173534-37-7|S-4048|(1S,3R,4R,5R)-1-[[(1R,2S)-2-(4-chlorophenyl)cyclopropyl]methoxy]-3,4-dihydroxy-5-[(Z)-3-imidazo[4,5-b]pyridin-1-yl-3-phenylprop-2-enoyl]oxycyclohexane-1-carboxylic acid|-范德生物科技公司

S-4048

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names：
(1S,3R,4R,5R)-1-[[(1R,2S)-2-(4-chlorophenyl)cyclopropyl]methoxy]-3,4-dihydroxy-5-[(Z)-3-imidazo[4,5-b]pyridin-1-yl-3-phenylprop-2-enoyl]oxycyclohexane-1-carboxylic acid
CAS号：
173534-37-7
MDL Number：
MF(分子式)： C32H30ClN3O7 MW(分子量)： 604.06
EINECS: Reaxys Number:
Pubchem ID: Brand:BIOFOUNT

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中文别名	(1S,3R,4R,5R)-1-[[(1R,2S)-2-(4-chlorophenyl)cyclopropyl]methoxy]-3,4-dihydroxy-5-[(Z)-3-imidazo[4,5-b]pyridin-1-yl-3-phenylprop-2-enoyl]oxycyclohexane-1-carboxylic acid
英文别名	S-4048; S 4048; S4048.
CAS号	173534-37-7
Inchi	InChI=1S/C32H30ClN3O7/c33-22-10-8-19(9-11-22)23-13-21(23)17-42-32(31(40)41)15-26(37)29(39)27(16-32)43-28(38)14-25(20-5-2-1-3-6-20)36-18-35-30-24(36)7-4-12-34-30/h1-12,14,18,21,23,26-27,29,37,39H,13,15-17H2,(H,40,41)/b25-14-/t21-,23+,26+,27+,29+,32-/m0/s1
InchiKey	MYXPHMOLFCUDIL-MLFVSVOESA-N
分子式 Formula	C32H30ClN3O7
分子量 Molecular Weight	604.06
溶解度Solubility
性状	Solid powder
储藏条件 Storage conditions	Dry, dark and store at 0-4℃ for short term (days to weeks) or -20℃ for long term (Store correctly 2-3years).

产品说明	S-4048(CAS:173534-37-7):仅限应用于工业或者科学研究过程中非医疗目的，不应用于人类或动物的临床诊断以及治过程疗，该产品非药用，非食用。
Introduction	S-4048 is a very potent inhibitor of glucose-6-phosphate translocase (G6P T1). S-4048 acts as a gatekeeper to transport glucose 6-phosphate into the endoplasmic reticulum and therefore plays an important role in the regulation of blood glucose levels.
Application1
Application2
Application3

警示图
危险性	Warning
危险性警示
安全声明
安全防护
备注

[1]Grefhorst A, Schreurs M, Oosterveer MH, Cortés VA, Havinga R, Herling AW, Reijngoud DJ, Groen AK, Kuipers F. Carbohydrate-response-element-binding protein (ChREBP) and not the liver X receptor α (LXRα) mediates elevated hepatic lipogenic gene expression in a mouse model of glycogen storage disease type [1]Biochem J. 2010 Dec 1;432(2):249-54. doi: 10.1042/BJ20101225. PubMed PMID: 20854262.

[2]Dubbelhuis PF, Van Sluijters DA, Blommaart EF, Gustafson LA, Van Woerkom GM, Herling AW, Burger HJ, Meijer AJ. Inhibition of autophagic proteolysis by inhibitors of phosphoinositide 3-kinase can interfere with the regulation of glycogen synthesis in isolated hepatocytes. Biochem J. 2002 Dec 15;368(Pt 3):827-33. PubMed PMID: 12371905; PubMed Central PMCID: PMC1223050.

[3] Hosokawa M, Thorens B. Glucose release from GLUT2-null hepatocytes: characterization of a major and a minor pathway. Am J Physiol Endocrinol Metab. 2002 Apr;282(4):E794-801. PubMed PMID: 11882499.

[4] Herling AW, Schwab D, Burger HJ, Maas J, Hammerl R, Schmidt D, Strohschein S, Hemmerle H, Schubert G, Petry S, Kramer W. Prolonged blood glucose reduction in mrp-2 deficient rats (GY/TR(-)) by the glucose-6-phosphate translocase inhibitor S 3025. Biochim Biophys Acta. 2002 Jan 15;1569(1-3):105-10. PubMed PMID: 11853963.

[5] Bandsma RH, Wiegman CH, Herling AW, Burger HJ, ter Harmsel A, Meijer AJ, Romijn JA, Reijngoud DJ, Kuipers F. Acute inhibition of glucose-6-phosphate translocator activity leads to increased de novo lipogenesis and development of hepatic steatosis without affecting VLDL production in rats. Diabetes. 2001 Nov;50(11):2591-7. PubMed PMID: 11679439.

6: Gustafson LA, Neeft M, Reijngoud DJ, Kuipers F, Sauerwein HP, Romijn JA, Herling AW, Burger HJ, Meijer AJ. Fatty acid and amino acid modulation of glucose cycling in isolated rat hepatocytes. Biochem J. 2001 Sep 15;358(Pt 3):665-71. PubMed PMID: 11535127; PubMed Central PMCID: PMC1222100.7: van Dijk TH, van der Sluijs FH, Wiegman CH, Baller JF, Gustafson LA, Burger HJ, Herling AW, Kuipers F, Meijer AJ, Reijngoud DJ. Acute inhibition of hepatic glucose-6-phosphatase does not affect gluconeogenesis but directs gluconeogenic flux toward glycogen in fasted rats. A pharmacological study with the chlorogenic acid derivative S4048. J Biol Chem. 2001 Jul 13;276(28):25727-35. Epub 2001 May 9. PubMed PMID: 11346646.8: Burger HJ, Schubert G, Hemmerle H, Kramer W, Herling AW. Pharmacological interference with hepatic glucose production. Ann N Y Acad Sci. 1999 Nov 18;89

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