Nutcracker Therapeutics Demonstrates Enhanced Functional Activity of Prostate Cancer Candidate NTX-470 at the 2024 AACR Annual Meeting
- Data showed NTX-470 successfully engaged CD3 T cells, while retaining low bystander activity and reduced off-tumor binding
- Another set of data detailed the design of LIGHT, an immunomodulatory cytokine that is a component of lead drug candidate NTX-250
- Company scientists engineered and iterated multiple RNA sequences for NTX-470 and LIGHT through its technology platform
Excerpt from the Press Release:
EMERYVILLE, Calif.–(BUSINESS WIRE)–Nutcracker Therapeutics, Inc., a biotechnology company dedicated to developing transformative RNA therapies through its proprietary technology platform, recently presented two posters at the American Association for Cancer Research (AACR) Annual Meeting in San Diego: one showcasing the latest preclinical data for the company’s mRNA drug candidate for prostate cancer, NTX-470; and the other highlighting data on the immunomodulatory cytokine, LIGHT.
“Nutcracker is building a strong slate of drug candidates for oncology indications, with NTX-470 being one of the highlights of our pipeline,” said Chief Executive Officer Igor Khandros, Ph.D. “Through our technology platform, Nutcracker scientists were able to engineer multiple variants of LIGHT and NTX-470 to investigate the activities of each molecule, and determine which has the most potential to be a clinical product candidate. This type of discovery process was made possible by the nature of RNA, and I look forward to sharing more progress our team has made on other drug candidates in the near future.”
NTX-470
There are limited treatment options for the 10 percent to 20 percent of prostate cancer patients who develop castration resistance. Bispecific T cell engagers targeting prostate-specific membrane antigen (PSMA) and six transmembrane epithelial antigen of the prostate 1 (STEAP1) have demonstrated promising preliminary clinical activity, but have faced challenges with durability and toxicity, primarily due to erroneous on-target, off-tumor binding.
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