DDInter927 DDInter905
Inotuzumab ozogamicin is an antibody-drug conjugate using linker and cytotoxic drug technology similar to that developed for the ground-breaking treatment Mylotarg (), which was approved by the US FDA in 2000 for the treatment of acute myeloid leukaemia. Inotuzumab ozogamicin consists of a recombinant humanised IgG4 kappa CD22-targeting monoclonal antibody covalently attached to calicheamicin derivative, N-acetyl-gamma-calicheamicin dimethylhydrazide, which is a potent DNA-binding cytotoxic agent. Developed by Pfizer and UCB, inotuzumab ozogamicin was granted approval by EU in June 2017 followed by FDA on August 17th, 2017 for the treatment of adults with relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). ALL is a rapidly progressing cancer of the bone marrow that is associated with
Idelalisib is a phosphoinositide 3-kinase inhibitor indicated in the treatment of chronic lymphocytic leukemia (CLL), relapsed follicular B-cell non-Hodgkin lymphoma (FL), and relapsed small lymphocytic lymphoma (SLL). For the treatment of relapsed CLL, it is currently indicated as a second-line agent in combination with rituximab in patients for whom rituximab alone would be considered appropriate therapy due to other co-morbidities, while in the treatment of FL and SLL it is intended to be used in patients who have received at least two prior systemic therapies. More specifically, idelalisib targets P110δ, the delta isoform of the enzyme phosphatidylinositol-4,5-bisphosphate 3-kinase, also known as PI-3K. The PI-3Ks are a family of enzymes involved in cellular functions such as cell growth, proliferation, differentiation, motility, survival and intracellular trafficking, which in turn are involved in cancer. In contrast to the other class IA PI3Ks p110α and p110β, p110δ is principally expressed in leukocytes (white blood cells) and is important for the function of T cells, B cell, mast cells and neutrophils. By inhibiting this enzyme, idelalisib induces apoptosis of malignant cells and inhibits several cell signaling pathways, including B-cell receptor (BCR) signaling and C-X-C chemokine receptors type 5 and type 4 signalling, which are involved in trafficking and homing of B-cells to the lymph nodes and bone marrow. Treatment of lymphoma cells with idelalisib has been shown to result in inhibition of chemotaxis and adhesion, and reduced cell viability.
Idelalisib {u} may cause a minor interaction that can limit clinical effects when taken with {v} Sibutramine
Idelalisib {u} may cause a minor interaction that can limit clinical effects when taken with {v} Cannabidiol
Idelalisib {u} may cause a moderate interaction that could exacerbate diseases when taken with {v} Eltrombopag
Idelalisib {u} may cause a moderate interaction that could exacerbate diseases when taken with {v} Satralizumab
Idelalisib {u} may lead to a major life threatening interaction when taken with {v} Baricitinib
Idelalisib {u} may lead to a major life threatening interaction when taken with {v} Vinorelbine
Idelalisib may cause a minor interaction that can limit clinical effects when taken with Sibutramine
Idelalisib may cause a minor interaction that can limit clinical effects when taken with Cannabidiol
Idelalisib may cause a moderate interaction that could exacerbate diseases when taken with Eltrombopag
Idelalisib may cause a moderate interaction that could exacerbate diseases when taken with Satralizumab
Idelalisib may lead to a major life threatening interaction when taken with Baricitinib
Idelalisib may lead to a major life threatening interaction when taken with Vinorelbine