Mechanism of action PI3Kδ is expressed in normal and malignant B-cells. By inhibiting it,<unk>  induces apoptosis and prevents proliferation in cell lines derived from malignant B-cells and in primary tumor cells. It also inhibits several cell signaling pathways, including B-cell receptor (BCR) signaling and the CXCR4 and CXCR5 signaling, which are involved in the trafficking and homing of B-cells to the lymph nodes and bone marrow. Idelisib reduces the levels of CD20 on the surface of malignant B lymphocytes by interfering with the IL4-STAT6, which might explain some of its repressive effects on the biology of B cells, but also impair its efficacy in combination with anti-CD20 antibodies (rituximab, ofatumumab etc). Binding profile<unk>  is a competitive inhibitor of the ATP binding site of the PI3Kδ catalytic domain. Its in vitro potency and selectivity relative to the other Class I PI3K isoforms is the following: PI3K isoform IC50, nM IC50-based PI3Kδ-fold selectivity PI3Kα 8,600 453 PI3Kβ 4,000 211 PI3Kγ 2,100 110 PI3Kδ 19 1
Idelalisib
Duvelisib
Alpelisib
Etalocib
Glasdegib
Enasidenib
Vismodegib
Ivosidenib