Molecular Sherlock

Molecular Sherlock

Share this post

Molecular Sherlock
Molecular Sherlock
CK-586 (cardiac myosin inhibitor) ✔️
Cardiovascular Disease

CK-586 (cardiac myosin inhibitor) ✔️

Cytokinetics

Jun 07, 2024
∙ Paid
2

Share this post

Molecular Sherlock
Molecular Sherlock
CK-586 (cardiac myosin inhibitor) ✔️
1
Share

Confirmed correct on February 15, 2025 via PubChem.

Hello everyone! It’s been a while but I’m back after finishing a grueling first year in med school. After being bombarded with exams every week, I’m happy to report that I survived (hooray)!

Today’s post is on how I figured out the structure of CK-586, a cardiac myosin inhibitor by Cytokinetics ( CYTK 0.00%↑) in phase 1 trials for hypertrophic cardiomyopathy/heart failure with preserved ejection fraction (NCT05877053). Funny enough, I ended my first year with the cardio block, so navigating the data on this compound brought back PTSD fond memories.

A housekeeping note: going forward, I’ll be keeping the 1 week paywall for free subscribers for the structure. After 1 week, I’ll reveal the structure as I’ve done but the process will be kept behind paywall.

Why have I chosen to do this? Well, it often takes me several hours to compile the data and then put it all together in a presentable format. I’m strapped for time these days, so I think it’s only reasonable to keep the process behind paywall. I hope you all can understand.

Without further ado…

CK-586 is a cardiac myosin inhibitor that is being developed by Cytokinetics (CYTK 0.00%↑) for hypertrophic cardiomyopathy. It is currently in phase 1 trials (NCT05877053).

HCM involves hypertrophy of the ventricles or intraventracular septum of the heart an results in heart failure with preserved ejection fraction (HFpEF). A subset of HCM, called hypertrophic obstructive cardiomyopathy (HOCM), is the most common inherited cardiomyopathy, affecting 1:250-500 people, and is a major contributor to sudden death in young people.

HCM can be caused by mutations in cardiac myosin genes that lead to hypercontractility of the sarcomere. This leads to pathololgicl hypertrophy and fibrosis.

So the thought behind a cardiac myosin inhibitor like CK-586 is that inhibition of cardiac myosin may be able to inhibit hypercontractility in HCM/HFpEF.

Molecular Sherlock is a reader-supported publication. Paid subscribers can see how I figured out the structure + 1 week advance on structure disclosure

This post is for paid subscribers

Already a paid subscriber? Sign in
© 2025 Victoria Yan
Market data by Intrinio
Privacy ∙ Terms ∙ Collection notice
Start writingGet the app
Substack is the home for great culture

Share