A Conversation with Bob Ladner,
CEO and Founder of CV6
Can you explain how your line “fish where no one else is fishing” defines your work?
In both fishing and science, the obvious places tend to be crowded. If you are willing to look more carefully in areas others have moved past, you can begin to see patterns that are not immediately obvious.
Early in my career, mentors in drug development, leaders in the field, encouraged me not to lose focus. I had cloned part of this biology when I was 24 years old, and they reinforced that some questions take years, even decades, to fully play out.
Much of this work came from following the biology over time, even when it was not the direction most people were pursuing. One of the outcomes of that is breadth of potential application. This approach may be relevant across multiple major cancers and inflammatory disease, which differs from therapies developed for molecularly narrow patient populations.
What was the inspiration for naming the company CV6 Therapeutics?
The name comes from the USS Enterprise, CV-6.
I was drawn to the ship’s resilience and its ability to continue operating under difficult conditions. Its persistence and consistency over time resonated with me.
I also admired the way the carrier approached challenges that were not always conventional. That willingness to do things differently contributed to its success and aligns with how we have pursued this work.
From the beginning, I understood that building a new category of medicine would require a long term commitment, persistence, discipline and a clear focus on the mission.
Another part of the carrier’s history has taken on additional meaning for me. After serving alongside the British Pacific Fleet as part of the Allied effort in the Pacific during World War II, the USS Enterprise, CV-6, received the British Admiralty Pennant in 1945. It was the only ship outside the Royal Navy to receive that honor. Given that CV6 Therapeutics is based in Belfast and our clinical trial is taking place across Northern Ireland and Great Britain, that connection feels especially meaningful to me.
You spent over a decade at the University of Southern California, where Charles Heidelberger worked on 5-fluorouracil. What did it mean to now build on that foundation?
We occupied Charles Heidelberger’s former laboratory for over a decade, reinforcing a sense of scientific continuity with the origins of 5-FU development. I had the opportunity to know many of his postdoctoral fellows and heard firsthand accounts of the discovery and development of 5-FU.
5-FU is still used around the world, and the vulnerability it creates in cancer cells is exactly what CV6-168 is designed to exploit.
As you got traction, you decided to move CV6 Therapeutics to Northern Ireland. Why?
The move to Northern Ireland was intentional. We needed an environment where the science could remain the focus and where we could build the right team around it.
Patrick Johnston was instrumental in supporting both the move and the vision for building a company around this work. We also brought continuity with us, including members of the original team, early advisors, and Board members, while expanding our network through Belfast and engaging leading experts across Europe.
There were practical advantages as well. Capital efficiency allowed us to build the company thoughtfully and deploy resources in a disciplined way, while still accessing international investment as the program advanced.
Why can this biology support a company and a pipeline, rather than a single drug?
I began studying dUTPase and uracil-DNA biology decades ago. Over time, that work led us to the Genomic Uracil Stress Response, or GUSR, and to the possibility that this biology could open more than one therapeutic opportunity.
In cancer, CV6-168 is designed to work in combination with thymidylate synthase inhibitors such as 5-FU. By inhibiting dUTPase while those treatments restrict thymidine, we aim to increase uracil in tumor DNA and trigger GUSR. Our preclinical studies have also shown immune-associated responses, which is why we are exploring combinations with immunotherapy.
We are also developing CV6-1271 for inflammatory diseases such as rheumatoid arthritis. In preclinical arthritis models, it showed activity on its own and enhanced the response to methotrexate.
That is why I see the potential for a pipeline: the science is opening distinct opportunities in cancer and inflammatory disease, and each program will have to establish its own evidence.
As you look at how far this has come, do you ever reflect on what Paddy Johnston might think of where things stand today?
Patrick Johnston played an important role in the early development of both the company and the broader scientific vision behind CV6. He was deeply knowledgeable in the field of 5-fluorouracil and translational oncology, and he immediately understood the long-term potential of targeting uracil-DNA biology, what we now call the Genomic Uracil Stress Response (GUSR), as a platform approach across multiple diseases.
At an important stage in the company’s development, Paddy strongly supported the move to Northern Ireland and helped create an environment where the science could continue to advance with the right institutional and clinical foundation around it. His role as Vice Chancellor of Queen’s University Belfast made that possible, and his encouragement, perspective, and confidence in the work were deeply influential during that period.
He was widely respected throughout the oncology community, both scientifically and personally, and his support carried real weight. Now that the company has advanced into clinical development and the Phase 1a study is progressing, there are many moments where I think he would have been genuinely encouraged to see how far the science and the program have evolved.