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Phosphoinositide 3-kinases (PI3Ks) are a family of lipid kinases that phosphorylate phosphatidylinositol lipids to regulate cell growth, survival, metabolism, and immune signaling. PI3K activation leads to downstream AKT and mTOR pathway signaling. Aberrant PI3K signaling is frequently observed in cancer due to PIK3CA mutations, PTEN loss, or receptor tyrosine kinase activation.

Class I PI3Ks include four catalytic isoforms: PI3Kα (PIK3CA) PI3Kβ (PIK3CB) PI3Kδ (PIK3CD) PI3Kγ (PIK3CG) PI3Kα and β are broadly expressed, while PI3Kδ and γ are enriched in leukocytes and play critical roles in immune regulation. Isoform selectivity is an important consideration in drug development due to toxicity and immune effects.

PI3K inhibitors can be classified as: Pan-PI3K inhibitors Isoform-selective inhibitors (α, β, δ, γ) Dual PI3K/mTOR inhibitors Irreversible inhibitors Selectivity influences therapeutic window and toxicity profile.

While PI3K inhibitors block upstream lipid kinase activity, mTOR inhibitors act downstream at the level of mTORC1 or mTORC2. Dual PI3K/mTOR inhibitors target both nodes of the pathway and may achieve broader pathway suppression.

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