Abstract: The invention provides methods, compositions, and kits containing a first therapeutic agent that is a substituted 2,3-dimethoxyquinone of Formula I, or a pharmaceutically acceptable salt thereof, for treating patients suffering from diabetic retinopathy, diabetic macular edema, and/or other diabetic retinal disorders and/or other disorders.

Abstract: Apurinic/apyrimidinic endonuclease 1 redox factor 1 (APE1/Ref-1) inhibitors for inhibiting ocular diseases are disclosed herein.

Abstract: Combination therapies including a Apurinic/Apyrimidinic Endonuclease/reduction-oxidation (redox) Factor-1 (APE1/Ref-1) inhibitor specific to inhibit the redox function of APE1/Ref-1 are disclosed herein. The Combination therapies can be used for treating various cancers, as well as other angiogenesis-mediated diseases (e.g., retinal diseases, cardiovascular diseases).

Abstract: [[(2E)-2-[(3-methoxy-1,4-dioxo-1,4-dihydronaphthalen-2-yl)methylidene]-N,N-diethylpentanamide] (APX2009) and (2E)-2-[(3-methoxy-1,4-dioxo-1,4-dihydronapthalen-2-yl)methylidene]-N-methoxypentanamide] (APX2014) for inhibiting ocular diseases are disclosed herein.

Abstract: Combination therapies including a Apurinic/Apyrimidinic Endonuclease/reduction-oxidation (redox) Factor-1 (APE1/Ref-1) inhibitor specific to inhibit the redox function of APE1/Ref-1 are disclosed herein. The Combination therapies can be used for treating various cancers, as well as other angiogenesis-mediated diseases (e.g., retinal diseases, cardiovascular diseases).

Abstract: Disclosed are novel methods for the therapeutic treatment of cancer and angiogenesis. The enzyme Ape1/Ref-1, via its redox function, enhances the DNA binding activity of transcription factors that are associated with the progression of cancer. The present disclosure describes the use of agents to selectively inhibit the redox function of Ape1/Ref-1 and thereby reduce tumor cell growth, survival, migration and metastasis. In addition, Ape1/Ref-1 inhibitory activity is shown to augment the therapeutic effects of other therapeutics and protect normal cells against toxicity. Further, Ape1/Ref-1 inhibition is shown to decrease angiogenesis, for use in the treatment of cancer as well other pathologic conditions of which altered angiogenesis is a component.

Abstract: Disclosed are novel methods for the therapeutic treatment of cancer and angiogenesis. The enzyme Ape1/Ref-1, via its redox function, enhances the DNA binding activity of transcription factors that are associated with the progression of cancer. The present invention describes the use of agents to selectively inhibit the redox function of Ape1/Ref-1 and thereby reduce tumor cell growth, survival, migration and metastasis. In addition, Ape1/Ref-1 inhibitory activity is shown to augment the therapeutic effects of other therapeutics and protect normal cells against toxicity. Further, Ape1/Ref-1 inhibition is shown to decrease angiogenesis, for use in the treatment of cancer as well other pathologic conditions of which altered angiogenesis is a component.

Abstract: Methods of reducing neuronal sensitivity, thereby reducing inflammation and chronic pain, in subjects having diabetes are disclosed herein. Particularly disclosed are methods of administrating the apurinic/apyrimidinic endonuclease 1 redox factor 1 (APE 1/Ref-1) inhibitor, APX3330, to enhance the DNA base excision repair (BER) pathway, thereby reducing neuronal sensitivity to inflammatory mediators and alleviating inflammatory or chronic pain.

Abstract: Disclosed are novel methods for the therapeutic treatment of cancer and angiogenesis. The enzyme Ape1/Ref-1, via its redox function, enhances the DNA binding activity of transcription factors that are associated with the progression of cancer. The present disclosure describes the use of agents to selectively inhibit the redox function of Ape1/Ref-1 and thereby reduce tumor cell growth, survival, migration and metastasis. In addition, Ape1/Ref-1 inhibitory activity is shown to augment the therapeutic effects of other therapeutics and protect normal cells against toxicity. Further, Ape1/Ref-1 inhibition is shown to decrease angiogenesis, for use in the treatment of cancer as well other pathologic conditions of which altered angiogenesis is a component.

Abstract: Methods of reducing inflammation and chronic pain in the gut of a subject suffering from inflammatory bowel disease (IBD) are disclosed herein. Particularly disclosed are methods of administrating the apurinic/apyrimidinic endonuclease 1 redox factor 1 (APE1/Ref-1) inhibitor, APX3330, which blocks APE1 and regulates transcription factors (TFs) involved in inflammation, thereby alleviating inflammatory or chronic pain.

Abstract: [[(2E)-2-[(3-methoxy-1,4-dioxo-1,4-dihydronaphthalen-2-yl)methylidene]-N,N-diethylpentanamide] (APX2009) and (2E)-2-[(3-methoxy-1,4-dioxo-1,4-dihydronapthalen-2-yl)methylidene]-N-methoxypentanamide] (APX2014) for inhibiting ocular diseases are disclosed herein.

Abstract: Compounds, compositions, and formulations, and accompanying methods useful for treating disorders arising from oxidative DNA damage, including oxidative DNA damage resulting from ionizing radiation or other therapy are described herein.

Abstract: Combination therapies including a Apurinic/Apyrimidinic Endonuclease/reduction-oxidation (redox) Factor-1 (APE1/Ref-1) inhibitor specific to inhibit the redox function of APE1/Ref-1 are disclosed herein. The Combination therapies can be used for treating various cancers, as well as other angiogenesis-mediated diseases (e.g., retinal diseases, cardiovascular diseases).

Abstract: Methods for targeting apurinic/apyrimidinic endonuclease1/redox effector factor 1 (APE1/Ref-1) are disclosed. More particularly, methods for inhibiting APE1/Ref-1 and hypoxia-mediated signaling for decreasing survival and invasion of tumor cells exposed to hypoxic conditions are disclosed.

Abstract: Methods of reducing neuronal sensitivity, thereby reducing inflammation and chronic pain, in subjects having diabetes are disclosed herein. Particularly disclosed are methods of administrating the apurinic/apyrimidinic endonuclease 1 redox factor 1 (APE 1/Ref-1) inhibitor, APX3330, to enhance the DNA base excision repair (BER) pathway, thereby reducing neuronal sensitivity to inflammatory mediators and alleviating inflammatory or chronic pain.

Abstract: Compounds, compositions, and formulations, and accompanying methods useful for treating disorders arising from oxidative DNA damage, including oxidative DNA damage resulting from ionizing radiation or other therapy are described herein.

Abstract: Compounds, compositions, and formulations, and accompanying methods useful for treating disorders arising from oxidative DNA damage, including oxidative DNA damage resulting from ionizing radiation or other therapy are described herein.

Abstract: Methods of using redox APE1/Ref-1 inhibitors to treat prostate cancer, and particularly, metastatic prostate cancer, are disclosed. Particularly, small molecule inhibitors of APE1/Ref-1 redox activity have been found to decrease cell proliferation and induce cell cycle arrest in metastatic prostate cancer cell lines. Further, these APE1/Ref-1 redox inhibitors can be used to reduce expression of survivin, which has been shown to be overexpressed in primary and metastatic tumors.

Abstract: Compounds, and methods and uses of compounds, and pharmaceutical compositions thereof, are described herein for treating myeloid malignancies. In particular, compounds, and methods and uses of compounds, and pharmaceutical compositions thereof, are described herein for treating acute myeloid leukemia (AML), myeloproliferative neoplasm (MPN), and/or myelodysplastic syndrome (MDS).

Abstract: Disclosed are novel methods for the therapeutic treatment of cancer and angiogenesis. The enzyme Ape1/Ref-1, via its redox function, enhances the DNA binding activity of transcription factors that are associated with the progression of cancer. The present disclosure describes the use of agents to selectively inhibit the redox function of Ape1/Ref-1 and thereby reduce tumor cell growth, survival, migration and metastasis. In addition, Ape1/Ref-1 inhibitory activity is shown to augment the therapeutic effects of other therapeutics and protect normal cells against toxicity. Further, Ape1/Ref-1 inhibition is shown to decrease angiogenesis, for use in the treatment of cancer as well other pathologic conditions of which altered angiogenesis is a component.