Qurient Co., Ltd. (KRX: 115180), a clinical-stage biotechnology company developing innovative cancer therapeutics, today announced the publication of a peer-reviewed study in Science Advances detailing how its selective CDK7 inhibitor, Q901 (mocaciclib), significantly enhances the antitumor activity of topoisomerase I inhibitor-based antibody-drug conjugates (TOP1i-ADCs).
The study, titled “Sensitizing tumor response to topoisomerase I antibody drug conjugate by selective CDK7 inhibition,” was conducted in collaboration with scientists at Pohang University of Science and Technology (POSTECH), the U.S. National Cancer Institute (NCI), and the University of Maryland.
The research demonstrates that Q901 suppresses MYC- and E2F-driven transcriptional programs, thereby impairing the expression of homologous recombination repair (HRR) genes. Consequently, this effect prolongs the persistence of TOP1-DNA protein crosslinks (TOP1-DPCs), drastically increasing tumor-cell sensitivity to both standalone TOP1 inhibitors and TOP1i-ADCs.
“While TOP1 inhibitor-based ADCs have emerged as one of the most effective cancer treatment modalities, there remains a critical opportunity to improve progression-free survival by inducing a transient HRR-deficient state,” said Kiyean Nam, Ph.D., Chief Executive Officer of Qurient and co-corresponding author of the study. “This publication elucidates the complementary molecular mechanism between CDK7 and TOP1 inhibition. We believe these findings provide a robust scientific rationale not only for combining Q901 with existing TOP1i-ADCs, but also for the development of our next-generation dual-payload ADCs that combine both CDK7 and TOP1 inhibitors into a single therapy.”
Key findings from the publication include:
- Highly Selective and Sustained CDK7 Inhibition: Q901 demonstrated exceptional selectivity for CDK7 across a kinome profiling panel, forming a covalent interaction with CDK7 at Cys312.
- Suppression of Oncogenic Transcription and DNA Damage Repair: Q901 successfully disrupted MYC- and E2F-driven transcriptional programs, leading to reduced expression of genes vital for DNA damage repair—specifically those associated with homologous recombination, checkpoint control, and DNA replication.
- Prolonged TOP1-DPC Persistence: The study revealed that CDK7 inhibition constrained RNA polymerase II (RNAPII) transcriptional elongation. This reduced the RNAPII-TOP1-DPC collisions that typically promote the proteasomal clearance of TOP1-DPCs. As a result, TOP1-DPCs persisted longer, amplifying lethal DNA damage within tumor cells.
- Enhanced Efficacy with Multiple TOP1i-ADCs: In preclinical models, Q901 significantly enhanced overall antitumor activity when administered in combination with leading ADCs, including trastuzumab deruxtecan (T-DXd) and sacituzumab govitecan (SG).
Ultimately, these findings provide a clear mechanistic framework for Qurient’s clinical strategy: augmenting current ADC treatments through combination therapies and advancing highly targeted dual-payload ADCs. Qurient is actively applying this framework to develop dual-payload ADCs across multiple antibody targets, establishing a highly scalable platform for internal pipeline expansion and future strategic partnerships.
About Qurient Co., Ltd.
Qurient Co., Ltd. (KRX: 115180) is a clinical-stage biotechnology company focused on the discovery and development of innovative therapeutics for cancer and infectious diseases. The company is advancing a robust pipeline of internally discovered small-molecule therapeutics and next-generation antibody-drug conjugates. This includes Q901 (mocaciclib), a selective CDK7 inhibitor, and QP101, a dual-payload ADC combining complementary cytotoxic mechanisms. Qurient is also pioneering a broader dual-payload ADC platform designed to seamlessly apply complementary payload combinations across a variety of antibody targets.
Website: www.qurient.com
View source version on businesswire.com: https://www.businesswire.com/news/home/20260930842516/en/
Media gallery
