Detail of "131918-61-1"

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Differential effects of very high doses of doxercalciferol and paricalcitol on serum phosphorus in hemodialysis patients

All Rights Reserved. Differential effects of very high doses of doxercalciferol and paricalcitol on serum phosphorus in hemodialysis patients. Joist, H. E.; Ahya, S. N.; Giles, K.; Norwood, K.; Slatopolsky, E.; Coyne, D. W. (Renal Division, Department of Internal Medicine, and the Chromalloy American Kidney Center, Washington University School of Medicine, St. Louis, MO, USA).There are some reagents with their cas registry numbers 7440-70-2 and 131918-61-1 are used in this study. Clinical Nephrology, 65(5), 335-341 (English) 2006 Dustri-Verlag Dr. Karl Feistle. CODEN: CLNHBI. ISSN: 0301-0430. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Background: Treatment of secondary hyperparathyroidism (SHPT) includes use of calcitriol (1,25D3) to suppress parathyroid hormone (PTH), but dosing of 1,25D3 is limited by the development of hypercalcemia and a high calcium ′ phosphorus (Ca ′ P) product due to gut absorption of calcium and phosphorus as well as enhanced bone resorption. The vitamin D analog 19-Nor-1,25(OH)2-vitamin D2 (paricalcitol) and the prohormone 1a-OH-vitamin D2 (doxercalciferol) have been proposed as alternatives which may cause less hypercalcemia and elevated Ca ′ P, while still suppressing PTH. Methods: We performed a prospective study to assess the acute bone mobilization effects of very high doses of paricalcitol and doxercalciferol. 13 Hemodialysis patients received 160 mcg of paricalcitol and 120 mcg of doxercalciferol on 2 sep. occasions in a research center while on a low calcium, low phosphorus diet, and sevelamer alone as a phosphorus binder. Changes in Ca, PO4, and PTH were measured over 36 h. Results: Serum phosphorus rose faster, and peaked significantly higher at 36 h following doxercalciferol (2.12 ± 0.11 mmol/l) than paricalcitol (1.85 ± 0.07 mmol/l; p = 0.025). Ca ′ P product also rose more following doxercalciferol than paricalcitol, and peaked higher at 36 h (5.02 ± 0.26 vs. 4.54 ± 0.21 mmol/l; p = 0.061). In contrast, suppression of PTH at 36 h was comparable (63% after paricalcitol and 65% with doxercalciferol). Conclusion: Consistent with animal studies, paricalcitol provides profound PTH suppression, while stimulating bone resorption and/or intestinal absorption less than doxercalciferol, resulting in less elevation of serum phosphorus and Ca ′ P. .

Effects of vitamin D analogs on the expression of plasminogen activator inhibitor-1 in human vascular cells

All Rights Reserved. Effects of vitamin D analogs on the expression of plasminogen activator inhibitor-1 in human vascular cells. Wu-Wong, J. Ruth; Nakane, Masaki; Ma, Junli (R4CM, AP52, Abbott Laboratories, Abbott Park, IL 60064, USA). Thrombosis Research, 118(6), 709-714 (English) 2006 Elsevier B.V. CODEN: THBRAA. ISSN: 0049-3848. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Vitamin D analogs such as paricalcitol and calcitriol have been shown to provide survival benefit for Stage 5 chronic kidney disease (CKD) patients, possibly due to their pos. impact on the cardiovascular system. Plasminogen activator inhibitor-1 (PAI-1) is one of the risk markers for coronary artery disease. Human coronary artery smooth muscle cells (SMC) and endothelial cells (CAEC) were treated with vitamin D analogs to assess the effects of the drugs on the expression of PAI-1 mRNA and protein. In SMC, both paricalcitol and calcitriol down-regulated the expression of PAI-1 mRNA and protein in a dose-dependent manner. The EC50 values of paricalcitol and calcitriol on suppressing PAI-1 mRNA were 3.0 and 2.8 nM, resp. Interestingly, these two drugs had no significant effect on the expression of PAI-1 protein or mRNA in CAEC. Further anal. showed that CAEC did not express functional vitamin D receptor (VDR) and paricalcitol failed to induce the expression of 25-hydroxyvitamin D-24-hydroxylase (CYP24A1) mRNA, a gene known to be regulated by VDR. 131918-61-1 and 32222-06-3 which are cas registry numbers of substances are two of reagents here. As a comparison, SMC expressed VDR and paricalcitol induced CYP24A1 mRNA in SMC (> 150-fold at 10 nM) dose-dependently. The effect of paricalcitol on suppressing PAI-1 in SMC was blocked by cycloheximide, suggesting that protein synthesis was involved. Conclusion: These results demonstrate that vitamin D analogs suppress PAI-1 in SMC, but not in CAEC. Suppression of PAI-1 in SMC may be one of the factors contributing to the survival benefits of vitamin D analog therapy in CKD patients. .