This site is operated by a business or businesses owned by Informa PLC and all copyright resides with them. Informa PLC's registered office is 5 Howick Place, London SW1P 1WG. Registered in England and Wales. Number 8860726.

13 Sep 2013

Amgen Highlights Data To Be Presented At 2013 European Cancer Congress

Amgen has announced that it will present new data from studies of marketed and pipeline products at the 17th ECCO — 38th ESMO — 32nd ESTRO European Cancer Congress happening 27 September to 1 October in Amsterdam.

"Amgen's continued focus on growth through innovation is highlighted by the data that we are presenting at the European Cancer Congress this year," said Sean E. Harper, MD, executive vice president of Research and Development at Amgen. "We are successfully advancing our pipeline, and using cutting-edge science to better understand each cancer's unique fingerprint and provide individualised care for patients."

Abstracts are available on the European Cancer Congress website at

Data presented on talimogene laherparepvec will include

• Secondary Endpoints from OPTiM: A Multicenter, Randomized Phase III Trial of Talimogene Laherparepvec versus GM-CSF for the Treatment of Unresected Stage IIIB/C and IV Melanoma
Abstract 3733 / P479, Poster Session, Monday, 30 September, 9:30–12:00 CEST (Hall 4)

Data presented on trebananib will include

• A Phase III, Randomised, Double-Blind Trial of Weekly Paclitaxel Plus the Angiopoietin 1 and 2 Inhibitor, Trebananib, or Placebo in Women With Recurrent Ovarian Cancer: TRINOVA-1
Abstract 41, Late Breaking Abstract, Proffered Papers Session, Tuesday, 1 October, 10:53–11:05 CEST (Hall 7.2)

Data presented on Vectibix (panitumumab) will include

• ASPECCT: A Randomised, Multicenter, Open-Label, Phase III Study of Panitumumab versus Cetuximab for Previously Treated Wild-Type KRAS Metastatic Colorectal Cancer
Abstract 18, Late Breaking Abstract, Proffered Papers Session, Saturday, 28 September, 12:47–14:10 CEST (RAI Auditorium)

• Tumor Genetic Analysis of PRIME: KRAS, NRAS, and BRAF Mutations as Predictive Biomarkers in Patients with Metastatic Colorectal Cancer Receiving First-Line Treatment With Panitumumab Plus FOLFOX4
Abstract 2275 / P157, Poster Session, Sunday, 29 September 14:00–16:30 CEST (Hall 4)

• Updated Overall Survival Analysis of Novel Predictive KRAS/NRAS Mutations Beyond KRAS Exon 2 in PEAK: A First-Line Phase II Study of FOLFOX6 plus Panitumumab or Bevacizumab in Metastatic Colorectal Cancer
Abstract 2262 / P144, Poster Session, Sunday, 29 September, 14:00–16:30 CEST (Hall 4)

About Talimogene Laherparepvec

Talimogene laherparepvec is an investigational oncolytic immunotherapy designed to selectively replicate in tumour tissue. Talimogene laherparepvec is injected directly into tumor tissue and then replicates until the membrane of the cancer cells rupture, thereby destroying the cells, in a process known as cell lysis. The virus that was contained in these cells is then released locally in the tumour tissue along with potential tumor antigens and GM-CSF, a white blood cell growth factor that the virus is engineered to express. This is intended to lead to the activation of a systemic immune response to kill tumor cells throughout the body.

About Trebananib

Trebananib is an investigational peptibody designed to inhibit the angiopoietin axis. The angiopoietin axis is involved in angiogenesis, a process used by the body to grow new blood vessels, which is also involved in the pathogenesis of several diseases including cancer. Trebananib is designed to bind to both angiopoietin-1 and -2 (Ang1 and Ang2), and is intended to inhibit their interaction with the Tie2 receptor.1–3 Ang1 and Ang2 each mediate separate actions upon binding with Tie2.4,5 Ang1 impacts vessel quality while Ang2 influences vessel quantity. The angiopoietins are also involved in lymphangiogenesis, the formation of new lymphatic vessels, which plays a key role in tumor metastasis.6

About Vectibix

Vectibix is the first fully human anti-EGFR antibody approved by FDA for the treatment of metastatic colorectal cancer (mCRC). Vectibix was approved in the US in September 2006 as a monotherapy for the treatment of patients with EGFR-expressing mCRC after disease progression on or following fluoropyrimidine-, oxaliplatin-, and irinotecan-containing chemotherapy regimens.

The effectiveness of Vectibix as a single agent for the treatment of EGFR-expressing mCRC is based on progression-free survival. Currently no data are available that demonstrate an improvement in disease-related symptoms or increased survival with Vectibix.

Vectibix is not indicated for the treatment of patients with KRAS mutation-positive mCRC or for whom KRAS mCRC status is unknown. Vectibix in combination with oxaliplatin-based chemotherapy is not indicated for the treatment of patients with RAS (KRAS or NRAS) mutation-positive mCRC or for whom RAS status is unknown.

In December 2007, the European Medicine Agency (EMA) granted a conditional marketing authorization for Vectibix as a monotherapy for the treatment of patients with EGFR-expressing mCRC with non-mutated (wild-type) KRAS after failure of fluoropyrimidine-, oxaliplatin-, and irinotecan-containing chemotherapy regimens. In July 2013, the indication was updated to the following:

Vectibix is indicated for the treatment of adult patients with wild-type RAS mCRC:
• in first-line in combination with FOLFOX.
• in second-line in combination with FOLFIRI for patients who have received first-line fluoropyrimidine-based chemotherapy (excluding irinotecan). 
• as monotherapy after failure of fluoropyrimidine-, oxaliplatin-, and irinotecan-containing chemotherapy regimens.

Vectibix is approved in more than 50 countries worldwide.


Arvind Sood, 805-447-1060 (investors)

1.  Herbst R.S., Expert Opin Emerg Drugs. 2006;11:635-650.
2.  Carmeliet P., Jain R.K., Nature. 2000;407:249-257.
3.  Folkman J., Nat Rev Drug Discov. 2007;6:273-286.
4.  Falcon B.L., Hashizume H., Koumoutsakos P., et al., Am J Pathol. 2009;175:2159-2170.
5.  Ahmad S.A., Liu W., Jung Y.D., et al., Cancer Res. 2001;61:1255-1259. 
6.  Huang H., Bhat A., Woodnutt G., et al.,  Nat Rev Cancer. 2010;10:575-585.

Related News