Canagliflozin

Manufactured by Merck Group

Sourced in United States

Canagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor, a class of medications used to lower blood glucose levels in individuals with type 2 diabetes. It works by inhibiting the SGLT2 protein in the kidneys, which is responsible for reabsorbing glucose from the urine, leading to increased excretion of glucose through the urine.

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Lab products found in correlation

Streptozocin, by Merck Group (3 mentions) Sucrose, by Merck Group (3 mentions) Nicotinamide, by Merck Group (3 mentions) Acarbose, by Merck Group (3 mentions) Ethyl acetate, by Thermo Fisher Scientific (2 mentions) Glucose, by Merck Group (2 mentions) Glibenclamide, by Merck Group (2 mentions) Buffer solution, by Merck Group (2 mentions) Methanol, by Thermo Fisher Scientific (2 mentions) Canagliflozin, by Apexbio (1 mentions) Dapagliflozin, by Apexbio (1 mentions) Compound c, by Apexbio (1 mentions) Keratinocyte serum free medium, by Thermo Fisher Scientific (1 mentions) Hk 2 cell, by American Type Culture Collection (1 mentions) Hk 2 cells, by Merck Group (1 mentions) Bafilomycin a, by Merck Group (1 mentions) Cisplatin, by Merck Group (1 mentions) Phloridzin, by Merck Group (1 mentions) Empagliflozin, by Merck Group (1 mentions) Trilobatin, by Merck Group (1 mentions)

7 protocols using canagliflozin

Investigating the Protective Role of SGLT2 Inhibitors in Cisplatin-Induced Cytotoxicity

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HK-2 cells (ATCC, Manassas, VA, USA), which were immortalized by transduction with human papillomavirus 16 E6/E7 genes, were maintained in a keratinocyte serum-free medium (Thermo Fisher Scientific, Waltham, MA, USA) supplemented with 5 ng/mL human recombinant epidermal growth factor 1–53 and 50 μg/mL bovine pituitary extract at 37 °C in a humidified 5% CO₂.
For analyzing the protective role of SGLT2 inhibitors in cisplatin-induced cytotoxicity, HK-2 cells were seeded in 6-well or 96-well plates and treated with 20 μM cisplatin (Sigma-Aldrich, St. Louis, MO, USA) in the absence or presence of 1–25 μM canagliflozin, dapagliflozin, or empagliflozin (APExBIO, Houston, TX, USA) for 24 h.
To test whether canagliflozin induces autophagy or modulates AMPK-mTOR pathway and whether the protective effect of canagliflozin on cisplatin-induced cytotoxicity occurs in autophagy or AMPK activation-dependent manner, the cells were seeded in 6-well or 96-well plates and treated with 20 μM cisplatin in the absence or presence of 10 μM canagliflozin and/or 10 μM chloroquine, 5 nM bafilomycin A (Sigma-Aldrich), or 1 μM compound C (APExBIO) for 24 h.

Park C.H., Lee B., Han M., Rhee W.J., Kwak M.S., Yoo T.H, & Shin J.S. (2022). Canagliflozin protects against cisplatin-induced acute kidney injury by AMPK-mediated autophagy in renal proximal tubular cells. Cell Death Discovery, 8, 12.

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Modulating T-cell Metabolic Pathways

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For certain experiments, IL-2 (10 ng/ml; Miltenyi) was added after 24 h. To bypass initial T cell receptor-dependent signalling, T-cells were activated using PMA (10 ng/ml; Merck) and ionomycin (500 ng/ml; Merck) for 4 h. For partial rescue, T-cells were activated in the presence and absence of canagliflozin, supplemented with dimethyl α-ketoglutarate (0.3 mM; Merck). For complex I inhibition experiments, T-cells were activated in the presence or absence of rotenone (1 μM; Merck) or metformin hydrochloride (10 mM; MedChemExpress). High-dose metformin hydrochloride was used to bypass any transporter-specific uptake. For combined inhibition of complex I and glutamate dehydrogenase, T-cells were activated in the presence and absence of piericidin A (500 nM; Enzo Life Sciences) and R162 (10 μM; Merck). To determine whether ERK inhibition or mTORC1 inhibition phenocopies canagliflozin treatment, T-cells were cultured in the presence of PD-98,059 (25 μM; Merck) and rapamycin (100 nM; Merck), respectively.

Jenkins B.J., Blagih J., Ponce-Garcia F.M., Canavan M., Gudgeon N., Eastham S., Hill D., Hanlon M.M., Ma E.H., Bishop E.L., Rees A., Cronin J.G., Jury E.C., Dimeloe S.K., Veale D.J., Thornton C.A., Vousden K.H., Finlay D.K., Fearon U., Jones G.W., Sinclair L.V., Vincent E.E, & Jones N. (2023). Canagliflozin impairs T cell effector function via metabolic suppression in autoimmunity. Cell metabolism, 35(7).

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Molecular Mechanisms of Trilobatin and Phloridzin

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Trilobatin, phloridzin, canagliflozin, empagliflozin were purchased from Sigma (Sigma, St. Louis, MO, USA). Cell-light EDU Appollo567 in vitro kit was purchased from RIBOBIO (Guangzhou, China). Rat SGLT2 primary antibody was obtained from Cell Signaling Technology (Danvers, MA, USA). HNF4α and HBXIP primary antibody was from Proteintech (Rosemont, IL, USA). Specific anti-mouse and anti-rabbit HRP-conjugated second antibodies were obtained from Santa Cruz Biotechnology (Texas, CA, USA). ECL Chemiluminescence Detection Reagent was obtained from Millipore Corporation (Billerica, MA, USA). BCA protein assay kit and other chemicals were purchased from Biyotime (Shanghai, China).

Wang L., Liu M., Yin F., Wang Y., Li X., Wu Y., Ye C, & Liu J. (2019). Trilobatin, a Novel SGLT1/2 Inhibitor, Selectively Induces the Proliferation of Human Hepatoblastoma Cells. Molecules, 24(18), 3390.

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Preparation of Antidiabetic Compounds

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Methanol (CC: 904903), ethyl acetate (CC:10382681), and petroleum ether (CC: 8032324) solvents were purchased from J.T. Baker^TM (Thermo Fisher Scientific, Waltham, MA, USA). Streptozocin (75% α-anomer basis, PN: S0130-5 G), nicotinamide (99.5%, PN: 47865-U), glucose (anhydrous, PN: D9434-1 Kg), sucrose (99.5% GC, PN: S9378-1 Kg), starch (CC 336155-1 Kg), acarbose (PN: PHR1253-500 mg), and canagliflozin (95%, PN:721174-1 G) were obtained from Sigma-Aldrich^® (Saint Louis, MO, USA). Silica gel (high purity grade (7734), pore size 60 Å, 70,230 mesh; CC: 391484-5 Kg) was purchased from Merck^® (Merck^®, Darmstadt, Germany).

Solares-Pascasio J.I., Ceballos G., Calzada F., Barbosa E, & Velazquez C. (2021). Antihyperglycemic and Lipid Profile Effects of Salvia amarissima Ortega on Streptozocin-Induced Type 2 Diabetic Mice. Molecules, 26(4), 947.

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Diabetic Compound Evaluation Protocol

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Streptozocin (≥75% α-anomer basis, PN: S0130-5G), nicotinamide (≥99.5%, PN: 47865-U), sucrose (≥99.5% GC, PN: S9378-1Kg), acarbose (PN: PHR1253-500MG), canagliflozin (95%, PN: 721174-1G), glibenclamide (PN: PHR1287-1G), metformin (PN: PHR1084-500MG) were purchased from Sigma-Aldrich^® (Sigma^®, Saint Louis, MO, USA). Buffer solution (citric acid/sodium hydroxide/hydrogen chloride, pH 4.00, CC: 109445) was purchased from Merck^® (Merck^®, Darmstadt, Germany).

Valdes M., Calzada F., Martínez-Solís J, & Martínez-Rodríguez J. (2023). Antihyperglycemic Effects of Annona cherimola Miller and the Flavonoid Rutin in Combination with Oral Antidiabetic Drugs on Streptozocin-Induced Diabetic Mice. Pharmaceuticals, 16(1), 112.

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Standardized Solvent and Reagent Preparation

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Ethanol anhydrous (Catalogue code: 15568604), ethyl acetate (CC:10382681), chloroform (CC: 15508564), and dichloromethane (CC:15594055) solvents were purchased from J.T. Baker™ (Thermo Fisher Scientific, Waltham, MA, USA). Farnesol (95%, CC: F203-25G), farnesal (≥85%, mixture of isomers, CC:46188-1ML-F), streptozocin (≥75% α-anomer basis, PN: S0130-5G ), nicotinamide (≥99.5%, PN: 47865-U), glucose (anhydrous, PN: D9434-1Kg), sucrose (≥99.5% GC, PN: S9378-1Kg), acarbose (PN: PHR1253-500MG), canagliflozin (95%, PN: 721174-1G ), and glibenclamide (PN: PHR1287-1G) were purchased from Sigma-Aldrich^® (Sigma^®, Saint Louis, MO, USA). Buffer solution (citric acid/sodium hydroxide/hydrogen chloride, pH 4.00, CC: 109445), silica gel high-purity grade (7734) pore size 60 Å, 70,230 mesh (CC: 391484-5KG), TLC glass plates L × W 20 cm × 20 cm, sílica gel 60 F₂₅₄, 2 mm (CC: Z292974) were purchased from Merck^® (Merck^®, Darmstadt, Germany). Saline solution 0.9% (solution 1000 mL) and DX-5 glucose solution 5% (solution 500 mL) were purchased from PISA^® Pharmaceutics (PISA^®, Mexico City, México). IR Spectrometer, Model: Tensor-27, Bruker^® (Bruker^®, Billerica, MA, USA); NMR Spectrometer, Model: Avance III, 400 MHz, Bruker^® (Bruker^®, Billerica, MA, USA).

Valdés M., Calzada F., Mendieta-Wejebe J.E., Merlín-Lucas V., Velázquez C, & Barbosa E. (2020). Antihyperglycemic Effects of Annona diversifolia Safford and Its Acyclic Terpenoids: α-Glucosidase and Selective SGLT1 Inhibitiors. Molecules, 25(15), 3361.

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Mesenteric Artery Vascular Reactivity Assay

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The vascular reactivity was measured as previously described.²⁴ Briefly after the mice or rats were anesthetized with pentobarbital sodium, the mesenteric vascular bed was removed and placed in cold (4 °C) Krebs solution (in mmol/L: 118 NaCl, 25 NaHCO₃, 11 d‐glucose, 4.7 KCl, 1.2 KH₂PO₄, 1.17 MgSO₄, and 2.5 CaCl₂, set to the pH of 7.4). The first branches of the mesenteric arteries (Mas) (for mice) and second branches of the Mas (for rats) were excised with the connective tissues, such as fat. Subsequently, 2‐mm MA segments were mounted on a myograph (Danish Myo Technology, Aarhus, Denmark). After incubation in 95% O₂ and 5% CO₂ at 37 °C, the MA segments were stretched to optimum baseline tension (1.8 mN for mouse Mas and 2.5 mN for rat Mas). The arteries were then equilibrated for 60 minutes before precontraction with 60 mmol/L KCl. After several washouts, each ring was treated with different vasoactive substances (phenylephrine, U46619, acetylcholine, or nitroglycerin, purchased from Sigma‐Aldrich) or other substances (Pyr3, canagliflozin, SN6, KB‐R7943, purchased from Sigma‐Aldrich or MedChemExpress, USA). All substances were dissolved in DMSO at a final concentration of 0.1%, and an equal amount of DMSO was negative control. Isometric contractions were recorded using a computerized data acquisition system (Power Lab/8SP; AD Instruments Pty Ltd, Castle Hill, Australia).

Zhao Y., Li L., Lu Z., Hu Y., Zhang H., Sun F., Li Q., He C., Shu W., Wang L., Cao T., Luo Z., Yan Z., Liu D., Gao P, & Zhu Z. (2022). Sodium‐Glucose Cotransporter 2 Inhibitor Canagliflozin Antagonizes Salt‐Sensitive Hypertension Through Modifying Transient Receptor Potential Channels 3 Mediated Vascular Calcium Handling. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 11(15), e025328.

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