HDAC6 is versatile protein responsible for cytosolic lysine deacetylation which regulates biological functions including cellular transport, cytoskeleton dynamics, misfolded protein clearance and immunomodulation.
Unlike other histone deacetylases, HDAC6 acts on non-epigenetic substrates, making its inhibition or even complete elimination from the body truly safe as demonstrated in vast literature and clinical evidence.
Coupling the proven safety of HDAC6 targeting with HDAX proprietary technology for enhanced therapeutic intervention, we exhibit an unparalleled efficacy and safety profile that allows us to address the root of the disease – whether in the central nervous system or periphery, in chronic or acute conditions, alone or in combination – the potential of our technology is endless.
Our innovative 2-site binding modality allows us to reverse disease phenotypes caused by aberrant HDAC6 activity.
We harness cutting-edge capabilities in rational drug design, by combining the use of structure-activity relationship studies, X-ray crystallography, molecular biology and computer aided drug discovery to engineer life-changing medicines.
By precisely inhibiting dysregulated HDAC6 activity at the epicentre of specific disease pathways, HDAX molecules deliver unparalleled efficacy, without the limitations seen in first-generation HDAC inhibitors and even the latest clinical candidates. Our innovative 2-site binding technology delivers treatments with high binding affinity, enabling low effective concentration and long duration of action, providing an intervention strategy for diseases with no or limited existing therapies.
Furthermore, we have shown the broad utility of our technology via the application as template for the discovery of novel HDAC6 inhibitors and degraders, with the know-how to expand into a platform for other targets as well.
HDAC6 plays a pivotal role in pathways which lead to nerve degeneration, axon transport impairment and inflammation in diseased states. Its hyperactivity ultimately results in impaired cargo transport and mitochondrial dysfunction found to cause neuropathy and neurodegeneration. HDAC6 inhibition restores the acetylation homeostasis, returning neurons to a healthy state and providing an avenue for neuroprotection and neuronal regeneration to reverse disease phenotypes.
Aberrant activity of HDAC6 has been linked to cardiovascular diseases including arrhythmia, infarction, hypertrophy, hypertension, fibrosis and chronic heart failure. Therapeutic intervention can modulate multiple interconnected pathways which regulate heart stiffness, contractility and boost cardiovascular well-being. HDAC6 inhibition can be used to provide cardioprotection and improve heart function by alleviating injury-induced remodelling in pathological conditions.
Apart from our immediate areas of interest, HDAC6 inhibition holds vast therapeutic promise across a wide spectrum of diseases, spanning metabolic disorders, inflammatory diseases, and beyond. With emerging insights into biological pathways and disease etiology, HDAX therapeutics’ proprietary platform offers endless opportunities to develop interventive strategies to augment patient outcomes in a myriad of complex diseases.
