Betahistine

136.19

136.19

227-086-4

X32KK4201D

42617

DTXSID3022665

C83554

N07CA01|N - Nervous system

2933399090

24.9

0.68

Solid

0.984 g/cm³

150-144

113-114 °C

206 °F

n20/D 1.518(lit.)

3.5, 9.7

3.5, 9.7

UN2735

2

36/37/38

26-37/39

UT5552000

Xi,C

P261-P305 + P351 + P338

H315-H319-H335

|Warning|H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]|P261, P264, P271, P280, P302+P352, P304+P340, P305+P351+P338, P312, P321, P332+P313, P337+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 45 companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Symptoms of an overdose with betahistine (< 640 mg) include dry mouth, nausea, dyspepsia, abdominal pain, and somnolence. Serious complications such as convulsions, pulmonary or cardiac effects may occur with higher doses (> 640 mg), especially during intentional overdoses and combination with other drugs. In the case of an overdose with betahistine, provide supportive therapy, and contact the local poison control center for further management.

The plasma protein binding of betahistine is reported to be less than 5%.

Betahistine is indicated for the reduction of recurrent vertigo episodes associated with Ménière's disease in patients 18 years old and above.|Treatment of peripheral vertigo

Through its actions on the histamine receptors, betahistine provides relief from vertigo associated with Ménière's disease.

Drugs used to cause dilation of the blood vessels. (See all compounds classified as Vasodilator Agents.)|Drugs that bind to and activate histamine receptors. Although they have been suggested for a variety of clinical applications histamine agonists have so far been more widely used in research than therapeutically. (See all compounds classified as Histamine Agonists.)

When given orally, betahistine is rapidly and almost completely absorbed from the gastrointestinal tract. In the fasted state, Cmax is achieved within 1 hour of administration; in the fed state, Cmax is delayed, but the total drug absorption is similar. Food, therefore, has little effect on the absorption of betahistine.[A220563,16388]|Betahistine is mainly excreted in the urine; with approximately 85-91% being detected in urine samples within 24 hours of administration.|In a pharmacokinetic study of rats, betahistine was found to be distributed throughout the body. Human data for betahistine's volume of distribution is not readily available.

Betahistine is metabolized primarily into the inactive metabolite 2-pyridylacetic acid. There is both clinical and in vitro evidence that monoamine oxidase enzymes are responsible for the metabolism of betahistine.

The half-life of betahistine is 3-4 hours.

Vertigo is a disturbing sensation of movement caused by dysfunction of the labyrinth (inner ear), vestibular nerve, cerebellum, brainstem, or Central Nervous System (CNS). Vestibular forms of vertigo are often accompanied by auditory dysfunctions such as hyperacusis, hearing loss, and tinnitus. In most cases, adaptive mechanisms of the CNS lead to functional recovery after episodes of vertigo, however, syndromes such as Ménière's disease tend to cause the recurrence of vertigo symptoms. This significantly impacts the quality of life and the ability to carry out daily activities. **H1-receptor activity** The mechanism of action of betahistine is multifactorial. Ménière's disease is thought to result from a disruption of endolymphatic fluid homeostasis in the ear. Betahistine mainly acts as a histamine H1-receptor agonist. The stimulation of H1-receptors in the inner ear causes a vasodilatory effect leading to increased permeability of blood vessels and a reduction in endolymphatic pressure; this action prevents the rupture of the labyrinth, which can contribute to the hearing loss associated with Ménière's disease. Betahistine is also purported to act by reducing the asymmetrical functioning of sensory vestibular organs and increasing vestibulocochlear blood flow, relieving symptoms of vertigo. **H3-receptor activity** In addition to the above mechanisms, betahistine also acts as a histamine H3-receptor antagonist, increasing the turnover of histamine from postsynaptic histaminergic nerve receptors, subsequently leading to an increase in H1-agonist activity. H3-receptor antagonism elevates levels of neurotransmitters including serotonin in the brainstem, inhibiting the activity of vestibular nuclei, thus restoring proper balance and decreasing vertigo symptoms.

Aequamen

2-Pyridineethanamine, N-methyl-: INACTIVE

Human Drugs -> EU pediatric investigation plans