Dual PI3K-δ and PI3K-γ inhibition1

COPIKTRA predominantly targets B cells and disrupts the tumor microenvironment1,2

View dual-isoform inhibition by clicking through the mechanism of action below.1,2,4,5

PI3K-δ

B-cell receptor (BCR) pathway

BCR signaling promotes cellular growth and proliferation, survival, and migration with involvement from multiple downstream kinases, including the PI3K pathway.

PI3K-δ inhibition with COPIKTRA

PI3K-δ inhibition prohibits proliferation and reduces viability in malignant B cells.

Malignant B cell

A genetically unstable B cell that inhibits anti-tumorigenic functions while enhancing the functions of other cells to aid in proliferation, survival, and immune evasion.

moa1

View dual-isoform inhibition by clicking through the mechanism of action below. 1,2,6,7

PI3K-γ

PI3K-γ inhibition with COPIKTRA

PI3K-γ inhibition blocks chemokine-mediated T-cell migration and M2 macrophage polarization.

Macrophages

A monocyte lineage that induces BCR signaling, promotes CLL cell survival, and attracts and retains CLL cells.

Myeloid-derived suppressor cells (MDSCs)

A major cell type found in the tumor microenvironment that incites tumor-supportive effects via suppression of immune responses.

CD4+ T cells

A major cell type that produces pro-survival cytokines and promotes tumor proliferation.

Tumor microenvironment

A network of nonneoplastic cells essential to malignant B-cell survival and proliferation.

moa2
  • CLL, chronic lymphocytic leukemia; δ, delta; γ, gamma; PI3K, phosphoinositide 3-kinase; SLL, small lymphocytic lymphoma.