AstraZeneca’s Baxfendy (baxdrostat) has
been approved in the US as a first-in-class aldosterone synthase inhibitor
(ASI) for the treatment of hypertension in combination with other
antihypertensive medications, to lower blood pressure in adults who are not
adequately controlled.
- Approval based on BaxHTN Phase III results
showing statistically significant and clinically meaningful reduction in
systolic blood pressure in patients with uncontrolled or resistant
hypertension
- Baxfendy 2mg lowered systolic blood pressure by
15.7 mmHg (9.8 mmHg placebo- adjusted) from baseline in BaxHTN trial
There are 1.4 billion people
worldwide living with hypertension.1 In the US, approximately
50% of patients living with hypertension who are already taking multiple
antihypertensive medications still struggle with persistently elevated blood
pressure,2 which is a leading risk factor for cardiovascular
disease and premature death.3,4 Hypertension is the most
prevalent and significant modifiable cardiovascular risk factor worldwide,
accounting for more deaths and disability than any other modifiable risk.5-7
Baxfendy is a
first-in-class, highly selective and potent ASI designed to lower blood
pressure in a new way by specifically inhibiting the production of aldosterone,8 a
hormone that raises blood pressure to unhealthy levels and increases the risk
of heart and kidney problems.9-11
The approval by the US Food and
Drug Administration (FDA) was based on positive results from the BaxHTN Phase
III trial,12 with Baxfendy demonstrating statistically
significant and clinically meaningful seated systolic blood pressure reduction
at both 2mg and 1mg doses in patients with uncontrolled and resistant
hypertension on two or more medications. Baxfendy was generally well-tolerated
with no unanticipated safety findings.
Dr. Bryan Williams, Chair of
Medicine at University College London, and BaxHTN primary investigator, said:
“We have been waiting for an innovative medication like Baxfendy for
hypertension for many years. Its novel way of lowering blood pressure has the potential
to transform clinical practice by targeting a root cause of persistently
uncontrolled hypertension. In addition, the nearly double-digit
placebo-adjusted systolic blood pressure reduction achieved with Baxfendy is
exciting and clinically meaningful for clinicians and patients. Epidemiological
data indicate that a 10 mmHg decrease in systolic blood pressure is associated
with a roughly 20% lower risk of serious cardiovascular events.”
John M. Clymer, Executive
Director, National Forum for Heart Disease & Stroke Prevention, said:
“Hypertension remains a staggeringly widespread silent killer and a leading
risk factor for stroke, heart attack, kidney damage and dementia. Tens of millions
of people struggle to control their blood pressure despite lifestyle changes
and currently available treatments. Innovative, new treatments could help
millions protect their heart, kidney and brain health.”
Ruud Dobber, Executive Vice
President, BioPharmaceuticals Business Unit, AstraZeneca, said: “The approval
of Baxfendy offers a much‑needed, first-in-class innovation for people living
with persistently uncontrolled hypertension who have not responded to or
tolerated existing medicines. In the US, about 23 million patients are
uncontrolled despite being on two or more medicines for hypertension, which is
a disease that has seen little therapeutic progress for the past two decades.”
In the BaxHTN Phase III trial,13 published
in the New England Journal of Medicine,12 Baxfendy
(baxdrostat) demonstrated statistically significant and clinically meaningful
efficacy for the treatment of patients with hypertension on top of standard of
care. At week 12, the absolute reduction from baseline in mean seated SBP was
15.7 mmHg (95% confidence interval [CI], -17.6 to -13.7) and placebo-adjusted
reduction was 9.8 mmHg (95% CI, -12.6 to -7.0; p<0.001) for the 2mg dose.
For the 1mg dose, the absolute reduction from baseline was 14.5 mmHg (95% CI,
-16.5 to -12.5) and placebo-adjusted reduction was 8.7 mmHg (95% CI, -11.5 to
-5.8; p<0.001). The reduction in mean seated SBP with placebo was 5.8 mmHg
(95% CI, -7.9 to -3.8). Results were consistent across both uncontrolled and
treatment-resistant subgroups.