Clemastine, also known asmeclastin, is a first-generationH1 histamine antagonist (antihistamine) withanticholinergic properties (drying) and sedative side effects.[1] Like all first-generation antihistamines, it is sedating.[2][3]
Patented in 1960, it came into medical use in 1967.[4]
Clemastine is used to relievehay fever andallergy symptoms, including sneezing; runny nose; and red, itchy, tearing eyes. Prescription strength clemastine is also used to relieve the itching and swelling ofhives.[5]
Continuous and/or cumulative use ofanticholinergic medications, including first-generation antihistamines, is associated with higher risk of cognitive decline and dementia in older people.[7][8]
Clemastine is an antihistamine withanticholinergic andsedative effects. Antihistamines competitively bind tohistamine receptor sites, thus reducing the neurotransmitter's effects.[9] Effects of histamine (which are countered by antihistamines) include:
Clemastine inhibits both thevasoconstrictor andvasodilator effects of histamine. Depending on the dose, the drug can produce paradoxical effects, including CNS stimulation or depression.
Most antihistamines exhibit some type ofanticholinergic activity. Antihistamines act by competitively binding to H1-receptor sites, thus blocking the binding of endogenous histamine. Antihistamines do not chemically inactivate or prevent the normal release of histamine.
Clemastine is rapidly absorbed from thegastrointestinal tract and peak plasma concentrations are attained in 2–4 hours. Antihistamines are thought to be metabolized in the liver, mostly by mono-/didemethylation and glucuronide conjugation. It is an inhibitor of cytochrome P450CYP2D6 and may interfere with other drugs metabolized by this isozyme.
Clemastine is a selective histamine H1 antagonist. It binds to the histamine H1 receptor, thus blocking the action ofendogenous histamine, which leads to temporary relief of the negative symptoms caused by histamine.[11]
Clemastine has been studied for its potential to treat several psychiatric and neurological disorders, including possibly promotingremyelination and myelin repair in conditions likemultiple sclerosis (MS).[13][14] Early phase II clinical trials showed promise for promoting remyelination in patients with MS, with clemastine improving nerve conduction velocity in the optic nerve.[15][16] However, a clinical trial (TRAP-MS) was halted in early 2024 after researchers found the disability progression was occurring at a significantly faster rate than anticipated in three participants with MS receiving clemastine.[17][18][19]
^Moghaddasi M, Nabovvati M, Koushki A, Soltansanjari M, Sardarinia M, Mohebi N, et al. (June 2020). "Randomized control trial of evaluation of Clemastine effects on visual evoked potential, nerve fiber layer and ganglion cell layer complex in patients with optic neuritis".Clinical Neurology and Neurosurgery.193: 105741.doi:10.1016/j.clineuro.2020.105741.PMID32145678.
