Ignite Creation Date:
2024-05-05 @ 5:03 PM
Last Modification Date:
2024-10-26 @ 9:27 AM
Study NCT ID:
NCT00375219
Status:
COMPLETED
Last Update Posted:
2021-11-15
First Post:
2006-09-08
Brief Title:
Homoharringtonine Omacetaxine Mepesuccinate in Treating Patients With Chronic Myeloid Leukemia CML With the T315I BCR-ABL Gene Mutation
Sponsor:
Teva Branded Pharmaceutical Products RD Inc
Organization:
Teva Branded Pharmaceutical Products RD Inc
Study Overview
Official Title:
A Phase II Open-Label Study of the Subcutaneous Administration of Homoharringtonine Omacetaxine CGX-635 in the Treatment of Patients With Chronic Myeloid Leukemia CML With the T315I BCR-ABL Gene Mutation
Status:
COMPLETED
Status Verified Date:
2021-11
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:
None
Brief Summary:
To evaluate the safety and efficacy of subcutaneous administration of omacetaxine mepesuccinate HHT in achieving a clinical response in CML patients in chronic accelerated or blast phase who have failed prior imatinib therapy and have the T315I kinase domain gene mutation
Detailed Description:
Point mutations within the ABL kinase domain of the BCR-ABL gene are emerging as the most frequent mechanism for resistance to imatinib and resultant reactivation of kinase activity The risk of mutation development is particularly high in patients who are beyond chronic phase as well as those with a long duration of disease prior to imatinib therapy
The T315I kinase domain KD point mutation has merited particular attention as T315I expressing CML cells are markedly resistant to imatinib CML patients with the T315I KD mutation therefore do not respond to continued treatment with imatinib and preliminary clinical data indicate that neither of two newer tyrosine kinase inhibitors will have activity in patients with T315I KD mutation either
Omacetaxine mepesuccinate HHT is a potent inducer of apoptosis programmed cell death in myeloid cells and inhibits angiogenesis blood vessel formation In Phase 2 studies HHT has demonstrated clinical activity in patients with CML both as a single agent and in-combination with other chemotherapeutic drugs HHT works via a different mechanism than imatinib or other tyrosine kinase inhibitors TKIs and HHT has been shown to inhibit in vitro CML cell lines which harbor the T315I KD mutation and are highly resistant to imatinib Therefore CML patients who have the T315I KD mutation may still respond to treatment with HHT HHT may therefore be an attractive therapeutic option for patients with the T315I KD mutation
On this basis a multicenter clinical trial is being conducted of HHT therapy for CML patients who have failed prior imatinib therapy and have the T315I KD mutation
Patients will be treated with an induction course consisting of subcutaneous SC HHT twice daily for 14 consecutive days every 28 days Patients who demonstrate a response may receive maintenance therapy for up to 24 months consisting of subcutaneous SC HHT twice daily for 7 days every 28 days
The T315I kinase domain KD point mutation has merited particular attention as T315I expressing CML cells are markedly resistant to imatinib CML patients with the T315I KD mutation therefore do not respond to continued treatment with imatinib and preliminary clinical data indicate that neither of two newer tyrosine kinase inhibitors will have activity in patients with T315I KD mutation either
Omacetaxine mepesuccinate HHT is a potent inducer of apoptosis programmed cell death in myeloid cells and inhibits angiogenesis blood vessel formation In Phase 2 studies HHT has demonstrated clinical activity in patients with CML both as a single agent and in-combination with other chemotherapeutic drugs HHT works via a different mechanism than imatinib or other tyrosine kinase inhibitors TKIs and HHT has been shown to inhibit in vitro CML cell lines which harbor the T315I KD mutation and are highly resistant to imatinib Therefore CML patients who have the T315I KD mutation may still respond to treatment with HHT HHT may therefore be an attractive therapeutic option for patients with the T315I KD mutation
On this basis a multicenter clinical trial is being conducted of HHT therapy for CML patients who have failed prior imatinib therapy and have the T315I KD mutation
Patients will be treated with an induction course consisting of subcutaneous SC HHT twice daily for 14 consecutive days every 28 days Patients who demonstrate a response may receive maintenance therapy for up to 24 months consisting of subcutaneous SC HHT twice daily for 7 days every 28 days
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| 2006-000176-32 | EUDRACT_NUMBER | None | None |