About Cyclacel Pharmaceuticals

Company Overview

Cyclacel's founding scientist, Professor Sir David Lane, a globally recognized authority in cell cycle biology, discovered p53, a key tumor suppressor gene that malfunctions in about two-thirds of human cancers. Cyclacel is using cell cycle control, transcriptional regulation and DNA damage response biology to develop innovative, targeted medicines for cancer and other proliferative diseases.

Under Professor Lane's guidance, our drug discovery and development programs are focused on CDK2/9 isoforms, which operate as key components of the p53 pathway.

These efforts resulted in bringing several molecules into clinical development: Fadraciclib, a second-generation CDK inhibitor, sapacitabine and CYC140, a highly selective inhibitor of a mitotic pathway enzyme polo-like kinase 1.

Fadraciclib – Second Generation CDK Inhibitor

Fadraciclib is a highly selective, orally- and intravenously available inhibitor of CDK2 and CDK9. It is differentiated from other inhibitors in development as inhibition of both CDK2 and CDK9 may contribute to fadraciclib's anti-oncogenic potential. It causes apoptotic death of cancer cells at sub-micromolar concentrations.


CYC140 is a highly selective inhibitor of a mitotic pathway enzyme polo-like kinase 1. Polo-like kinase 1 (PLK1) is a serine/threonine kinase with a central role in cell division, or mitosis, and is an important regulator of the DNA damage checkpoint. Removal of Plk1 gene leads to embryonic lethality in mice signifying the functional utility of this kinase. Plk1 is an oncogene and when overexpressed, causes cellular transformation, overrides the DNA damage checkpoint, contributes to checkpoint adaptation, supports invasion through the extracellular matrix and paves the way for aneuploidy. Development of an inhibitor to PLK1 to control aberrant tumor growth is therefore a reasonable proposition. CYC140 is a novel, small molecule inhibitor being developed against PLK1.


Sapacitabine is a nucleoside analogue that demonstrated potent anti-tumor activity in various preclinical studies. The metabolite of sapacitabine, 2'-C-cyano-2'-deoxy-1-?-D-arabino-pentofuranosylcytosine (CNDAC), is also an active compound and exerts a cytotoxic effect against cancer cells. Sapacitabine is therefore a prodrug of CNDAC. CNDAC has a significantly longer resident time in the blood when produced through natural metabolism than when administered directly and contributes to the efficacy and influences the overall therapeutic index of sapacitabine.

Research & Development