Captor's EIC Accelerator Targets a Protein That Broke Rivals

MCL-1 is one of the proteins that stop a cancer cell from killing itself, and cancers that survive treatment often do so by making more of it. Drugs that blocked MCL-1 looked promising and then damaged patients' hearts, which ended several clinical programmes. Captor Therapeutics, based in Wrocław and Basel, does something different: its molecule tags MCL-1 for destruction by the cell's own disposal machinery, a technique called targeted protein degradation, and the company says it achieved almost complete degradation in cynomolgus monkeys with no effect on cardiac safety biomarkers.

The EIC Accelerator selected the project, CT-03, at its October 2024 cut-off for blended finance, and CORDIS records a grant of €2,499,875 from January 2026 to December 2027, the latest-finishing award of the cut-off. The goal is to show safety and the absence of cardiotoxicity in humans in a phase Ia/Ib trial in patients with acute myeloid leukaemia who have become resistant to Venclexta, and then to out-license the asset.

Degrading what others tried to block

The scientific argument is specific. Blocking MCL-1 with an inhibitor leaves the protein in place; degrading it removes both its anti-apoptotic function and its role in the DNA damage response, Captor's pipeline page says. Its MCL-1 degraders kill patient-derived leukaemia cells outside the body and inhibit tumour growth in a mouse model of AML, and an independent contractor's study in mice with human AML xenografts produced tumour regression at 75 and 150mg per kilogram once daily.

The commercial logic is resistance. Venclexta is the standard for AML patients too frail for intensive chemotherapy or a stem cell transplant, and nearly all of them eventually stop responding. Captor presented CT-03p at the American Society of Hematology meeting in 2025 as a cardio-safe degrader that overcomes venetoclax resistance in AML, which is the claim the trial would test.

One of five programmes

CT-03 sits in a pipeline of five public programmes: a triple degrader of GSPT1, NEK7 and SALL4 for liver, lung and neuroendocrine tumours, a brain-penetrant NEK7 degrader for neuroinflammation in Parkinson's disease and ALS, a systemic NEK7 programme for autoimmune disease, the MCL-1 degrader, and a PKC-theta degrader. None is listed as being in a clinical phase. The company's own stage columns run from discovery through preclinical and trial-application-enabling studies to phase Ia/Ib.

The pattern in its claims is consistent and worth noting: almost all the evidence is degradation levels in monkeys and efficacy in mouse models, which is normal for this stage and also means nothing has yet been tested in a person.

1. Cardio-safe degradation in primatesReportedNear-complete MCL-1 degradation with no cardiac biomarker effect, per the company.
2. Efficacy against resistant AMLPreclinicalPatient-derived cells ex vivo and a mouse model; ASH 2025 poster.
3. Clinical trial applicationNot confirmedFiling was targeted for the end of 2025; no confirmation found.
4. First patient dosedNot yetNo programme listed in a clinical phase.

A listed company taking a small grant

Captor is unusual among EIC beneficiaries in being publicly listed, with periodic reports, analyst coverage and a dividend policy page. The €2.5 million grant is small against the cost of a phase I trial in leukaemia, and the project explicitly plans to fund the rest of the company from an out-licensing deal rather than from equity. The award was blended finance and no EIC Fund investment has been announced. The company also has Polish national funding for CT-03, with a second project phase reported to run to July 2026, and a 2022 collaboration with Ono Pharmaceutical on a different target.

Its news page lists an item from 19 November 2025 headed "Captor Therapeutics Enters into a Strategic Agreement with a Pharmaceutical Partner"; the partner is not named there, and no deal terms for CT-03 are public.

A Polish company on a target the big firms dropped

MCL-1 is a textbook case of a target the industry abandoned for safety reasons rather than biology, which makes it a reasonable thing for public money to re-attempt: the science is validated, the clinical risk is specific and known, and a smaller company with a different modality can test it for a fraction of what the failures cost. For the EU, funding a Wrocław-based degrader company also puts EIC money into a part of Europe that sees relatively little of it.