Promising data on MEK162 in an ongoing Phase 2 trial of patients with
BRAF and NRAS mutated advanced melanoma was presented today at the
American Society of Clinical Oncology (ASCO) Annual Meeting in Chicago,
Illinois. MEK162, a small molecule selective inhibitor of the kinases
MEK1 and MEK2, showed clinical activity and good tolerability in this
patient population. This is the first targeted therapy to show activity
in patients with NRAS mutated melanoma.
Array BioPharma Inc. (NASDAQ: ARRY) invented MEK162 and licensed
worldwide rights to develop and commercialize MEK162 to Novartis in
April 2010. The ongoing Phase 2 open-label trial is being conducted by
Novartis and continues to enroll patients.
Since February 2012, the study has shown that, of the 35 patients with
BRAF mutations evaluable for response, eight had partial responses,
including two confirmed partial responses and 13 patients demonstrated
stable disease. The disease control rate was 60 percent among these
patients with at least two scans. Of the 28 patients with NRAS mutations
who were evaluable for response, six had partial responses, including
three confirmed partial responses and 13 patients demonstrated stable
disease. The disease control rate was 68 percent among these patients
with at least two scans. The median progression-free survival was 3.55
months [95% CI 2.00 - 3.81 months] for patients with BRAF mutation and
3.65 months [95% CI 2.53 - 5.39 months] for patients with NRAS mutations.
Common adverse events of all grades were consistent with data reported
for the MEK inhibitor class and included rash, diarrhea, acneiform
dermatitis, edema, creatine phosphokinase elevation, central serous
retinopathy-like events, nausea, and fatigue.
"Significant treatment progress has been achieved for patients with
advanced melanoma, particularly those with BRAF mutations, over the past
few years," said Paolo A. Ascierto, MD, Director of the Unit of Medical
Oncology and Innovative Therapy, National Tumor Institute Fondazione G.
Pascale. "However, for patients with NRAS mutations, no targeted
treatment has been available and prognosis is poor. MEK162 has shown for
the first time efficacy in the NRAS mutated melanoma population. This is
another important brick in the wall we are building to stop melanoma."
In conclusion, MEK162, the first targeted therapy to show activity in
patients with NRAS mutant melanoma, showed clinical activity and good
tolerability in patients with BRAF and NRAS mutated advanced melanoma.
Novartis is evaluating the development options of MEK162 in melanoma.