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2. CRAF dimerization with ARAF regulates KRAS-driven tumor growth

3. ARAF mutations confer resistance to the RAF inhibitor belvarafenib in melanoma

4. Activation Mechanism of Oncogenic Deletion Mutations in BRAF, EGFR, and HER2

5. Data from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900

6. Supplemental Figure 5 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900

7. Supplemental Figure 8 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900

8. Supplemental Figure 6 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900

9. Supplemental Figure 3 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900

10. Supplemental Figure 7 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900

11. Supplemental Figure 4 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900

12. Supplemental Figure 2 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900

13. Supplemental Figure 1 from Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900

15. Structure-based optimization of hydroxylactam as potent, cell-active inhibitors of lactate dehydrogenase

16. RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth

17. Targeting KRAS Mutant Cancers via Combination Treatment: Discovery of a Pyridopyridazinone pan-RAF Kinase Inhibitor

18. Targeting KRAS Mutant Cancers via Combination Treatment: Discovery of a 5-Fluoro-4-(3H)-quinazolinone Aryl Urea pan-RAF Kinase Inhibitor

20. Pharmacological Induction of RAS-GTP Confers RAF Inhibitor Sensitivity in KRAS Mutant Tumors

21. Abstract 874: Pharmacologically induced RAS-GTP levels and CRAF-BRAF hetero-dimerization drive sensitization to Type II pan-RAF inhibitors in KRAS mutant cancer

23. ARAFmutations confer resistance to the RAF inhibitor belvarafenib in melanoma

24. Optimization of 5-(2,6-dichlorophenyl)-3-hydroxy-2-mercaptocyclohex-2-enones as potent inhibitors of human lactate dehydrogenase

25. Abstract 4967: RAF kinase inhibition synergizes with MEK inhibitors in KRAS mutant tumors

28. Identification of substituted 3-hydroxy-2-mercaptocyclohex-2-enones as potent inhibitors of human lactate dehydrogenase

30. Identification of substituted 2-thio-6-oxo-1,6-dihydropyrimidines as inhibitors of human lactate dehydrogenase

31. Discovery of a Potent and Selective in Vivo Probe (GNE-272) for the Bromodomains of CBP/EP300

32. Discovery of a Noncovalent, Mutant-Selective Epidermal Growth Factor Receptor Inhibitor

33. Cell Active Hydroxylactam Inhibitors of Human Lactate Dehydrogenase with Oral Bioavailability in Mice

34. Metabolic plasticity underpins innate and acquired resistance to LDHA inhibition

35. Abstract 4374: Activation mechanism of oncogenic C-helix shifting mutations in BRAF, EGFR, and HER2

36. Kinases as Molecular Switches: Catalytic and Non‐catalytic Functions of BRAF Reveal Novel Insights into Oncogenic Activation

37. Correction to Noncovalent Mutant Selective Epidermal Growth Factor Receptor Inhibitors: A Lead Optimization Case Study

38. 4-Aminoindazolyl-dihydrofuro[3,4- d ]pyrimidines as non-covalent inhibitors of mutant epidermal growth factor receptor tyrosine kinase

39. Pyridones as Highly Selective, Noncovalent Inhibitors of T790M Double Mutants of EGFR

40. Noncovalent Mutant Selective Epidermal Growth Factor Receptor Inhibitors: A Lead Optimization Case Study

41. Mitigation of Acetylcholine Esterase Activity in the 1,7-Diazacarbazole Series of Inhibitors of Checkpoint Kinase 1

42. Discovery of Selective and Noncovalent Diaminopyrimidine-Based Inhibitors of Epidermal Growth Factor Receptor Containing the T790M Resistance Mutation

43. Combination Drug Scheduling Defines a “Window of Opportunity” for Chemopotentiation of Gemcitabine by an Orally Bioavailable, Selective ChK1 Inhibitor, GNE-900

46. Abstract B14: Inherent resistance to BRAF inhibitors in BRAFV600E colorectal tumors is driven by ligand-dependent activation of the EGFR pathway

49. Abstract 5753: RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth

50. Abstract B90: Understanding the effects of RAF inhibitors on RAF signaling in B‐RAF V600E mutant versus wild type tumors

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