Ercalcitriol - CAS 60133-18-8
Catalog number:
60133-18-8
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C28H44O3
Molecular Weight:
428.65
COA:
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Targets:
VD/VDR
Description:
Ercalcitriol is a active metabolite of vitamin D2. It exhibits equipotent antirachitic activity in rats as calcitriol.
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Purity:
>98%
Synonyms:
1α,25-Dihydroxy Vitamin D2
MSDS:
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1.The effect of topical diclofenac 3% and calcitriol 3 μg/g on superficial basal cell carcinoma (sBCC) and nodular basal cell carcinoma (nBCC): A phase II, randomized controlled trial.
Brinkhuizen T1, Frencken KJ2, Nelemans PJ3, Hoff ML4, Kelleners-Smeets NW2, Hausen AZ5, van der Horst MP5, Rennspiess D5, Winnepenninckx VJ5, van Steensel MA6, Mosterd K2. J Am Acad Dermatol. 2016 Apr 7. pii: S0190-9622(16)00130-4. doi: 10.1016/j.jaad.2016.01.050. [Epub ahead of print]
BACKGROUND: Nonsteroidal anti-inflammatory drugs and vitamin-D derivatives can target signaling pathways activated in basal cell carcinoma (BCC).
2.Evaluation of responses to vitamin D3 (cholecalciferol) in patients on dialysis: a systematic review and meta-analysis.
Xu C1, Li YC1, Zhao SM1, Li ZX2. J Investig Med. 2016 Apr 13. pii: jim-2015-000032. [Epub ahead of print]
Vitamin D plays a key role in mineral metabolism and its deficiency is often noted in patients on dialysis for end-stage renal disease (ESRD). We evaluated the efficacy and responses to vitamin D3 (cholecalciferol) in patients undergoing dialysis for ESRD. Randomized controlled trials or prospective studies comparing vitamin D3 supplementation to placebo in patients with ESRD on dialysis were searched from medical databases using the terms, 'Calcitriol/Cholecalciferol, vitamin D, chronic kidney disease, hemodialysis, serum calcium, parathyroid hormones (PTH), phosphorus, 25(OH)D, and 1,25(OH)2D'. The outcomes analyzed were serum calcium, PTH, phosphorus, 25(OH)D, and 1,25(OH)2D levels. Of the 259 records identified, 9 studies with a total of 368 patients were chosen for the current meta-analysis. The number of patients, age, and gender distribution among the groups were comparable. Results reveal a greater increase in both 25(OH)D (Pooled difference in means=0.
3.Vascular Calcification Induced by Chronic Kidney Disease Is Mediated by an Increase of 1α-Hydroxylase Expression in Vascular Smooth Muscle Cells.
Torremadé N1, Bozic M1, Panizo S2, Barrio-Vazquez S2, Fernandez-Martín JL2, Encinas M3, Goltzman D4, Arcidiacono MV1, Fernandez E1, Valdivielso JM1. J Bone Miner Res. 2016 Apr 13. doi: 10.1002/jbmr.2852. [Epub ahead of print]
Vascular calcification (VC) is a complication of chronic kidney disease which predicts morbidity and mortality. Uremic serum promotes VC, but the mechanism involved is unknown. A role for 1,25(OH)2 D3 on VC has been proposed, but the mechanism is unclear because both, low and high levels have been shown to increase it. In this paper we investigate the role of 1,25(OH)2 D3 produced in vascular smooth muscle cells (VSMCs) on VC. Rats with subtotal nephrectomy and kidney recipient patients showed increased arterial expression of 1α-hydroxylase in vivo. VSMCs exposed in vitro to serum obtained from uremic rats also showed increased 1α-hydroxylase expression. Those increases were parallel to an increase in VC. After 6 days with high phosphate media, VSMCs overexpressing 1α-hydroxylase show significantly higher calcium content and RUNX2 expression than control cells. 1α-hydroxylase null mice (KO) with subtotal nephrectomy and treated with calcitriol (400 ng/kg) for two weeks showed significantly lower levels of vascular calcium content, alizarin red staining and RUNX2 expression than wild type (WT) littermates.
4.Vitamin D in patients with chronic kidney disease: a position statement of the Working Group "Trace Elements and Mineral Metabolism" of the Italian Society of Nephrology.
Morrone LF1, Bolasco P2, Camerini C3, Cianciolo G4, Cupisti A5, Galassi A6, Mazzaferro S7, Russo D8, Russo L8, Cozzolino M9. J Nephrol. 2016 Apr 9. [Epub ahead of print]
In the late 1970s, calcitriol was introduced into clinical practice for the management of secondary renal hyperparathyroidism in chronic kidney disease (CKD). Since then, the use of calcifediol or other native forms of vitamin D was largely ignored until the publication of the 2009 Kidney Disease Improving Global Outcomes (KDIGO) recommendations. The guidelines suggested that measurement of circulating levels of 25(OH)D (calcifediol) and its supplementation were to be performed on the same basis as for the general population. This indication was based on the fact that the precursors of active vitamin D had provided to CKD patients considerable benefits in survival, mainly due to their pleiotropic effects on the cardiovascular system. However, despite the long-term use of various classes of vitamin D in CKD, a clear definition is still lacking concerning the most appropriate time for initiation of therapy, the best compound to prescribe (active metabolites or analogs), the proper dosage, and the most suitable duration of therapy.
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CAS 60133-18-8 Ercalcitriol

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