It is mostly (96.6%) circulating in its original form; only a small proportion is metabolized by the liver enzymes UGT1A1 and UGT1A3, resulting in a glucuronide.The drug is mainly excreted via the faeces (93.3%). Less than 2% is found in the urine. Chemistry
Letermovir is used as the free acid. It is a white to off-white, amorphous powder that is slightly hygroscopic, very slightly soluble in water, and very soluble in acetonitrile, acetone, dimethylacetamide, ethanol, and 2-propanol.The molecule has one asymmetric carbon atom, which is in S configuration. References
External links
"Letermovir". Drug Information Portal. U.S. National Library of Medicine. "Letermovir Injection". MedlinePlus.
It also may be induced temporarily by disorientation (such as on roller coaster rides or when a person has been spinning in circles) or by some drugs (alcohol, lidocaine, and other central nervous system depressants, inhalant drugs, stimulants, psychedelics, and dissociative drugs). Early-onset nystagmus
Early-onset nystagmus occurs more frequently than acquired nystagmus. It can be insular or accompany other disorders (such as micro-ophthalmic anomalies or Down syndrome). Early-onset nystagmus itself is usually mild and non-progressive. The affected persons are usually unaware of their spontaneous eye movements, but vision can be impaired depending on the severity of the eye movements. Types of early-onset nystagmus include the following, along with some of their causes:

Infantile:
Albinism
Aniridia
Bilateral congenital cataract
Bilateral optic nerve hypoplasia
Idiopathic
Lebers congenital amaurosis
Optic nerve or macular disease
Persistent tunica vasculosa lentis
Rod monochromatism
Visual-motor syndrome of functional monophthalmus
Latent nystagmus
Noonan syndrome
Nystagmus blockage syndromeX-linked infantile nystagmus is associated with mutations of the gene FRMD7, which is located on the X chromosome.Infantile nystagmus is also associated with two X-linked eye diseases known as complete congenital stationary night blindness (CSNB) and incomplete CSNB (iCSNB or CSNB-2), which are caused by mutations of one of two genes located on the X chromosome. In CSNB, mutations are found in NYX (nyctalopin). CSNB-2 involves mutations of CACNA1F, a voltage-gated calcium channel that, when mutated, does not conduct ions. Acquired nystagmus
Nystagmus that occurs later in childhood or in adulthood is called acquired nystagmus. The cause is often unknown, or idiopathic, and thus referred to as idiopathic nystagmus.