Home Metabolism FXR inhibitor Sevelamer HCl

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Sevelamer HCl FXR inhibitor

Cat.No.S4129

Sevelamer HCl is a phosphate binding drug used to treat hyperphosphatemia via binding to dietary phosphate and prevents its absorption.
Sevelamer HCl FXR inhibitor Chemical Structure

Chemical Structure

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Quality Control

Batch: Purity: 98.47%
98.47

Solubility

In vitro
Batch:

4-Methylpyridine : 5 mg/mL

DMSO : Insoluble
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : Insoluble

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In vivo
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Chemical Information, Storage & Stability

Molecular Weight Formula

(C3H7N.C3H5ClO.HCl)x

 Storage (From the date of receipt)
CAS No. 152751-57-0 Download SDF Storage of Stock Solutions

Synonyms N/A Smiles C=CCN.C1C(O1)CCl.Cl

Mechanism of Action

In vivo
Sevelamer is as effective as CaCO3 in reducing serum phosphorus, calcium-phosphorus product, and attenuating secondary hyperparathyroidism in nephrectomized rats (U) fed high phosphorus (HP) diet. Sevelamer results in markedly lower calcium deposition in the myocardium and aorta compared to control rats. Sevelamer suppresses calcification of the aorta media, and also the osteoid volume, fibrosis volume, and porosity ratio of femurs in chronic renal failure rats. Sevelamer results in a significantly lower degree of atherosclerosis and vascular calcification in uremic mice when compared with uremic control mice. Sevelamer exerts an effect on both intima and media calcification in uremic mice. Sevelamer treatment controlled serum P independent of increases in serum Ca, thus reducing serum calcium-phosphate product and further deterioration of renal function, as indicated by the highest creatinine clearances in uremic rats. Sevelamer is as effective as CaCO3 in the control of high-P-induced SH, as shown by similar serum PTH levels, parathyroid (PT) gland weight, and markers of PT hyperplasia. Sevelamer causes a dramatic reduction of renal Ca deposition compared with both uremic + high-P diet (U-HP) and the U-HP+CaCO3 diet. Sevelamer hydrochloride results in a fall in urine pH, as well as an increase in urinary ammonium and calcium excretion consistent with an increase in net acid excretion in animal model.
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/15296506/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01220843 Completed
Chronic Renal Failure
Centre Hospitalier Universitaire Amiens|Genzyme a Sanofi Company
 October 2010 Phase 3
NCT01191762 Completed
Hyperparathyroidism|Chronic Kidney Disease
Kenneth R. Phelps M.D.|Genzyme a Sanofi Company|Phelps Kenneth R. M.D.
 April 2010 Phase 3
NCT01011699 Terminated
Chronic Renal Failure|Hemodialysis
Centre Hospitalier Universitaire Amiens
 January 2010 Phase 3
NCT00853242 Completed
Kidney Failure Chronic
Genzyme a Sanofi Company|Sanofi
 February 2009 Phase 2

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