The present invention provides use of a multi-target protein kinase inhibitor compound A or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for treating leukemia, and provides a method for treating acute myeloid leukemia, especially acute myeloid leukemia with FLT3 mutation, with compound A. In clinical trials, compound A has certain efficacies both on acute myeloid leukemia with FLT3-ITD mutation and/or FLT3-TKD mutation, and on DEK-CAN positive acute myeloid leukemia with FLT3-ITD mutation. Patients with relapsed and/or refractory acute myeloid leukemia who have failed treatment previously with Type II FLT3 inhibitors (e.g., sorafenib) can still clinically benefit from the treatment with compound A.

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The present invention provides use of a multi-target protein kinase inhibitor compound A or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for treating leukemia, and provides a method for treating acute myeloid leukemia, especially acute myeloid leukemia with FLT3 mutation, with compound A. In clinical trials, compound A has certain efficacies both on acute myeloid leukemia with FLT3-ITD mutation and/or FLT3-TKD mutation, and on DEK-CAN positive acute myeloid leukemia with FLT3-ITD mutation. Patients with relapsed and/or refractory acute myeloid leukemia who have failed treatment previously with Type II FLT3 inhibitors (e.g., sorafenib) can still clinically benefit from the treatment with compound A.

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The instant invention relates to therapeutic combinations of LSD1 inhibitors and one or more other active pharmaceutical ingredient(s) or pharmaceutically acceptable salts thereof. The combinations are particularly useful for treating neoplastic diseases, such as cancer, particularly small cell lung cancer (SCLC).

The instant invention relates to therapeutic combinations of LSD1 inhibitors and one or more other active pharmaceutical ingredient(s) or pharmaceutically acceptable salts thereof. The combinations are particularly useful for treating neoplastic diseases, such as cancer, particularly small cell lung cancer (SCLC).

The present invention provides a novel use and methods comprising antibodies, or antigen-binding fragments thereof, which bind to a CCR7 receptor for use as a novel combination therapy with a BTK inhibitor and/or a Bcl-2 inhibitor in treatment of hyperproliferative blood malignancies, preferably in B-cell lymphomas, such as CLL. The combination can be used as first line, or in naïve patients not treated before with a BTK inhibitor and/or Bcl-2 inhibitor, or in patients with a BTK-inhibitor and/or Bcl-2-inhibitor refractory/relapsed disease. The antibodies and antigen-binding fragments are capable of selectively depleting ex vivo or in vitro malignant cells expressing CCR7 and are capable of impairing/blocking migration of said tumor cells towards CCR7 ligands. These effects are not related to previous or contemporary treatments with a BTK inhibitor and/or a Bcl-2 inhibitor. Similarly, the efficacy of the antibodies is not affected in patients that have relapsed/refractory disease. The use of said antibodies as a monotherapy or as a combination with a BTK inhibitor and/or a Bcl-2 inhibitor for depleting, killing and impairing/blocking migration and activation of tumor cells expressing CCR7 cells is disclosed, thus providing an alternative therapy treating hyperproliferative blood cancers.

The present invention provides a novel use and methods comprising antibodies, or antigen-binding fragments thereof, which bind to a CCR7 receptor for use as a novel combination therapy with a BTK inhibitor and/or a Bcl-2 inhibitor in treatment of hyperproliferative blood malignancies, preferably in B-cell lymphomas, such as CLL. The combination can be used as first line, or in naïve patients not treated before with a BTK inhibitor and/or Bcl-2 inhibitor, or in patients with a BTK-inhibitor and/or Bcl-2-inhibitor refractory/relapsed disease. The antibodies and antigen-binding fragments are capable of selectively depleting ex vivo or in vitro malignant cells expressing CCR7 and are capable of impairing/blocking migration of said tumor cells towards CCR7 ligands. These effects are not related to previous or contemporary treatments with a BTK inhibitor and/or a Bcl-2 inhibitor. Similarly, the efficacy of the antibodies is not affected in patients that have relapsed/refractory disease. The use of said antibodies as a monotherapy or as a combination with a BTK inhibitor and/or a Bcl-2 inhibitor for depleting, killing and impairing/blocking migration and activation of tumor cells expressing CCR7 cells is disclosed, thus providing an alternative therapy treating hyperproliferative blood cancers.

The disclosure relates to methods for treating cancer. More particularly, the disclosure relates to use of chimeric non-natural synthetic proteins, in combination with non-tyrosine targeting kinase inhibitors (NTKIs), in treating cancer and preventing intrinsic and/or acquired resistance to NTKIs.

The disclosure relates to methods for treating cancer. More particularly, the disclosure relates to use of chimeric non-natural synthetic proteins, in combination with non-tyrosine targeting kinase inhibitors (NTKIs), in treating cancer and preventing intrinsic and/or acquired resistance to NTKIs.

Provided is a degrader for injured mitochondria based on an autophagy mechanism, the degrader including a compound or a salt thereof, the compound containing a ligand capable of binding to or accumulating in mitochondria and a substituent represented by the following general formula (1): ##STR00001##
where R.sup.1, R.sup.2, and R.sup.3 are identical to or different from each other, and each represent a hydrogen atom or the like.

Methods of treating malignant lymphoproliferative disorders in a patient, comprising administering an effective amount of a GSK-3β inhibitor, for example 9-ING-41, are provided. Also provided are methods for treating malignant lymphoproliferative disorders comprising administering a ({umlaut over (.Math.)}8K-3β inhibitor, for example 9-ING-41, in combination with a second or multiple therapeutic agents.