sensitivity without increasing adverse events .

Case Study 2: Cardiovascular Outcomes

In a cohort study analyzing data from the RECORD trial, researchers assessed the long-term cardiovascular effects of this compound in patients with type 2 diabetes. The study concluded that while there was an increased risk for heart failure, overall cardiovascular mortality rates were comparable to those receiving other antidiabetic therapies .

Data Summary

Application AreaFindings
Diabetes ManagementReduces hemoglobin A1c by 1.2-1.5%, improves insulin sensitivity (16%-24%)
Cardiovascular RiskIncreased risk of myocardial infarction (OR=1.28); no significant increase in mortality
Additional BenefitsPotential anti-inflammatory effects; may protect against diabetic retinopathy

Mechanism of Action

Rosiglitazone exerts its effects by activating the intracellular receptor class of peroxisome proliferator-activated receptors, specifically PPAR-gamma. This activation influences the production of gene products involved in glucose and lipid metabolism. This compound is a selective ligand of PPAR-gamma and does not bind to PPAR-alpha. Apart from its effect on insulin resistance, it also appears to have anti-inflammatory effects by modulating nuclear factor kappa-B levels .

Comparison with Similar Compounds

Structural Analogs

Compound Structural Similarity Key Differences Biological Effects Source
Pioglitazone Shares thiazolidinedione core; differs in side chain (pyridine vs. pyrimidine in rosiglitazone) - Higher selectivity for PPARα/γ dual activation
- Reduced cardiovascular risk profile
- Superior triglyceride reduction in fasting/postprandial states
- Similar glycemic control
Lobeglitazone Derived from this compound backbone; pyrimidine moiety substituted with methoxyphenol - Enhanced PPARγ binding affinity due to methoxyphenol group - Greater glucose-lowering efficacy
- Improved lipid metabolism modulation
TZD Derivatives Retain 2,4-thiazolidinedione core; modified side chains (e.g., hexane rings) - Variable hydrogen-bonding interactions with PPARγ LBD - Comparable or superior insulin-sensitizing effects in preclinical models

Key Findings :

  • Pioglitazone’s PPARα activation contributes to its triglyceride-lowering effects, unlike this compound’s exclusive PPARγ focus .
  • Lobeglitazone’s structural modifications enhance PPARγ binding, improving therapeutic efficacy .

Functional Analogs (Non-TZD PPARγ Agonists)

Compound Class Key Similarities Key Differences Biological Effects Source
AFC (N-Acetylfarnesylcysteine) Farnesyl cysteine analog - Induces PPARγ target genes (Angptl4, Adrp) similarly to this compound - Partial agonism: weaker aP2 induction - Adipogenesis promotion without full PPARγ activation
Red Wine Polyphenols Natural ligands (e.g., ellagic acid, ECG) - Bind PPARγ with affinity comparable to this compound - Dose-dependent effects achievable via dietary intake - Cardiovascular benefits linked to PPARγ activation
Balanol Analogs Synthetic kinase inhibitors - Occupy PPARγ LBD similarly to this compound - Covalent binding via enone moiety (unlike this compound’s non-covalent binding) - Dual kinase/PPARγ modulation potential

Key Findings :

  • AFC partially mimics this compound’s gene regulation, suggesting utility in conditions requiring moderate PPARγ activation .

Key Findings :

  • This compound’s binding to cardiac ion channels (e.g., L-type calcium channels) may underlie its CV risks, unlike pioglitazone’s neuronal receptor affinity .
  • Both TZDs inhibit BSEP, but clinical DILI risk remains low compared to drugs like ritonavir .

Mitochondrial and Metabolic Effects

Compound Mitochondrial Targets Metabolic Outcomes Source
This compound - CISD1/2 inhibitor; induces mitophagy - Improves insulin sensitivity but increases adipogenesis
NL1 - CISD1/2 inhibitor - Similar mitophagy induction to this compound
GW7647 - PPARα agonist - Larger plasma metabolite changes vs. This compound (e.g., lipid remodeling)

Key Findings :

  • This compound and NL1 rescue mitochondrial dysfunction in Parkinson’s models via CISD1/2 inhibition .
  • GW7647’s PPARα activation drives distinct lipid metabolic shifts compared to this compound’s PPARγ focus .

Biological Activity

Rosiglitazone, a thiazolidinedione, is primarily used in the management of type 2 diabetes mellitus (T2DM). Its biological activity is largely attributed to its role as a selective agonist for the peroxisome proliferator-activated receptor gamma (PPAR-γ), which influences glucose metabolism, insulin sensitivity, and various cellular functions. This article delves into the biological mechanisms, therapeutic effects, and associated risks of this compound, supported by relevant research findings and case studies.

PPAR-γ Agonism
this compound activates PPAR-γ, leading to enhanced transcription of genes involved in glucose and lipid metabolism. This activation improves insulin sensitivity in peripheral tissues, particularly adipose tissue and muscle, facilitating better glucose uptake and utilization .

Nitric Oxide Synthesis
Research indicates that this compound stimulates nitric oxide (NO) synthesis in endothelial cells via AMP-activated protein kinase (AMPK) activation. This process enhances endothelial function and may contribute to cardiovascular protective effects .

Glucose Uptake in Podocytes
In glomerular podocytes, this compound has been shown to increase glucose uptake by promoting the translocation of glucose transporter 1 (GLUT1) to the plasma membrane. This effect is crucial for maintaining podocyte function in diabetic nephropathy, suggesting a protective role against renal complications associated with diabetes .

Clinical Efficacy

Glycemic Control
this compound has demonstrated significant reductions in fasting plasma glucose (FPG), 2-hour postprandial glucose (2hPG), and glycated hemoglobin (HbA1c) levels in patients with T2DM. A meta-analysis of randomized controlled trials showed that patients receiving this compound achieved better glycemic control compared to those on placebo or other antidiabetic agents .

Study Population Duration Outcome Measures Results
RECORD Study4,447 patients18 monthsHbA1c levelsSignificant reduction in HbA1c with combination therapy
Meta-analysis35,531 patientsVariesMI and mortality ratesIncreased risk of myocardial infarction but improved glycemic control

Case Studies

  • Cardiovascular Risks
    A comprehensive meta-analysis indicated that this compound treatment was associated with an increased risk of myocardial infarction (MI) by approximately 43% compared to controls. This raised concerns about its cardiovascular safety profile, leading to restrictions on its use in clinical practice .
  • Cancer Risk Assessment
    A meta-analysis assessing the incidence of cancer among this compound users found no significant increase in cancer risk; however, results were inconclusive across different studies. Some studies suggested a potential protective effect against certain malignancies due to PPAR-γ activation .

Safety Profile

Despite its efficacy in glycemic control, this compound is associated with several adverse effects:

  • Cardiovascular Events: Increased risk of heart failure and MI has been documented. The hazard ratios for these events compared to pioglitazone were statistically significant .
  • Weight Gain: Patients on this compound often experience weight gain due to fluid retention and increased fat accumulation .
  • Bone Fractures: Long-term use has been linked to an elevated risk of bone fractures, particularly in women .

Q & A

Basic Research Questions

Q. What analytical methods are validated for quantifying rosiglitazone in pharmaceutical formulations, and how can researchers ensure specificity in complex matrices?

  • Methodology : Spectrophotometric and high-performance thin-layer chromatography (HPTLC) methods have been validated for simultaneous quantification of this compound maleate and metformin hydrochloride. Key steps include wavelength selection (e.g., 317 nm for this compound) and optimization of mobile phases (e.g., chloroform:methanol:ammonia 8:2:0.1 v/v for HPTLC) to resolve interference from excipients .
  • Critical Considerations : Validation parameters (linearity, accuracy, precision) should adhere to ICH guidelines. Matrix effects can be mitigated using standard addition methods or gradient elution in HPLC .

Q. How should researchers design randomized controlled trials (RCTs) to evaluate this compound’s glycemic efficacy while controlling for cardiovascular confounders?

  • Experimental Design : Use a double-blind, placebo-controlled approach with active comparators (e.g., metformin). Primary endpoints should include HbA1c reduction, insulin sensitivity (HOMA-IR), and beta-cell function. For cardiovascular safety, pre-specify adjudicated endpoints like myocardial infarction (MI) and heart failure (HF) .
  • Example : In a 26-week RCT, metformin-rosiglitazone combination therapy reduced HbA1c by 1.2% (8 mg dose) but required monitoring of weight gain (+2.2 kg vs. placebo) and LDL cholesterol .

Advanced Research Questions

Q. How can conflicting evidence on this compound’s cardiovascular risk be reconciled across meta-analyses and long-term trials?

  • Data Contradiction Analysis :

  • Nissen & Wolski (2007) : Reported 43% increased MI risk (OR 1.43, 95% CI 1.03–1.98) and borderline cardiovascular mortality (OR 1.64, 95% CI 0.98–2.74) .
  • RECORD Trial : Found no significant increase in cardiovascular mortality (HR 1.11, 95% CI 0.93–1.32) but 2.15× higher HF risk .
    • Methodological Insights : Differences arise from trial inclusion criteria (e.g., follow-up duration, adjudication rigor) and statistical models (fixed-effects vs. time-to-event analysis). Sensitivity analyses and individual patient data (IPD) meta-analyses are recommended to address heterogeneity .

Q. What molecular mechanisms underlie this compound’s PPARγ-mediated effects, and how can they be experimentally dissected from off-target outcomes?

  • Advanced Techniques :

  • TR-FRET Assays : Quantify corepressor (NCoR/SMRT) displacement and coactivator (p300/CBP) recruitment to PPARγ ligand-binding domains .
  • ChIP Analysis : Assess promoter-specific binding of PPARγ-coregulator complexes (e.g., PEPCK gene in adipocytes) under this compound treatment .
    • Functional Correlates : Link transcriptional changes to metabolic outcomes (e.g., insulin sensitivity, adipose tissue browning) using knockout models or RNA-seq .

Q. Does this compound exhibit dose-dependent pleiotropic effects, such as anti-aging properties, and how can these be investigated preclinically?

  • Preclinical Models : In aging mice, low-dose this compound (1–5 mg/kg) improved insulin sensitivity, reduced adipose fibrosis, and induced white fat browning via UCP1 upregulation. These effects were absent at higher doses, suggesting a therapeutic window .
  • Methodological Framework : Use aging-accelerated models (e.g., SAMP8 mice) with longitudinal metrics for inflammation (IL-6, TNF-α) and mitochondrial function (Seahorse assays) .

Q. Methodological Guidance

Q. How can researchers mitigate bias in meta-analyses evaluating this compound’s safety profile?

  • Best Practices :

  • Include unpublished data from registries (e.g., ClinicalTrials.gov , GSK Study Register) to address publication bias .
  • Use GRADE criteria to assess evidence certainty, emphasizing studies with independent adjudication of endpoints .
    • Case Study : A 2010 FDA meta-analysis of 54 this compound trials found 28% had zero cardiovascular events, highlighting the need for IPD and competing risk analysis .

Q. What strategies ensure reproducibility in this compound-related pharmacological studies?

  • Protocol Standardization :

  • In Vivo Studies : Report dosing regimens, vehicle controls, and diet composition (e.g., high-fat vs. chow) to contextualize metabolic outcomes .
  • In Vitro Work : Use PPARγ-specific antagonists (e.g., T0070907) to confirm on-target effects .
    • Data Transparency : Share raw datasets (e.g., RNA-seq, clinical adjudication records) via repositories like FigShare, adhering to FAIR principles .

Q. Emerging Research Frontiers

Q. Can this compound’s potential anticancer properties be mechanistically validated despite conflicting epidemiological data?

  • Evidence Synthesis : A meta-analysis of 80 RCTs found no increased cancer risk (OR 0.91, 95% CI 0.71–1.16) but noted lower incidence vs. controls (0.23 vs. 0.44 cases/100 patient-years; p < 0.05) .
  • Research Gaps : Conduct preclinical studies using PPARγ-inducible knockout models to isolate this compound’s role in tumorigenesis pathways (e.g., apoptosis, angiogenesis) .

Properties

IUPAC Name

5-[[4-[2-[methyl(pyridin-2-yl)amino]ethoxy]phenyl]methyl]-1,3-thiazolidine-2,4-dione
Source PubChem
URL https://pubchem.ncbi.nlm.nih.gov
Description Data deposited in or computed by PubChem

InChI

InChI=1S/C18H19N3O3S/c1-21(16-4-2-3-9-19-16)10-11-24-14-7-5-13(6-8-14)12-15-17(22)20-18(23)25-15/h2-9,15H,10-12H2,1H3,(H,20,22,23)
Source PubChem
URL https://pubchem.ncbi.nlm.nih.gov
Description Data deposited in or computed by PubChem

InChI Key

YASAKCUCGLMORW-UHFFFAOYSA-N
Source PubChem
URL https://pubchem.ncbi.nlm.nih.gov
Description Data deposited in or computed by PubChem

Canonical SMILES

CN(CCOC1=CC=C(C=C1)CC2C(=O)NC(=O)S2)C3=CC=CC=N3
Source PubChem
URL https://pubchem.ncbi.nlm.nih.gov
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Molecular Formula

C18H19N3O3S
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URL https://pubchem.ncbi.nlm.nih.gov
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DSSTOX Substance ID

DTXSID7037131
Record name Rosiglitazone
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Molecular Weight

357.4 g/mol
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Physical Description

Solid
Record name Rosiglitazone
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Color/Form

Colorless crystals from methanol

CAS No.

122320-73-4
Record name Rosiglitazone
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Record name 5-(4-(2-(N-METHYL-N-(2-PYRIDYL)AMINO)ETHOXY)BENZYL)THIAZOLIDINE-2,4 -DIONE
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Melting Point

122-123 °C, 153-155 °C
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Synthesis routes and methods I

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Synthesis routes and methods II

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Retrosynthesis Analysis

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Feasible Synthetic Routes

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