Technologies
This technology is a KDM1A inhibitor that improves carcinoma sensitivity to FDA-approved antibody-drug conjugates by epigenetically reprogramming tumor cell to increase surface expression of antigens.
Antibody-drug conjugates (ADCs) deliver cytotoxic payloads to tumor cells by recognizing specific cell surface antigens, enabling improved efficacy at the treatment site with fewer side effects. However, many tumors exhibit low or heterogeneous expression of these target antigens, limiting ADC effectiveness and leading to treatment resistance. While several ADCs have been approved for metastatic cancers, their benefit is often restricted to patients with sufficient antigen expression. There is a need for strategies that increase target antigen expression to improve ADC efficacy and expand treatment opportunities for patients with ADC-resistant tumors.
This technology is a KDM1A (lysine-specific demethylase 1A) inhibitor that epigenetically reprograms carcinoma cells to overexpress the ADC-targeted antigens NECTIN4 and/or TROP2 to increase their sensitivity to ADC therapies across bladder, breast, and other carcinomas. As such, a greater proportion of these tumors, even those expressing low levels of ADC-targeted antigens, can be altered to improve the targetability of ADCs, thereby increasing delivery of the chemotherapeutic drug to maximize cancer-killing potential.
This technology has been validated in human patient-derived bladder cancer organoids. Treatment with KDM1A inhibitors (including GSK-LSD1 and ORY-1001) led to increased expression of NECTIN4 and TROP2. In combination with FDA-approved ADCs Enfortumab vedotin and Sacituzumab govitecan, this technology enhanced tumor sensitivity compared to ADC treatment alone.
Patent Pending(WO/2026/076330)
IR CU24095
Licensing Contact: Joan Martinez