Company: WHWK
Filing Date: 2025-01-31
Form Type: DEFM14A
Source: 0001193125-25-018470
Chunk: 288

Company: Whitehawk Therapeutics, Inc.
Filing Date: 2025-01-31
Form: DEFM14A
Chunk 288
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| • |     | “a” Indicates groupings of preferred terms defined by standardized queries in the Medical Dictionary 
 for Regulatory Activities.                                                                           |

| • |     | Additional G3 TRAEs were 6% hypokalemia, and 3% each of AST/ALT, amylase, hypophosphatemia, insomnia, lipase, 
 lymphocyte, skin infection, vomiting. No G4 TRAEs were reported.                                              |

In December 2017, we received Orphan Drug Designation (“ODD”) for FYARRO for the treatment of PEComa. In October 2018, the FDA granted Fast Track designation for FYARRO for the treatment of patients with advanced (metastatic or locally advanced) malignant PEComa. In December 2018, the FDA granted Breakthrough Therapy Designation (“BTD”) for FYARRO for the treatment of patients with advanced (metastatic or locally advanced) malignant PEComa. The FDA accepted the NDA in July 2021 and granted full approval on November 22, 2021. In January 2023, the FDA granted us orphan drug exclusivity (“ODE”) for FYARRO for the treatment of patients with advanced malignant PEComa. As a result of ODE for FYARRO in the advanced malignant PEComa indication, the FDA may not approve any other application to market the same drug for the same indication for a period of seven years from NDA approval of FYARRO (November 22, 2028), except in limited circumstances, such as a showing of clinical superiority over the product with orphan exclusivity. FYARRO in combination with KRAS G12Cinhibitors for KRAS G12Cmutated cancer xenografts In 2022, we conducted preclinical studies to investigate the antitumor activity of mTOR inhibitors, FYARRO or everolimus, in combination with KRASG12C inhibitors, sotorasib or adagrasib, in KRAS G12C-mutated cancer xenografts. KRAS is frequently mutated in non-small cell lung cancer (NSCLC) and other tumor types, with the KRAS G12Cpresent in approximately 9% of NSCLC patients. The mTOR pathway is often activated in patients with the KRAS mutation and contributes to adaptive resistance to KRAS inhibitors. We conducted these studies to determine