Vadimezan


Vadimezan is a tumor-vascular disrupting agent that attacks the blood supply of a cancerous tumor to cause tumor regression.

Clinical trials

Non-small cell lung cancer

Despite positive results at the preclinical stage, vadimezan failed in human clinical trials. Studies have demonstrated the reason for the inefficacy. Vadimezan was shown to target the STING pathway, however, this effect is mouse specific; it has no effect on human STING. A single amino acid difference at position 162 of the cyclic-dinucleotide-binding site of STING makes mouse STING sensitive to the drug, whereas human STING remains insensitive.
Vadimezan had been studied in combination with chemotherapy in at least two Phase II trials for advanced non-small cell lung cancer and showed survival extensions of around 5 months when compared to chemotherapy alone.
In April 2008, a Phase III trial started. In March 2010, the phase III trial of use as a first line therapy for NSCLC gave poor results. Interim results on another phase III trial as second-line therapy for NSCLC were completed in 2011. In November 2010, the second trial also gave poor interim results.

Other cancers

Vadimezan has also been studied for the treatment of prostate cancer and HER2-negative metastatic breast cancer.

History

Vadimezan was discovered by Bruce Baguley and William Denny and their teams at the Auckland Cancer Society Research Centre at the University of Auckland in New Zealand. It was licensed to Antisoma in 2001. Novartis acquired the worldwide rights for it in 2007 and it underwent development by Antisoma and Novartis.