Abstract: The present technology relates to processes, compounds, compositions, and methods useful for coupling reactions. Also, the present disclosure provides for novel intermediates, compositions of matter, and processes relating to the Chk1 inhibitor, SRA737.

Abstract: Herein disclosed are methods of treatment administering SRA737 as a monotherapy or in a combination therapy useful for treating patients with cancer.

Abstract: Disclosed herein are methods of treatment by administering SRA737 as a monotherapy or in a combination therapy that is useful for treating patients with cancer.

Abstract: Herein disclosed are combinations of Checkpoint Kinase 1 (Chk1) inhibitors and PARP inhibitors useful for inhibiting the growth of tumors such as those in patients with cancer. In particular, the combination demonstrates remarkable synergistic effects on cancer cells that are representative models for tumors. Also provided for are methods for treating disorders or diseases mediated or affected by Chk1 and/or PARP activity.

Abstract: Herein disclosed are combinations of Checkpoint Kinase 1 (Chk1) inhibitors and PARP inhibitors useful for inhibiting the growth of tumors such as those in patients with cancer. In particular, the combination demonstrates remarkable synergistic effects on cancer cells that are representative models for tumors. Also provided for are methods for treating disorders or diseases mediated or affected by Chk1 and/or PARP activity.

Abstract: This disclosure provides methods of using a checkpoint kinase 1 (Chk1) inhibitor in the treatment of cancer in a subject having at least an intermediate tumor mutational burden (TMB), or a genetic abnormality in one or more particular genes associated with replicative stress. Accordingly, methods of treating cancer in a subject having at least an intermediate tumor mutational burden (TMB-I) are provided. Also provided are methods of treating cancer in a subject having a genetic abnormality in one or more particular genes selected from cell cycle regulation genes, replication stress genes, oncogenic driver mutations and DNA damage response and repair network genes. Methods of selecting subjects for Chk1 inhibition therapy are provided. The methods can include administering to the subject an effective amount of a SRA737 compound, in some cases in combination with low dose gemcitabine.