MedPath

Dosing Study of Ara-C/EL625/Idarubicin in Refractory and Relapsed AML

Phase 2
Completed
Conditions
Acute Myelogenous Leukemia
Interventions
Registration Number
NCT00074737
Lead Sponsor
Eleos, Inc.
Brief Summary

The principal goal of this clinical trial is to assess the ability of cenersen sodium (EL625) to improve cancer responsiveness to the established AML therapeutic agent Idarubicin used alone or in combination with Cytarabine (Ara-C).

Cenersen sodium is a drug that is designed to block the effects of a protein called p53. Laboratory evidence shows that blocking p53 will make many types of cancer, including acute myelogenous leukemia (AML), more sensitive to a variety of established cancer therapeutics while making normal tissues more resistant to the toxic effects of these agents.

Detailed Description

This clinical trial is designed to assess the ability of cenersen sodium (EL625) in combination with Idarubicin alone or with Cytarabine to either: (1) induce remissions in patients who have previously failed to go into remission in response to chemotherapy; or (2) provide patents who have relapsed after going into a chemotherapy-induced remission with a longer remission.

Cenersen sodium is one of a new class of drugs called antisense oligonucleotides (oligos). Oligos are designed to block the production of specific proteins and thereby inhibit their function. Cenersen sodium targets p53, a widely studied protein.

In cancer, p53 occurs either in the un-mutated ("normal") or mutated forms. The majority of participants in this trial are expected to have un-mutated p53. Cenersen sodium is anticipated to sensitize cancers with un-mutated p53 to most established cancer therapeutics.

p53 has a pivotal role in protecting the body from cells that have suffered genetic damage and, as a result, do not function properly. The protein first senses the level of the damage and then forces the damaged cell to respond to the damage either by repairing itself or committing suicide. In general, the greater the level of damage the more likely the cellular response will be suicide.

Many cancer therapeutics, including both chemotherapy and radiation, cause the types of genetic damage that activate p53 and, consequently, cause either damage repair or cellular suicide. Laboratory studies suggest that cancer cells have a host of defenses that reduce the chances that these cells will respond to genetic damage by committing suicide. So compared to normal cells, cancer cells are more likely to repair the damage caused by cancer therapeutics while normal cells are more likely to commit suicide. Thus, blocking un-mutated p53 is more likely to prevent repair in cancer cells while preventing suicide in normal cells. This provides the basis for a differential effect of cenersen sodium on cancer cells verses normal cells.

When p53-dependent repair is prevented in cancer cells they begin to copy their damaged genetic information in preparation for cell division. This copying of the genetic damage triggers a p53-independent backup suicide mechanism and, as a result, the cancer cells are eliminated. This is the presumed mechanism whereby cenersen sodium is able to sensitize cancer cells with normal p53 function to numerous cancer therapeutics.

At higher doses however, chemotherapy sometimes blocks cells from copying their genes in preparation for division. Thus, it is possible that a chemotherapeutic agent used at a high dose could block any sensitizing effect that cenersen sodium might otherwise have on the cancer.

The chemotherapeutic agent Idarubicin is known to produce the type of genetic damage that effects p53 expression, causes p53-dependent responses and has been shown to be made more effective at killing cancer cells by cenersen sodium. Cytarabine (Ara-C) is the most widely used chemotherapeutic agent for AML. Cenersen sodium does not appear to sensitize cancer cells to Cytarabine and at higher doses Cytarabine may reduce the capacity of cenersen sodium to sensitize cancer cells.

Hence, this AML study will examine the effects of Cenersen sodium used in combination with Idarubicin and one of three different doses of Cytarabine (i.e. 0, 0.1 and 1.0 gm/m2/day), on the responsiveness of participants to these chemotherapeutic agents.

Recruitment & Eligibility

Status
COMPLETED
Sex
All
Target Recruitment
53
Inclusion Criteria

Not provided

Exclusion Criteria
  • Subjects with M3 AML.
  • Subjects receiving other anti-leukemia investigational agents (i.e., unapproved drugs). However, individual cases will be considered on a case-by-case basis for other investigational agents (e.g., antibiotics, antifungals).
  • Pregnant or lactating subjects. Chemotherapy (including hydroxyurea) within three (3) weeks prior to initiation of therapy, unless there is evidence of rapidly progressive disease; then subjects may be enrolled with a minimum of two (2) weeks from previous treatments.

Prohibited Medications during the first week of each course:

  • Acetaminophen
  • Hi-Dose antioxidants (e.g., Vitamins C, E; Multivitamins)

Study & Design

Study Type
INTERVENTIONAL
Study Design
SINGLE_GROUP
Arm && Interventions
GroupInterventionDescription
cenersen, idarubicin, HDACCytarabinecenersen, idarubicin, HDAC (high dose cytarabine)
cenersen, idarubicincenersencenersen, idarubicin, no cytarabine
cenersen, idarubicinIdarubicincenersen, idarubicin, no cytarabine
cenersen, idarubicin, cytarabinecenersencenersen, idarubicin, standard dose cytarabine
cenersen, idarubicin, cytarabineIdarubicincenersen, idarubicin, standard dose cytarabine
cenersen, idarubicin, cytarabineCytarabinecenersen, idarubicin, standard dose cytarabine
cenersen, idarubicin, HDACcenersencenersen, idarubicin, HDAC (high dose cytarabine)
cenersen, idarubicin, HDACIdarubicincenersen, idarubicin, HDAC (high dose cytarabine)
Primary Outcome Measures
NameTimeMethod
Determine the effective dose of Cytarabine chemotherapy to be used in combination with EL625 and Idarubicin.6 months

Cenersen plus standard of care

Secondary Outcome Measures
NameTimeMethod
Determine the safety profile for the combination of EL625 and Idarubicin +/- Cytarabine.6 months

Standard of care plus cenersen

Determine the Complete Response Rate and Time to Progression.6 months

Standard of care plus cenersen

Trial Locations

Locations (6)

University of California, San Diego

🇺🇸

La Jolla, California, United States

University of Miami Health Center

🇺🇸

Miami, Florida, United States

North Shore University Hospital

🇺🇸

Lake Success, New York, United States

Washington University Medical Center (Siteman Cancer Center)

🇺🇸

St. Louis, Missouri, United States

M. D. Anderson Cancer Center

🇺🇸

Houston, Texas, United States

Roswell Park Cancer Institute

🇺🇸

Buffalo, New York, United States

© Copyright 2025. All Rights Reserved by MedPath