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1. Structure-based optimization of aminothiadiazole inhibitors of AKT

3. Data from CC-223, a Potent and Selective Inhibitor of mTOR Kinase: In Vitro and In Vivo Characterization

4. Supplementary Figures S1-S3, Tables S1-S7 from CC-223, a Potent and Selective Inhibitor of mTOR Kinase: In Vitro and In Vivo Characterization

5. Supplemental Methods; Supplemental Tables S1-S7; and Supplemental Figures S1-S6 from Synthetic Lethal Strategy Identifies a Potent and Selective TTK and CLK1/2 Inhibitor for Treatment of Triple-Negative Breast Cancer with a Compromised G1–S Checkpoint

6. Supplementary Figure 5 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

7. Supplementary Figure 4 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

8. Supplementary Data from Pleiotropic Impact of DNA-PK in Cancer and Implications for Therapeutic Strategies

9. Supplementary Figure 1 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

10. Supplementary Figure Legend from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

11. Supplementary Figure 3 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

12. Data from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

13. Supplementary Figure 2 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

14. Supplementary Tables from Pleiotropic Impact of DNA-PK in Cancer and Implications for Therapeutic Strategies

15. Data from Pleiotropic Impact of DNA-PK in Cancer and Implications for Therapeutic Strategies

16. Supplementary Figure 6 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

17. Supplementary Figure 7 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

21. Modulation of CD47-SIRPα innate immune checkpoint axis with Fc-function detuned anti-CD47 therapeutic antibody

24. Pleiotropic Impact of DNA-PK in Cancer and Implications for Therapeutic Strategies

25. Synthetic Lethal Strategy Identifies a Potent and Selective TTK and CLK1/2 Inhibitor for Treatment of Triple-Negative Breast Cancer with a Compromised G1–S Checkpoint

27. Abstract 4694: The humanized anti-CD47 monclonal antibody, CC-90002, has antitumor activity in vitro and in vivo

28. Optimization of a Series of Triazole Containing Mammalian Target of Rapamycin (mTOR) Kinase Inhibitors and the Discovery of CC-115

29. Discovery of Mammalian Target of Rapamycin (mTOR) Kinase Inhibitor CC-223

30. CC-223, a Potent and Selective Inhibitor of mTOR Kinase: In Vitro and In Vivo Characterization

32. CC-122 Has Potent Anti-Lymphoma Activity through Destruction of the Aiolos and Ikaros Transcription Factors and Induction of Interferon Response Pathways

35. The Novel mTOR Kinase Inhibitor CC-223 Demonstrates Significant Activity In In Vitro Models Of Multiple Myeloma (MM), Both As a Single Agent and In Combination With The Approved Agents, Dexamethasone, Lenalidomide and Pomalidomide

37. The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas

38. Sotatercept, an Activin Receptor IIa Ligand Trap, Acts Through Bone Marrow Accessory Cells to Promote Late-Stage Erythropoiesis and a Rapid Induction of Red Blood Cell Number and Hemoglobin

39. Effect of mutant alpha-synuclein on dopamine homeostasis in a new human mesencephalic cell line.

40. The Synthetic Compound CC-5079 Is a Potent Inhibitor of Tubulin Polymerization and Tumor Necrosis Factor-α Production with Antitumor Activity

50. The Novel mTOR Kinase Inhibitor CC-223 Demonstrates Significant Activity In In VitroModels Of Multiple Myeloma (MM), Both As a Single Agent and In Combination With The Approved Agents, Dexamethasone, Lenalidomide and Pomalidomide

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