Mechanism Of Action of Palbociclib & PFS Benefit



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A Phase II Randomized Controlled Trial of Palbociclib & Tamoxifen/Fulvestrant in Postmenopausal Women and Men With Hormone-Receptor Positive, HER2- Negative Metastatic Breast Cancer (MBC) Protocol Chair: Vered Stearns, M.D. Co-investigators: Ciara O Sullivan, M.D. Ben Ho Park, M.D, Ph.D Akhilesh Pandey, M.D, Ph. D Biostatistics: Zhe Zhang, M.S

Background Despite new targeted therapies, approx. 40,000 women will die of MBC in the US in 2014 75% of MBC is hormone receptor (HR)-positive (ER+ and/or PR+) Endocrine therapy (ET) is cornerstone of treatment, but all pts progress & few cured due to development endocrine resistance. 35-40% patients have HR+HER2- disease & are not eligible for HER2-directed therapies. Renewed interest in combining chemo/experimental therapies with ET to overcome endocrine resistance & expand treatment options Recent strategies: addition of mtor inhibitors and cyclin-dependent kinase 4/6 inhibitors (CDK4/6i), e.g. palbociclib

Mechanism Of Action of Palbociclib & PFS Benefit Doubling of PFS noted in PALOMA-1 trial (Palbociclib & letrozole vs. letrozole alone): 20.2 months vs.10.2 months Minimal toxicity

Study Hypothesis Eligible patients with HR-positive, HER2- negative MBC treated with palbociclib and tamoxifen/fulvestrant have a significant improvement in PFS vs. patients treated with tamoxifen /fulvestrant alone. The presence/absence of ER mutations may be a predictive biomarker of response to treatment.

Study Schema

Study Objectives Primary Compare PFS in postmenopausal women and men with ERpositive, HER2-negative MBC treated with tamoxifen /fulvestrant and palbociclib vs. tamoxifen /fulvestrant alone in pts who have progressed on at least one line of endocrine therapy in the metastatic setting Secondary Compare measures of disease control, including response rate (RR), and clinical benefit rate (CBR) between treatment arms. Compare safety and tolerability between treatment arms

Correlative Objectives Exploratory Prospectively follow plasma tumor DNA levels in patients Describe alterations in genes and gene products relevant to the cell cycle, drug targets, tumor sensitivity and resistance Aim to identify several pathway markers that are predictive of response to CDK4/6 inhibition, considering variables such as ER mutational status, ER- positivity and phosphoproteomics.

Correlates New/fresh biopsies of metastatic site Baseline/Pre-treatment for confirmation of ER+HER2- MBC Surgical specimen Study bloods Pharmacogenomics (optional) ptdna levels (baseline, after every 2 cycles (i.e. 8 week intervals) PKs (1 and 2 hours post-dose on day 1, pre-dose weeks 4/7/10) Imaging All patients must receive restaging CT CAP every 2 cycles (i.e.8 week intervals)

Inclusion Criteria Postmenopausal females & men Stage IV breast cancer ER and/or PR-positive Evaluable/measurable disease by RECIST 1.1 ECOG 0-2 Progressed on at least one line of prior ET in the metastatic setting Use adjuvant TAM/ aromatase inibitor permitted (stopped >6 months prior to devt MBC) Adequate end organ function CNS mets allowed if treated 4 wks from starting study drug & have recovered from toxicities Disease free of invasive malignancies 5 years (except BCC/ SCC skin or CIN) Bisphosphonates allowed if started before trial entry If baseline biopsy cannot be obtained, pt is still eligible for trial

Exclusion Criteria Concurrent CYP2D6 inhibitors (moderate/strong)* Inhibitors/inducers of CYP3A4 Medications that prolong QTc Medical/Psych comorbidities affecting compliance or posing increased risk to pt Other current experimental therapy Uncontrolled intercurrent illness Pts developing MBC within 6 months of adjuvant tx Pts who have had more than one line of prior treatment for MBC (chemo,hormones, experimental therapy).

Statistical Plan & Study Design Non-blinded, randomized phase II study 3:1 randomization to palbociclib and tamoxifen/fulvestrant vs. tamoxifen/fulvestrant alone (n=100; 70-80 pts P & T, 20-30 pts T ) 28 day cycle - Tamoxifen 20mg orally daily / Fulvestrant 500mg loading dose, then 250mg I.M monthly - Palbociclib 125mg orally days 1-21, then 7 days off Patients on tamoxifen/fulvestrant alone arm can cross over to palbociclib at progression

Significance The combination of palbociclib and letrozole has already shown to double PFS in patients with HR-positive, HER2-negative MBC who have already progressed on one prior line of ET. Therefore, CDK4/6 inhibitors are very promising agents in the treatment of this subgroup of patients given these impressive results and the favorable toxicity profile. This trial will evaluate the efficacy of other ET/palbociclib combinations in this setting and aim to identify predictive biomarkers of treatment response.