Reports this week that Pfizer intends to shelve the development of its oral PCSK9 inhibitor suggest the future of this therapy may remain in injectables.
In its Q2 earnings report earlier this week Pfizer President Mikael Dolston said: “We don’t think that the oral PCSK9 profile would be competitive with the strong LDL lowering seen with PCSK9 antibodies, observed in many phase 3 trials.”
In a session today on Novel therapies in atherosclerosis Associate Professor David Sullivan from the Department of Clinical Biochemistry at the Royal Prince Alfred Hospital in Sydney said oral drugs were usually preferred by patients; however, some trials in PCSK9 inhibitors had come up with some “interesting observations”.
For instance, some patients had expressed a preference to injectables, including indigenous cultures who believed injections to be a “stronger therapy”.
Injections also offered useful dosing regiments to address CVD survival gap in mental health patients, he said.
PCSK9 antibodies required less frequent dosing, compared to something like insulin, meaning this may be less of a problem with these sorts of agents, he said.
“I think the trend is going to be towards a decrease in injection frequency and therefore it would become an extremely convenient treatment – not unlike some of the osteoporotic treatments, Dr Sullivan told delegates.
“At the moment there are still a few logistic issues with the injections as they exist at the moment – they are very viscous, and they are still a reasonable volume”.
“I think at the moment there would have been a place for such an oral agent now, but by the time they [Pfizer] developed it there wouldn’t be,” he added.
He concluded that cardiology clinics in Australia will likely use PCSK9 antibodies according to the following adverbs: sparingly, economically, safely and optimistically.
“There’s a good case that they will be largely used in combination and they might need to be used as a last resort,” he added.
The PBAC recommend the listing of the PCSK9 inhibitor for the homozygous familial hypercholesterolaemia population (but not the heterozygous FH population). The restriction includes the requirement for a diagnosis defined by either a score of 7 or more in the Dutch Lipid Clinic criteria or by genetic test prior to treatment.