NCT01536743

A Open Label Study of the Efficacy and Safety of PD0332991 a Selective Inhibitor of the Cyclin Dependent Kinases 4 and 6 in Patients With Recurrent Ovarian Cancer Demonstrating Rb-proficiency and Low p16 Expression

Completed Phase 2 Last updated 5 June 2020

What this trial tests

Phase 2 trial testing PD0332991 in Ovarian Epithelial Carcinoma in 26 participants. Completed in 24 February 2020.

Timeline

15 December 2011

Primary endpoint
24 February 2020

24 February 2020

Quick facts

Lead sponsor	Jonsson Comprehensive Cancer Center
Phase	Phase 2
Status	Completed
Study type	INTERVENTIONAL
Allocation	na
Design	single group
Masking	none
Primary purpose	treatment
Enrollment	26
Start date	15 December 2011
Primary completion	24 February 2020
Estimated completion	24 February 2020
Sites	1 location across United States

Drugs / interventions tested

• PD0332991 (pd0332991) — full drug profile →

Conditions studied

• Ovarian Epithelial Carcinoma — all drugs for Ovarian Epithelial Carcinoma →

Sponsor

Jonsson Comprehensive Cancer Center — full company profile →

Who can join

18 and older, female only, with Ovarian Epithelial Carcinoma. Patients with the condition only — healthy volunteers not accepted.

Sponsor's own description

The purpose of this study is to obtain an estimate of the biochemical response rate as determined by CA125 response using the Gynecologic Cancer Intergroup (GCIG) response criteria of PD0332991 in patients with recurrent ovarian epithelial carcinoma. CA125 response is defined as ≥ 50% decrease from the baseline CA125 level and confirmed ≥ 21 days after initial evaluation (baseline is defined as the higher value of 2 pre-treatment CA125 assessments).

Publications & conference data

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

1. Cyclin D1, cancer progression, and opportunities in cancer treatment.
   Qie S, Diehl JA. · · 2016 · cited 527× · PMID 27695879 · DOI 10.1007/s00109-016-1475-3
2. The Strange Case of CDK4/6 Inhibitors: Mechanisms, Resistance, and Combination Strategies.
   Knudsen ES, Witkiewicz AK. · · 2017 · cited 218× · PMID 28303264 · DOI 10.1016/j.trecan.2016.11.006
3. CDK4/6 inhibition promotes immune infiltration in ovarian cancer and synergizes with PD-1 blockade in a B cell-dependent manner.
   Zhang QF, Li J, Jiang K, Wang R, et al · · 2020 · cited 129× · PMID 32929370 · DOI 10.7150/thno.44871
4. Clinical potential of novel therapeutic targets in breast cancer: CDK4/6, Src, JAK/STAT, PARP, HDAC, and PI3K/AKT/mTOR pathways.
   Hosford SR, Miller TW. · · 2014 · cited 109× · PMID 25206307 · DOI 10.2147/pgpm.s52762
5. The application and prospect of CDK4/6 inhibitors in malignant solid tumors.
   Du Q, Guo X, Wang M, Li Y, et al · · 2020 · cited 105× · PMID 32357912 · DOI 10.1186/s13045-020-00880-8
6. Paradigm Shift: A Comprehensive Review of Ovarian Cancer Management in an Era of Advancements.
   Tavares V, Marques IS, Melo IG, Assis J, et al · · 2024 · cited 85× · PMID 38339123 · DOI 10.3390/ijms25031845
7. Biological functions of CDK5 and potential CDK5 targeted clinical treatments.
   Shupp A, Casimiro MC, Pestell RG. · · 2017 · cited 85× · PMID 28077789 · DOI 10.18632/oncotarget.14538
8. Intrinsic and acquired resistance to CDK4/6 inhibitors and potential overcoming strategies.
   Xu XQ, Pan XH, Wang TT, Wang J, et al · · 2021 · cited 54× · PMID 32504067 · DOI 10.1038/s41401-020-0416-4