Deoxycytidine Kinase (dCK) has been implicated in cancer cell proliferation. Our dCK inhibitor, TRE-515, has been chemically engineered to improve bioavailability and demonstrates robust anti-tumor activity in combination therapies.
TRE-515, a first-in-class inhibitor for treatment of blood cancers
TRE-515 is a small molecule, deoxycytidine kinase (dCK) inhibitor with nanomolar affinity and is being developed for a combination therapy to treat myelodyspastic syndromes (MDS), acute myeloid leukemia (AML), and potentially other hematological neoplasms and solid tumor indications.
TRE-515 will qualify as an Orphan Indication in both the US and Europe. Trethera has secured a robust intellectual property position around TRE-515 in the US and in all major markets abroad.
A dual attack on cancer
dCK catalyzes the rate-limiting reaction in the deoxyribonucleoside salvage pathway, one of two biosynthetic pathways that generate the precursors of DNA. The other biosynthetic pathway is the de novo pathway. Trethera’s founders discovered that certain cancer cells can dynamically shift production between these two pathways, allowing the cancer cells to escape single pathway inhibition. Trethera has developed TRE-515 for use in combination with de novo pathway inhibitors, thereby enabling a dual-blockade of nucleotide synthesis that precisely targets a metabolic vulnerability of these cancer cells. The dual blockade of nucleotide synthesis holds the potential to improve treatment efficacy and minimize the development of drug resistance.