Buspar Dividose

Buspar Dividose Uses, Dosage, Side Effects, Food Interaction and all others data.

Buspar Dividose exerts anxiolytic activity through high affinity for serotonin 5-HT1A and 5-HT2 receptors. It has moderate affinity for dopamine D2 receptors but no affinity for GABA receptors.

The clinical effect of buspirone in alleviating the symptoms of generalized anxiety disorders typically takes 2 to 4 weeks to achieve. The delayed onset of action of buspirone suggests that the therapeutic effectiveness in generalized anxiety may involved more than its molecular mechanism of action at the 5-HT1A receptors, or buspirone may induce adaptations of 5-HT1A receptors. Buspar Dividose was not shown to alter the psychomotor or cognitive function in healthy volunteers, and the risk of developing sedation is relatively low compared to other anxiolytics, such as benzodiazepines. Unlike benzodiazepines and barbiturates used in anxiety disorders, buspirone is not associated with a risk for developing physical dependence or withdrawal, or any significant interaction with central nervous system depressants such as ethanol. This is due to the lack of effects on GABA receptors. Buspar Dividose also does not exhibit any anticonvulsant or muscle-relaxing properties, but may interfere with arousal reactions due to its inhibitory action on the aactivity of noradrenergic locus coerulus neurons.

Despite its clinical effectiveness in generalized anxiety, buspirone demonstrated limited clinical effectiveness on panic disorders, severe anxiety, phobias, and obsessive compulsive disorders. The clinical effectiveness of the long-term use of buspirone, for more than 3 to 4 weeks, has not demonstrated in controlled trials but there were no observable significant adverse events in patients receiving buspirone for a year in a study of long-term use.

Buspar Dividose
Uses
Dosage
Side Effect
Precautions
Interactions
Uses during Pregnancy
Uses during Breastfeeding
Accute Overdose
Food Interaction
Half Life
Volume of Distribution
Clearance
Interaction With other Medicine
Contradiction
Storage

Trade Name	Buspar Dividose
Availability	Prescription only
Generic	Buspirone
Buspirone Other Names	Buspiron, Buspirona, Buspirone, Buspironum
Related Drugs	sertraline, escitalopram, fluoxetine, alprazolam, duloxetine, Lexapro, Zoloft, Xanax, Cymbalta, Prozac
Type	Oral
Formula	C₂₁H₃₁N₅O₂
Weight	Average: 385.5031 Monoisotopic: 385.247775261
Protein binding	Based on the findings of an in vitro protein binding study, approximately 86% of buspirone is bound to plasma proteins. It is mainly bound to serum albumin and alpha-1-acid glycoprotein.
Groups	Approved, Investigational
Therapeutic Class	Miscellaneous sedatives & hypnotics
Manufacturer
Available Country	United States
Last Updated:	September 19, 2023 at 7:00 am

Uses

Buspar Dividose is used for short-term management of anxiety.

Buspar Dividose is also used to associated treatment for these conditions: Anxiety Disorders, Depression

How Buspar Dividose works

The therapeutic action of buspirone in generalized anxiety disorders is thought to be mainly derived from its interaction with two major 5-HT_1A receptor subtypes that are involved in the brain's anxiety and fear circuitry to enhance the serotonergic activity in these brain areas. Buspar Dividose acts as a full agonist at presynaptic 5-HT_1A receptors, or 5-HT_1A autoreceptors, expressed at dorsal raphe while acting as a partial agonist at the postsynaptic 5-HT_1A receptors expressed on hippocampus and cortex. 5-HT_1A receptors function as inhibitory autoreceptors by being expressed on the soma or dendrites of serotonergic neurons or mediate postsynaptic actions of 5-HT by being highly expressed on the corticolimbic circuits. They are inhibitory G-protein coupled receptors that couple to Gi/Go proteins. When activated, presynaptic 5-HT_1A autoreceptors causes neuron hyperpolarization and reduces the firing rate of the serotonergic neuron, thereby decreasing extracellular 5-HT levels in the neuron's projection areas. Activated postsynaptic 5-HT_1A receptors promote hyperpolarization to released 5-HT on pyramidal neurons.

The anxiolytic action of buspirone is mainly thought to arise from the interaction at presynaptic 5-HT_1A autoreceptors. Acting as a potent agonist in these receptors, buspirone initially causes activation of these autoreceptors and inhibition of 5-HT release. It is proposed that buspirone induces desensitization of somatodendritic autoreceptors over time, which may explain the delayed onset of action of the drug. Desensitization of the autoreceptors ultimately results in heightened excitation of serotonergic neurons and enhanced 5-HT release. Buspar Dividose also displays a weak affinity for serotonin 5HT2 receptors and acts as a weak antagonist on dopamine D2 autoreceptors, although there is not much evidence that the action at these receptors contribute to the anxiolytic effect of buspirone. It acts as an antagonist at presynaptic dopamine D3 and D4 receptors and may bind to alpha-1 adrenergic receptors as a partial agonist.

Dosage

Buspar Dividose dosage

Initially, 5 mg bid/tid increased by 5 mg increments at intervals of 2-3 days. Max: 45 mg daily in divided doses.

Side Effects

Dizziness, nausea, headache, nervousness, lightheadedness, excitement, paraesthesia, sleep disturbances, chest pain, tinnitus, nasal congestion, sore throat. Less sedation and lower potential for dependence compared to other anxiolytics.

Toxicity

The oral LD₅₀ of buspirone is 196 mg/kg in rat, 655 mg/kg in mouse, 586 mg/kg in dog, and 356 mg/kg in monkey. The intraperitoneal LD₅₀ is 136 mg/kg in rat and 146 mg/kg in mouse.

In clinical pharmacology trials, administration of buspirone at the dose of 375 mg/day resulted in symptoms of nausea, vomiting, dizziness, drowsiness, miosis, and gastric distress. Few cases of overdosage that have been reported usually resulted in complete recovery. In case of overdose, the use of general symptomatic and supportive treatment is recommended along with immediate gastric lavage and monitoring of respiration, pulse, and blood pressure.

Precaution

Preceding co-administration of MAOIs, decreased hepatic or renal function. In patients on benzodiazepines, withdraw the drug gradually. May impair ability to drive or operate machinery.

Interaction

Enhanced sedative effects with alcohol or CNS depressants. Increases serum haloperidol. Concurrent admin with MAOIs may lead to increase in BP.

Food Interaction

Avoid alcohol. Alcohol may cause additive CNS depressant effects.
Avoid grapefruit products. Grapefruit increases the plasma concentrations of the drug.
Take at the same time every day. Take consistently at the same time in regard to meals.
Take with or without food. Take drug always with or always without food in a consistent manner.

[Moderate] GENERALLY AVOID: Alcohol may potentiate some of the pharmacologic effects of buspirone.

Use in combination may result in additive central nervous system depression and
ADJUST DOSING INTERVAL: In a small, randomized, crossover study, the consumption of large amounts of grapefruit juice (compared to water) was associated with significantly increased plasma buspirone concentrations, slightly prolonged elimination half-lives, and delayed times to reach peak drug concentration.

The perceived pharmacodynamic effect of buspirone, as measured by subjective drowsiness and overall subjective drug effect, was also enhanced by grapefruit juice.

These alterations may stem from the delay of gastric emptying as well as inhibition of CYP450 3A4-mediated first-pass metabolism in the gut wall induced by certain compounds present in grapefruits.

MANAGEMENT: Patients receiving buspirone should be advised to avoid consumption of alcohol.

Patients also should preferably avoid the consumption of large amounts of grapefruits and grapefruit juice to prevent any undue fluctuations in plasma drug levels.

If this is not possible, the buspirone dose should be taken at least 2 hours before or 8 hours after grapefruit or grapefruit juice.

Monitoring for increased CNS depression is recommended.

Buspar Dividose Drug Interaction

Major: duloxetine, duloxetine, escitalopram, escitalopram, sertraline, sertralineModerate: pregabalin, pregabalin, alprazolam, alprazolam, cetirizine, cetirizineUnknown: omega-3 polyunsaturated fatty acids, omega-3 polyunsaturated fatty acids, cyanocobalamin, cyanocobalamin, ascorbic acid, ascorbic acid, cholecalciferol, cholecalciferol

Buspar Dividose Disease Interaction

Major: depression, renal/liver diseaseModerate: glaucoma, liver disease, drug dependence

Volume of Distribution

In a pharmacokinetic study assessing buspirone over the dose range of 10 to 40 mg, the volume of distribution was 5.3 L/kg.

Elimination Route

Buspar Dividose is rapidly absorbed following oral administration. Bioavailability is low and variable (approximately 5%) due to extensive first pass metabolism. While absorption of buspirone is decreased with concomitant food intake, the first-pass metabolism of the drug is also decreased, resulting in an increased bioavailability as well as increased Cmax and AUC. Following oral administration of single oral doses of 20 mg, the Cmax ranged from 1 to 6 ng/mL and the Tmax ranged from 40 to 90 minutes.

Half Life

In a single-dose pharmacokinetic study of 14C-labeled buspirone, the average elimination half-life of unchanged buspirone following administration of single doses ranging from 10 to 40 mg was about 2 to 3 hours.

Clearance

In a pharmacokinetic study assessing buspirone over the dose range of 10 to 40 mg, the systemic clearance was 1.7 L/h/kg.

Elimination Route

A single-dose pharmacokinetic studies using 14C-labeled buspirone demonstrated that about 29-63% of the dose administered was excreted in the urine within 24 hours, primarily in the form of metabolites. About 18% to 38% of the dose was eliminated via fecal excretion.

Pregnancy & Breastfeeding use

Pregnancy Category B. Either animal-reproduction studies have not demonstrated a fetal risk but there are no controlled studies in pregnant women or animal-reproduction studies have shown an adverse effect (other than a decrease in fertility) that was not confirmed in controlled studies in women in the 1st trimester (and there is no evidence of a risk in later trimesters).