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1. Metabolism-driven in vitro/in vivo disconnect of an oral ERɑ VHL-PROTAC

2. Table S4 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations

3. Figure 6 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations

4. Supplementary Figures S1-S16 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations

5. Figure 5 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations

6. Figure 3 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations

7. Figure 1 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations

8. Supplementary Tables from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations

9. Figure 4 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations

10. Data from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations

11. Figure 2 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations

13. Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations

14. Multiomic profiling of breast cancer cells uncovers stress MAPK-associated sensitivity to AKT degradation

15. Drug mechanism‐of‐action discovery through the integration of pharmacological and CRISPR screens

16. Abstract 5321: Large scale pan cancer drug combination screening to identify effective and actionable combinations and biomarker hypothesis

18. Supplementary Figures 1-5 from Tumors with AKT1E17K Mutations Are Rational Targets for Single Agent or Combination Therapy with AKT Inhibitors

19. Data from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel

20. Supplementary Materials text from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel

21. Supplementary Figure Legends 1-5 from Preclinical Pharmacology of AZD5363, an Inhibitor of AKT: Pharmacodynamics, Antitumor Activity, and Correlation of Monotherapy Activity with Genetic Background

22. Supplementary Figure 1 from Preclinical Pharmacology of AZD5363, an Inhibitor of AKT: Pharmacodynamics, Antitumor Activity, and Correlation of Monotherapy Activity with Genetic Background

24. Supplementary Table 1 from Preclinical Pharmacology of AZD5363, an Inhibitor of AKT: Pharmacodynamics, Antitumor Activity, and Correlation of Monotherapy Activity with Genetic Background

26. Supplementary Tables 1-3 and Figure 1-7 from Inhibition of PI3Kβ Signaling with AZD8186 Inhibits Growth of PTEN-Deficient Breast and Prostate Tumors Alone and in Combination with Docetaxel

28. Data from Combined Inhibition of mTOR and CDK4/6 Is Required for Optimal Blockade of E2F Function and Long-term Growth Inhibition in Estrogen Receptor–positive Breast Cancer

30. Supplementary figures and tables from Combined Inhibition of mTOR and CDK4/6 Is Required for Optimal Blockade of E2F Function and Long-term Growth Inhibition in Estrogen Receptor–positive Breast Cancer

31. Supplementary Figure legends from Tumors with AKT1E17K Mutations Are Rational Targets for Single Agent or Combination Therapy with AKT Inhibitors

34. Supplementary Figure 2 from Preclinical Pharmacology of AZD5363, an Inhibitor of AKT: Pharmacodynamics, Antitumor Activity, and Correlation of Monotherapy Activity with Genetic Background

35. Supplementary Figure 3 from Preclinical Pharmacology of AZD5363, an Inhibitor of AKT: Pharmacodynamics, Antitumor Activity, and Correlation of Monotherapy Activity with Genetic Background

36. Supplementary Figure 5 from Preclinical Pharmacology of AZD5363, an Inhibitor of AKT: Pharmacodynamics, Antitumor Activity, and Correlation of Monotherapy Activity with Genetic Background

37. Supplementary Figure 4 from Preclinical Pharmacology of AZD5363, an Inhibitor of AKT: Pharmacodynamics, Antitumor Activity, and Correlation of Monotherapy Activity with Genetic Background

45. Multi-omic profiling of breast cancer cells uncovers stress MAPK-associated sensitivity to AKT degradation

48. Assembly of nuclear dimers of PI3K regulatory subunits is regulated by the Cdc42-activated tyrosine kinase ACK

50. Discovery of PROTAC molecules that selectively degrade the IRAK3 pseudokinase

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