CBP501

Our lead product, CBP501, safely potentiates Cisplatin efficacy in first-line treatment of late-stage solid tumors. A synthetic dodecapeptide of 1929.1 molecular mass, CBP501 is covered by composition of matter patents with exclusivity through 2023. The compound was originally identified through our phenotype screen, which selects for G2 checkpoint abrogation.

In addition to abrogating the G2 checkpoint, CBP501 also acts by increasing intracellular concentration of Cisplatin in tumor cells over normal cells. Higher levels of intracellular Cisplatin cause increased platinum-DNA adduct formation, the mechanism by which DNA is damaged. Increased DNA-platinum-adduct formation has been correlated with anti-tumor efficacy of Cisplatin in man. CBP501 raises intracellular levels of Cisplatin, resulting in higher DNA-platinum adduct formation in tumor but not normal cells.

Randomized Phase II clinical trials are currently ongoing in two indications, malignant pleural mesothelioma (MPM) and non-small cell lung cancer (NSCLC)

Phase I studies have been completed in ovarian cancer.

To read more about CBP501:

• [Related News Release - PDF] CanBas' Phase II Anti-Cancer Drug CBP501 Mechanisms Include Calmodulin Binding; CBS9106 Inhibits CRM1 [April 5, 2011].
• 1. NAOKI MINE, Sayaka Yamamoto, Naoya Saito, Donald W. Kufe, Daniel D. VonHoff, and Takumi Kawabe: CBP501-calmodulin binding contributes to sensitizing tumor cells to CDDP and BLM. AACR Meeting, Abstract #2635, Apr 2011.