Heart Failure Epidemiology

Heart failure classification consists of two primary forms of the disease: Heart Failure with Reduced Ejection Fraction (HFrEF) and Heart Failure with Preserved Ejection Fraction (HFpEF), which each represent approximately 50% of the overall HF patient population.

There are treatments available for patients with HFrEF, but clinical progression and death still occur.  For HFpEF, there is not a single approved drug or device to date – half of all HF patients have no treatment option available to them.


Neuregulin-1, also known as NRG-1 or simply neuregulin, is a growth factor that has shown great promise as a treatment for heart failure.

In animal studies, neuregulin has been shown to improve heart function in a variety of different models of heart failure.

In clinical studies, the growth factor by itself showed the ability to improve ejection fraction in HFrEF patients by nearly 10% absolute improvement at higher doses – a statistically significant and clinically meaningful improvement.

Improvement in left ventricular ejection fraction following NRG-1 administration

Improvement in left ventricular ejection fraction following NRG-1 administration

Vermeulen et al., ErbB2 signaling at the crossing between heart failure and cancer,
Basic Res Cardiol (2016) 111:60

However, NRG-1 by itself has a short half-life in circulation.  This requires higher doses to be administered, which have shown signs of toxicity, or for administration over a prolonged period of time – 10 hours per day for 10 consecutive days in Phase III studies.

NRG-1 dosing has also been limited by gastrointestinal (GI) side-effects and a theoretical risk of stimulating cancer progression.

Researchers have shown the NRG-1 acts through two different pathways – HER3 and HER4.  The HER3 pathway appears primarily responsible for the GI side-effects and the cancer risk, while the HER4 pathway appears primarily responsible for the regenerative effects in the heart.

There is a belief in the research community that selectively activating HER4 without activating HER3 could yield a wider therapeutic window and better clinical effects.

JK07 Design

  • NRG-1 fusion domain can stimulate HER3 and HER4
  • Anti-HER3 antibody blocks HER3 signaling
  • Overall effect is selective stimulation of HER4 with a favorable pharmacokinetic profile
JK07 has shown potent regenerative potential in large and small animal models of heart failure, including HFrEF and HFpEF, and potent anti-tumor activity in a xenograft model of cancer.

Clinical Trials

We are currently studying JK07 in a Phase 1 trial to evaluate the safety, pharmacokinetics, and activity of JK07 in heart failure patients with reduced ejection fraction.

We have an esteemed group of institutions and clinical researchers working with us on the study.

Please see our trial listing at www.clinicaltrials.gov for details on this study and how to participate if you are interested.