CI

At a glance

ClinicalIndex Comparison Record
Phase 2Completed· 21 enrolled
Drug / intervention
Fabrazyme (agalsidase beta)biological
Likely dose
1.0 mg/kg Fabrazyme intravenously every two weeks for 6 months, then 0.3 mg/kg every two weeks for 18 monthsAI-extracted
Key inclusion· 4
  • Clinical manifestations of Fabry disease documented in patient's history
  • Plasma α-galactosidase A activity <1.5 nmol/hr/mL OR leukocyte α-galactosidase A activity <4 nmol/hr/mg
  • Male gender and age ≥16 years
  • Written informed consent from patient or parent/guardian prior to study procedures
Key exclusion· 6
  • Renal insufficiency defined as serum creatinine ≥2.2 mg/dL (194.7 μmol/L) AND/OR estimated GFR <80 mL/min using MDRD equation
  • History of kidney transplantation or current dialysis treatment
  • Clinically significant organic disease or unstable condition (excluding Fabry-related symptoms) that would preclude trial participation in Investigator's opinion
  • Prior enzyme replacement therapy for Fabry disease

Standardized by ClinicalIndex from the ClinicalTrials.gov record · verify against the source.

Search/NCT00196716
NCT00196716Phase 2Completed

A Multicenter, Open-label Study of Low Dose Maintenance Treatment of Fabrazyme (Recombinant Human Alpha-Galactosidase A (R-h Alpha-GAL)) Replacement Therapy in Patients With Fabry Disease

Genzyme, a Sanofi Company·interventional·Posted Sep 20, 2005·Updated Apr 3, 2015

In Brief

A Phase 2 clinical trial evaluating Fabrazyme (agalsidase beta) for Fabry Disease. Completed, enrolled 21 participants across 4 sites in 4 countries.

Detailed Summary

People with Fabry disease have an alteration in their genetic material (DNA) which causes a deficiency of the alpha-galactosidase A enzyme. This enzyme helps to break down and remove certain types of fatty substances called "glycolipids." These glycolipids are normally present within the body in most cells. In people with Fabry disease, glycolipids build up in various tissues such as the liver, kidney, skin, and blood vessels because alpha-galactosidase A is not present, or is present in small quantities. The build up of glycolipid levels (also referred to as "globotriaosylceramide" or "GL-3") in these tissues is thought to cause the clinical symptoms that are common to Fabry disease. Symptoms commonly appear during childhood with pain in the hands and feet. This trial is designed to evaluate the efficacy of a lower dose of Fabrazyme in patients who initially received 1.0 mg/kg every 2 weeks of Fabrazyme by investigating if the achieved clearance of glycosphingolipid deposits in the vascular endothelium of the kidney can be maintained at a lower dose.

Study Details

Study Typeinterventional
Allocation--
Masking--
Primary Purpose--
ConditionsFabry Disease
CountriesCzechia, Estonia, Poland, Slovakia
Collaborators--

Timeline

Phase 2CompletedFinished
2003200420052006200720082009201020112012201320142015201620172018201920202021202220232024202520262027
First PostedSep 20, 2005
Enrollment StartJun 1, 2003
Primary CompletionApr 1, 2006
Study CompletionMar 1, 2007
TodayJul 2, 2026
Enrollment to primary: 2.8 yearsPosted 20.8 years ago

Interventions

Fabrazyme (agalsidase beta)biological

1.0 mg/kg Fabrazyme every two weeks for approximately six months followed by 0.3 mg/kg Fabrazyme every two weeks for approximately 18 months