Other Programs
Our expertise in cell cycle biology has potential applications in a number of diseases outside of cancer. We have developed compound series with potential for use in several other diseases, including kidney disease, Type 2 diabetes and HIV/AIDS.
Inflammatory Kidney Disease and CDK inhibitors
As in cancer, certain kidney diseases are characterized by abnormal cell proliferation and dysregulation of the cell cycle. Glomerulonephritis is a major cause of kidney failure or End-Stage Renal Disease (ESRD), the treatment of which requires dialysis or kidney transplantation. Approximately $17 billion is spent annually to treat ESRD in the USA alone, one of few medical conditions to have received dedicated funding by act of Congress. Glomerulonephritis is often associated with other conditions which lead to kidney injury, such as viral infection, Systemic Lupus Erythematosus and exposure to toxic substances. In multiple preclinical studies, Cyclacel has demonstrated that the pharmacological inhibition of CDKs blocks or slows the progression of chronic and acute forms of glomerulonephritis.
GSK-3 Inhibitors in Type 2 Diabetes
Cyclacel has developed lead compounds that inhibit the Glycogen Synthase Kinase-3, a target that plays an important role in controlling the body’s glucose levels. Research indicates that GSK-3 is inhibited in healthy patients as part of the signaling pathway triggered by insulin when it binds to its receptor, but in patients with adult onset or Type 2 Diabetes, GSK-3 is not inhibited because the insulin receptor is not operating properly. In contrast with other GSK-3 inhibitors, our compounds do not induce the accumulation of beta-catenin, a protein associated with tumor growth.
HIV Cell Cycle Inhibitors
Cyclacel has designed a number of compounds that inhibit the HIV/AIDS virus by blocking the replication of HIV/AIDS infected cells. Research suggests that our compounds inhibit CDKs as well as uniquely inhibit kinases involved in mitosis. This provides a distinct approach to viral treatment because the compounds act on the host target as opposed to a viral target. This program builds on a body of literature that suggests that CDK inhibitors have been effective in a number of HIV/AIDS molecules in preclinical studies.

