International study confirms a more effective treatment is available for women with advanced HER2-positive breast cancer
Updated results from a pivotal study, CLEOPATRA, demonstrate that adding Perjeta® (pertuzumab) to the current standard
treatment of advanced HER2-positive breast cancer, Herceptin® (trastuzumab) and chemotherapy, extends patients’ average
survival by almost 16 months. The results were presented at the European Society for Medical Oncology (ESMO) meeting.1
Roche Products New Zealand General Manager, Lance Baldo M.D., commented, “It is timely and exciting to be able to
present these updated data on Perjeta during Breast Cancer Awareness Month. HER2-positive breast cancer is an aggressive
form of the disease. While it is reassuring to know that women in New Zealand are surviving their cancer for longer,
there remains a recognised need for more effective treatments, as highlighted in recent data from the Auckland Breast
• Final data from the Phase III CLEOPATRA study showed that patients with previously untreated advanced
HER2-positive breast cancer who received Perjeta, Herceptin and docetaxel chemotherapy lived an average of 15.7 months
longer than those who received Herceptin and chemotherapy (56.5 months compared to 40.8 months).1
• The average length of survival of almost five years is the longest observed to date in patients with advanced
HER2-positive breast cancer. 1
• The results confirm that for women diagnosed with advanced HER2 positive breast cancer, a more effective
treatment is available which can significantly and meaningfully extend their lives.1
“Adding Perjeta to treatment with Herceptin and chemotherapy resulted in the longest survival observed to date in a
clinical study of people with HER2-positive advanced breast cancer,” said Sandra Horning, M.D., Roche’s Chief Medical
Officer and Head, Global Product Development. “The median survival of nearly five years for women who received the
Perjeta regimen is 15.7 months longer than for people who received Herceptin and chemotherapy alone, a magnitude of
improvement we rarely see in clinical trials in advanced cancer.”
Perjeta in combination with Herceptin and docetaxel chemotherapy is licensed in New Zealand for patients with previously
untreated advanced HER2-positive breast cancer.3 Perjeta is not funded by PHARMAC which means patients seeking access
will have to pay for their treatment. An application for funding has been made to PHARMAC.
About the CLEOPATRA Study4
CLEOPATRA (CLinical Evaluation Of Pertuzumab And TRAstuzumab) was an international, Phase III, randomised, double-blind,
placebo-controlled study. The study compared the combination of Perjeta, Herceptin and docetaxel chemotherapy with
placebo, Herceptin and chemotherapy in 808 patients with previously untreated advanced HER2-positive breast cancer, or
with advanced HER2-positive breast cancer that had come back after prior therapy for early breast cancer.
The final results showed:1
• The risk of death was reduced by 32 percent for patients who received the Perjeta regimen compared to those who
received Herceptin and chemotherapy, resulting in a 15.7 month improvement in survival.
• The average time before the cancer got worse was also improved in patients who received Perjeta; 18.7 months
compared to 12.4 months for those who received Herceptin and chemotherapy, a 6.3 month improvement.
• The most common side effects seen in patients who received Perjeta were diarrhoea, rash, mucosal inflammation,
headache, upper respiratory tract infection, itching, low white blood cell count with fever, dry skin and muscle spasms.
• The most common severe side effects were low white blood cell count, low white blood cell count with fever and a
decrease in a certain type of white blood cells.
Perjeta is a medicine that targets the HER2 receptor, a protein found on the outside of many normal cells and in high
quantities on the outside of cancer cells in HER2-positive cancers. Perjeta is designed specifically to prevent the HER2
receptor from pairing (or “dimerising”) with other HER receptors (EGFR/HER1, HER3 and HER4) on the surface of cells, a
process that is believed to play a role in tumour growth and survival. Binding of Perjeta to HER2 may also signal the
body’s immune system to destroy the cancer cells. The mechanisms of action of Perjeta and Herceptin are believed to
complement each other, as both bind to the HER2 receptor, but to different places. The combination of Perjeta and
Herceptin is thought to provide a more comprehensive blockade of HER signaling pathways. 5,6
About Roche’s medicines for HER2-positive breast cancer
Roche has been leading research into the HER2 pathway for over 30 years and is committed to improving the health,
quality of life and survival for patients with both early and advanced HER2-positive disease.
Roche has developed three innovative medicines that have helped transform the treatment of HER2-positive breast cancer:
Herceptin, Perjeta and Kadcyla® (trastuzumab emtansine). HER2-positive breast cancer is a particularly aggressive form
of the disease that affects approximately 20 percent of patients.7 Over the past 15 years, the outlook for patients with
HER2-positive disease has improved to the extent that patients with the disease, treated with these innovative
medicines, now typically experience better outcomes than those patients with the less aggressive HER2-negative disease.8
1.) Swain S. et al. Final overall survival (OS) analysis from the CLEOPATRA study of first-line (1L) pertuzumab (Ptz),
trastuzumab (T), and docetaxel (D) in patients (pts) with HER2-positive metastatic breast cancer (MBC). European Society
for Medical Oncology 2014, abstract #350O_PR
3) Perjeta Data Sheet 26 September 2013. www.medsafe.govt.nz
4.) F. Hoffmann-La Roche. ClinicalTrials.gov NCT00567190. National Library of Medicine. Available at: http://clinicaltrials.gov/ct2/show/NCT00567190
5. Franklin MC, Carey KD, Vaidos FF, et al. Insights into ErbB signaling from the structure of the ErbB2-pertuzumab
complex.Cancer Cell, 2004; 5:317–328.
6. Baselga J and Swain SM. Novel anticancer targets: revisiting ERBB2 and discovering ERBB3. Nat Rev Cancer, 2009;
7.) Wolff A.C. et al. Arch Pathol Lab Med 2007; 131:18-34
8.) Dawood S. et al. J Clin Oncol 2010; 28:92