Pfizer Inc. (NYSE:PFE) today announced the publication of the detailed results from PALOMA-1, a randomized Phase 2 study of palbociclib in combination with letrozole versus letrozole alone, in The Lancet Oncology.
As previously disclosed, PALOMA-1 achieved its primary endpoint with the combination of palbociclib and letrozole significantly prolonging progression-free survival (PFS) compared with letrozole alone in post-menopausal women with estrogen receptor positive (ER+), human epidermal growth factor receptor 2 negative (HER2-) locally advanced or metastatic breast cancer.
A New Drug Application (NDA) for palbociclib was accepted for filing and granted Priority Review by the United States Food and Drug Administration (FDA). This NDA is based on the final results of PALOMA-1. The Prescription Drug User Fee Act (PDUFA) goal date for a decision by the FDA is April 13, 2015. IBRANCETM is the proposed trade name for palbociclib.
“The publication of the PALOMA-1 data in The Lancet Oncology marks another important milestone in the path to bring IBRANCETM, the proposed trade name for palbociclib, to women with ER+, HER2- metastatic breast cancer, who haven’t seen a first-line treatment advance in more than 10 years,” said Dr. Mace Rothenberg, Senior Vice President of Clinical Development and Medical Affairs and Chief Medical Officer for Pfizer Oncology.
Results from PALOMA-1 were presented by lead author Dr. Richard Finn at the American Association for Cancer Research (AACR) Annual Meeting 2014. PALOMA-1 was conducted in collaboration with the Jonsson Comprehensive Cancer Center’s Revlon/UCLA Women’s Cancer Research Program, led by Dr. Dennis Slamon.
For more information on clinical trials of palbociclib in breast cancer and other tumor types, please visitwww.clinicaltrials.govExternal Links icon.
About IBRANCETM (palbociclib)
IBRANCETM, the proposed trade name for palbociclib, is not approved for any indication in any market. Palbociclib is an investigational oral targeted agent that selectively inhibits cyclin-dependent kinases (CDKs) 4 and 6 to regain cell cycle control and block tumor cell proliferation.1
Loss of cell cycle control is a hallmark of cancer and CDK 4/6 are overactivated in numerous cancers, leading to loss of proliferative control.2,3CDK 4/6 are key regulators of the cell cycle that trigger cellular progression from growth phase (G1) into phases associated with DNA replication (S).4,5 CDK 4/6, whose increased activity is frequent in estrogen receptor-positive (ER+) breast cancer (BC), are key downstream targets of ER signaling in ER+ BC.6,7 Preclinical data suggest that dual inhibition of CDK 4/6 and ER signaling is synergistic, and it has been shown to stop growth of ER+ BC cell lines in the G1 phase.