Theralase Technologies Inc. announced that in preclinical research, it's lead drug formulation, Rutherrin has been proven effective in increasing the efficacy of chemotherapy and reducing multidrug resistance. Chemotherapy is currently one of the principal treatment methods for cancer, along with radiation and surgery. Clinically, many tumours undergo a satisfactory response, when first exposed to chemotherapeutic drugs; however, despite the initial success of these treatments, growing resistance to treatment with these drugs becomes a common occurrence.

This results in the steady loss of therapeutic response over time for cancer patients, despite the wide spectrum of drugs and treatments available. This phenomenon is termed Multi-Drug Resistance ("MDR"). Although there are several different mechanisms associated with the development of MDR in patients, a common cause is believed to be the overexpression of a plasma membrane superfamily of transporter proteins, called the ATP-Binding Cassette ("ABC") transporter, which act as an energy-dependent drug efflux pump, preventing adequate intracellular accumulation of a broad range of cytotoxic drugs.

In other words, the chemotherapeutic drugs are expelled by the cancer cells, before they have a chance to be effective. This underlines the critical importance of identifying compounds that could inhibit the efflux pump activities. In order to determine the effect of Rutherrin on MDR in cancer cells, cells were treated with Rutherrin, before addition of one of the following drugs: Hoechst 33342 (nuclear dye commonly used to study ABC transporter drug efflux) - Temozolomide (chemotherapy used to treat brain cancer) - Gemcitabine (chemotherapy used to treat various cancers) - Cisplatin (platinum-based chemotherapy used to treat various cancers).

Following incubation, cells were washed and the amount of intracellular drug was quantified using High-Performance Liquid Chromatography coupled with Mass Spectrometry. The amount of drug was normalized to cells, which were not treated with Rutherrin, as a control. Treatment with Rutherrin significantly enhanced the retention of all tested chemotherapeutic drugs, presumably through the inhibition of the ABC transporter efflux pump, resulting in higher intracellular drug accumulation, which would increase exposure of the cancer cells to the respective chemotherapy and consequently improve overall treatment efficacy.

To further investigate this phenomenon and to demonstrate cancer cell kill, in vitro cells were treated with Rutherrin, before addition of various chemotherapeutic drugs to analyze cell survival. These chemotherapeutic drugs included: Vandetanib (chemotherapy used to treat thyroid cancer) - Vemurafenib (chemotherapy used to treat melanoma) - Vinblatine (chemotherapy used to treat lymphoma, breast cancer and testicular cancer) - Cisplatin (platinum-based chemotherapy used to treat various cancers) - Temozolomide (chemotherapy used to treat brain cancer) - Gemcitabine (chemotherapy used to treat various cancers). Addition of Rutherrin significantly increased the cancer cell kill for all tested chemotherapeutic drugs, suggesting a universal effect of Rutherrin on chemotherapeutic drugs in their destruction of cancer cells, rendering the cancer cells more susceptible to chemotherapy.

To further validate the research, a mouse animal model was utilized, where the mice were injected subcutaneously with mouse colorectal cancer cells and divided into four treatment groups; specifically: Untreated Control, Rutherrin only, Vinblastine only and Rutherrin combined with Vinblastine. The combination of Rutherrin and Vinblastine significantly delayed tumor volume progression and enhanced overall animal survival, compared to control or either treatment alone. This research was completed using Rutherrin with no light or radiational activation.