NCT00642031

A Phase I Study of Triciribine Phosphate Monohydrate (TCN-PM, VD-0002) in Adult Patients With Advanced Hematologic Malignancies

Completed Phase 1 Last updated 6 August 2016

What this trial tests

Phase 1 trial testing Triciribine in Hematologic Malignancies in 20 participants. Completed in 1 October 2012.

Timeline

1 August 2006

Primary endpoint
1 October 2012

1 October 2012

Quick facts

Lead sponsor	Prescient Therapeutics, Ltd.
Phase	Phase 1
Status	Completed
Study type	INTERVENTIONAL
Allocation	na
Design	single group
Masking	none
Primary purpose	treatment
Enrollment	20
Start date	1 August 2006
Primary completion	1 October 2012
Estimated completion	1 October 2012
Sites	2 locations across United States

Drugs / interventions tested

• Triciribine — full drug profile →

Conditions studied

• Hematologic Malignancies — all drugs for Hematologic Malignancies →
• Leukemia — all drugs for Leukemia →

Sponsor

Prescient Therapeutics, Ltd. — full company profile →

Who can join

Eligibility, any sex, with Hematologic Malignancies or Leukemia. Patients with the condition only — healthy volunteers not accepted.

What's being measured

Primary outcomes are the specific endpoints the trial is designed to prove or disprove.

• Maximum tolerated dose (MTD) of TCN-PM (Triciribine)
  Time frame: 28 day cycle
  The MTD is the highest dose level in which \<2 patients of 6 develop first cycle dose-limiting toxicity (DLT). Evaluations after each dose level (28 day cycle).

Sponsor's own description

Primary objective:

To determine the dose limiting toxicity (DLT) and maximum tolerated dose (MTD) of TCN-PM (Triciribine) when administered as an approximately one-hour intravenous infusion on a weekly schedule on days 1, 8 and 15 in a 28 day cycle in patients with advanced hematologic malignancies;

To determine the pharmacokinetics (PK) of Triciribine following study drug administration.

Secondary objective:

To observe the anti-tumor effects of Triciribine, if any occur

Publications & conference data

7 peer-reviewed publications reference this trial (live from Europe PMC):

1. Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: how mutations can result in therapy resistance and how to overcome resistance.
   McCubrey JA, Steelman LS, Chappell WH, Abrams SL, et al · · 2012 · cited 242× · PMID 23085539 · DOI 10.18632/oncotarget.659
2. Role of the PI3K/AKT and mTOR signaling pathways in acute myeloid leukemia.
   Park S, Chapuis N, Tamburini J, Bardet V, et al · · 2010 · cited 229× · PMID 19951971 · DOI 10.3324/haematol.2009.013797
3. Maximising the potential of AKT inhibitors as anti-cancer treatments.
   Brown JS, Banerji U. · · 2017 · cited 184× · PMID 27919797 · DOI 10.1016/j.pharmthera.2016.12.001
4. Concise Review: Chronic Myeloid Leukemia: Stem Cell Niche and Response to Pharmacologic Treatment.
   Arrigoni E, Del Re M, Galimberti S, Restante G, et al · · 2018 · cited 52× · PMID 29418079 · DOI 10.1002/sctm.17-0175
5. Therapeutic Modulation of Autophagy in Leukaemia and Lymphoma.
   Djavaheri-Mergny M, Giuriato S, Tschan MP, Humbert M. · · 2019 · cited 34× · PMID 30704144 · DOI 10.3390/cells8020103
6. Phase I clinical, pharmacokinetic, and pharmacodynamic study of the Akt-inhibitor triciribine phosphate monohydrate in patients with advanced hematologic malignancies.
   Sampath D, Malik A, Plunkett W, Nowak B, et al · · 2013 · cited 33× · PMID 23993427 · DOI 10.1016/j.leukres.2013.07.034
7. Molecular targeted approaches in mantle cell lymphoma.
   Weniger MA, Wiestner A. · · 2011 · cited 16× · PMID 21782064 · DOI 10.1053/j.seminhematol.2011.05.001