Trial Outcomes & Findings for Study of RAD001 in Soft Tissue Extremity and/or Retroperitoneal Sarcomas (NCT NCT01048723)

NCT ID: NCT01048723

Last Updated: 2013-12-16

Results Overview

PD markers of RAD001 on downstream signaling pathways in patients with sarcomas: p70S6K, S6-RP, P-AKT, cleaved PARP and PCNA by Western blot, quantitative multiplex assays and immunohistochemical studies measured pre and post the 2 week treatment of RAD001. Patients were to be separated into two groups, responders and non responders based on PD results and downstream up regulation of the referenced pathways. Mean fractional inhibition of each PD marker for the responding and non-responding groups were to be calculated. Our planned analysis was for 40 participants.

Recruitment status

TERMINATED

Study phase

PHASE2

Target enrollment

2 participants

Primary outcome timeframe

Pre and post the 2 week treatment

Results posted on

2013-12-16

Participant Flow

40 patients were to be treated with RAD001 in a neoadjuvant pre-resection manner 10mg po daily x 2 weeks with resection of their extremity or retroperitoneal tumors within 2 weeks after the conclusion of therapy. All patients with resectable sarcomas by CT or MRI imaging without evidence of distant metastases would be eligible for the trial.

The sarcomas must be amenable to percutaneous needle core biopsy prior to initiation of RAD001 therapy.

Participant milestones

Participant milestones
Measure
RAD001 Administration
RAD001 was administered orally as once daily dose of 10 mg PO daily x 2 weeks (14 X 10 mg tablets) continuously from study day 1 until the end of therapy (2 weeks later) or unacceptable toxicity.
Overall Study
STARTED
2
Overall Study
COMPLETED
2
Overall Study
NOT COMPLETED
0

Reasons for withdrawal

Withdrawal data not reported

Baseline Characteristics

Study of RAD001 in Soft Tissue Extremity and/or Retroperitoneal Sarcomas

Baseline characteristics by cohort

Baseline characteristics by cohort
Measure
RAD001 Administration
n=2 Participants
RAD001 was administered orally as once daily dose of 10 mg PO daily x 2 weeks (14 X 10 mg tablets) continuously from study day 1 until the end of therapy (2 weeks later) or unacceptable toxicity.
Age, Categorical
<=18 years
0 Participants
n=5 Participants
Age, Categorical
Between 18 and 65 years
2 Participants
n=5 Participants
Age, Categorical
>=65 years
0 Participants
n=5 Participants
Sex: Female, Male
Female
0 Participants
n=5 Participants
Sex: Female, Male
Male
2 Participants
n=5 Participants
Region of Enrollment
United States
2 participants
n=5 Participants

PRIMARY outcome

Timeframe: Pre and post the 2 week treatment

PD markers of RAD001 on downstream signaling pathways in patients with sarcomas: p70S6K, S6-RP, P-AKT, cleaved PARP and PCNA by Western blot, quantitative multiplex assays and immunohistochemical studies measured pre and post the 2 week treatment of RAD001. Patients were to be separated into two groups, responders and non responders based on PD results and downstream up regulation of the referenced pathways. Mean fractional inhibition of each PD marker for the responding and non-responding groups were to be calculated. Our planned analysis was for 40 participants.

Outcome measures

Outcome data not reported

SECONDARY outcome

Timeframe: Post the 2 week treatment

Quantitative in vivo and ex vivo assessments of PD markers (p70S6K, S6-RP, P-AKT, cleaved PARP and PCNA) were to be normalized within the same sample. The extent of inhibition is defined as the fractional inhibition in each patient calculated as \[(PreRx normalized PD marker - PostRx normalized PD marker) / PreRx normalized PD marker\] x 100. Same definition would apply to each of these markers. Our planned analysis was for 40 participants.

Outcome measures

Outcome data not reported

SECONDARY outcome

Timeframe: Post the 2 week treatment

We planned to determine pathological response in terms of tumor necrosis and apoptosis assessed on the resected specimens after 2 weeks of RAD001 therapy. Percent necrosis was to be reported based on the routine H and E staining. In addition to cleaved PARP analysis, TUNEL assays were to be performed judging the amount of apoptosis in the specimens after treatment. Our planned analysis was for 40 participants.

Outcome measures

Outcome data not reported

SECONDARY outcome

Timeframe: Pre and Post the 2 week treatment

Memory CD8 T cell enhanced production as determined by fluorescence activated cell sorter (FACS) analysis on blood and tumor core biopsy specimens taken before and after therapy with RAD001. Our planned analysis was for 40 participants.

Outcome measures

Outcome data not reported

Adverse Events

RAD001 Administration

Serious events: 0 serious events
Other events: 2 other events
Deaths: 0 deaths

Serious adverse events

Adverse event data not reported

Other adverse events

Other adverse events
Measure
RAD001 Administration
n=2 participants at risk
RAD001 was administered orally as once daily dose of 10 mg PO daily x 2 weeks (14 X 10 mg tablets) continuously from study day 1 until the end of therapy (2 weeks later) or unacceptable toxicity.
Blood and lymphatic system disorders
Platelets
100.0%
2/2 • Number of events 2 • 1 year
Blood and lymphatic system disorders
Leukocytes (total WBC)
50.0%
1/2 • Number of events 1 • 1 year
Blood and lymphatic system disorders
Neutrophils/granulocytes (ANC/AGC)
50.0%
1/2 • Number of events 1 • 1 year
Ear and labyrinth disorders
Tinnitus
50.0%
1/2 • Number of events 1 • 1 year
General disorders
Fatigue
50.0%
1/2 • Number of events 1 • 1 year
Skin and subcutaneous tissue disorders
Rash
50.0%
1/2 • Number of events 1 • 1 year
Gastrointestinal disorders
Mucositis/stomatitis
50.0%
1/2 • Number of events 3 • 1 year
Metabolism and nutrition disorders
Creatinine
50.0%
1/2 • Number of events 1 • 1 year
Metabolism and nutrition disorders
Glucose, serum-high (hyperglycemia)
50.0%
1/2 • Number of events 1 • 1 year
Respiratory, thoracic and mediastinal disorders
Dyspnea (shortness of breath)
50.0%
1/2 • Number of events 1 • 1 year

Additional Information

Jonathan Zager, M.D.

H. Lee Moffitt Cancer Center and Research Institute

Phone: 813-745-1085

Results disclosure agreements

  • Principal investigator is a sponsor employee
  • Publication restrictions are in place