PPARγ (Kd = 40 nM); PPARγ (EC50 = 60 nM); TRPC5 (EC50 = 30 μM); TRPM3

多能 C3H10T1/2 干细胞通过罗格列酮（0.1–10 μM，72 小时）分化为脂肪细胞 [1]。当与 NF-α1 启动子结合时，罗格列酮（1 μM，24 小时）会刺激 PPARγ，进而激活神经元中的基因转录 [3]。罗格列酮（1 μM，24 小时）可以保护海马神经元和 Neuro2A 细胞免受氧化应激，同时还能以 NF-κ1 依赖性方式增加 BCL-2 的表达 [3]。罗格列酮（0.01-100 μM，15 分钟）的 IC50 值为 9.5 和 4.6 μM，可抑制 TRPM3，从而分别阻止 PregS 和硝苯地平诱导的活性 [4]。罗格列酮（0.5-50 μM，7 天）可抑制卵巢癌细胞的增殖[7]。在 A2780 和 SKOV3 细胞中，罗格列酮（5 μM，7 天）抑制奥拉帕尼诱导的细胞衰老改变并刺激细胞凋亡 [7]。

在糖尿病大鼠中，口服罗格列酮（5 mg/kg，每天一次，持续 8 周）可降低血糖水平 [5]。通过激活 PPARγ 和 RXRα，罗格列酮（腹腔注射，3 mg/kg/天）可降低雄性 Wistar 大鼠的血糖并抑制 M1 巨噬细胞极化引起的气道炎症 [6]。在 A2780 和 SKOV3 动物皮下异种移植模型中，罗格列酮（腹腔注射，10 mg/kg，每 2 天）可抑制皮下卵巢癌的生长 [7]。

在这里，我们报告噻唑烷二酮类是过氧化物酶体增殖物激活受体γ（PPAR-γ）的强效和选择性激活剂，PPAR-γ是核受体超家族的成员，最近被证明在脂肪生成中起作用。这些药物中最有效的是BRL49653，它以约40nM的Kd与PPARγ结合。用BRL49653处理多能性C3H10T1/2干细胞可有效分化为脂肪细胞。这些数据首次证明了高亲和力PPAR配体，并提供了强有力的证据，表明PPAR-γ是噻唑烷二酮类脂肪生成作用的分子靶点。此外，这些数据提出了一种有趣的可能性，即PPAR-γ是这类化合物治疗作用的靶点。[1]
通过聚合酶链式反应扩增编码PPARγ1氨基酸174-475的cDNA，并将其插入细菌表达载体pGEX-2T中。GST-PPARγLBD在BL21（DE3）plysS细胞和提取物中表达。对于饱和结合分析，在存在或不存在未标记的罗格列酮的情况下，将细菌提取物（100μg蛋白质）在4°C下在含有10 mM Tris（pH 8.0）、50 mM KCl、10 mM二硫苏糖醇和[3H]-BRL49653（比活度，40 Ci/mmol）的缓冲液中孵育3小时。通过1-mL Sephadex G-25脱盐柱洗脱，将结合放射性与游离放射性分离。结合放射性在柱空隙体积中洗脱，并通过液体闪烁计数进行定量[1]。

细胞增殖测定[7]
细胞类型： A2780 和 SKOV3 细胞
测试浓度： 0.5-50 μM
孵育时间： 1-7 天
实验结果： 以时间依赖性和浓度依赖性的方式抑制细胞增殖。

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蛋白质印迹分析[3]
细胞类型： 海马神经元
测试浓度： 1 μM
孵育时间：24小时
实验结果：NF-α1和BCL-2蛋白水平增加。

Animal/Disease Models: Streptozotocin (STZ)-induced diabetic rats[5]
Doses: 5 mg/kg
Route of Administration: Oral administration, daily for 8 weeks.
Experimental Results: diminished 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.

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Animal/Disease Models: Male Wistar rats[6]
Doses: 3 mg/kg/day
Route of Administration: intraperitoneal (ip)injection, twice a day, 6 days Consecutive per week for 12 weeks
Experimental Results: 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 diminished the ratio of M1/M2.

Absorption, Distribution and Excretion
The absolute bioavailability of rosiglitazone is 99%. Peak plasma concentrations are observed about 1 hour after dosing. Administration of rosiglitazone with food resulted in no change in overall exposure (AUC), but there was an approximately 28% decrease in Cmax and a delay in Tmax (1.75 hours). These changes are not likely to be clinically significant; therefore, rosiglitazone may be administered with or without food. Maximum plasma concentration (Cmax) and the area under the curve (AUC) of rosiglitazone increase in a dose-proportional manner over the therapeutic dose range.
Following oral or intravenous administration of [14C]rosiglitazone maleate, approximately 64% and 23% of the dose was eliminated in the urine and in the feces, respectively.
17.6 L [oral volume of distribution Vss/F]
13.5 L [population mean, pediatric patients]
Oral clearance (CL) = 3.03 ± 0.87 L/hr [1 mg Fasting]
Oral CL = 2.89 ± 0.71 L/hr [2 mg Fasting]
Oral CL = 2.85 ± 0.69 L/hr [8 mg Fasting]
Oral CL = 2.97 ± 0.81 L/hr [8 mg Fed]
3.15 L/hr [Population mean, Pediatric patients]
In a study in healthy volunteers, the absorption of rosiglitazone was relatively rapid, with 99% oral bioavailability after oral absorption.
Severe forms of non-alcoholic fatty liver disease (NAFLD) adversely affect the liver physiology and hence the pharmacokinetics of drugs. Here, we investigated the effect of NAFLD on the pharmacokinetics of rosiglitazone, an insulin sensitizer used in the treatment of type 2 diabetes. Male C57BL/6 mice were divided into two groups. The first group (n=14) was fed with normal chow feed and the second group (n=14) was fed with 60% high-fat diet (HFD) and 40% high fructose liquid (HFL) for 60 days to induce NAFLD. The development of NAFLD was confirmed by histopathology, liver triglyceride levels and biochemical estimations, and used for pharmacokinetic investigations. Rosiglitazone was administered orally at 30 mg/kg dose. At predetermined time points, blood was collected and rosiglitazone concentrations were determined using LC/MS/MS. Plasma concentrations were subjected to non-compartmental analysis using Phoenix WinNonlin (6.3), and the area under the plasma concentration-time curve (AUC) was calculated by the linear-up log-down method. HFD and HFL diet successfully induced NAFLD in mice. Rosiglitazone pharmacokinetics in NAFLD animals were altered significantly as compared to healthy mice. Rosiglitazone exposure increased significantly in NAFLD mice (2.5-fold higher AUC than healthy mice). The rosiglitazone oral clearance was significantly lower and the mean plasma half-life was significantly longer in NAFLD mice as compared to healthy mice. The NAFLD mouse model showed profound effects on rosiglitazone pharmacokinetics. The magnitude of change in rosiglitazone pharmacokinetics is similar to that observed in humans with moderate to severe liver disease. The present animal model can be utilized to study the NAFLD-induced changes in the pharmacokinetics of different drugs.
The absolute bioavailability of rosiglitazone is 99%. Peak plasma concentrations are observed about 1 hour after dosing. Administration of rosiglitazone with food resulted in no change in overall exposure (AUC), but there was an approximately 28% decrease in Cmax and a delay in Tmax (1.75 hours). These changes are not likely to be clinically significant; therefore, Avandia may be administered with or without food.
The mean (CV%) oral volume of distribution (Vss/F) of rosiglitazone is approximately 17.6 (30%) liters, based on a population pharmacokinetic analysis. Rosiglitazone is approximately 99.8% bound to plasma proteins, primarily albumin.
For more Absorption, Distribution and Excretion (Complete) data for Rosiglitazone (8 total), please visit the HSDB record page.

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Metabolism / Metabolites
Hepatic. 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.
The main metabolites observed in humans are also observed in rats; however, the clearance in rats was almost ten times higher than in humans, probably due to the higher levels of CYP2C in rat microsomes.
In vitro data demonstrate that rosiglitazone is predominantly metabolized by Cytochrome P450 (CYP) isoenzyme 2C8, with CYP2C9 contributing as a minor pathway.
Rosiglitazone is extensively metabolized with no unchanged drug excreted in the urine. The major routes of metabolism were N-demethylation and hydroxylation, followed by conjugation with sulfate and glucuronic acid. All the circulating metabolites are considerably less potent than parent and, therefore, are not expected to contribute to the insulin-sensitizing activity of rosiglitazone.
Rosiglitazone has known human metabolites that include N-Desmethylrosiglitazone, ortho-hydroxyrosiglitazone, and para-hydroxyrosiglitazone.

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Biological Half-Life
3-4 hours (single oral dose, independent of dose)
The elimination half-life of rosiglitazone was 3-4 hours and was independent of dose. The time to Cmax and the elimination half-life for two metabolites in plasma were significantly longer than for rosiglitazone itself (4-6 hours versus 0.5-1 hours, and about 5 days versus 3-7 hours).
The plasma half life of (14)C-related material ranged from 103 to 158 hours.

Toxicity Summary
IDENTIFICATION AND USE: Rosiglitazone is a solid. It is used as an antidiabetic agent as an adjunct to diet and exercise to improve glycemic control in patients with type 2 diabetes mellitus. HUMAN STUDIES: Thiazolidinediones, including rosiglitazone, alone or in combination with other antidiabetic agents, can cause fluid retention and may lead to or exacerbate congestive heart failure (CHF). Use of thiazolidinediones is associated with an approximately twofold increased risk of CHF. No evidence of hepatotoxicity has been noted with rosiglitazone in clinical studies to date, including a long-term (4-6 years) study in patients with recently diagnosed type 2 diabetes mellitus. However, hepatitis, elevations in hepatic enzymes to at least 3 times the upper limit of normal, and liver failure with or without fatalities have been reported during postmarketing experience with rosiglitazone. Rosiglitazone was not mutagenic or clastogenic in the in vitro chromosome aberration test in human lymphocytes. ANIMAL STUDIES: Rosiglitazone was not carcinogenic in the mouse. There was an increase in incidence of adipose hyperplasia in the mouse at doses >/= 1.5 mg/kg/day. Heart weights were increased in mice (3 mg/kg/day), rats (5 mg/kg/day), and dogs (2 mg/kg/day) with rosiglitazone treatments. Effects in juvenile rats were consistent with those seen in adults. Morphometric measurement indicated that there was hypertrophy in cardiac ventricular tissues, which may be due to increased heart work as a result of plasma volume expansion. Rosiglitazone had no effects on mating or fertility of male rats given up to 40 mg/kg/day. In juvenile rats dosed from 27 days of age through to sexual maturity (at up to 40 mg/kg/day), there was no effect on male reproductive performance, or on estrous cyclicity, mating performance, or pregnancy incidence in females. Rosiglitazone was not mutagenic or clastogenic in the in vitro bacterial assays for gene mutation, the in vivo mouse micronucleus test, and the in vivo/in vitro rat UDS assay. There was a small (about 2-fold) increase in mutation in the in vitro mouse lymphoma assay in the presence of metabolic activation.

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Hepatotoxicity
In contrast to troglitazone, rosiglitazone is not associated with an increased frequency of aminotransferase elevations during therapy. In clinical trials, ALT elevations above 3 times the ULN occurred in only 0.25% of patients on rosiglitazone, compared to 0.25% of placebo recipients (and 1.9% of troglitazone recipients in similar studies). In addition, clinically apparent liver injury attributed to rosiglitazone is very rare, fewer than a dozen cases having been described in the literature despite extensive use of this agent. The liver injury usually arises between 1 and 12 weeks after starting therapy (thus, a shorter latency than typically occurs with troglitazone) and all patterns of serum enzyme elevations have been described including hepatocellular, cholestatic and mixed. Allergic phenomena are rare and autoantibodies have not been typically present. Fatal instances have been reported usually in cases with a hepatocellular pattern of injury. In most instances, recovery is complete within 1 to 2 months.
Likelihood score: C (probable rare cause of clinically apparent liver injury).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
No information is available on the clinical use of rosiglitazone during breastfeeding. Rosiglitazone is over 99% protein bound in plasma, so it is unlikely to pass into breastmilk in clinically important amounts. The manufacturer recommends avoiding breastfeeding during rosiglitazone use, so pioglitazone might be a better choice of the drugs in this class for nursing mothers.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
99.8% bound to plasma proteins, primarily albumin.

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Interactions
An inhibitor of CYP2C8 (e.g., gemfibrozil) may increase the AUC of rosiglitazone and an inducer of CYP2C8 (e.g., rifampin) may decrease the AUC of rosiglitazone. Therefore, if an inhibitor or an inducer of CYP2C8 is started or stopped during treatment with rosiglitazone, changes in diabetes treatment may be needed based upon clinical response.
/The authors/ investigated the possible effect of ketoconazole on the pharmacokinetics of rosiglitazone in humans. Ten healthy Korean male volunteers were treated twice daily for 5 days with 200 mg ketoconazole or with placebo, using a randomized, open-label, two-way crossover study. On day 5, a single dose of 8 mg rosiglitazone was administered orally, and plasma rosiglitazone concentrations were measured. Ketoconazole increased the mean area under the plasma concentration-time curve for rosiglitazone by 47%[P = 0.0003; 95% confidence interval (CI) 23, 70] and the mean elimination half-life from 3.55 to 5.50 hr (P = 0.0003; 95% CI in difference 1.1, 2.4). The peak plasma concentration of rosiglitazone was increased by ketoconazole treatment by 17% (P = 0.03; 95% CI 5, 29). The apparent oral clearance of rosiglitazone decreased by 28% after ketoconazole treatment (P = 0.0005; 95% CI 18, 38). This study revealed that ketoconazole affected the disposition of rosiglitazone in humans, probably by the inhibition of CYP2C8 and CYP2C9, leading to increasing rosiglitazone concentrations that could increase the efficacy of rosiglitazone or its adverse events.
Endothelial dysfunction is implicated in the initiation and progression of atherosclerosis. Whether atorvastatin combined with rosiglitazone has synergistic effects on endothelial function improvement in the setting of dyslipidemia is unknown. Dyslipidemia rat model was produced with high-fat and high-cholesterol diet administration. Thereafter, atorvastatin, rosiglitazone or atorvastatin combined with rosiglitazone were prescribed for 2 weeks. At baseline, 6 weeks of dyslipidemia model production, and 2 weeks of medical intervention, fasting blood was drawn for parameters of interest evaluation. At the end, myocardium was used for 15-deoxy-delta-12,14-PGJ2 (15-d-PGJ2) assessment. Initially, there was no significant difference of parameters between sham and dyslipidemia groups. With 6 weeks' high-fat and high-cholesterol diet administration, as compared to sham group, serum levels of triglyceride (TG), total cholesterol (TC) and low density lipoprotein-cholesterol (LDL-C) were significantly increased. Additionally, nitric oxide (NO) production was reduced and serum levels of malondialdehyde (MDA), C-reactive protein (CRP) and asymmetric dimethylarginine (ADMA) were profoundly elevated in dyslipidemia group. After 2 weeks' medical intervention, lipid profile was slightly improved in atorvastatin and combined groups as compared to control group. Nevertheless, in comparison to control group, NO production was profoundly increased and serum levels of MDA, CRP and ADMA were significantly decreased with atorvastatin or rosiglitazone therapy. 15-d-PGJ2 expression of myocardium was also significantly elevated with atorvastatin or rosiglitazone treatment. Notably, these effects were further enhanced with combined therapy, suggesting that atorvastatin and rosiglitazone had synergistic effects on endothelial protection, and inflammation and oxidation amelioration. Atorvastatin and rosiglitazone therapy had synergistic effects on endothelium protection as well as amelioration of oxidative stress and inflammatory reaction in rats with dyslipidemia.
Avandia (2 mg twice daily) taken concomitantly with glyburide (3.75 to 10 mg/day) for 7 days did not alter the mean steady-state 24-hour plasma glucose concentrations in diabetic patients stabilized on glyburide therapy. Repeat doses of Avandia (8 mg once daily) for 8 days in healthy adult Caucasian subjects caused a decrease in glyburide AUC and Cmax of approximately 30%. In Japanese subjects, glyburide AUC and Cmax slightly increased following coadministration of Avandia.
Rifampin administration (600 mg once a day), an inducer of CYP2C8, for 6 days is reported to decrease rosiglitazone AUC by 66%, compared with the administration of rosiglitazone (8 mg) alone.

[1]. 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]. 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]. Rosiglitazone-activated PPARγ induces neurotrophic factor-α1 transcription contributing to neuroprotection. J Neurochem. 2015 Aug;134(3):463-70.

[4]. Rapid and contrasting effects of rosiglitazone on transient receptor potential TRPM3 and TRPC5 channels. Mol Pharmacol. 2011 Jun;79(6):1023-30.

[5]. Beneficial effects of rosiglitazone and losartan combination in diabetic rats. Can J Physiol Pharmacol. 2018 Mar;96(3):215-220.

[6]. 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]. Rosiglitazone ameliorates senescence and promotes apoptosis in ovarian cancer induced by olaparib. Cancer Chemother Pharmacol. 2020 Feb;85(2):273-284.

Therapeutic Uses
Antidiabetic agent
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Rosiglitazone is included in the database.
Rosiglitazone is used as monotherapy or in combination with a sulfonylurea, metformin hydrochloride, or a sulfonylurea and metformin as an adjunct to diet and exercise to improve glycemic control in patients with type 2 diabetes mellitus. Rosiglitazone in fixed combination with metformin hydrochloride is used as an adjunct to diet and exercise to improve glycemic control in patients with type 2 diabetes mellitus. Rosiglitazone also is used in fixed combination with glimepiride as an adjunct to diet and exercise for the management of type 2 diabetes mellitus. /Included in US product label/
/EXPL THER/ 1-Methyl-4-phenylpyridinium ion (MPP(+)), an inhibitor of mitochondrial complex I, has been widely used as a neurotoxin because it elicits a severe Parkinson's disease-like syndrome with elevation of intracellular reactive oxygen species (ROS) level and apoptotic death. Rosiglitazone, a peroxisome proliferator-activated receptor (PPAR)-gamma agonist, has been known to show various non-hypoglycemic effects, including anti-inflammatory, anti-atherogenic, and anti-apoptotic. In the present study, /the authors/ investigated the protective effects of rosiglitazone on MPP(+) induced cytotoxicity in human neuroblastoma SH-SY5Y cells, as well as underlying mechanism. /Their/ results suggested that the protective effects of rosiglitazone on MPP(+) induced apoptosis may be ascribed to its anti-oxidative properties, anti-apoptotic activity via inducing expression of SOD and catalase and regulating the expression of Bcl-2 and Bax. These data indicated that rosiglitazone might provide a valuable therapeutic strategy for the treatment of progressive neurodegenerative disease such as Parkinson's disease.

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Drug Warnings
/BOXED WARNING/ WARNING: CONGESTIVE HEART FAILURE. Thiazolidinediones, including rosiglitazone, cause or exacerbate congestive heart failure in some patients. After initiation of Avandia, and after dose increases, observe patients carefully for signs and symptoms of heart failure (including excessive, rapid weight gain; dyspnea; and/or edema). If these signs and symptoms develop, the heart failure should be managed according to current standards of care. Furthermore, discontinuation or dose reduction of Avandia must be considered. Avandia is not recommended in patients with symptomatic heart failure. Initiation of Avandia in patients with established NYHA Class III or IV heart failure is contraindicated.
Thiazolidinediones, including rosiglitazone, alone or in combination with other antidiabetic agents, can cause fluid retention and may lead to or exacerbate congestive heart failure (CHF). Use of thiazolidinediones is associated with an approximately twofold increased risk of CHF. Patients should be observed for signs and symptoms of CHF (e.g., dyspnea, rapid weight gain, edema, unexplained cough or fatigue), especially during initiation of therapy and dosage titration. If signs and symptoms of CHF develop, the disorder should be managed according to current standards of care. In addition, a decrease in the dosage of rosiglitazone or discontinuance of the drug should be considered.
Thiazolidinedione use is associated with bone loss and fractures in women and possibly in men with type 2 diabetes mellitus. In long-term comparative clinical trials in patients with type 2 diabetes mellitus, the incidence of bone fracture was increased in patients (particularly women) receiving rosiglitazone versus comparator agents (glyburide and/or metformin). Such effects were noted after the first year of treatment and persisted throughout the study. The majority of fractures observed in patients taking thiazolidinediones were in a distal upper limb (i.e., forearm, hand, wrist) or distal lower limb (i.e., foot, ankle, fibula, tibia). In an observational study in the United Kingdom in men and women (mean age: 60.7 years) with diabetes mellitus, use of pioglitazone or rosiglitazone for approximately 12-18 months (as estimated from prescription records) was associated with a twofold to threefold increase in fractures, particularly of the hip and wrist. The overall risk of fracture was similar among men and women and was independent of body mass index, comorbid conditions, diabetic complications, duration of diabetes mellitus, and use of other oral antidiabetic drugs.145 Risk of fractures should be considered when initiating or continuing thiazolidinedione therapy in female patients with type 2 diabetes mellitus. Bone health should be assessed and maintained according to current standards of care. Although increased risk of fracture may also apply to men, the risk appears to be higher among women than men.
Because rosiglitazone requires endogenous insulin for activity, it should not be used in patients with type 1 diabetes mellitus or diabetic ketoacidosis.
For more Drug Warnings (Complete) data for Rosiglitazone (19 total), please visit the HSDB record page.

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Pharmacodynamics
When rosiglitazone is used as monotherapy, it is associated with increases in total cholesterol, LDL, and HDL. It is also associated with decreases in free fatty acids. Increases in LDL occurred primarily during the first 1 to 2 months of therapy with AVANDIA and LDL levels remained elevated above baseline throughout the trials. In contrast, HDL continued to rise over time. As a result, the LDL/HDL ratio peaked after 2 months of therapy and then appeared to decrease over time.

C18H19N3O3S

357.43

357.114

C, 60.49; H, 5.36; N, 11.76; O, 13.43; S, 8.97

122320-73-4

Rosiglitazone maleate;155141-29-0;Rosiglitazone hydrochloride;302543-62-0;Rosiglitazone potassium;316371-84-3;Rosiglitazone-d3;1132641-22-5

77999

Colorless crystals from methanol

1.3±0.1 g/cm3

585.0±35.0 °C at 760 mmHg

153-155ºC

307.6±25.9 °C

0.0±1.6 mmHg at 25°C

1.642

2.56

96.83

1

6

7

25

469

0

S1C(N([H])C(C1([H])C([H])([H])C1C([H])=C([H])C(=C([H])C=1[H])OC([H])([H])C([H])([H])N(C([H])([H])[H])C1=C([H])C([H])=C([H])C([H])=N1)=O)=O

YASAKCUCGLMORW-UHFFFAOYSA-N

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)

5-(4-(2-(methyl(pyridin-2-yl)amino)ethoxy)benzyl)thiazolidine-2,4-dione

HSDB7555; TDZ 01; HSDB 7555; HSDB-7555; BRL 49653; BRL49653; BRL-49653; TDZ-01; TDZ01; Rosiglitazone. trade name Avandia; rosiglitazone; 122320-73-4; Avandia; Rosiglizole; 5-(4-(2-(Methyl(pyridin-2-yl)amino)ethoxy)benzyl)thiazolidine-2,4-dione; Brl-49653; Brl 49653; Rezult; .

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

配方 1 中的溶解度: 2.5 mg/mL (6.99 mM) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 悬浮液；超声助溶。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL 澄清 DMSO 储备液加入900 μL 玉米油中，混合均匀。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (6.99 mM) (饱和度未知) in 5% DMSO + 40% PEG300 + 5% Tween80 + 50% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.5 mg/mL (6.99 mM) (饱和度未知) in 5% DMSO + 95% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 4 中的溶解度: ≥ 2.08 mg/mL (5.82 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 20.8 mg/mL澄清的DMSO储备液加入400 μL PEG300中，混匀；再向上述溶液中加入50 μL Tween-80，混匀；然后加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 5 中的溶解度: ≥ 2.08 mg/mL (5.82 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100μL 20.8mg/mL澄清的DMSO储备液加入到900μL 20％SBE-β-CD生理盐水中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 6 中的溶解度: 4% DMSO+30% PEG 300+5% Tween 80+ddH2O: 5mg/mL

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配方 7 中的溶解度: 10 mg/mL (27.98 mM) in 0.5% CMC-Na/saline water (这些助溶剂从左到右依次添加，逐一添加), 悬浊液; 超声助溶。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。