Cancer
The main use of cyclophosphamide is with other chemotherapy agents in the treatment of lymphomas, some forms of brain cancer, neuroblastoma, leukemia and some solid tumors.Oncovet C (Chemovet S.A.), is the first-based drug approved in Latin America for veterinary use for canine and feline cancer (carcinomas of anal sacs, bladder carcinomas, urethral carcinomas, hemangiosarcomas, lymphomas, mast cell tumor, osteosarcomas, soft tissue sarcoma), feline cancers (mammary carcinomas, hemangiosarcomas, lymphomas, plasmacytomas, chronic lymphocytic leukemia, acute myelogenous leukemia, mast cell tumor). It can be administered in different treatment schemes, such as induction therapy, adjuvant, neoadjuvant, maintenance and metronomic chemotherapy. Autoimmune diseases
Cyclophosphamide decreases the immune systems response, and although concerns about toxicity restrict its use to patients with severe disease, it remains an important treatment for life-threatening autoimmune diseases where disease-modifying antirheumatic drugs (DMARDs) have been ineffective. For example, systemic lupus erythematosus with severe lupus nephritis may respond to pulsed cyclophosphamide. Cyclophosphamide is also used to treat minimal change disease, severe rheumatoid arthritis, granulomatosis with polyangiitis, Goodpasture syndrome and multiple sclerosis.Because of its potential side effects such as amenorrhea or ovarian failure, cyclophosphamide is used for early phases of treatment and later substituted by other medications, such as mycophenolic acid or ACA. AL amyloidosis
Cyclophosphamide, used in combination with thalidomide or lenalidomide and dexamethasone has documented efficacy as an off-label treatment of AL amyloidosis. It appears to be an alternative to the more traditional treatment with melphalan in people who are ill-suited for autologous stem cell transplant.
In 2020, viloxazine was reported to have significant affinity for the serotonin 5-HT2B and 5-HT2C receptors (Ki = 3,900 nM and 6,400 nM) and to act as an antagonist and agonist of these receptors, respectively. It also showed weak antagonistic activity at the serotonin 5-HT7 receptor and the α1B- and β2-adrenergic receptors. These actions, although relatively weak, might be involved in its effects and possibly its therapeutic effectiveness in the treatment of ADHD. Pharmacokinetics
Absorption
The bioavailability of extended-release viloxazine relative to an instant-release formulation was about 88%. Peak and AUC levels of extended-release viloxazine are proportional over a dosage range of 100 to 400 mg once daily. The time to peak levels is 5 hours with a range of 3 to 9 hours after a single 200 mg dose. A high-fat meal modestly decreases levels of viloxazine and delays the time to peak by about 2 hours. Steady-state levels of viloxazine are released after 2 days of once-daily administration and no accumulation occurs. Levels of viloxazine are approximately 40 to 50% higher in children age 6 to 11 years compared to children age 12 to 17 years. Distribution
The plasma protein binding of viloxazine is 76 to 82% over a concentration range of 0.5 to 10 μg/mL. Metabolism
The metabolism of viloxazine is primarily via the cytochrome P450 enzyme CYP2D6 and the UDP-glucuronosyltransferases UGT1A9 and UGT2B15. The major metabolite of viloxazine is 5-hydroxyviloxazine glucuronide. Viloxazine levels are slightly higher in CYP2D6 poor metabolizers relative to CYP2D6 extensive metabolizers. Elimination
The elimination of viloxazine is mainly renal.