Treatment of systolic heart failure without increased heart rate (tachycardia)

This technology is a small molecule protein therapeutic for systolic heart failure, which improves contractility without an unwanted rise in a patient’s heart rate.

Unmet Need: Therapeutics which increase cellular calcium levels without heart rate increases

Advanced systolic heart failure is a serious condition, often treated with inotropes. These medications work to increase cardiac output and contractility; however, due to a lack of selectivity, these mediations also target the cardiac conduction system, causing increased heart rate. This significant off-target effect can result in dangerous tachycardia which can lead to a cardiac arrest or even death. Although inotropes are effective, there are currently no medications or therapeutics which are selective enough to avoid these potentially disastrous side effects.

The Technology: Selective small-molecule therapeutic for systolic heart failure

This therapeutic is a small molecule protein which selectively targets and regulates calcium ion channels present in cardiovascular tissues. This allows an increase in calcium levels in cardiac muscles cells without affecting the overall cardiac conduction system, or a patient’s heart rate. Due to its precision and selectivity, this protein is advantageous over conventional inotropes used to treat systolic heart failure. As such, this technology has potential for use as a therapeutic for systolic heart failure and other calcium ion-channel related diseases.

Applications:

• Small molecule therapy for systolic heart failure
• Treatment of cardiogenic shock
• Regulation of calcium channels
• Research tool for studying calcium-dependent cardiac function

Advantages:

• Selective cardiac regulation of calcium channels
• Site-specific and tight small-molecule binding
• Improvement in cardiac contractility
• Reduced presence of unwanted tachycardia (elevated heart rate)

Lead Inventor:

[Alexander Kushnir, M.D., Ph.D.]

Patent Information:

Patent Pending (US20220397567)

Related Publications:

• Liu G, Papa A, Katchman AN, Zakharov SI, Roybal D, Hennessey JA, Kushner J, Yang L, Chen BX, Kushnir A, Dangas K, Gygi S, Pitt GS, Colecraft HM, Ben-Johny M, Kalocsay M, Marx SO. “Mechanism of adrenergic Cav1.2 stimulation revealed by proximity proteomics” Nature. 2020 Jan; 577: 695-700.

Tech Ventures Reference:

• IR CU19251

• Licensing Contact: Joan Martinez