Voriconazole, sold under the brand name Vfend among others, is an antifungal medication used to treat a number of fungal infections. This includes aspergillosis, candidiasis, coccidioidomycosis, histoplasmosis, penicilliosis, and infections by Scedosporium or Fusarium. It can be taken by mouth or used by injection into a vein.Common side effects include vision problems, nausea, abdominal pain, rash, headache, and seeing or hearing things that are not present. Use during pregnancy may result in harm to the baby. It is in the triazole family of medications. It works by affecting fungal metabolism and fungal cell membranes.Voriconazole was patented in 1990 and approved for medical use in the United States in 2002. It is on the World Health Organizations List of Essential Medicines. Medical uses
Voriconazole is used to treat invasive aspergillosis and candidiasis and fungal infections caused by Scedosporium and Fusarium species, which may occur in immunocompromised patients, including people undergoing allogeneic bone marrow transplant (BMT), who have  hematologic cancers or who undergo organ transplants.It is also used to prevent fungal infection in people as they undergo BMT.It is also the recommended treatment for the CNS fungal infections transmitted by epidural injection of contaminated steroids.It can be taken by mouth or given in a doctors office or clinic by intravenous infusion. Contraindications
It is toxic to the fetus; pregnant women should not take it and women taking it should not become pregnant.People who have hereditary intolerance for galactose,  Lapp lactase deficiency, or glucose-galactose malabsorption should not take this drug.
CD20 is widely expressed on B cells, from early pre-B cells to later in differentiation, but it is absent on terminally differentiated plasma cells. Although the function of CD20 is unknown, it may play a role in Ca2+ influx across plasma membranes, maintaining intracellular Ca2+ concentration and allowing activation of B cells. Rituximab is relatively ineffective in elimination of cells with low CD20 cell-surface levels. It tends to stick to one side of B cells, where CD20 is, forming a cap and drawing proteins over to that side. The presence of the cap changes the effectiveness of natural killer (NK) cells in destroying these B cells. When an NK cell latched onto the cap, it had an 80% success rate at killing the cell. In contrast, when the B cell lacked this asymmetric protein cluster, it was killed only 40% of the time.The following effects have been found:
The Fc portion of rituximab mediates antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). Rituximab has a general regulatory effect on the cell cycle. Preferential elimination of malignant B cells with high CD20 levels and high BCR signaling propensity, especially in chronic lymphocytic leukemia (CLL). It increases MHC II and adhesion molecules LFA-1 and LFA-3 (lymphocyte function-associated antigen). It elicits shedding of CD23. It downregulates the B cell receptor. It induces apoptosis of CD20+ cells.