This compound and its uses are investigational and have not been approved by the US Food and Drug Administration. Efficacy and safety have not been established. The information presented should not be construed as a recommendation for use. The relevance of findings in preclinical studies to humans is currently being evaluated.
Ipatasertib is an investigational, orally administered, ATP-competitive, selective AKT inhibitor. AKT is a key component of the PI3K/AKT pathway. This pathway is dysregulated in many malignancies, often through acquisition of activating mutations in AKT and phosphatidylinositol 3-kinase (PI3K), loss of the tumor suppressor phosphatase and tensin homolog (PTEN), or amplification of AKT and PI3K.1,2
Some cancer treatments have led to the aberrant activation of the PI3K/AKT pathway, which resulted in the survival and proliferation of tumor cells.1-4 In various preclinical models, PI3K/AKT/mammalian target of rapamycin (mTOR) signaling was shown to become activated following chemotherapy or antihormonal therapy.2,3
Ipatasertib is designed to target and bind to the adenosine triphosphate (ATP)–binding pocket of the 3 activated isoforms of AKT, potentially inhibiting downstream signaling.1 Ipatasertib is being investigated in combination with various treatment modalities (eg, antihormonal therapy, chemotherapy).1,3
FOXO=Forkhead box O; GSK3=glycogen synthase kinase 3; mTORC=mammalian target of rapamycin complex; PDK1=phosphoinositide-dependent kinase-1; PI4,5P2=phosphatidylinositol 4,5-bisphosphate; PIP3=phosphatidylinositol 3,4,5-trisphosphate; RTK=receptor tyrosine kinase.
Watch how ipatasertib inhibits hyperactive PI3K/AKT pathway in cancer.
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