Novartis Rydapt®(midostaurin) to be listed on the Pharmaceutical Benefits Scheme on 1 December 2018 for Acute Myeloid Leukaemia (AML) patients with FLT3 gene mutation
Rydapt® is the first targeted therapy approved for newly diagnosed FLT3 gene mutated AML1and the first major therapeutic breakthrough for the treatment of AML in more than 25 years2,3.
AML is the most common acute leukaemia in adults; it accounts for approximately 25% of all adult leukaemias worldwide, with the highest incidence rates occurring in the US, Europe and Australia4. It also has the lowest survival rate of all adult leukaemias4.
In Australia, about 1070 people are estimated to be diagnosed with AML per year5 and approximately one-third of these patients will have a mutation affecting the FLT36.
Sydney, November 30 2018 – Novartis today announced Rydapt® (midostaurin) will be listed on the Pharmaceutical Benefits Scheme (PBS) on 1 December 2018 for the treatment of adult patients with newly diagnosed Acute Myeloid Leukaemia (AML) who have a specific genetic mutation called FLT3, in combination with chemotherapy and as single agent maintenance therapy in patients responding to initial therapy1.
AML is a rare but aggressive cancer of the blood and bone marrow. In Australia, about 1070 people are estimated to have been diagnosed with AML in 20165. Approximately one-third of these patients will have a mutation affecting the FLT3 gene6, which is one of the most common and important gene abnormalities in AML and routinely assessed at diagnosis6.
"Novartis is committed to bringing new treatment options to patients with rare diseases including AML," said Lauren Carey, General Manager Oncology and Country President, Novartis Australia and New Zealand. "We acknowledge the Australian Government for their commitment to providing access to medicines for patients in Australia."
"The arrival of Rydapt onto the PBS in Australia is the culmination of a multinational clinical research journey that began over a decade ago" said A/Prof Andrew Wei, Head of Leukaemia Research at Alfred Hospital. "Rydapt is the first of a new generation of targeted drugs aiming to re-shape the treatment landscape of AML and bring new hope to patients with this aggressive disease."
Mutations affecting FLT3 result in overactivity of the cell-surface kinase receptor, leading to accelerated growth of leukaemia and earlier disease progression, resulting in lower rates of survival than other forms of AML. Rydapt functions by blocking FLT3, as well as other kinase receptors, augmenting the efficacy of chemotherapy and improving the survival of patients with this mutation1.
"This is a much needed and long awaited step forward for newly diagnosed AML patients", said Bill Petch, Chief Executive Officer, Leukaemia Foundation. "To now have access to this precision medicine is vital for improving the quality of life for the many Australians who have this particular type of acute myeloid leukaemia".
"As part of our commitment to patients and caregivers, Novartis has been supplying Rydapt7through an access program to eligible patients over the last 14 months," Ms Carey added. "These patients will now transition over to the PBS from 1 December."
References
[1] Rydapt® (midostaurin) Product Information
[2] Schiller GJ. High-risk acute myelogenous leukemia: treatment today ... and tomorrow. Hematology Am Soc Hematol Educ Program. 2013; 2013:201-208.
[3] Lin TL, Levy MY. Acute myeloid leukemia: focus on novel therapeutic strategies. Clin Med Insights Oncol. 2012;6:205-217.
[4] Deschler B, Lübbert M. Acute myeloid leukemia: epidemiology and etiology. Cancer. 2006;107(9):2009-2107.
[5] Cancer Australia, Acute Myeloid Leukaemia, https://canceraustralia.gov.au/affected-cancer/cancer-types/leukaemia/acute-myeloid-leukaemia-statistics. Accessed 19 November 2018
[6] Patel JP, Gönen M, Figueroa ME, et al. Prognostic relevance of integrated genetic profiling in acute myeloid leukemia. N Engl J Med. 2012; 22;366(12):1079-1089.
[7] This product is not listed on the PBS. It will be listed on the PBS on 1 December 2018.
