Ark Therapeutics has withdrawn the MAA for its lead gene-based treatment for operable malignant glioma, Cerepro®. The move follows a request by the EMEA’s Scientific Advisory Group on Oncology (SAG-O) for an additional clinical trial with the treatment.
Ark says that it is now reviewing its portfolio of assets and has initiated discussions with a number of parties that might lead to a takeover bid. The firm stressed that an offer is by no means a certainty, and it is considering alternative strategies and options to optimize shareholder value.
The SAG-O’s re-evaluation of the Cerepro marketing application concluded that existing trial data did not provide sufficiently reliable evidence of a clinical benefit. In particular, concerns related to the lack of standardized decision-making with respect to re-intervention following tumor recurrence. This meant that data on the primary endpoint could not be considered reliable, despite the use of a blinded re-intervention committee and the Phase III data showing no evidence of bias on all available re-intervention related study measurements, the company notes.
“We are naturally disappointed with this news,” comments Nigel Parker, Ark’s CEO. “Whilst there are differences of opnion concerning the data relating to the re-intervention endpoint, we are in a unique position, with all the barriers in relation to approval of the gene medicine components of Cerepro behind us, and the recommendation for a further trial to resolve outstanding concerns is the logical way forward to secure marketing approval.”
The MAA application for Cerepro was filed in November 2008 and underwent formal review via the centralized procedure. The European Committee for Medicinal Products for Human Use (CHMP) adopted a negative opinion on the MAA in December 2009. In February Ark filed documentation with the EMEA relating to its request for re-examination of the MAA.
In January Ark confirmed it was reprioritizing its product development programs and would cut jobs to preserve cash. Pipeline reprioritization included the decision to put further Phase III development of its cancer cachexia drug candidate, Vitor™, on hold, while continuing with Phase III development of Trinam®, a gene-based therapy to prevent blood-vessel blocking in kidney dialysis patients who have undergone vascular access graft surgery.
The firm also aimed to push on with taking its key preclinical programs into Phase I/IIa development. These include EG011 in refractory angina, EG016 in peripheral vascular disease, and EG013 in fetal growth retardation.