ロシグリタゾン
概要
説明
ロシグリタゾンは、チアゾリジンジオン系薬剤に属する合成化合物です。主に2型糖尿病患者の血糖コントロールを改善するための抗糖尿病薬として使用されます。 ロシグリタゾンは、脂肪細胞のペルオキシソーム増殖因子活性化受容体に結合することによりインスリン感受性を高める作用を有し、細胞のインスリンに対する応答性を高めます .
製法
合成ルートと反応条件
ロシグリタゾンの合成には、いくつかの重要なステップが含まれます。
2-クロロピリジンと2-メチルアミノエタノールの反応: この反応はトリチルナトリウムによって触媒され、2-[N-メチル-N-(2-ピリジン)アミノ]エタノールが生成されます。
ウィリアムソン合成反応: N-置換ベンズアルデヒドと4-フルオロベンズアルデヒドは、ビス（トリメチルシリル）アミノカリウムによって触媒されるウィリアムソン合成反応を受け、4-[2-[N-メチル-N-(2-ピリジン)アミノ]エトキシ]ベンズアルデヒドを生成します。
縮合反応: 得られた化合物は、チアゾリン-2,4-ジケトンと縮合して、5-{4-[2-[N-メチル-N-(2-ピリジン)アミノ]エトキシ]ベンジリデン}チアゾリン-2,4-ジケトンを生成します。
工業生産方法
工業生産では、ロシグリタゾンの合成は、スケーラビリティと効率性を高めるために最適化されています。このプロセスには、2-クロロピリジン、N-メチルエタノールアミン、4-フルオロベンズアルデヒド、1,3-チアゾリジン-2,4-ジオンなどの市販の出発物質を使用した5段階の合成ルートが含まれます。 この工程には、環化、アルキル化、エーテル化、縮合、還元が含まれ、全体の収率は約40％です .
作用機序
ロシグリタゾンは、ペルオキシソーム増殖因子活性化受容体の細胞内受容体クラス、特にPPAR-ガンマを活性化することにより作用を発揮します。この活性化は、グルコースと脂質の代謝に関与する遺伝子産物の産生に影響を与えます。ロシグリタゾンはPPAR-ガンマの選択的リガンドであり、PPAR-アルファには結合しません。 インスリン抵抗性への影響に加えて、核因子カッパBレベルを調節することにより、抗炎症作用も示すようです .
科学的研究の応用
Rosiglitazone has a wide range of scientific research applications:
Chemistry: Used as a model compound in studies of thiazolidinedione synthesis and reaction mechanisms.
Biology: Investigated for its effects on insulin sensitivity and glucose metabolism.
Medicine: Primarily used to treat type 2 diabetes mellitus by improving insulin sensitivity.
Industry: Utilized in the pharmaceutical industry for the production of antidiabetic medications.
生化学分析
Biochemical Properties
Rosiglitazone works by activating the intracellular receptor class of the peroxisome proliferator-activated receptors (PPARs), specifically PPARγ . It is a selective ligand of PPARγ, and has no PPARα-binding action . Apart from its effect on insulin resistance, it appears to have an anti-inflammatory effect .
Cellular Effects
Rosiglitazone has been shown to suppress the growth of human glioma cell lines U87 and U251 . It also induces cell cycle arrest and apoptosis . In addition, rosiglitazone has been found to exhibit anti-inflammatory properties and can target cardiomyocytes secreting CXCL10, under interferon (IFN)γ and tumor necrosis factor (TNF)α challenge .
Molecular Mechanism
The mechanism of action of rosiglitazone is by activation of the intracellular receptor class of the peroxisome proliferator-activated receptors (PPARs), specifically PPARγ . Rosiglitazone is a selective ligand of PPARγ, and has no PPARα-binding action . Apart from its effect on insulin resistance, it appears to have an anti-inflammatory effect: nuclear factor kappa-B (NFκB) levels fall and inhibitor (IκB) levels increase in patients on rosiglitazone .
Temporal Effects in Laboratory Settings
Rosiglitazone has been shown to have a significant effect on the reduction of glucose and HbA1c treatment effects in rats . This effect was observed over a period of 6 weeks of treatment with rosiglitazone .
Dosage Effects in Animal Models
In animal models, rosiglitazone has been shown to be the most effective treatment in thiazolidinediones (TZDs) not only for its hypoglycemic effect but also for its additional effects such as anti-inflammatory and anti-cancer capabilities, retinopathy, and ischemia–reperfusion injury protection effects .
Metabolic Pathways
Rosiglitazone is extensively metabolized in the liver to inactive metabolites via N-demethylation, hydroxylation, and conjugation with sulfate and glucuronic acid . In vitro data have shown that Cytochrome (CYP) P450 isoenzyme 2C8 (CYP2C8) and to a minor extent CYP2C9 are involved in the hepatic metabolism of rosiglitazone .
Transport and Distribution
Rosiglitazone is primarily distributed in the liver, where it is extensively metabolized . It is also distributed in fat cells, where it works as an insulin sensitizer, by binding to the PPAR in fat cells and making the cells more responsive to insulin .
Subcellular Localization
Rosiglitazone acts at the level of the nucleus, where it binds to the peroxisome proliferator-activated receptors (PPARs), specifically PPARγ . This binding activates the PPARγ, leading to the transcription of insulin-responsive genes involved in the control of glucose production, transport, and utilization .
準備方法
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 rosiglitazone.
Industrial Production Methods
For industrial production, the synthesis of rosiglitazone 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% .
化学反応の分析
反応の種類
ロシグリタゾンは、次のような様々な化学反応を受けます。
一般的な試薬と条件
水素化ホウ素ナトリウム: 還元段階で使用されます。
塩化コバルト六水和物とジメチルグリオキシム: 還元反応の触媒。
トリチルナトリウム: 2-クロロピリジンと2-メチルアミノエタノールの反応の触媒。
ビス（トリメチルシリル）アミノカリウム: ウィリアムソン合成反応の触媒.
生成される主要な生成物
これらの反応から生成される主要な生成物は、ロシグリタゾンそのものであり、2-[N-メチル-N-(2-ピリジン)アミノ]エタノールや4-[2-[N-メチル-N-(2-ピリジン)アミノ]エトキシ]ベンズアルデヒドなどの中間体が含まれます .
科学研究への応用
ロシグリタゾンは、様々な科学研究に幅広く応用されています。
類似化合物との比較
類似化合物
ピオグリタゾン: 2型糖尿病の治療に使用される別のチアゾリジンジオン。
トログリタゾン: 肝毒性に関する懸念から市場から撤退したチアゾリジンジオン。
ロシグリタゾンの独自性
ロシグリタゾンは、PPAR-アルファに影響を与えることなく、PPAR-ガンマに特異的に結合するという点で独特です。 ピオグリタゾンと比較して、ロシグリタゾンは心筋梗塞とうっ血性心不全のリスクが高いことが示されており、安全性に関する懸念が生じています . それでも、ロシグリタゾンは有効なインスリン感受性増強剤であり、糖尿病治療以外の追加の治療用途について研究されています .
特性
IUPAC Name |
5-[[4-[2-[methyl(pyridin-2-yl)amino]ethoxy]phenyl]methyl]-1,3-thiazolidine-2,4-dione |
Source
|
|---|---|---|
| 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
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
InChI Key |
YASAKCUCGLMORW-UHFFFAOYSA-N |
Source
|
| 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
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Molecular Formula |
C18H19N3O3S |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
DSSTOX Substance ID |
DTXSID7037131 |
Source
|
| Record name | Rosiglitazone | |
| Source | EPA DSSTox | |
| URL | https://comptox.epa.gov/dashboard/DTXSID7037131 | |
| Description | DSSTox provides a high quality public chemistry resource for supporting improved predictive toxicology. | |
Molecular Weight |
357.4 g/mol |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Physical Description |
Solid |
Source
|
| Record name | Rosiglitazone | |
| Source | Human Metabolome Database (HMDB) | |
| URL | http://www.hmdb.ca/metabolites/HMDB0005031 | |
| Description | The Human Metabolome Database (HMDB) is a freely available electronic database containing detailed information about small molecule metabolites found in the human body. | |
| Explanation | HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications. | |
Mechanism of Action |
Rosiglitazone acts as a highly selective and potent agonist at peroxisome proliferator activated receptors (PPAR) in target tissues for insulin action such as adipose tissue, skeletal muscle, and liver. Activation of PPAR-gamma receptors regulates the transcription of insulin-responsive genes involved in the control of glucose production, transport, and utilization. In this way, rosiglitazone enhances tissue sensitivity to insulin., Because osteoblasts and marrow adipocytes are derived from a common mesenchymal progenitor, increased adipogenesis may occur at the expense of osteoblasts, leading to bone loss. Our previous in vitro studies indicated that activation of the proadipogenic transcription factor peroxisome proliferator-activated receptor isoform gamma 2 with rosiglitazone suppressed osteoblast differentiation. Here, we show that 5-month-old Swiss-Webster mice receiving rosiglitazone for 28 day exhibited bone loss associated with an increase in marrow adipocytes, a decrease in the ratio of osteoblasts to osteoclasts, a reduction in bone formation rate, and a reduction in wall width--an index of the amount of bone formed by each team of osteoblasts. Rosiglitazone had no effect on the number of early osteoblast or osteoclast progenitors, or on osteoblast life span, but decreased the expression of the key osteoblastogenic transcription factors Runx2 and Osterix in cultures of marrow-derived mesenchymal progenitors. These effects were associated with diversion of bipotential progenitors from the osteoblast to the adipocyte lineage, and suppression of the differentiation of monopotential osteoblast progenitors. However, rosiglitazone had no effect on osteoblastic cells at later stages of differentiation. Hence, rosiglitazone attenuates osteoblast differentiation and thereby reduces bone formation rate in vivo, leading to bone loss. These findings provide a mechanistic explanation for the recent evidence that peroxisome proliferator-activated receptor isoform gamma activation is a negative regulator of bone mass and suggest that the increased production of oxidized fatty acids with age may indeed be an important mechanism for age-related osteoporosis in humans., Brain peroxisome proliferator-activated receptor gamma (PPARgamma), a member of the nuclear receptor superfamily of ligand-dependent transcription factors, is involved in neuroprotection. It is activated by the drug rosiglitazone, which then can increase the pro-survival protein B-cell lymphoma 2 (BCL-2), to mediate neuroprotection. However, the mechanism underlying this molecular cascade remains unknown. Here, we show that the neuroprotective protein neurotrophic factor-a1 (NF-a1), which also induces the expression of BCL-2, has a promoter that contains PPARgamma-binding sites that are activated by rosiglitazone. Treatment of Neuro2a cells and primary hippocampal neurons with rosiglitazone increased endogenous NF-a1 expression and prevented H2 O2 -induced cytotoxicity. Concomitant with the increase in NF-a1, BCL-2 was also increased in these cells. When siRNA against NF-a1 was used, the induction of BCL-2 by rosiglitazone was prevented, and the neuroprotective effect of rosiglitazone was reduced. These results demonstrate that rosiglitazone-activated PPARgamma directly induces the transcription of NF-a1, contributing to neuroprotection in neurons. We proposed the following cascade for neuroprotection against oxidative stress by rosiglitazone: Rosiglitazone enters the neuron and binds to peroxisome proliferator-activated receptor gamma (PPARgamma) in the nucleus. The PPARgamma-rosiglitazone complex binds to the neurotrophic factor-a1 (NF-a1) promoter and activates the transcription of NF-a1 mRNA which is then translated to the protein. NF-a1 is the secreted, binds to a cognate receptor and activates the extracellular signal-regulated kinases (ERK) pathway. This in turn enhances the expression of the pro-survival protein, B-cell lymphoma 2 (BCL-2) and inhibition of caspase 3 (Csp-3) to mediate neuroprotection under oxidative stress. Akt, protein kinase B (PKB)., Rosiglitazone, a member of the thiazolidinedione class of antidiabetic agents, improves glycemic control by improving insulin sensitivity. Rosiglitazone is a highly selective and potent agonist for the peroxisome proliferator-activated receptor-gamma (PPARgamma). In humans, PPAR receptors are found in key target tissues for insulin action such as adipose tissue, skeletal muscle, and liver. Activation of PPARgamma nuclear receptors regulates the transcription of insulin-responsive genes involved in the control of glucose production, transport, and utilization. In addition, PPARgamma- responsive genes also participate in the regulation of fatty acid metabolism, Rosiglitazone acts principally by increasing insulin sensitivity in target tissues, as well as decreasing hepatic gluconeogenesis. Rosiglitazone is a peroxisome proliferator-activated receptorgamma (PPARgamma) agonist that increases transcription of insulin-responsive genes and increases insulin sensitivity. Rosiglitazone, like other thiazolidinediones, ameliorates insulin resistance associated with type diabetes mellitus without stimulating insulin release from pancreatic beta cells, thus avoiding the risk of hypoglycemia. Because rosiglitazone does not lower glucose concentrations below euglycemia, the drug is appropriately referred to as an antidiabetic agent rather than a hypoglycemic agent. Some evidence suggests that the glucoregulatory effects of thiazolidinediones are mediated in part via reduced systemic and tissue lipid availability. Circulating concentrations of insulin and C-peptide are reduced during rosiglitazone therapy. |
Source
|
| Record name | Rosiglitazone | |
| Source | DrugBank | |
| URL | https://www.drugbank.ca/drugs/DB00412 | |
| Description | The DrugBank database is a unique bioinformatics and cheminformatics resource that combines detailed drug (i.e. chemical, pharmacological and pharmaceutical) data with comprehensive drug target (i.e. sequence, structure, and pathway) information. | |
| Explanation | Creative Common's Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/legalcode) | |
| Record name | Rosiglitazone | |
| Source | Hazardous Substances Data Bank (HSDB) | |
| URL | https://pubchem.ncbi.nlm.nih.gov/source/hsdb/7555 | |
| Description | The Hazardous Substances Data Bank (HSDB) is a toxicology database that focuses on the toxicology of potentially hazardous chemicals. It provides information on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, nanomaterials, and related areas. The information in HSDB has been assessed by a Scientific Review Panel. | |
Color/Form |
Colorless crystals from methanol | |
CAS No. |
122320-73-4 |
Source
|
| Record name | Rosiglitazone | |
| Source | CAS Common Chemistry | |
| URL | https://commonchemistry.cas.org/detail?cas_rn=122320-73-4 | |
| Description | CAS Common Chemistry is an open community resource for accessing chemical information. Nearly 500,000 chemical substances from CAS REGISTRY cover areas of community interest, including common and frequently regulated chemicals, and those relevant to high school and undergraduate chemistry classes. This chemical information, curated by our expert scientists, is provided in alignment with our mission as a division of the American Chemical Society. | |
| Explanation | The data from CAS Common Chemistry is provided under a CC-BY-NC 4.0 license, unless otherwise stated. | |
| Record name | Rosiglitazone [INN:BAN] | |
| Source | ChemIDplus | |
| URL | https://pubchem.ncbi.nlm.nih.gov/substance/?source=chemidplus&sourceid=0122320734 | |
| Description | ChemIDplus is a free, web search system that provides access to the structure and nomenclature authority files used for the identification of chemical substances cited in National Library of Medicine (NLM) databases, including the TOXNET system. | |
| Record name | Rosiglitazone | |
| Source | DrugBank | |
| URL | https://www.drugbank.ca/drugs/DB00412 | |
| Description | The DrugBank database is a unique bioinformatics and cheminformatics resource that combines detailed drug (i.e. chemical, pharmacological and pharmaceutical) data with comprehensive drug target (i.e. sequence, structure, and pathway) information. | |
| Explanation | Creative Common's Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/legalcode) | |
| Record name | rosiglitazone | |
| Source | DTP/NCI | |
| URL | https://dtp.cancer.gov/dtpstandard/servlet/dwindex?searchtype=NSC&outputformat=html&searchlist=758698 | |
| Description | The NCI Development Therapeutics Program (DTP) provides services and resources to the academic and private-sector research communities worldwide to facilitate the discovery and development of new cancer therapeutic agents. | |
| Explanation | Unless otherwise indicated, all text within NCI products is free of copyright and may be reused without our permission. Credit the National Cancer Institute as the source. | |
| Record name | Rosiglitazone | |
| Source | EPA DSSTox | |
| URL | https://comptox.epa.gov/dashboard/DTXSID7037131 | |
| Description | DSSTox provides a high quality public chemistry resource for supporting improved predictive toxicology. | |
| Record name | 5-(4-(2-(N-METHYL-N-(2-PYRIDYL)AMINO)ETHOXY)BENZYL)THIAZOLIDINE-2,4 -DIONE | |
| Source | European Chemicals Agency (ECHA) | |
| URL | https://echa.europa.eu/information-on-chemicals | |
| Description | The European Chemicals Agency (ECHA) is an agency of the European Union which is the driving force among regulatory authorities in implementing the EU's groundbreaking chemicals legislation for the benefit of human health and the environment as well as for innovation and competitiveness. | |
| Explanation | Use of the information, documents and data from the ECHA website is subject to the terms and conditions of this Legal Notice, and subject to other binding limitations provided for under applicable law, the information, documents and data made available on the ECHA website may be reproduced, distributed and/or used, totally or in part, for non-commercial purposes provided that ECHA is acknowledged as the source: "Source: European Chemicals Agency, http://echa.europa.eu/". Such acknowledgement must be included in each copy of the material. ECHA permits and encourages organisations and individuals to create links to the ECHA website under the following cumulative conditions: Links can only be made to webpages that provide a link to the Legal Notice page. | |
| Record name | ROSIGLITAZONE | |
| Source | FDA Global Substance Registration System (GSRS) | |
| URL | https://gsrs.ncats.nih.gov/ginas/app/beta/substances/05V02F2KDG | |
| Description | The FDA Global Substance Registration System (GSRS) enables the efficient and accurate exchange of information on what substances are in regulated products. Instead of relying on names, which vary across regulatory domains, countries, and regions, the GSRS knowledge base makes it possible for substances to be defined by standardized, scientific descriptions. | |
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| Record name | Rosiglitazone | |
| Source | Hazardous Substances Data Bank (HSDB) | |
| URL | https://pubchem.ncbi.nlm.nih.gov/source/hsdb/7555 | |
| Description | The Hazardous Substances Data Bank (HSDB) is a toxicology database that focuses on the toxicology of potentially hazardous chemicals. It provides information on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, nanomaterials, and related areas. The information in HSDB has been assessed by a Scientific Review Panel. | |
| Record name | Rosiglitazone | |
| Source | Human Metabolome Database (HMDB) | |
| URL | http://www.hmdb.ca/metabolites/HMDB0005031 | |
| Description | The Human Metabolome Database (HMDB) is a freely available electronic database containing detailed information about small molecule metabolites found in the human body. | |
| Explanation | HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications. | |
Melting Point |
122-123 °C, 153-155 °C |
Source
|
| Record name | Rosiglitazone | |
| Source | DrugBank | |
| URL | https://www.drugbank.ca/drugs/DB00412 | |
| Description | The DrugBank database is a unique bioinformatics and cheminformatics resource that combines detailed drug (i.e. chemical, pharmacological and pharmaceutical) data with comprehensive drug target (i.e. sequence, structure, and pathway) information. | |
| Explanation | Creative Common's Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/legalcode) | |
| Record name | Rosiglitazone | |
| Source | Hazardous Substances Data Bank (HSDB) | |
| URL | https://pubchem.ncbi.nlm.nih.gov/source/hsdb/7555 | |
| Description | The Hazardous Substances Data Bank (HSDB) is a toxicology database that focuses on the toxicology of potentially hazardous chemicals. It provides information on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, nanomaterials, and related areas. The information in HSDB has been assessed by a Scientific Review Panel. | |
Synthesis routes and methods I
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Synthesis routes and methods II
Procedure details
Retrosynthesis Analysis
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