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US 2016O166697A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2016/0166697 A1 Bender (43) Pub. Date: Jun. 16, 2016 (54) METHOD OF TREATING CANCER A619/00 (2006.01) A647/4 (2006.01) (71) Applicant: Intensity Therapeutics, Inc., Westport, A647/8 (2006.01) CT (US) A6II 45/06 (2006.01) A619/08 (2006.01) (72) Inventor: Lewis H. Bender, Redding, CT (US) A 6LX3/555 (2006.01) (52) U.S. Cl. (21) Appl. No.: 15/052,326 CPC. A61K47/12 (2013.01); A61 K9/08 (2013.01); 1-1. A61K 33/24 (2013.01); A61 K3I/555 (22) Filed: Feb. 24, 2016 (2013.01); A61 K47/14 (2013.01); A61K47/18 Related U.S. Application Data (2013.01); A61K 45/06 (2013.01); also (63) Continuation of application No. 14/280,036, filed on May 16, 2014, which is a continuation of application (57) ABSTRACT No. PCT/US2013/059841, filed on Sep. 15, 2013. The invention provides a method for treating cancer using a (60) Provisional application No. 61/779,509, filed on Mar. coadministration strategy that combines local codelivery of a 13, 2013, provisional application No. 61/707,733, therapeutic agent and an intracellular penetration enhancing filed on Sep. 28, 2012, provisional application No. agent, and optionally in further combination with local 61/703,890, filed on Sep. 21, 2012. administration of an immunotherapeutic agent, such as a cancer vaccine or NKTagonist. The invention also provides a Publication Classification method for treating cancer using an intracellular penetration enhancing agent. The methods of the invention aim to Sub (51) Int. Cl. stantially kill and/or destroy the target tumor cells, as well as A6 IK 47/12 (2006.01) those cancerous cells that have metastasized to other parts of A6 IK33/24 (2006.01) the body. Patent Application Publication Jun. 16, 2016 Sheet 1 of 10 US 2016/O166697 A1 : : s Patent Application Publication Jun. 16, 2016 Sheet 2 of 10 US 2016/O166697 A1 FG. 2 FG. 3 Patent Application Publication Jun. 16, 2016 Sheet 3 of 10 US 2016/O166697 A1 Cage in nor Biointinescence over tire 120E-01 - 100E+01 \ u', or 8,00E-00 * al- s 6.00E-00 c-AK-2V 222 - 4.00E+00 ya r *" — O.8 1 5 2 2. 3. 3.5 ine Days -- rancer achie r Er Cisplatin V 0.120 mg r;x-Pt O.045 mg -- Pi + Enhancer 0.045rng Relative Change in B waites low dose of its attano'ai cispati 15 1.30 2-8 s - u 1 1. 21-J ----- is O.90. ...-...-...--Allae./ -1 Irelaaaaaaaa... ------ 0 0.5 5 2 2.5 3 3.5 bays since first dose - - Efrancer aire -- Cisplatin V 0.120 mgimouse -- Cisplatin IT -%- Enhancer & Cisplatin IT (37% of W (37% of IV dose) dose) FG. 5 Patent Application Publication Jun. 16, 2016 Sheet 4 of 10 US 2016/O166697 A1 Charge in nor Bioininescence overtine 1.40E+04: 4.30E-01 2----------------------------------------------------------------------------------------------------------------------------------------------------------------------- 1,10E+01 .00+0- 3.0CE+00 8.00E-00---Y 7.00E+00. S-1 is - es is re 6,00E+00. ...?...........If......................... 5.00E+09-i-or- ...?ts. 4.00E+00 - 8 A. 8 3 O 6 hr time point of shown fine bays -(-Enhancer alone - C - Cisplatin V ri-Cisplatin T-3- Cisplatin & Entarcer F.G. 6 Relative Change in 8. 0.40 3. 5. 7 9 6 hr time point ays since first dose not show -XX-Enhance alone - - Cisplatin W - {x - Cisplatin IT -X- Cisplatin & Enhancer FG. 7 Patent Application Publication Jun. 16, 2016 Sheet 5 of 10 US 2016/O166697 A1 Change in Body Weight uring Stady 23.00 - 22.00 - says since first dose -(-Enhancer alone -i- Cisplatin V-ryx" Cisplatin -x- Cisplatin & Enhancer r FG. 8 Patent Application Publication Jun. 16, 2016 Sheet 6 of 10 US 2016/O166697 A1 sÁed Patent Application Publication Jun. 16, 2016 Sheet 7 of 10 US 2016/O166697 A1 :6di1039--~~~~~~~~#--#- c & s is sei.e. 3.838 Patent Application Publication Jun. 16, 2016 Sheet 8 of 10 US 2016/O166697 A1 ~~~~£-- ~/~~•×*~~~~~~ Á#0.3}{300 ----?~-------- Patent Application Publication Jun. 16, 2016 Sheet 9 of 10 US 2016/O166697 A1 ---{}{}{3 8€è#0.*** 3. A Qia. Patent Application Publication Jun. 16, 2016 Sheet 10 of 10 US 2016/O166697 A1 3 of oil. US 2016/01 66697 A1 Jun. 16, 2016 METHOD OF TREATING CANCER ceuticals, cytotoxic agents, monoclonal antibodies; or tran sarterial chemo immobilization (TACE), and combinations CROSS-REFERENCE TO RELATED thereof pursuant to specific regimens based on the specific APPLICATIONS type and stage of cancer under treatment. However, these 0001. This application is a continuation of U.S. Ser. No. therapies are associated with Substantially high costs. In addi 14/280,036, filed May 16, 2014 which is a continuation of tion, current treatment options are highly invasive, are asso PCT/US2013/05984, filed Sep. 15, 2013, which claims pri ciated with significant toxicities, and result in an overall poor ority to, and the benefit of, U.S. Provisional Application No. quality of life for patients. 61/779,509, filed Mar. 13, 2013, U.S. Provisional Application 0008 Standard of care cancer therapies typically couple No. 61/707,733, filed Sep. 28, 2012, and U.S. Provisional surgical removal of the affected tissue with chemotherapy or Application No. 61/703,890, filed Sep. 21, 2012. Each of radiation treatments. Standard approaches for administering these applications is hereby incorporated by reference in their chemotherapeutics are through the blood, e.g., systemic entirety. delivery, which can be achieved by various routes such as intravenous and/or gastrointestinal delivery. However, toxic ity is a major drawback associated with systemically deliv BACKGROUND OF THE INVENTION ered chemotherapeutic drugs. Standard of care Surgical treat 0002 1. Field of the Invention ments also introduce problems, including dislodgement of 0003. The present invention relates to novel methods for cancer cells into the blood and/or lymph systems, which treating cancer. The methods involve treating a carcinoma or results in the opportunity for cancer cells to metastasize to sarcoma using a coadministration strategy that combines other sites in the body and cause additional tumors to form. local codelivery of a therapeutic agent and an intracellular 0009. When surgery is not possible, the accepted treat penetration enhancing agent, optionally in combination with ment for cancer is to use radiation or chemotherapy. But at least one additional therapeutic agent (e.g., local or sys Survival rates for inoperable cancer are low when compared to temic administration of an immunotherapeutic agent). The the Survival rate for cancers that are Surgically removed prior methods of the invention reduce the growth, shrink, and/or to chemotherapy or radiation. eradicate a target tumor, as well as those cancerous cells that 0010 Regional chemotherapy represents a recent advance have metastasized to other parts of the body. in the chemotherapeutic treatment of cancer. This approach 0004 2. Background involves delivering the chemotherapeutic agent directly to the 0005. It is currently believed that cancer cells routinely tumor, e.g., proximal to, adjacent to, or intratumorally, as arise in our bodies but are continuously destroyed by a opposed to introducing the toxic agent into the bloodstream. healthy immune system. It is thought that cancer tumors form One goal of regional chemotherapy is to minimize the toxic when the immune system fails to destroy these routinely side effects typically associated with systemic chemothera formed diseased cells. The word "cancer' is used to describe peutic administration. a number of diseases in which there is uncontrolled division 0011. However, regional chemotherapeutic approaches of abnormal cells. Cancer may initially arise in virtually any generally have not been satisfactory. A general problem with tissue or organ in the body and forms as a result of a complex chemotherapy—including regional chemotherapy—is that interaction of both innate genetic factors and environmental cancer cells are highly resistant to penetration by chemo factors, such as one's diet or exposure to radiation, toxins, and therapeutic agents. For example, certain platinum com the like. Despite advances in medicine and the understanding pounds are mainly taken into cancer cells by an active trans of the molecular basis of cancer, the exact causes of any given port process using the CTR1 pathway (see Holzer et al., type of cancer are largely unknown, especially in a particular Molecular Pharmacology 70: 1390-1394 (2006)). In addi individual. Given this lack of knowledge, it is not Surprising tion, chemotherapeutic agents generally are delivered by the that it remains highly difficult to find effective cancer treat blood, they should be soluble in the blood, making them mentS. generally water soluble. Water soluble materials such as che 0006 Finding effective treatments is also made challeng motherapeutic agents do not effectively pass through lipid ing because cancer often develops resistance to various thera cell membranes passively, and thus, are not readily deliver peutic strategies. In addition, effective means for treating able to the intracellular space of cancer cells especially at low cancer become an even greater challenge in view of the capac concentrations. Further, once inside, tumor cells have mecha ity for certain types of cancers to spread from their primary nisms and various processes designed to excrete the chemo Source. This process, called metastasis, enables cancer cells therapeutic agents. For example, tumor cells are able to rid to spread to other vital parts of the body through the blood and themselves of chemical agents using glutathione and/or met lymph systems. Some experts estimate that only a single cell allothioneins complexing and have innate DNA repair in a million can Survive long enough to help form a metastatic mechanisms to overcome chemotherapies.
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