- Draft Recommendation Confirms that Eculizumab is Very Effective and Only Treatment for aHUS -
- NICE Evaluation Committee Recommends Funding for Treatment of Patients with aHUS Subject to Conditions, Including Establishment of an Expert Center and a Robust System to Monitor Patients Receiving Treatment -
- Alexion Remains Committed to Working to Ensure Patients with aHUS in England Will Have Sustained Access to Eculizumab -
- Final Evaluation Decision Expected in Q4 2014 -
In the second Evaluation Consultation Document (ECD) released today, the NICE EC again confirmed the 2013
- Coordination of the use of eculizumab through an expert center;
- Monitoring systems to record the number of people with a diagnosis of atypical hemolytic uremic syndrome, the number of people who receive eculizumab, and the dose and duration of treatment for these people;
- A national protocol for starting and stopping eculizumab for clinical reasons;
- And a research programme with robust methods to evaluate when stopping treatment or dose adjustment might occur.
"We are pleased that NICE has once again confirmed that patients with aHUS are at constant risk of sudden, progressive and life-threatening damage to vital organs including the kidney and other organs, and that eculizumab is a significant breakthrough for patients with this devastating disorder," said
Currently, new and existing patients with aHUS in
About aHUS
aHUS is a chronic, ultra-rare, and life-threatening disease in which a life-long and permanent genetic deficiency in one or more complement regulatory genes causes chronic uncontrolled complement activation, resulting in complement-mediated thrombotic microangiopathy (TMA), the formation of blood clots in small blood vessels throughout the body.1,2 Permanent, uncontrolled complement activation in aHUS causes a life-long risk for TMA, which leads to sudden, catastrophic, and life-threatening damage to the kidney, brain, heart, and other vital organs, and premature death.1,3 Sixty-five percent of all patients with aHUS die, require kidney dialysis or have permanent kidney damage within the first year after diagnosis despite plasma exchange or plasma infusion (PE/PI).4,5 The majority of patients with aHUS who receive a kidney transplant commonly experience subsequent systemic TMA, resulting in a 90 percent transplant failure rate in these TMA patients.6
aHUS affects both children and adults. Complement-mediated TMA also causes reduction in platelet count (thrombocytopenia) and red blood cell destruction (hemolysis). While mutations have been identified in at least ten different complement regulatory genes, mutations are not identified in 30-50 percent of patients with a confirmed diagnosis of aHUS.7
About Soliris® (eculizumab)
Soliris is a first-in-class terminal complement inhibitor developed from the laboratory through regulatory approval and commercialization by Alexion. Soliris is approved in the U.S. (2007),
More information including the full U.S. prescribing information on Soliris is available at: http://soliris.net/sites/default/files/assets/soliris_pi.pdf.
The full prescribing information on Soliris in
Important Safety Information
The U.S. product label for Soliris includes a boxed warning: "Life-threatening and fatal meningococcal infections have occurred in patients treated with Soliris. Meningococcal infection may become rapidly life-threatening or fatal if not recognized and treated early [see Warnings and Precautions (5.1)]. Comply with the most current
In patients with PNH, the most frequently reported adverse events observed with Soliris treatment in clinical studies were headache, nasopharyngitis (runny nose), back pain and nausea. Soliris treatment of patients with PNH should not alter anticoagulant management because the effect of withdrawal of anticoagulant therapy during Soliris treatment has not been established. In patients with aHUS, the most frequently reported adverse events observed with Soliris treatment in clinical studies were headache, diarrhea, hypertension, upper respiratory infection, abdominal pain, vomiting, nasopharyngitis, anemia, cough, peripheral edema, nausea, urinary tract infections, pyrexia. Soliris is not indicated for the treatment of patients with Shiga-toxin E. coli-related hemolytic uremic syndrome (STEC-HUS). Please see full prescribing information for Soliris, including BOXED WARNING regarding risk of serious meningococcal infection.
About Alexion
Alexion is a biopharmaceutical company focused on serving patients with severe and rare disorders through the innovation, development and commercialization of life-transforming therapeutic products. Alexion is the global leader in complement inhibition and has developed and markets Soliris® (eculizumab) as a treatment for patients with PNH and aHUS, two debilitating, ultra-rare and life-threatening disorders caused by chronic uncontrolled complement activation. Soliris is currently approved in nearly 50 countries for the treatment of PNH and in nearly 40 countries for the treatment of aHUS. Alexion is evaluating other potential indications for Soliris in additional severe and ultra-rare disorders beyond PNH and aHUS, and is developing other highly innovative biotechnology product candidates, including asfotase alfa, across multiple therapeutic areas. This press release and further information about Alexion can be found at: www.alexionpharma.com.
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Safe Harbor Statement
This news release contains forward-looking statements, including statements related to potential health and medical benefits of Soliris® (eculizumab) for the treatment of patients with aHUS and PNH, pricing for Soliris in
References:
(1) Benz K, Amann K. Thrombotic microangiopathy: new insights. Curr
(2) Ariceta G, Besbas N, Johnson S, et al. Guideline for the investigation and initial therapy of diarrhea-negative hemolytic uremic syndrome. Pediatr Nephrol. 2009;24:687-96.
(3) Tsai HM. The molecular biology of thrombotic microangiopathy. Kidney Int. 2006;70(1):16-23.
(4) Caprioli J, Noris M, Brioschi S, et al. The impact of MCP, CFH, and IF mutations on clinical presentation, response to treatment, and outcome. Blood. 2006;108:1267-9.
(5) Loirat C, Garnier A, Sellier-Leclerc AL, Kwon T. Plasmatherapy in atypical hemolytic uremic syndrome. Semin Thromb Hemost. 2010;36:673-81.
(6) Bresin E, Daina E, Noris M, et al. Outcome of renal transplantation in patients with non-Shiga toxin-associated hemolytic uremic syndrome: prognostic significance of genetic background. Clin J Am Soc Nephrol. 2006;1:88-99.
(7) Noris M, Caprioli J, Bresin E, et al. Relative role of genetic complement abnormalities in sporadic and familial aHUS and their impact on clinical phenotype. Clin J Am Soc Nephrol. 2010;5:1844-59.
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