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. Dose escalation is continuing, with no dose-limiting toxicities observed to date.
Scientific Focus
Our science centers on uracil-DNA metabolism, an underexplored area of biology drawing growing scientific interest, including recent published work showing that uracil in DNA can drive replication stress.
The mechanism runs in four steps. Thymidylate stress depletes the thymine cells need to copy their DNA. Blocking dUTPase allows uracil to build up and enter DNA in its place. The result is Genomic Uracil Stress. The cell’s response, GUSR, spans DNA damage and repair, replication stress, cell-death pathways and, where supported by data, inflammatory and immune signaling.
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.