Programs
Our programs are built on one mechanism. CV6 medicines target dUTPase, a key regulator of nucleotide-pool integrity, to drive uracil into the DNA of diseased cells and exploit how those cells respond, the Genomic Uracil Stress Response (GUSR).
In cancer, CV6-168 turns the stress created by thymidylate synthase inhibitors such as 5-fluorouracil (5-FU) into lethal genomic damage. In inflammatory disease, CV6-1271 applies the same biology alongside methotrexate.
CV6-168 is being evaluated in an ongoing Phase 1a trial in combination with infusional 5-FU.
SCIENTIFIC FOCUS: GUSR
CV6 is developing medicines that exploit the connection between nucleotide metabolism, DNA integrity and cellular survival.
In cancer, thymidylate synthase inhibitors restrict the supply of thymidine nucleotides needed for DNA synthesis. CV6-168 inhibits dUTPase, a metabolic safeguard that limits uracil incorporation into DNA. Together, these interventions are designed to increase the dUTP:dTTP ratio and promote extensive DNA uracilation.
This combination is designed to create a metabolic synthetic lethal effect, driving replication stress, DNA damage and cancer cell death in preclinical models. CV6 preclinical studies also show immune-associated responses, supporting investigation of combinations with immune checkpoint inhibitors.
Oncology
Cornerstone chemotherapies such as 5-FU create a vulnerability in cancer cells. Our GUSR medicines are designed to exploit it.
Inflammatory Diseases
Methotrexate anchors rheumatoid arthritis care, yet many patients respond inadequately. We are extending the same GUSR platform to reach them.
Pipeline
CV6 is building a pipeline of first-in-class medicines on a single platform, led by CV6-168 in oncology and CV6-1271 in inflammatory disease.
Further programs extend the GUSR platform into new combinations and disease areas.
