CKD-504 / Chong Kun Dang - LARVOL DELTA

Therapeutic Potential of CKD-504, a Novel Selective Histone Deacetylase 6 Inhibitor, in a Zebrafish Model of Neuromuscular Junction Disorders. (PubMed, Mol Cells) - "In the present study, we demonstrated that HDAC6 inhibition was sufficient to enhance movement by restoring NMJ impairments observed in a zebrafish disease model. We found that CKD-504, a novel HDAC6 inhibitor, was effective in repairing NMJ defects, suggesting that treatment of neurodegenerative diseases via NMJ targeting is possible."

Epigenetic controller • Journal • CNS Disorders • Genetic Disorders • Pain

HDAC6 Inhibition Corrects Electrophysiological and Axonal Transport Deficits in a Human Stem Cell-Based Model of Charcot-Marie-Tooth Disease (Type 2D). (PubMed, Adv Biol (Weinh)) - "Treatment with histone deacetylase 6 inhibitors, tubastatin A and CKD504, improves mitochondrial movement and α-tubulin acetylation in these cells. Furthermore, CKD504 treatment enhances population-level electrophysiological activity, highlighting its potential as an effective treatment for CMT2D."

Journal • CNS Disorders • Genetic Disorders • Pain

A novel histone deacetylase 6 inhibitor improves myelination of Schwann cells in a model of Charcot-Marie-Tooth disease type 1A. (PubMed, Br J Pharmacol) - "A novel HDAC6 inhibitor, CKD-504, has potent therapeutic efficacy for CMT1A."

Journal • CNS Disorders • Genetic Disorders • Pain • HSP90AA1

CKD-504 in SAD and MAD in Healthy Korean and Caucasian Adult Male and Female Subjects (clinicaltrials.gov) - P1; N=88; Recruiting; Sponsor: Chong Kun Dang Pharmaceutical; Trial completion date: Feb 2020 ➔ Dec 2020; Trial primary completion date: Nov 2019 ➔ Dec 2020

Clinical • Trial completion date • Trial primary completion date

Acetylation changes tau interactome to degrade tau in Alzheimer's disease animal and organoid models. (PubMed, Aging Cell) - "We found a histone deacetylase 6 (HDAC6) inhibitor, CKD-504, changed the tau interactome dramatically to degrade pathological tau not only in AD animal model (ADLP ) brains containing both amyloid plaques and neurofibrillary tangles but also in AD patient-derived brain organoids...We also identified the responsible acetylation sites on tau. These dramatic tau-interactome changes may result in tau degradation, leading to the recovery of synaptic pathology and cognitive decline in the ADLP mice."

Journal • Preclinical