Novartis' new blood pressure drug no better than the rest?
not be the blockbuster success Novartis hoped for after a new study
claims it is no more effective than current therapies.
Novartis' Tekturna (aliskiren) was only approved two months ago, having been developed in conjunction with Speedel. The drug is designed to reduce blood pressure by directly inhibiting a protein called renin. However, a review of six large clinical trials, published in the May issue of the Elsevier's American Journal of Hypertension, claims that because the body secretes more renin in response to the drug, its efficacy is limited. Novartis estimates that nearly 1bn people worldwide suffer from hypertension and the condition is uncontrolled in nearly 70 per cent of patients and so, although there are seven classes of drugs used to reduce high blood pressure, there is still a need for new therapies. When the US Food and Drug Administration (FDA) approved the drug in March this year, industry analysts predicted peak sales of over $1bn (€739m) a year. The authors report that, in trials involving over 5000 hypertensive patients, Tekturna was no more effective than other classes of drugs that block the same renin-angiotensin system - namely converting enzyme inhibitors (CEI), angiotensin receptor blockers (ARB) or diuretics. Although Tekturna lowered blood pressure to a greater extent when combined with a CEI or an ARB or a diuretic, blood pressure control was achieved by less than 50 per cent of patients. The authors put these "very disappointing" results down to the drug's "unexpectedly strong stimulation of kidney renin secretion" - more so than CEIs or ARBs. Therefore, its antihypertensive capabilities could be counteracted by large increases in plasma renin concentration, which is particularly likely at higher doses. "[Tekturna's] pervasive stimulation of varying degrees of renin secretion could especially be a problem for those hypertensive patients who have hyper reactive renin systems such as patients with renovascular, advanced or malignant hypertension, all of whom were excluded from the trials," said Jean Sealey and John Laragh in the article. "Their reactive renin responses might be so great as to induce a rise in blood pressure. Until the possibility of aliskiren inducing increases in blood pressure is eliminated it seems safer, and simple and wiser to stick to the less expensive, equally effective and widely available generic drugs for treating hypertensive disorders."
