Pharmacodynamics Relative to other SNRIs,<unk> , as well as milnacipran, differ in that they are much more balanced reuptake inhibitors of serotonin and norepinephrine. To demonstrate, the serotonin:norepinephrine ratios of SNRIs are as follows: venlafaxine = 30:1, duloxetine = 10:1, desvenlafaxine = 14:1, milnacipran = 1.6:1, and<unk>  = 1:2. The clinical implications of more balanced elevations of serotonin and norepinephrine are unclear, but may include improved effectiveness, though also increased side effects.<unk>  is selective for the serotonin and norepinephrine transporters, lacking significant affinity for over 23 off-target sites. However, it does show some affinity for the dizocilpine (MK-801/) 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,<unk>  is an NMDA receptor antagonist at high concentrations.<unk>  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 Alzheimer's disease. Pharmacokinetics<unk>  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.<unk>  is excreted in urine.
Levomilnacipran
Ciltacabtagene autoleucel
Brexucabtagene autoleucel
Lisocabtagene maraleucel
Milnacipran
Pivhydrazine
Darvadstrocel
Damoctocog alfa pegol