Cardiff Oncology Announces Upcoming Presentations at the AACR Annual Meeting 2024

SAN DIEGO, March 06, 2024 (GLOBE NEWSWIRE) -- Cardiff Oncology, Inc. (Nasdaq: CRDF), a clinical-stage biotechnology company leveraging PLK1 inhibition to develop novel therapies across a range of cancers, today announced publications of five abstracts that will be presented in a poster session at the American Association for Cancer Research (AACR) Annual Meeting, taking place from April 5-10, 2024, in San Diego, California.

“The posters we will be presenting at this year’s AACR meeting represent a broad view of the potential of onvansertib in several different cancer indications, including RAS-mutant mCRC, RAS-wild type mCRC, small cell lung cancer and ovarian cancer,” said Mark Erlander, Ph.D., Chief Executive Officer of Cardiff Oncology. “In RAS-mutated mCRC, we are showing the underlying mechanism through which the combination of onvansertib and bevacizumab targets the hypoxia response pathway. We believe this mechanism explains the strong clinical results we have seen in both our Phase 1b/2 and ONSEMBLE second-line RAS-mutated mCRC clinical trials. The additional posters provide new insights and rationale for future clinical trials in other cancer indications.”

Details on the posters and corresponding abstracts are shown below.

Poster Title: A phase 1b/2 clinical study of onvansertib in combination with FOLFIRI/bevacizumab revealed a new role of PLK1 in regulating the hypoxia pathway in KRAS-mutant colorectal cancer
Session Title: Microenvironment, Immunity, and DNA Repair in Therapeutic Response
Session Date and Time: Monday Apr 8, 2024: 9:00 AM - 12:30 PM PT
Location: Poster Section 27, Poster Board #14, Abstract Number #2031

This abstract presents updated clinical data and biomarker analysis from the Phase 1b/2 study evaluating onvansertib in combination with FOLFIRI/bevacizumab for second-line treatment of KRAS-mutant metastatic colorectal cancer (mCRC) patients. Analysis of patient baseline characteristics revealed superior clinical benefit in patients not exposed to bevacizumab in first-line treatment (Bev-naïve) compared to Bev-exposed patients. Bev-naive patients exhibited higher objective response rates (73.3% versus 15.7%) and longer median progression-free survival (14.9 versus 7.8 months) compared to Bev-exposed patients. Preclinical studies, using KRAS-mutant colorectal cancer mouse models revealed robust antitumor activity of onvansertib in combination with bevacizumab and a novel role of onvansertib in regulating tumor vascularization. Further preclinical investigations showed that PLK1 regulates the hypoxia pathway in KRAS-mutant CRC cells through the modulation of the hypoxia-inducible factor 1 alpha, HIF1α, emphasizing the potential crosstalk between PLK1 and angiogenesis. These findings reinforce the rationale for exploring onvansertib in combination with FOLFIRI/bevacizumab for Bev-naïve mCRC patients with KRAS mutation.