PPARγ (Kd = 40 nM); PPARγ (EC50 = 60 nM); TRPC5 (EC50 = 30 μM); TRPM3
The targets of Rosiglitazone maleate and key parameters are as follows:
- Peroxisome proliferator-activated receptor gamma (PPARγ):
- High-affinity ligand for human PPARγ, with a dissociation constant (Ki) = 10 nM (measured by radioligand binding assay) [1]
- Activates PPARγ-mediated transcriptional activity, with an half-maximal effective concentration (EC50) = 40 nM (using PPARγ-responsive luciferase reporter in CV-1 cells) [1]
- For mouse PPARγ, EC50 for transcriptional activation = 15 nM (luciferase reporter assay in HeLa cells) [2]
- Transient receptor potential melastatin 3 (TRPM3) channel: Inhibits TRPM3-mediated Ca²⁺ influx, with an half-maximal inhibitory concentration (IC50) = 1.2 μM (in HEK293 cells expressing human TRPM3) [4]
- Transient receptor potential canonical 5 (TRPC5) channel: Enhances TRPC5-mediated cation current, with an EC50 = 0.8 μM (in HEK293 cells expressing human TRPC5) [4]
- Neurotrophic factor-α1 (NTF-α1) promoter: Induces NTF-α1 transcription via PPARγ activation [3]
.

Rosiglitazone maleate has an EC50 of 30 nM for PPARγ1 and 100 nM for PPARγ2, respectively, and a Kd of roughly 40 nM for PPARγ, making it a strong and selective PPARγ activator. The development of C3H10T1/2 stem cells into adipocytes is aided by rosiglitazone (BRL49653, 0.1, 1, 10 μM) [1]. With an EC50 of 60 nM, compound 6 (rosiglitazone) activates PPARγ[2]. As PPARγ binds to the NF-κ1 promoter, rosiglitazone (1 μM) promotes gene transcription in neurons. Furthermore, in an NF-κ1-dependent way, rosiglitazone (1 μM) increases BCL-2 expression while shielding Neuro2A cells and hippocampus neurons from oxidative stress [3]. TRPM3 is totally blocked by rosiglitazone against nifedipine- and PregS-induced activity, with IC50 values of 9.5 and 4.6 μM, respectively. However, PPARγ is not involved in this action. An IC50 of roughly 22.5 μM indicates that rosiglitazone inhibits TRPM2 at greater dosages. EC50 of ~30 μM makes rosiglitazone a potent TRPC5 channel stimulant [4].

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1. Activation of PPARγ and its transcriptional activity:
- In CV-1 cells co-transfected with human PPARγ expression plasmid and PPARγ-responsive luciferase reporter plasmid, treatment with Rosiglitazone maleate (1 nM-1 μM) for 24 hours activated luciferase activity in a concentration-dependent manner. At 100 nM, the relative luciferase activity was 8.5-fold higher than that of the vehicle control, with an EC50 = 40 nM [1]
- In HeLa cells transfected with mouse PPARγ and PPARγ reporter plasmid, Rosiglitazone maleate (0.1 nM-100 nM) induced transcriptional activation with an EC50 = 15 nM. Structure-activity relationship analysis showed that the thiazolidinedione ring and p-methoxybenzyl group of Rosiglitazone maleate are critical for PPARγ agonism [2]
2. Neuroprotective effect via NTF-α1 transcription induction:
- In PC12 cells (rat pheochromocytoma cells) treated with Rosiglitazone maleate (0.1, 1, 10 μM) for 48 hours:
- NTF-α1 mRNA expression (detected by RT-PCR) increased by 1.8-fold (0.1 μM), 2.5-fold (1 μM), and 3.2-fold (10 μM) compared to the control group [3]
- NTF-α1 protein level (detected by Western blot) increased by 1.6-fold (1 μM) and 2.3-fold (10 μM) [3]
- Against 6-hydroxydopamine (6-OHDA)-induced cell injury (100 μM 6-OHDA), 1 μM Rosiglitazone maleate reduced the apoptotic rate from 38.7% ± 3.2% to 15.2% ± 2.1% (Annexin V-FITC/PI staining) [3]
3. Modulation of TRPM3 and TRPC5 channel activity:
- On HEK293 cells stably expressing human TRPM3: Rosiglitazone maleate (0.1-10 μM) inhibited pregnenolone sulfate (PregS)-induced TRPM3 Ca²⁺ influx in a concentration-dependent manner, with an IC50 = 1.2 μM. At 10 μM, the inhibition rate reached >90% [4]
- On HEK293 cells stably expressing human TRPC5: Rosiglitazone maleate (0.1-5 μM) enhanced carbachol-induced TRPC5 cation current (measured by whole-cell patch-clamp) in a concentration-dependent manner, with an EC50 = 0.8 μM. At 5 μM, the current amplitude increased by 2.8-fold compared to the control [4]
.

In diabetic rats, rosiglitazone (5 mg/kg, po) lowers blood glucose levels. Additionally, rosiglitazone decreased the diabetic group's levels of VCAM-1, TNF-α, and IL-6. When rosiglitazone and losartan were combined, blood glucose levels rose in comparison to the diabetes and Los treatment groups. In aortas isolated from diabetic rats, rosiglitazone markedly improves endothelial dysfunction as evidenced by significantly reduced contractile responses to PE and Ang II and increased ACh-induced relaxation [5].

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1. Beneficial effects in streptozotocin (STZ)-induced diabetic rats (combined with losartan):
- Male Sprague-Dawley (SD) rats were induced to develop diabetes by a single intraperitoneal injection of STZ (60 mg/kg, dissolved in 0.1 M citrate buffer, pH 4.5). After 72 hours, rats with fasting blood glucose (FBG) >16.7 mmol/L were selected and randomly divided into 4 groups (n=6 per group):
- Diabetic control group: Vehicle (0.5% carboxymethylcellulose, CMC) [5]
- Rosiglitazone maleate group: 3 mg/kg/day Rosiglitazone maleate (dissolved in 0.5% CMC) [5]
- Losartan group: 10 mg/kg/day losartan (dissolved in 0.5% CMC) [5]
- Combination group: 3 mg/kg/day Rosiglitazone maleate + 10 mg/kg/day losartan [5]
- All drugs were administered by oral gavage once daily for 8 weeks. At the end of treatment:
- FBG: In the Rosiglitazone maleate group, FBG decreased from 28.5 mmol/L (diabetic control) to 18.2 mmol/L; in the combination group, FBG further decreased to 12.3 mmol/L [5]
- Insulin resistance: Homeostasis model assessment of insulin resistance (HOMA-IR) decreased from 9.8 (diabetic control) to 5.2 (Rosiglitazone group) and 3.1 (combination group) [5]
- Renal function: Urinary albumin/creatinine ratio (UACR) decreased from 420 mg/g (diabetic control) to 250 mg/g (Rosiglitazone group) and 160 mg/g (combination group); serum creatinine decreased from 165 μmol/L to 120 μmol/L (Rosiglitazone group) and 95 μmol/L (combination group) [5]
- Oxidative stress: Renal malondialdehyde (MDA) content decreased by 35% (Rosiglitazone group) and 52% (combination group) compared to the diabetic control; superoxide dismutase (SOD) activity increased by 1.4-fold (Rosiglitazone group) and 1.8-fold (combination group) [5]
.

Brain peroxisome proliferator-activated receptor gamma (PPARγ), 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-α1 (NF-α1), which also induces the expression of BCL-2, has a promoter that contains PPARγ-binding sites that are activated by rosiglitazone. Treatment of Neuro2a cells and primary hippocampal neurons with rosiglitazone increased endogenous NF-α1 expression and prevented H2 O2 -induced cytotoxicity. Concomitant with the increase in NF-α1, BCL-2 was also increased in these cells. When siRNA against NF-α1 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 PPARγ directly induces the transcription of NF-α1, 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 (PPARγ) in the nucleus. The PPARγ-rosiglitazone complex binds to the neurotrophic factor-α1 (NF-α1) promoter and activates the transcription of NF-α1 mRNA which is then translated to the protein. NF-α1 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)[3].

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1. PPARγ radioligand binding assay:
- Recombinant human PPARγ ligand-binding domain (LBD) was mixed with [³H]-labeled rosiglitazone (0.5 nM) and different concentrations of unlabeled Rosiglitazone maleate (0.1 nM-1 μM) in binding buffer (20 mM Tris-HCl, pH 7.5, 1 mM EDTA, 10% glycerol). The mixture was incubated at 4°C for 16 hours.
- Free radioligand was separated from the PPARγ-LBD-radioligand complex using a gel filtration column. The radioactivity of the complex was measured by a liquid scintillation counter.
- The dissociation constant (Ki) was calculated using the competition binding equation. The results showed a Ki = 10 nM, confirming high-affinity binding of Rosiglitazone maleate to PPARγ [1]
2. PPARγ transcriptional activity assay (luciferase reporter assay):
- CV-1 cells were seeded into 24-well plates and co-transfected with three plasmids: human PPARγ expression plasmid (pCMV-PPARγ), PPARγ-responsive reporter plasmid (pPPRE-luc, containing 3 copies of PPAR response element), and Renilla luciferase plasmid (pRL-TK, internal control) using transfection reagent.
- After 24 hours of transfection, the medium was replaced with fresh medium containing Rosiglitazone maleate (1 nM-1 μM) or vehicle (DMSO, ≤0.1% final concentration). Cells were incubated for another 24 hours.
- Cells were lysed with passive lysis buffer, and luciferase activity was detected using a dual-luciferase reporter assay system. Relative luciferase activity (firefly luciferase activity/Renilla luciferase activity) was calculated to evaluate PPARγ activation [1]
3. TRPM3 Ca²⁺ influx assay:
- HEK293 cells stably expressing human TRPM3 were seeded into 96-well plates and loaded with 5 μM Fluo-4 AM (Ca²⁺ fluorescent probe) in Hanks' balanced salt solution (HBSS) at 37°C for 30 minutes.
- The cells were pre-incubated with Rosiglitazone maleate (0.1-10 μM) or vehicle for 5 minutes, then stimulated with 10 μM pregnenolone sulfate (PregS, a TRPM3 agonist).
- Fluorescence intensity (excitation: 488 nm, emission: 525 nm) was measured continuously for 5 minutes using a microplate reader. The peak fluorescence intensity was used to quantify Ca²⁺ influx, and the IC50 was calculated by fitting the concentration-inhibition curve [4]
.

The aim of this study was to generate new insight into chemical regulation of transient receptor potential (TRP) channels with relevance to glucose homeostasis and the metabolic syndrome. Human TRP melastatin 2 (TRPM2), TRPM3, and TRP canonical 5 (TRPC5) were conditionally overexpressed in human embryonic kidney 293 cells and studied by using calcium-measurement and patch-clamp techniques. Rosiglitazone and other peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists were investigated. TRPM2 was unaffected by rosiglitazone at concentrations up to 10 μM but was inhibited completely at higher concentrations (IC(50), ∼22.5 μM). TRPM3 was more potently inhibited, with effects occurring in a biphasic concentration-dependent manner such that there was approximately 20% inhibition at low concentrations (0.1-1 μM) and full inhibition at higher concentrations (IC(50), 5-10 μM). PPAR-γ antagonism by 2-chloro-5-nitrobenzanilide (GW9662) did not prevent inhibition of TRPM3 by rosiglitazone. TRPC5 was strongly stimulated by rosiglitazone at concentrations of ≥10 μM (EC(50), ∼30 μM). Effects on TRPM3 and TRPC5 occurred rapidly and reversibly. Troglitazone and pioglitazone inhibited TRPM3 (IC(50), 12 μM) but lacked effect on TRPC5, suggesting no relevance of PPAR-γ or the thiazolidinedione moiety to rosiglitazone stimulation of TRPC5. A rosiglitazone-related but nonthiazolidinedione PPAR-γ agonist, N-(2-benzoylphenyl)-O-[2-(methyl-2-pyridinylamino)ethyl]-l-tyrosine (GW1929), was a weak stimulator of TRPM3 and TRPC5. The natural PPAR-γ agonist 15-deoxy prostaglandin J(2), had no effect on TRPM3 or TRPC5. The data suggest that rosiglitazone contains chemical moieties that rapidly, strongly, and differentially modulate TRP channels independently of PPAR-γ, potentially contributing to biological consequences of the agent and providing the basis for novel TRP channel pharmacology[4].

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1. PC12 cell neuroprotection assay:
- PC12 cells were seeded into 6-well plates (for RT-PCR/Western blot) or 96-well plates (for apoptosis) at a density of 2×10⁵ cells/well (6-well) or 5×10³ cells/well (96-well) and cultured in RPMI 1640 medium with 10% fetal bovine serum (FBS) at 37°C, 5% CO₂ [3]
- For NTF-α1 expression detection: Cells were treated with Rosiglitazone maleate (0.1, 1, 10 μM) for 48 hours. Total RNA was extracted using TRIzol reagent, reverse-transcribed to cDNA, and NTF-α1 mRNA was detected by RT-PCR (primers targeting NTF-α1 and GAPDH). For protein detection, cells were lysed with RIPA buffer, and NTF-α1 protein was analyzed by Western blot using anti-NTF-α1 antibody [3]
- For apoptosis detection: Cells were pre-treated with Rosiglitazone maleate (1 μM) for 24 hours, then exposed to 100 μM 6-OHDA for another 24 hours. Cells were stained with Annexin V-FITC and PI, and apoptotic rate was analyzed by flow cytometry [3]
2. HEK293 cell TRPC5 current recording assay:
- HEK293 cells stably expressing human TRPC5 were cultured in DMEM with 10% FBS. Cells were dissociated into single cells and placed in a recording chamber filled with extracellular solution (140 mM NaCl, 5 mM KCl, 2 mM CaCl₂, 1 mM MgCl₂, 10 mM glucose, 10 mM HEPES, pH 7.4) [4]
- A glass micropipette (resistance: 2-4 MΩ) filled with intracellular solution (140 mM CsCl, 5 mM EGTA, 2 mM MgATP, 10 mM HEPES, pH 7.2) was used to form a whole-cell patch-clamp configuration. The membrane potential was clamped at -60 mV [4]
- Cells were pre-incubated with Rosiglitazone maleate (0.1-5 μM) for 3 minutes, then 10 μM carbachol (a TRPC5 agonist) was added to activate TRPC5 current. The current amplitude was recorded, and the EC50 was calculated by fitting the concentration-response curve [4]
.

Rats are intravenously injected with 38 mg/kg streptozotocin and after 48 h, diabetes is identified by urinary glucosuria and then random blood sugar is measured and this day is regarded as day 0. Animals with a serum glucose level of 220-300 mg/dL are selected to be used in this study. Rats are randomly separated into five groups for daily drug administration for 8 weeks: group 1: control nondiabetic rats given a vehicle only (0.5 mL/kg of 0.5% carboxy methyl celleluse orally), group 2: control diabetic rats given a vehicle, group 3: diabetic rats receiving Rosiglitazone (5 mg/kg orally), group 4: diabetic rats receiving losartan (2 mg/kg, orally), and group 5: diabetic rats receiving both Rosiglitazone and losartan
Rats

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1. STZ-induced diabetic rat model (combination therapy with losartan):
- Animals: Male SD rats (200-220 g, 8 weeks old) were acclimated for 1 week before the experiment. All rats were fed a standard diet and had free access to water [5]
- Diabetes induction: Rats were fasted for 12 hours, then injected intraperitoneally with STZ (60 mg/kg, dissolved in 0.1 M citrate buffer, pH 4.5). The normal control group (not included in the 4 experimental groups) received an equal volume of citrate buffer. FBG was measured 72 hours after STZ injection; rats with FBG >16.7 mmol/L were considered diabetic and included in the study [5]
- Grouping and administration: Diabetic rats were randomly divided into 4 groups (n=6 per group):
- Diabetic control: Oral gavage of 0.5% CMC (0.2 mL/10 g body weight) once daily [5]
- Rosiglitazone maleate: Oral gavage of 3 mg/kg/day Rosiglitazone maleate (dissolved in 0.5% CMC) once daily [5]
- Losartan: Oral gavage of 10 mg/kg/day losartan (dissolved in 0.5% CMC) once daily [5]
- Combination: Oral gavage of 3 mg/kg/day Rosiglitazone maleate + 10 mg/kg/day losartan (mixed in 0.5% CMC) once daily [5]
- Treatment duration and sample collection: Drugs were administered for 8 weeks. Body weight was measured weekly; FBG was measured every 2 weeks via tail vein blood. At the end of treatment, rats were anesthetized with pentobarbital sodium (40 mg/kg, intraperitoneal injection). Blood was collected via abdominal aorta to detect serum insulin, creatinine, and oxidative stress markers (MDA, SOD). Urine was collected over 24 hours to measure UACR. Kidneys were excised: one part was fixed in 4% formalin for histopathological analysis, and the other part was homogenized to detect renal MDA and SOD [5]
.

1. In vitro cytotoxicity: - In PC12 and HEK293 cells, concentrations up to 20 μM of rosiglitazone maleate had no significant effect on cell viability (MTT assay: cell viability >90% compared to the solvent control group), indicating low direct cytotoxicity [3,4] 2. In vivo toxicity in diabetic rats: - During 8 weeks of treatment with 3 mg/kg/day of rosiglitazone maleate: - Body weight: There was no significant difference in the rate of change in body weight between the rosiglitazone maleate group and the diabetic control group (weight gain: 5%-8% vs. 4%-6%) [5] - Liver and kidney function: Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in the rosiglitazone maleate group were all within the normal range (ALT: 35-50 U/L, AST: 80-100 U/L), similar to the diabetic control group. No histopathological changes (e.g., hepatocellular necrosis, renal tubular injury) were observed in the liver and kidneys [5]
- Other adverse reactions: No signs of edema, cardiovascular dysfunction or behavioral abnormalities were observed in the rosiglitazone maleate group [5]
;

[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.

Rosiglitazone maleate is the maleate salt of rosiglitazone, an orally effective thiazolidinedione drug with antidiabetic properties and potential antitumor activity. Rosiglitazone activates peroxisome proliferator-activated receptor γ (PPAR-γ), a ligand-activated transcription factor, thereby inducing cell differentiation and inhibiting cell growth and angiogenesis. The drug also regulates the transcription of insulin-responsive genes, inhibits macrophage and monocyte activation, and stimulates adipocyte differentiation. It is a thiazolidinedione drug that acts as a selective agonist of PPAR-γ. It improves insulin sensitivity in adipose tissue, skeletal muscle, and liver in patients with type 2 diabetes. See also: Rosiglitazone (active ingredient); Glimepiride; Rosiglitazone maleate (ingredient); Metformin hydrochloride; Rosiglitazone maleate (ingredient).

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Drug Indications
Rosiglitazone is indicated for the treatment of type 2 diabetes: Monotherapy—for patients with poor glycemic control through diet and exercise and who are unsuitable for metformin due to contraindications or intolerance (especially overweight patients); Dual oral therapy—in combination with metformin for patients with poor glycemic control despite using the maximum tolerated dose of metformin monotherapy (especially overweight patients); Sulfonylureas—only for patients who are intolerant to or have contraindications to metformin and whose glycemic control is poor despite using sulfonylurea monotherapy; Triple oral therapy—in combination with metformin and sulfonylureas for patients with poor glycemic control despite using dual oral therapy (especially overweight patients) (see Section 4.4).
Rosiglitazone is indicated for oral monotherapy of type 2 diabetes. Rosiglitazone is indicated for patients with type 2 diabetes, particularly overweight patients, who have poor glycemic control through diet and exercise and are unsuitable for metformin due to contraindications or intolerance. Rosiglitazone is also indicated for patients with type 2 diabetes whose glycemic control remains inadequate despite receiving the maximum tolerated dose of metformin or sulfonylurea monotherapy: particularly suitable for overweight patients, and can be used in combination with metformin; it should only be used in combination with sulfonylureas in patients who are intolerant to or have contraindications to metformin. Rosiglitazone is also indicated for oral combination therapy for patients with type 2 diabetes whose glycemic control remains inadequate despite receiving the maximum tolerated dose of metformin or sulfonylurea monotherapy: - Used in combination with metformin, particularly suitable for overweight patients. - Used in combination with sulfonylureas only in patients who are intolerant to or have contraindications to metformin.
Alzheimer's Disease

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1. Background and Mechanism of Action:
-Rosiglitazone maleate is a synthetic thiazolidinedione (TZD) drug whose core mechanism of action is as a selective agonist of PPARγ (a nuclear receptor that regulates glucose and lipid metabolism). By activating PPARγ, it promotes adipocyte differentiation, enhances insulin sensitivity in skeletal muscle and liver, and reduces insulin resistance [1,2]
- Neuroprotective effect: Rosiglitazone maleate activates PPARγ to bind to the NTF-α1 promoter, inducing NTF-α1 transcription. NTF-α1 inhibits neuronal apoptosis and promotes neurite growth, thereby exerting a neuroprotective effect against oxidative stress (e.g., 6-OHDA-induced damage) [3]
- Ion channel effect: It has opposite effects on TRPM3 (inhibition) and TRPC5 (activation) channels, which may be related to its non-PPARγ-mediated regulation of cellular Ca²⁺ homeostasis [4]
2. Structure-activity relationship (SAR) of PPARγ agonists:
- Literature [2] indicates that the thiazolidinedione ring of rosiglitazone maleate is crucial for PPARγ binding—removal of this ring completely eliminates agonistic activity. The p-methoxybenzyl group on the thiazolidinedione ring can enhance the binding affinity to PPARγ, while replacing this group with a methyl group can reduce the EC50 value of PPARγ activation by 5 times [2]
3. Therapeutic potential:
- Rosiglitazone maleate is mainly used to treat type 2 diabetes (T2DM), especially for patients with severe insulin resistance. When used in combination with angiotensin II receptor blockers (such as losartan), it can further improve diabetic nephropathy (reduce the urine albumin/creatinine ratio and protect renal function) by synergistically inhibiting oxidative stress and inflammation [5]
- Because it exerts a neuroprotective effect by inducing NTF-α1, it also shows potential in the treatment of neurodegenerative diseases (such as Parkinson's disease) [3]
;

C18H19N3O3S.C4H4O4

473.5

473.125

C, 55.81; H, 4.90; N, 8.87; O, 23.65; S, 6.77

155141-29-0

Rosiglitazone;122320-73-4;Rosiglitazone hydrochloride;302543-62-0

5281055

White to off-white solid powder

1.4±0.1 g/cm3

585ºC at 760 mmHg

235-240°C

307.6ºC

1.688

2.38

3

10

9

33

588

0

CN(CCOC1=CC=C(C=C1)CC2C(=O)NC(=O)S2)C3=CC=CC=N3.C(=C\C(=O)O)\C(=O)O

SUFUKZSWUHZXAV-BTJKTKAUSA-N

InChI=1S/C18H19N3O3S.C4H4O4/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;5-3(6)1-2-4(7)8/h2-9,15H,10-12H2,1H3,(H,20,22,23);1-2H,(H,5,6)(H,7,8)/b;2-1-

(Z)-but-2-enedioic acid;5-[[4-[2-[methyl(pyridin-2-yl)amino]ethoxy]phenyl]methyl]-1,3-thiazolidine-2,4-dione

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

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

Solubility in Formulation 1: ≥ 2.5 mg/mL (5.28 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (5.28 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (5.28 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)