NCT01266954

An Open Label Study To Investigate the Pharmacokinetics and Pharmacodynamics of Repeat Escalating Doses of the Oral AKT Inhibitor GSK2141795 by 18F FDG PET Analysis in Subjects With Ovarian Cancer

Completed Phase 1 Last updated 9 November 2017

What this trial tests

Phase 1 trial testing GSK2141795 in Solid Tumours in 36 participants. Completed in 1 September 2011.

Timeline

1 June 2010

Primary endpoint
1 September 2011

1 September 2011

Quick facts

Lead sponsor	GlaxoSmithKline
Phase	Phase 1
Status	Completed
Study type	INTERVENTIONAL
Allocation	non randomized
Design	single group
Masking	none
Primary purpose	treatment
Enrollment	36
Start date	1 June 2010
Primary completion	1 September 2011
Estimated completion	1 September 2011
Sites	1 location across United Kingdom

Drugs / interventions tested

• GSK2141795 — full drug profile →

Conditions studied

• Solid Tumours — all drugs for Solid Tumours →

Sponsor

GlaxoSmithKline — full company profile →

Who can join

Adults 18 to 85, female only, with Solid Tumours. Patients with the condition only — healthy volunteers not accepted.

Sponsor's own description

The purpose of this study is to explore the potential dose response relationship between the pharmacokinetics of GSK2141795 and \[18F\] FDG PET pharmacodynamic markers of glucose metabolism in tumor tissue. Three to six subjects will be enrolled in each cohort and dosed with repeat escalating doses of GSK2141795. \[18F\] FDG PET imaging and optional tumor biopsies will be done prior to initiation of dosing and sequentially at select time points during the first five weeks of dosing. The maximal dose of a given schedule evaluated in this study will not exceed the maximal tolerated dose established in the first-time-in-human trial PCS112689 for the same schedule.

Publications & conference data

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

1. Role of PI3K/AKT pathway in cancer: the framework of malignant behavior.
   Jiang N, Dai Q, Su X, Fu J, et al · · 2020 · cited 419× · PMID 32333246 · DOI 10.1007/s11033-020-05435-1
2. 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
3. The Warburg effect: evolving interpretations of an established concept.
   Chen X, Qian Y, Wu S. · · 2015 · cited 177× · PMID 25277420 · DOI 10.1016/j.freeradbiomed.2014.08.027
4. PI3K-AKT-mTOR and NFκB Pathways in Ovarian Cancer: Implications for Targeted Therapeutics.
   Ghoneum A, Said N. · · 2019 · cited 118× · PMID 31284467 · DOI 10.3390/cancers11070949
5. Clear cell carcinoma of the ovary: molecular insights and future therapeutic perspectives.
   Mabuchi S, Sugiyama T, Kimura T. · · 2016 · cited 98× · PMID 27029752 · DOI 10.3802/jgo.2016.27.e31
6. Clinical implications of the interaction between PD-1/PD-L1 and PI3K/AKT/mTOR pathway in progression and treatment of non-small cell lung cancer.
   Quan Z, Yang Y, Zheng H, Zhan Y, et al · · 2022 · cited 81× · PMID 36313041 · DOI 10.7150/jca.77619
7. Targeting the PI3K/AKT/mTOR pathway in epithelial ovarian cancer, therapeutic treatment options for platinum-resistant ovarian cancer.
   Rinne N, Christie EL, Ardasheva A, Kwok CH, et al · · 2021 · cited 80× · PMID 35582310 · DOI 10.20517/cdr.2021.05
8. The Akt signaling pathway: an emerging therapeutic target in malignant melanoma.
   Madhunapantula SV, Mosca PJ, Robertson GP. · · 2011 · cited 68× · PMID 22157148 · DOI 10.4161/cbt.12.12.18442