Ignite Creation Date:
2024-05-06 @ 1:26 PM
Last Modification Date:
2024-10-26 @ 1:14 PM
Study NCT ID:
NCT04027309
Status:
ACTIVE_NOT_RECRUITING
Last Update Posted:
2023-06-15
First Post:
2019-07-18
Brief Title:
A Study of Gilteritinib Versus Midostaurin in Combination With Induction and Consolidation Therapy Followed by One-year Maintenance in Patients With Newly Diagnosed Acute Myeloid Leukemia or Myelodysplastic Syndromes With Excess Blasts-2 With FLT3 Mutations Eligible for Intensive Chemotherapy
Sponsor:
Stichting Hemato-Oncologie voor Volwassenen Nederland
Organization:
Stichting Hemato-Oncologie voor Volwassenen Nederland
Study Overview
Official Title:
A Phase 3 Multicenter Open-label Randomized Study of Gilteritinib Versus Midostaurin in Combination With Induction and Consolidation Therapy Followed by One-year Maintenance in Patients With Newly Diagnosed Acute Myeloid Leukemia AML or Myelodysplastic Syndromes With Excess Blasts-2 MDS-EB2 With FLT3 Mutations Eligible for Intensive Chemotherapy HOVON 156 AML AMLSG 28-18
Status:
ACTIVE_NOT_RECRUITING
Status Verified Date:
2023-06
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
HOVON 156 AML
Brief Summary:
Activating mutations in the fms like tyrosine kinase 3 FLT3 gene are observed in approximately 30 of patients with newly diagnosed acute myeloid leukemia AML Addition of the multitargeted kinase inhibitor midostaurin to standard chemotherapy prolongs event-free survival EFS and overall survival OS in patients with a FLT3 mutation Gilteritinib is a more potent and more specific inhibitor of mutant FLT3 in comparison to midostaurin and has shown promising clinical activity in AML
Detailed Description:
AML and MDS-EB2 are malignant diseases of the bone marrow The standard treatment for these diseases is chemotherapy A subgroup of these diseases is characterized by a specific error in the DNA of the leukemic cells This is the FLT3 mutation which leads to a change of a certain protein FLT3 on the blasts This altered protein plays an important role in the development of leukemia and the survival of leukemic cells
FLT3 can be inhibited by the drug midostaurin Adding midostaurin to chemotherapy leads to better treatment results in patients with AML Therefore the standard treatment for AML or MDS-EB2 with a FLT3 mutation FLT3-AML is a combination of chemotherapy and midostaurin
Gilteritinib is also a drug that inhibits FLT3 In laboratory studies gilteritinib was found to be significantly more specific and potent than midostaurin in inhibiting FLT3
Gilteritinib has subsequently been studied in patients with AML who relapsed after previous treatment with chemotherapy This resulted in a much larger number of complete remissions than previously seen when comparable patients were treated with midostaurin
FLT3 can be inhibited by the drug midostaurin Adding midostaurin to chemotherapy leads to better treatment results in patients with AML Therefore the standard treatment for AML or MDS-EB2 with a FLT3 mutation FLT3-AML is a combination of chemotherapy and midostaurin
Gilteritinib is also a drug that inhibits FLT3 In laboratory studies gilteritinib was found to be significantly more specific and potent than midostaurin in inhibiting FLT3
Gilteritinib has subsequently been studied in patients with AML who relapsed after previous treatment with chemotherapy This resulted in a much larger number of complete remissions than previously seen when comparable patients were treated with midostaurin
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
False
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| Pasha | OTHER | Astellas | None |
| 2018-000624-33 | EUDRACT_NUMBER | None | None |
| AMLSG 28-18 | OTHER | None | None |