A targeted oral inhibitor of PI3K delta, to be used in combination with rituximab for the treatment of relapsed CLL.
Acts by interfering with key signaling events that are activated in CLL cells within the microenvironment acting very lymphoid tissues such as lymph nodes and spleen.
Interactions between the leukemia cells in the microenvironment activate the B-cell sectors on the CLL cells, which induces sequential activation of downstream signaling molecules,, such as the spleen tyrosine kinase, Bruton’s tyrosine kinase and PI3 kinases, promoting survival and proliferation of CLL.
The p11odelta-isoform of PI3K is overexpressed in CLL B-cells and blocks survival signals provided by the microenvironment.
Approved for the treatment of patients with B-cell follicular lymphoma who have received at least 2 prior therapies.
Approved for the treatment of patients with small lymphocytic lymphoma who have received at least 2 prior therapies.
The addition of idelalisib to rituximab improves overall survival in refractory CLL patients by 72% and progression free survival by 82% versus placebo and rituximab.
Single agent idelalisib has an overall response rate of 54% as a single agent for refractory follicular lymphoma and 61% for small lymphocytic lymphoma
Dose 150 mg start, administered orally twice a day.
Indicated in combination with rituximab for the treatment of adults with relapsed CLL.
When added to rituximab, and bendamustine in relapsed
or refractory CLL patients it reduces disease progression and death.
Generally well-tolerated.
It does not substantially affect the patient’s blood counts.
Fatal and/or serious hepatotoxicity has occurred and 14% of treated patients: Monitoring hepatic function prior to and during treatment is recommended.
Fatal and/or serious and severe diarrhea or colitis occurs and 14% of patients.
Fatal and serious pneumonitis can occur.
Fatal and serious intestinal perforation can occur.
Neutropenic fever can occur.
A strong CYP3A inhibitor other CYP3A inhibitor and inducer drugs should be avoided.