Common adverse drug reactions (≥1% of people) include confusion, dizziness, drowsiness, headache, insomnia, agitation, and/or hallucinations. Less common adverse effects include vomiting, anxiety, hypertonia, cystitis, and increased libido.Like many other NMDA antagonists, memantine behaves as a dissociative anesthetic at supratherapeutic doses. Despite isolated reports, recreational use of memantine is rare due to the drugs long duration and limited availability. Also memantine seems to lack effects such as euphoria or hallucinations.Memantine appears to be generally well tolerated by children with autism spectrum disorder. Pharmacology
Glutamate
A dysfunction of glutamatergic neurotransmission, manifested as neuronal excitotoxicity, is hypothesized to be involved in the etiology of Alzheimers disease. Targeting the glutamatergic system, specifically NMDA receptors, offers a novel approach to treatment in view of the limited efficacy of existing drugs targeting the cholinergic system.Memantine is a low-affinity voltage-dependent uncompetitive antagonist at glutamatergic NMDA receptors. By binding to the NMDA receptor with a higher affinity than Mg2+ ions, memantine is able to inhibit the prolonged influx of Ca2+ ions, particularly from extrasynaptic receptors, which forms the basis of neuronal excitotoxicity. The low affinity, uncompetitive nature, and rapid off-rate kinetics of memantine at the level of the NMDA receptor-channel, however, preserves the function of the receptor at synapses, as it can still be activated by physiological release of glutamate following depolarization of the postsynaptic neuron. The interaction of memantine with NMDA receptors plays a major role in the symptomatic improvement that the drug produces in Alzheimers disease.
In studies this corresponds to higher incidences of severe neutropenia and diarrhea.In 2004, a clinical study was performed that both validated prospectively the association of the *28 variant with greater toxicity and the ability of genetic testing in predicting that toxicity before chemotherapy administration.In 2005, the FDA made changes to the labeling of irinotecan to add pharmacogenomics recommendations, such that irinotecan recipients with a homozygous (both of the two gene copies) polymorphism in UGT1A1 gene, to be specific, the *28 variant, should be considered for reduced drug doses. Irinotecan is one of the first widely used chemotherapy agents that is dosed according to the recipients genotype. Approval
Irinotecan received accelerated approval from the U.S. Food and Drug Administration (FDA) in 1996, and full approval in 1998. Names
During development, it was known as CPT-11. Formulations
A liposome encapsulated version of irinotecan sold as Onivyde by Merrimack Pharmaceuticals, was approved by FDA in October 2015, to treat metastatic pancreatic cancer. It was approved for medical use in the European Union in October 2016. See also
Etirinotecan pegol, an experimental derivative of irinotecan with a longer half-life in the human body

References
Further reading
Dean L (2015). "Irinotecan Therapy and UGT1A1 Genotype". In Pratt VM, McLeod HL, Rubinstein WS,  et al. (eds.). Medical Genetics Summaries. National Center for Biotechnology Information (NCBI). PMID 28520360. Bookshelf ID: NBK294473. External links
"Irinotecan". Drug Information Portal. U.S. National Library of Medicine. "Irinotecan hydrochloride". Drug Information Portal. U.S. National Library of Medicine. Irinotecan Pathway on PharmGKB