The Class IA Phosphoinositol-3-Kinases (PI3K) are heterodimeric lipid kinases, each composed of a regulatory subunit and a p110 catalytic subunit with three isoforms: α, β, and δ.

Class IA PI3Ks are activated by growth factor receptor tyrosine kinases.

PI3Ks generate the lipid second messenger phosophatydilinositol-3,4,5-triphosphate (PIP3), leading to the activation of AKT.

AKT activation leads to the phosphorylation of several targets, including the complex mTORC1.

PI3K signaling has numerous downstream effects on cell survival, growth, protein synthesis, and the inhibition of apoptosis.

The dysregulated activity of PI3Ks may promote tumor cell survival in cancer.

In particular, the PI3Kδ isoform plays a key role in survival and development of B lymphocytes.

PI3Kδ is upregulated and has been shown to be a critical driver of growth and survival in B-cell malignancies, including chronic lymphocytic leukemia (CLL), mantle cell lymphoma (MCL), and non-Hodgkin's lymphoma (NHL).

Incyte is developing inhibitors of PI3Kδ signaling.

PI3Kδ is an important anticancer target implicated in malignant B-cell growth, survival, and migration.

It may also play a role in the development of resistance to currently available therapies and may influence the tumor microenvironment by modulating cytokine production. Emerging data suggest that PI3Kδ may be an important target in hematologic malignancies as well as solid tumors.

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