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(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date i - 10 March 2011 (10.03.2011) W 2011/026219 Al (51) International Patent Classification: AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, A61K 33/24 (2006.01) A61K 31/404 (2006.01) CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, A61K 31/122 (2006.01) A61K 31/555 (2006.01) DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, A61K 31/136 (2006.01) A61P 35/00 (2006.01) HN, HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, A61K 31/282 (2006.01) KR, KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, (21) International Application Number: NO, NZ, OM, PE, PG, PH, PL, PT, RO, RS, RU, SC, SD, PCT/CA20 10/00 1327 SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, (22) International Filing Date: TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. 1 September 2010 (01 .09.2010) (84) Designated States (unless otherwise indicated, for every (25) Filing Language: English kind of regional protection available): ARIPO (BW, GH, GM, KE, LR, LS, MW, MZ, NA, SD, SL, SZ, TZ, UG, (26) Publication Language: English ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, MD, RU, TJ, (30) Priority Data: TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, DK, ΓΓ 61/272,208 1 September 2009 (01 .09.2009) US EE, ES, FI, FR, GB, GR, HR, HU, IE, IS, , LT, LU, 61/272,479 29 September 2009 (29.09.2009) US LV, MC, MK, MT, NL, NO, PL, PT, RO, SE, SI, SK, 61/344,064 17 May 2010 (17.05.2010) US SM, TR), OAPI (BF, BJ, CF, CG, CI, CM, GA, GN, GQ, GW, ML, MR, NE, SN, TD, TG). (72) Inventor; and (71) Applicant : LU, Qing-Bin [CA/CA]; 414 Woodrow Declarations under Rule 4.17 : Drive, Waterloo, Ontario N2T 2V7 (CA). — as to applicant's entitlement to apply for and be granted a patent (Rule 4.1 7(H)) (74) Agents: RAOUL, Jennifer, M . et al; BORDEN LAD- NER GERVAIS LLP, World Exchange Plaza, 100 Queen — of inventorship (Rule 4.1 7(iv)) Street, Suite 1100, Ottawa, Ontario KIP 1J9 (CA). Published: (81) Designated States (unless otherwise indicated, for every — with international search report (Art. 21(3)) kind of national protection available): AE, AG, AL, AM, (54) Title: COMBINATION THERAPY FOR CANCER COMPRISING A PLATINUM -BASED ANTINEOPLASTIC AGENT © AND A BIOCOMPATIBLE ELECTRON DONOR (57) Abstract: The combination of a biocompatible electron donor and a platinum-based antineoplastic agent exhibits improved efficacy in treating cancer This improved activity appears to be the result of electron transfer from the aforementioned donor com pound to the platinum-based antineoplastic agent As the electron donor alone has no chemotherapeutic utility in treating cancer, the resulting combinations appear to be synergistic in nature In select preferred embodiments, the biocompatible electron donor is an amine (such as N,N,N',N'-tetramehtyl-p-phenylene diamine or indocyanine green), a phenolic compound (such as a flavanol or catechin), or a quinone (such as an aromatic quinone), while the antineoplastic is cisplatin. COMBINATION THERAPY FOR CANCER COMPRISING A PLATINUM-BASED ANTINEOPLASTIC AGENT AND A BIOCOMPATIBLE ELECTRON DONOR CROSS REFERENCE TO RELATED APPLICATIONS This application claims the benefit of priority of U.S. Provisional Patent Application No. 61/272,208 filed September 1 , 2009, U.S. Provisional Patent Application No. 61/272,479 filed September 29, 2009, and U.S. Provisional Patent Application No. 61/344,064 filed May 17, 2010, each of which is incorporated herein by reference in its entirety. FIELD OF THE DISCLOSURE The present disclosure relates to a combination treatment for cancer comprising a platinum-based antineoplastic agent and a biocompatible electron donor. BACKGROUND Current cancer therapy generally involves treatment with surgery, radiation therapy, chemotherapy, or a combination of these approaches, each of which has significant drawbacks and limitations. Chemotherapy generally refers to the treatment of cancer with one or more antineoplastic (e.g. anticancer) agents. Many antineoplastic agents act by impairing mitosis and thereby target rapidly-dividing cells, a hallmark property of most cancer cells. Some agents stop the cells from dividing and others kill the cells, e.g. by triggering apoptosis. Certain newer agents are being developed to provide a more targeted therapy, for example, those targeting specific proteins expressed on cancer cells. Some antineoplastic agents, such as bioreductive agents, become preferentially active at the site of a tumor, e.g. under hypoxic conditions. While a variety of antineoplastic agents are available, nearly all are toxic. Chemotherapy generally causes significant, and often dangerous, side effects, including severe nausea and vomiting, bone marrow depression, immunosuppression, cytopenia, pain and fatigue. Additional side-effects can include cachexia, mucositis, alopecia, cutaneous complications, such as hypersensitivity reactions, as well as neurological, pulmonary, cardiac, reproductive and endocrine complications. Side effects associated with antineoplastic agents are generally the major factor in defining a dose-limiting toxicity (DLT) for the agent. Managing the adverse side effects induced by chemotherapy is of major importance in the clinical management of cancer treatment. In addition, many tumor cells are resistant, or develop resistance, to antineoplastic agents, e.g. through multi-drug resistance. Combination therapeutic approaches that permit the use of lower doses of antineoplastic agents than doses conventionally used in monotherapy, while maintaining anticancer efficacy, are highly desirable. In many combinations, there is no synergistic interaction between the combined agents, for instance, the two agents may act via different mechanisms of action, or target different pathways, thereby achieving an additive therapeutic effect while reducing the side effects associated with each individual agent. In some combinations, a synergistic effect may be achieved between two or more agents, where the combined effect is greater than the additive effect of the individual agents. For example, a beneficial interaction between the agents may occur in vivo. Synergistic combinations are desirable but rare. In some combination therapies, each agent administered exerts therapeutic effects. However, in other combination therapies, a therapeutic agent may be administered in combination with a non-therapeutic agent that directly or indirectly enhances the activity of the therapeutic agent or otherwise modifies its effects in a beneficial manner. Effective combination therapies, including anticancer therapies, are desirable, since they can lead to a decrease in the frequency and/or severity of adverse side effects and an improved quality of life for the patient. Benefits of reducing the incidence of side effects include improved patient compliance, a reduction in the number of hospitalizations needed for the treatment of adverse effects, and a decrease in the administration of analgesic agents needed to treat pain associated with the adverse effects. Where dose-limiting toxicity is not an issue, combination therapy can also maximize the therapeutic effects of antineoplastic agents administered at higher doses. In addition to increased anticancer efficacy, such approaches may reduce or overcome the development of resistance. The identification of new antineoplastic agents remains a somewhat empirical process, generally involving screening a large number of compounds in order to identify a very small number of potential candidate molecules for further investigation. Thus, there is a need for a more rational and efficient approach to the design of novel antineoplastic agents. The same applies for the development of novel combinations of agents for enhanced chemotherapy. While various drug discovery tools are available, such as binding-based screening, inhibitor-based screening and structure-based drug design, a major hindrance has been lack of understanding of the precise molecular mechanisms of action of most anticancer drugs currently in use or in clinical trials. Without a specific mechanistic understanding, it is difficult to learn from the successes and failures of individual therapies. Furthermore, the development of successful combination therapies, particularly ones where synergy may be achieved, is effectively reduced to trial and error. Thus, there is a need for enhanced mechanistic understanding of anticancer drug action and subsequent rational design of effective anticancer therapies, including combination therapies. SUMMARY The present disclosure relates to a treatment for cancer comprising a combination of a platinum-based antineoplastic agent and a biocompatible electron donor. The present inventor has revealed the molecular mechanisms of action of cisplatin in inducing DNA damage and in combination with radiotherapy. The inventor then hypothesized that the cytotoxic activity of platinum-based anticancer agents could be enhanced in the presence of a biocompatible molecule capable of donating one or more electrons to the anticancer agent. It has now been demonstrated that contacting cancer cells with a platinum- based antineoplastic agent in the presence of a biocompatible electron donor in vitro or in vivo provides an enhanced anticancer effect. In a first aspect, the present disclosure provides a method for the treatment of a cancer. The method comprises administering to a subject