In draft guidance, NICE fails to back Clovis's PARP inhibitor Rubraca
Despite the EMA’s endorsement of Clovis’s cancer treatment Rubraca last year, the UK’s cost-effectiveness watchdog NICE has recommended against the adoption of the drug in the National Health Service (NHS).
Rubraca is approved for use in the EU as monotherapy for the maintenance treatment of adult patients with high-grade epithelial ovarian, fallopian tube, or primary peritoneal cancer who have relapsed after platinum-based chemotherapy. The drug was originally developed at Newcastle University, with a team involving researchers from the Northern Institute for Cancer Research and Cancer Research UK-funded scientists. It generated second-quarter sales of $33 million globally.
In its draft guidance, NICE suggested that while Rubraca extends the time until cancer progresses compared with routine care — the magnitude of this benefit is uncertain because mature trial data are not available yet.
In addition, the agency said its cost-effectiveness estimates surpass what NICE typically considers acceptable.
Rubraca is one of three approved poly-ADP ribose polymerase (PARP) inhibitors. PARP is a protein used by damaged cells to initiate repair, and PARP inhibitors — including Rubraca, AstraZeneca’s $AZN Lynparza and GSK’s $GSK Zejula — are engineered to prevent cancer cells from repairing themselves, thereby catalyzing their destruction.
Last month, NICE backed the use of Zejula in the same patient group as a maintenance treatment as well as adopting Lynparza in patients that carry the BRCA mutation.
When NICE compared the use of Rubraca versus Lynparza in BRCA patients who had undergone three lines of platinum-based chemotherapy — the analysis suggested Rubraca cost more and worked equally as well as Lynparza, the agency said.
NICE consultees have until August 27 to comment on the draft recommendations. Endpoints News has contacted Clovis for comment.
So far, PARP inhibitors have been primarily used in ovarian cancers containing BRCA mutations, but trial data show they sometimes work in a broader group of patients. This could be because while the assault on DNA repair is being waged, these drugs are also attacking ribosomes — the machinery that makes proteins, scientists theorized in the journal Molecular Cell last month.