However, it does show some affinity for the dizocilpine (MK-801/PCP) site of the NMDA receptor (Ki = 1.7 μM), and has been found to inhibit NR2A and NR2B subunit-containing NMDA receptors with respective IC50 values of 5.62 and 4.57 μM. As such, levomilnacipran is an NMDA receptor antagonist at high concentrations.Levomilnacipran has recently been found to act as an inhibitor of beta-site amyloid precursor protein cleaving enzyme-1 (BACE-1), which is responsible for β-amyloid plaque formation, and hence may  be a potentially useful drug in the treatment of Alzheimers disease. Pharmacokinetics
Levomilnacipran has a high oral bioavailability of 92% and a low plasma protein binding of 22%. It is metabolized in the liver by the cytochrome P450 enzyme CYP3A4, thereby making the medication susceptible to grapefruit-drug interactions. The drug has an elimination half-life of approximately 12 hours, allowing for once-daily administration. Levomilnacipran is excreted in urine. History
Levomilnacipran was developed by Forest Laboratories and Pierre Fabre Group, and was approved by the Food and Drug Administration in July 2013. References
External links
 Media related to Levomilnacipran at Wikimedia Commons
"Levomilnacipran". Drug Information Portal. U.S. National Library of Medicine.
The epithelium of the trachea, bronchi, or gastrointestinal tract may be involved in SJS and TEN. Ocular symptoms are the most common complication in TEN, experienced by 20–79% of those with TEN, even by those who do not experience immediate ocular manifestations. These can include dry eyes, photophobia, symblepharon, corneal scarring or xerosis, subconjunctival fibrosis, trichiasis, decreased visual acuity, and blindness. Cause
Drug reactions have been reported to cause 80–95% of TEN cases.The drugs most often implicated in TEN are:

antibiotics
sulfonamides (sulfamethoxazole, sulfadiazine, sulfapyridine)
beta-lactams (cephalosporins, penicillins, carbapenems)
nonsteroidal anti-inflammatory drugs
allopurinol
antimetabolites (methotrexate)
antiretroviral drugs (nevirapine)
corticosteroids
anxiolytics (chlormezanone)
anticonvulsants (phenobarbital, phenytoin, carbamazepine, lamotrigine, and valproic acid).TEN has also been reported to result from infection with Mycoplasma pneumoniae or dengue virus. Contrast agents used in imaging studies as well as transplantation of bone marrow or organs have also been linked to TEN development. HIV
HIV-positive individuals have 1000 times the risk of developing SJS/TEN compared to the general population. The reason for this increased risk is not clear. Genetics
Certain genetic factors are associated with increased risk of TEN. For example, certain HLA-types such as, HLA-B*1502, HLA-A*3101, HLA-B*5801, and HLA‐B*57:01 have been seen to be linked with TEN development when exposed to specific drugs. Pathogenesis
The immune systems role in the precise pathogenesis of TEN remains unclear. It appears that a certain type of immune cell (cytotoxic CD8+ T cell) is primarily responsible for keratinocyte death and subsequent skin detachment. Keratinocytes are the cells found lower in the epidermis and specialize in holding the surrounding skin cells together.