Chemotherapy-induced Neutropenia

More than half of all patients diagnosed with cancer receive chemotherapy that, by definition, is cytotoxic. The key market drivers in cytotoxics include Taxotere, Gemzar and Eloxatin. The dose required for these drugs to be effective causes a high level of toxicity and of associated neutropenia. In order to overcome these negative side effects, the drug dose has to be decreased to below optimal levels for treatment or the chemotherapy regime has to be delayed. Such reduction in dose intensity often compromises the long-term treatment outcome for patients. The unmet market need calls for the identification, formulation and evaluation of drugs with a greater degree of selectivity for cancer cells.

As a form of myelosuppression, chemotherapy-induced neutropenia (CIN) remains one of the most common side effects caused by chemotherapy and it can quickly result in life-threatening infections and complications in patients. Until the 1990s, the only option for managing CIN was the reduction or delay of chemotherapeutic doses. Since then, clinical management of CIN has progressed significantly through the introduction of granulocyte-macrophage colony-stimulating factors (GM-CSF) and granulocyte colony-stimulating factors (G-CSF) into the market. Currently, there are limited therapeutic options in preventing and curing CIN. In 2006, the total global sales for CIN treatment were just over $4.2 billion, about 93% of which came from Amgen’s two leading G-CSF drugs, Neupogen and Neulasta. These are expensive drugs that have to be injected by health care professionals. In the United States, the cost of Neulasta is between $3,000 and $7,000.00 per syringe. As well, they may promote further cancer cell proliferation during treatment and the build up of resistance to the chemotherapy. With up to 50% of cancer patients that undergo chemotherapy developing neutropenia, the CIN treatment market has an unmet, high priority need.

An earlier study by Welichem indicated that an oral administration of WBI-2100 could significantly boost the number of neutrophils in the peripheral blood of mice that were being treated with Cyclophosphamide, a commonly used chemotherapeutic drug that causes CIN. This is highly significant since there is no existing drug in the market that has the dual activity of targeting certain cancers while also suppressing CIN.

WBI-2100 is a small molecule compound that is anticipated to be easy to administer, rapid acting and cost significantly less than biologics. In preliminary animal studies, it enhanced the chemotherapeutic benefit of leading chemotherapeutic drugs against solid tumours and showed effects comparable with the commonly used G-CSF, but without the undesirable side effects. By inhibiting cancer growth while stimulating neutrophils, WBI-2100 has the potential to be marketed as a new generation of cancer treatment agent that is more effective and better tolerated than those currently on the market. The formal pre-clinical study will be completed within the year.