With a €6.26M round, QLi5 doubles down on proteasome-based ADC payloads

The QLi5-Qurient story: where the company comes from

QLi5 Therapeutics did not originate as an ADC company. Its roots are in academic and translational work on the proteasome, a cellular complex responsible for regulated protein degradation. Early proteasome inhibitors such as bortezomib demonstrated that blocking this pathway could be effective, but they also revealed that systemic proteasome inhibition can cause significant toxicity.

At the Max Planck Institute for Biochemistry, Robert Huber, who won the 1988 Nobel Prize in Chemistry for solving the structure of a photosynthetic reaction centre, later contributed to proteasome research. That work fed into drug discovery programs at the Lead Discovery Center (LDC), the translational arm linked to the Max Planck Society. LDC’s aim was not to revisit first-generation proteasome drugs, but to explore whether more selective and controllable ways of exploiting proteasome biology could be pursued.

QLi5 was then created in 2019 as a joint venture to take that work forward in a focused company setting. Qurient was involved as co-founder from the outset, bringing drug-development experience and an interest in building a platform rather than using the technology inside a single oncology candidate.

The Seoul-based biotech has been building its own oncology pipeline while developing small-molecule programs, and today it contributes again to the German company. Indeed, Qurient isn’t only injecting capital, it is increasing its voting stake in this round, suggesting a desire to play an active role in shaping QLi5’s strategic direction as the platform matures. 

QLi5’s technology: using ADC delivery to unlock proteasome inhibition

QLi5’s approach is about delivering proteasome inhibition more precisely. Indeed, according to the company, the first-generation proteasome inhibitor caused toxicity because of the lack of precision in the delivery. QLi5 wants to avoid the compound from being distributed in the bloodstream to widen the therapeutic window. Instead of administering proteasome inhibitors systemically, the company is developing them as payloads for ADCs, so that the drug is largely inactive in circulation and only released once inside targeted tumor cells.

In 2025,  QLi5 and Qurient presented preclinical data on proteasome inhibitor-based ADCs at the AACR–NCI–EORTC conference, and the PI-ADC payloads showed anti-tumor activity, including in settings where tumors had shown resistance to existing ADCs. 

Where QLi5 fits in the ADC payload landscape

Most approved ADCs today still rely on a relatively narrow set of payload mechanisms, dominated by microtubule inhibitors and, more recently, topoisomerase 1 inhibitors that have driven much of the latest clinical momentum. That concentration is one reason the field has been exploring next payload classes that could sidestep shared resistance mechanisms or broaden the settings where ADCs work.

In that light, proteasome inhibition remains rare in ADC formats, meaning QLi5 is operating in a relatively uncrowded space, but it also means clinical validation is still ahead. A cautionary example is carfilzomib, a clinically used proteasome inhibitor that was tested as an ADC payload and found to be unsuitable because it was rapidly inactivated by lysosomal enzymes. Academic groups have explored alternative proteasome-inhibitor scaffolds, such as carmaphycins, as potential ADC payload candidates, but these efforts have largely remained at a preclinical proof-of-concept stage. 

The field remains early, with proteasome inhibition still rarely explored in ADC formats, so QLi5 and Qurient still have a lot of work ahead.