It is a controlled substance in the United States and is considered to have a low misuse potential. Pharmacology
Pharmacodynamics
Lemborexant is a dual antagonist of the orexin OX1 and OX2 receptors. It associates and dissociates from the orexin receptors more rapidly than certain other orexin receptor antagonists, such as suvorexant, and this may cause it to have a shorter duration of action. Pharmacokinetics
The bioavailability of lemborexant is good and is at least 87%. The time to peak levels of lemborexant is 1 to 3 hours. A high-fat and high-calorie meal has been found to delay the time to peak levels by 2 hours. Its plasma protein binding in vitro is 94%. Lemborexant is metabolized primarily by CYP3A4 and to a lesser extent by CYP3A5. The "effective" half-life of lemborexant is 17 to 19 hours while its terminal elimination half-life is 55 hours. The medication is excreted in feces (57%) and to a lesser extent urine (29%). Although lemborexant has a longer terminal elimination half-life than suvorexant, it appears to be more rapidly cleared than suvorexant in the earlier phases of elimination. In addition, lemborexant dissociates from the orexin receptors more rapidly than does suvorexant. These differences may allow for comparatively reduced next-day effects such as daytime somnolence with lemborexant. History
In June 2016, Eisai initiated Phase III clinical trials in the United States, France, Germany, Italy, Japan, Poland, Spain and the UK.In December 2019, lemborexant was approved for use in the United States based on results from the SUNRISE 1 and SUNRISE 2 Phase III clinical trials.
Sneddons syndrome is a form of arteriopathy characterized by several symptoms, including:

Severe, transient neurological symptoms or stroke
Livedo reticularis, or livedo racemosa

Signs and symptoms
Sneddons syndrome generally manifests with stroke or severe, transient neurological symptoms, and a skin rash (livedo reticularis). Livedo reticularis appears as a bluish-purple, netlike mottling of the skin. Sneddons syndrome may instead present with livedo racemosa, which involves larger, less organized patches of bluish-purple mottling of the skin. Both are generally found first in the extremities, both worsen in cold and either may occur without Sneddons Syndrome or any other systemic disease.Sneddons Syndrome can be characterized by: transient amnesia, transient aphasia, palsy, headaches, hypertension, transient ischemic attacks (TIA), stroke, coronary disease and dementia. The skin manifestations may precede the neurologic symptoms by years. Pathogenesis
Sneddons syndrome is a progressive, noninflammatory arteriopathy leading to the characteristic skin condition and to cerebrovascular problems, including stroke, transient ischemic attack (TIA), severe but transient neurological symptoms thought to be caused by cerebral vasospasm, coronary disease and early-onset dementia. Progressive compromise of arterial linings in Sneddons produces clotting, for which high-dose warfarin is most commonly prescribed, and can also cause the development of systemic arterial plaque when cholesterol levels are normal. Diagnosis
There are no diagnostic tests on which all Sneddons patients will have abnormal results, although brain MRI and skin biopsy are often abnormal. The diagnosis is based on a detailed history and physical examination. About 40-60% of patients with the syndrome test positive for antiphospholipid antibodies.