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Rapid and sustained clearance of GL-3 in the kidney, heart, and skin1,2

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Potential reduction of life-threatening events by 61%3
 

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Protection from long-term progression of renal function decline4

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Improved cardiac function5

 

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Fabrazyme® cleared GL-3 in the kidney, heart, and skin in as quickly as 6 months after initiation6

Adapted from Germain D et al. 2007.6

A potential reduction of life threatening events by 61%3

61% relative risk reduction of renal, cardiac and cerebrovascular life-threatening events and death in Fabrazyme®-treated patients vs. placebo.3 A smaller percentage of Fabrazyme®- treated patients (27%) experienced clinical events vs. placebo (42%).3 (Absolute risk reduction = 14%).3

Fabrazyme® substantially lowered the rate of renal, cardiac, and cerebrovascular clinical events among Fabrazyme®-treated vs. placebo-treated patients (risk reduction = 53% ITT population [HR 95% CI: 0.47 (0.21–1.03); p=0.06.3]; risk reduction = 61% per-protocol population [HR 95% CI: 0.39 (0.16–0.93); p=0.034.3]).3

The time-to-event analyses for the composite end point in both treatment groups in the per-protocol population3

Results are from the population of protocol-adherent patients who followed all of the clinical study guidelines after adjustment for baseline proteinuria.3
Adapted from Banikazemi M et al. 2007.3

Protection from long term progression of renal function decline4

70.9% slower rate of eGFR decrease in Fabrazyme®-treated patients than a comparable untreated patient, after adjusting for the noted imbalances in gender and proteinuria.4 Fabrazyme®-treated classic Fabry disease patients experience a slower median eGFR decrease (2.46 mL/min/1.73m2/year, 95% CI: [0.63–4.29]; p=0.0087) than comparable untreated patients.4

Forest plot comparing the adjusted median eGFR slopes in Fabrazyme®-treated versus untreated patients4

Adjusted median eGFR slopes and IQR for the overall treated and untreated groups and the individual studies.
Adapted from Ortiz A et al. 2021.4

Early initiation with Fabrazyme®, before development of fibrosis, could help improve cardiac morphology, function, and exercise capacity5

Change in left ventricular mass during 3 years of ERT.5

Adapted from Weidemann F et al. 2009.5

Change in exercise capacity during 3 years of ERT5

Adapted from Weidemann F et al. 2009.5
A mild but significant improvement in exercise capacity could be demonstrated for patients
with no fibrosis (p=0.014).5

Did you know?

Fabry disease starts early in the kidney and is a silent threat. Progressive accumulation of globotriaocylceramide (GL-3) leads to cellular changes and histological damage.8 Fabry nephropathy shows similarities to other proteinuric nephropathies of metabolic origin.3 Once the mechanisms leading to tissue injury are activated, the progression of Fabry nephropathy becomes irreversible.9,10

Learn more about Fabrazyme®

Fabrazyme® safety profile


Find out more about the safety and tolerability profile for Fabrazyme®.

Treatment with Fabrazyme®


Discover more about treatment with Fabrazyme® for patients living with Fabry disease.

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Fabrazyme® safety profile


Find out more about the safety and tolerability profile for Fabrazyme®.

Treatment with Fabrazyme®


Discover more about treatment with Fabrazyme® for patients living with Fabry disease.


 

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Do you have questions or need support? We are here to help you.

Resources

Quantifying the effect of Fabrazyme® on the preservation of renal function in Fabry disease

Learning from the Canadian Fabry Disease Initiative
 

Understanding the impact of Fabrazyme® on long-term renal function

 

References

  1. Eng CM et al. N Engl J Med 2001; 345(1): 9–16.

  2. Thurberg B et al. Circulation 2009; 119(19): 2561–2567.

  3. Banikazemi M et al. Ann Intern Med 2007; 146: 77–86.

  4. Ortiz A et al. Clinical Kidney Journal 2021; 14 (4): 1136–1146.

  5. Weidemann F et al. Circulation 2009; 119(4): 524–529.

  6. Germain D et al. J Am Soc Nephrol 2007; 18(5): 1547–1557.

  7. Eng CM et al. N Engl J Med 2001; 345(1): 9–16.

  8. Waldek S and Ferriozi S. BMC Nephrol. 2014;15:72.

  9. Ortiz A, et al. Mol Genet Metab. 2018;123(4):416–27.

  10. Van der Veen SJ, et al. Mol Genet Metab. 2022;135(2):163–69

MAT-XU-2400636 (v1.0) Date of preparation: March 2024