As of the most recent check, shares of Cyclacel Pharmaceuticals, Inc. (NASDAQ: CYCC) had increased 32.82% during pre-market activity, to $13.03. The dramatic increase comes after the business published fresh findings from independent clinical studies that show the encouraging outcomes of plogosertib, its PLK1 inhibitor, in a number of cancer models.
Positive Findings in the Study of Biliary Tract Cancer
In the journal Cancer Research, Cyclacel highlighted a preclinical study titled “Evaluation of Antitumor Effects of Plogosertib, PLK1 Inhibitor in Biliary Tract Cancer with BUBR1 as a Potential Biomarker.” The results, which were first reported at the annual conference of the American Association for Cancer Research in 2025, showed that plogosertib, both alone and in combination, was sensitive to many biliary tract cancer (BTC) cell lines.
Mechanistically, it was demonstrated that plogosertib stimulates the development of the mitotic checkpoint complex (MCC) during prometaphase, which results in mitotic arrest and BTC cell death. Importantly, the study found that BUBR1, a crucial mitotic checkpoint protein, may be a biomarker, and that elevated BUBR1 expression is associated with greater treatment sensitivity.
A Biomarker for Increased Efficacy: BUBR1
According to the study’s findings, BTC cells with higher BUBR1 expression reacted better to plogosertib and showed synergistic advantages when paired with an ATR inhibitor. These results suggest that PLK1 targeting may be an effective BTC therapeutic approach, particularly for individuals whose tumors show a high level of BUBR1.
Potential Breakthrough in Fibrolamellar Carcinoma
In a related development recently, Cyclacel also highlighted research published in the peer-reviewed journal Gut, titled “DNAJ-PKAc Fusion Heightens PLK1 Inhibitor Sensitivity in Fibrolamellar Carcinoma”. The study demonstrated that the DNAJ-PKAc fusion oncoprotein, a driver of Fibrolamellar hepatocellular carcinoma (FLC), renders tumors highly sensitive to plogosertib.
Researchers discovered that PLK1 plays a critical role in FLC cell survival. In patient-derived in vitro and in vivo xenograft models, pharmacologic inhibition with plogosertib markedly inhibited the development of FLC tumors while preserving normal liver cells. These results provide credence to plogosertib’s further assessment in preclinical and clinical studies as a possible FLC therapy.
