드로페리돌, 펜타닐

Pharmaceuticals -> Nervous system -> Anesthetics

Pharmaceuticals -> Listed in ZINC15

log Kow = 3.50

2.8

3.5

1 g soluble in 5.5 mL chloroform, 600 mL alcohol, 10,000 mL water; slightly soluble in ether

9.66e-02 g/L

33.4 [ug/mL] (The mean of the results at pH 7.4)

Breast Feeding; Lactation; Milk, Human; Antiemetics; Antipsychotic Agents; Butyrophenones; Dopamine Antagonists; Gastrointestinal Agents

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

Pharmaceuticals

145-146.5

145-146 °C

MP: 144-148 °C (after vacuum drying at 70 °C for 4 hr)

145.75 °C

Warning

H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]

P264, P270, P301+P317, P330, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 40 reports by companies from 2 notifications to the ECHA C&L Inventory.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including droperidol, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

Droperidol and fentanyl citrate injection is a sterile solution containing 20 mg of droperidol and 0.4 mg of fentanyl citrate per cubic centimeter. ... It is used in dogs as an analgesic and tranquilizer and for general anesthesia. /Droperidol and fentanyl citrate injection/

The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Droperidol is included on this list.

Droperidol injection is physically and/or chemically incompatible with some drugs (e.g., parenteral barbiturates), but the compatibility depends on several factors (e.g., concentrations of the drugs, specific diluents used, resulting pH, temperature). Specialized references should be consulted for specific compatibility information.

As with all fires, evacuate personnel to a safe area. Firefighters should use self-contained breathing equipment and protective clothing.

Water spray, dry chemical, carbon dioxide, or foam as appropriate for surrounding fire and materials.

Commercially available droperidol injection should be protected from light and stored at room temperature (15-25 °C).

Store in tight, light-resistant container as defined in the USP-NF. This material should be handled and stored per label instructions to ensure product integrity. Store in a cool place. Store under nitrogen.

Wear approved respiratory protection, chemically compatible gloves, and protective clothing. Wipe up spillage or collect spillage using a high-efficiency vacuum cleaner. Avoid breathing dust. Place spillage in appropriately labeled container for disposal. Wash spill site.

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

As a general rule, when handling USP Reference Standards, avoid all contact and inhalation of dust, mists, and/or vapors associated with the material. Wash thoroughly after handling.

As with all dry powders, it is advisable to ground mechanical equipment in contact with dry material to dissipate the potential buildup of static electricity.

Respiratory protection: Use a NIOSH-approved respirator, if it is determined to be necessary by an industrial hygiene survey involving air monitoring. In the event that a respirator is not required, an approved dust mask should be used. Gloves: Chemically compatible. Eye protection: Safety glasses or goggles. Protective clothing: Protect exposed skin.

Engineering controls such as exhaust ventilation are recommended

Any drug known to have the potential to prolong the QT interval should not be used together with droperidol. Possible pharmacodynamic interactions can occur between droperidol and potentially arrhythmogenic agents such as class I or III antiarrhythmics, antihistamines that prolong the QT interval, antimalarials, calcium channel blockers, neuroleptics that prolong the QT interval, and antidepressants.

Caution should be used when patients are taking concomitant drugs known to induce hypokalemia or hypomagnesemia as they may precipitate QT prolongation and interact with droperidol. These would include diuretics, laxatives and supraphysiological use of steroid hormones with mineralocorticoid potential.

CNS depressant drugs (e.g. barbiturates, tranquilizers, opioids and general anesthetics) have additive or potentiating effects with droperidol. When patients have received such drugs, the dose of droperidol required will be less than usual. Following the administration of droperidol, the dose of other CNS depressant drugs should be reduced.

To report a case of QT prolongation associated with concomitant cyclobenzaprine and fluoxetine administration followed by torsade de pointes potentiated by droperidol. A 59-year-old white woman who had been receiving long-term fluoxetine and cyclobenzaprine therapy was admitted for Achilles tendon repair. Baseline QTc was prolonged at 497 msec. Prior to surgery, the patient received droperidol, an agent known to prolong the QT interval. During surgery the patient developed torsade de pointes, which progressed into ventricular fibrillation. On postoperative day 1, after cyclobenzaprine discontinuation, the QTc decreased toward normal (440 msec). Cyclobenzaprine shares anticholinergic effects, tachycardia, and dysrhythmic potential with the tricyclic antidepressants (TCAs). Fluoxetine is a known inhibitor of the CYP2D6 isoenzyme (along with CYP3A4 and CYP2C) and has been shown to increase TCA serum concentrations. The combination of cyclobenzaprine and fluoxetine resulted in significant QT prolongation in our patient that progressed to torsade de pointes after preoperative droperidol administration. Resolution of QT abnormalities after cyclobenzaprine discontinuation provided further evidence of a drug-induced etiology. Other possible medical and drug-related causes of torsade de pointes are reviewed and ruled out. ...

For more Interactions (Complete) data for DROPERIDOL (12 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 820(SRC), determined from a log Kow of 3.50(2) and a regression-derived equation(3), indicates that droperidol is expected to have low mobility in soil(SRC). The pKa of droperidol is 7.46(4), indicating that this compound will exist partially in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5). Volatilization of the neutral species of droperidol from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.7X10-15 atm-cu m/mole(SRC), using a fragment constant estimation method(6). Droperidol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.9X10-10 mm Hg at 25 °C(SRC), determined from a fragment constant method(7). Biodegradation data in soil were not available(SRC, 2012).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 820(SRC), determined from a log Kow of 3.50(2) and a regression-derived equation(3), indicates that droperidol is expected to adsorb to suspended solids and sediment(SRC). Volatilization of the neutral species from water surfaces is not expected(4) based upon an estimated Henry's Law constant of 2.7X10-15 atm-cu m/mole(SRC), developed using a fragment constant estimation method(5). A pKa of 7.46(6) indicates droperidol will exist partially in the cation form at pH values of 5 to 9 and therefore volatilization from water surfaces is not expected to be an important fate process(SRC). According to a classification scheme(7), an estimated BCF of 25(SRC), from its log Kow(2) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data in water were not available(SRC, 2012).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), droperidol, which has an estimated vapor pressure of 1.9X10-10 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase droperidol may be removed from the air by wet or dry deposition(SRC). Droperidol contains chromophores that absorb at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

The Koc of droperidol is estimated as 820(SRC), using a log Kow of 3.50(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that droperidol is expected to have low mobility in soil. The pKa of droperidol is 7.46(4), indicating that this compound will exist partially in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5).

/HUMAN EXPOSURE STUDIES/ The sensitivity of the respiratory center following a single 0.3 mg X kg-1 iv dose of droperidol was determined in eight healthy volunteers by using carbon dioxide (CO2) rebreathing and mouth occlusion pressure measurements (P0.1). There were no significant differences in the mean slopes of the minute ventilation/partial pressure of CO2 (VE/PCO2) and log P0.1/PCO2 relationships between control measurements and those made 30, 60, 90, 150, and 240 min after droperidol administration. However, individual variations in response were present, one subject showing significant (approximately 50%) depression of respiratory drive.

/HUMAN EXPOSURE STUDIES/ In a double-blind, placebo-controlled study, both the incidence of akathisia and its relationship to the dose of droperidol (0.5 or 1 mg) /were investigated/. One hundred and twenty healthy women undergoing day-case gynaecological surgery were anaesthetised with propofol, fentanyl, isoflurane and droperidol according to group. Patients were assessed by structured telephone interview at 24 hr. There was an increasing incidence of both restlessness (p = 0.01) and unpleasant restlessness (p = 0.02) between the groups on Chi-squared testing. Compared to the control group, those women given droperidol 1 mg suffered more restlessness (p = 0.001) and unpleasant restlessness (p < 0.01). No statistical difference could be demonstrated between the two droperidol groups. /The authors/ conclude that droperidol may commonly cause akathisia and may not, therefore, be an appropriate prophylactic antiemetic for day-case anaesthesia.

/HUMAN EXPOSURE STUDIES/ ... /The authors/ investigated, if neuroleptanalgesic doses of droperidol led to QT prolongation and cardiac arrhythmias in children undergoing cardiac surgery. /Investigators/ retrospectively analyzed electrocardiogram rhythm strips that were obtained before and in time increments after a 100 ug x kg(-1) intravenous bolus of droperidol in 20 children undergoing cardiac surgery. The longest QT interval was determined in each ECG and corrected for heart rate (QTc). All arrhythmias were recorded. Droperidol led to a significant increase in QTc time that was still present at 15 min but had resolved within 30 min after the bolus. No associated arrhythmias were observed. The statistically significant prolongation of QTc time after a sedative dose of droperidol is of concern because it may increase the risk for malignant cardiac arrhythmias. A large, prospective study is necessary to identify the true risk for arrhythmias after droperidol in this patient population, but our study suggests that any arrhythmogenic risk, if present, will be very transient, since the increase in QTc time was limited to a period of less than 30 min after the bolus.

/HUMAN EXPOSURE STUDIES/ This was a randomized, double-blinded, two-period, placebo-controlled crossover trial that utilized a standard driver-training program with computerized scoring. /Investigators/ solicited 20 paid volunteers who were pre-screened with a 12-lead EKG to evaluate QT length. For the first driving simulation, subjects were randomly assigned to receive either 2.5 mg of DROP IM or an equal volume of normal saline (NS). At least 72 hours later, the same subjects participated in a second driving simulation. For the second driving simulation, the assignment of DROP, 2.5 mg IM, or normal saline was reversed: (If a subject received DROP, 2.5 mg IM, in the first simulation, the subject received normal saline in the second simulation; conversely, if a subject received normal saline in the first simulation, the subject received DROP, 2.5 mg IM, in the second simulation). Thirty minutes later, participants drove the 20-minute simulation and received an average score based on the errors made in 4 categories: accelerating, braking, steering, and signaling. Post-testing, participants evaluated their degree of drowsiness and driving impairment using a visual analog scale and compared their perception of impairment to that caused by alcohol ingestion. Data were analyzed using analysis-of-variance, Pearson chi-square and Fischer's exact test with alpha set at p = 0.05. Twenty subjects (11 males and 9 females) completed the protocol. The mean age was 30 years with a range of 20 to 46 years, and the mean weight was 80 kg. The mean driving experience was 12 years. Participants who received DROP felt significantly drowsier (38.6 mm +/- 9.0) than those receiving NS (13.2 mm +/- 9.0), the mean difference was 25.4 mm p = 0.009. Subjects receiving DROP were also more likely to feel that their driving would be impaired as rated on the VAS (DROP: 34.6 +/- 5.2; NS: 3.2 +/- 5.2; p = 0.0005), and DROP subjects reported impairment equivalent to 1-4 drinks more frequently than those receiving placebo (61% vs. 16.7%, p < 0.001). These subjective feelings of impairment were confirmed by their driving performance on the simulator. The mean driving score, using the driving simulator, was 68.8% with DROP vs. 73.6% with NS; p = 0.013. Subjects receiving modest doses of IM DROP report increased perceptions of drowsiness, driving impairment, and intoxication; these perceptions are confirmed on objective testing.

For more Human Toxicity Excerpts (Complete) data for DROPERIDOL (17 total), please visit the HSDB record page.

Drug Induced Liver Injury Rank (DILIrank 2.0)

Droperidol

vNo-DILI-concern

0

No match

DOI:10.1016/j.drudis.2016.02.015

An estimated BCF of 25 was calculated in fish for droperidol(SRC), using a log Kow of 3.50(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Henry's Law constant for the neutral species of droperidol is estimated as 2.7X10-17 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that droperidol is expected to be essentially nonvolatile from water and moist soil surfaces(2). Droperidol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.9X10-10 mm Hg(SRC), determined from a fragment constant method(3).

/LABORATORY ANIMALS: Acute Exposure/ In rabbits /droperidol/... is reported to cause a preliminary small rise of ocular pressure, then a reduction.

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Droperidol administered intravenously has been shown to cause a slight increase in mortality of the newborn rat at 4.4 times the upper human dose. At 44 times the upper human dose, mortality rate was comparable to that for control animals. Following intramuscular administration, increased mortality of the offspring at 1.8 times the upper human dose is attributed to CNS depression in the dams who neglected to remove placentae from their offspring. Droperidol has not been shown to be teratogenic in animals.

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ An oral study in rats revealed no impairment of fertility in either males or females at 0.63, 2.5 and 10 mg/kg doses (approximately 2, 9 and 36 times maximum recommended human iv/im dosage).

/GENOTOXICITY/ The micronucleus test in female rats revealed no mutagenic effects in single oral doses as high as 160 mg/kg.

Neuroleptic analgesia should not be used for patients with Parkinson's disease.

Droperidol should be used with caution in patients with impaired hepatic and renal function.

Severe hypertension and tachycardia have occurred in patients with diagnosed or suspected pheochromocytoma after administration of droperidol.

Droperidol should be administered with extreme caution to patients who may be at risk for development of prolonged QT syndrome (e.g., congestive heart failure, bradycardia, use of a diuretic, cardiac hypertrophy, hypokalemia, hypomagnesemia, or administration of other drugs known to increase the QT interval). Other risk factors may include age over 65 years, alcohol abuse, and use of agents such as benzodiazepines, volatile anesthetics, and IV opiates. Droperidol should be initiated at a low dose and adjusted upward, with caution, as needed to achieve the desired effect.

Droperidol is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(1). Droperidol contains chromophores that absorb at wavelengths >290 nm(1) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 3,340 workers (2,588 of these were female) were potentially exposed to droperidol in the US(1). Occupational exposure to droperidol may occur through dermal contact with this compound at workplaces where droperidol is produced or administered. Exposure to droperidol among the general population may be limited to those administered the drug(SRC).

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including droperidol, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

Droperidol and fentanyl citrate injection is a sterile solution containing 20 mg of droperidol and 0.4 mg of fentanyl citrate per cubic centimeter. ... It is used in dogs as an analgesic and tranquilizer and for general anesthesia. /Droperidol and fentanyl citrate injection/

The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Droperidol is included on this list.

N05AD08

N - Nervous system

QN - Nervous system

Droperidol produces marked tranquilization and sedation. It allays apprehension and provides a state of mental detachment and indifference while maintaining a state of reflex alertness. Droperidol produces an antiemetic effect as evidenced by the antagonism of apomorphine in dogs. It lowers the incidence of nausea and vomiting during surgical procedures and provides antiemetic protection in the postoperative period. Droperidol potentiates other CNS depressants. It produces mild alpha-adrenergic blockade, peripheral vascular dilatation and reduction of the pressor effect of epinephrine. It can produce hypotension and decreased peripheral vascular resistance and may decrease pulmonary arterial pressure (particularly if it is abnormally high). It may reduce the incidence of epinephrine-induced arrhythmias, but it does not prevent other cardiac arrhythmias.

The exact mechanism of action is unknown, however, droperidol causes a CNS depression at subcortical levels of the brain, midbrain, and brainstem reticular formation. It may antagonize the actions of glutamic acid within the extrapyramidal system. It may also inhibit cathecolamine receptors and the reuptake of neurotransmiters and has strong central antidopaminergic action and weak central anticholinergic action. It can also produce ganglionic blockade and reduced affective response. The main actions seem to stem from its potent Dopamine(2) receptor antagonism with minor antagonistic effects on alpha-1 adrenergic receptors as well.

Within the CNS, droperidol acts principally at subcortical levels and exhibits a strong sedative effect. The drug also inhibits sympathetic postganglionic alpha-adrenergic receptor binding sites; however, therapeutic dosages of droperidol do not appear to completely block these receptors. Droperidol has antiemetic activity, but does not appear to exhibit analgesic activity.

Because of its inhibitory effects on alpha-adrenergic receptor binding sites, droperidol attenuates the cardiovascular response to sympathomimetic amines. Droperidol also produces direct peripheral vasodilation, which alone or in conjunction with its alpha-adrenergic blocking activity may cause hypotension and decreased peripheral vascular resistance. Droperidol may decrease pulmonary arterial pressure (particularly in patients with preexisting elevations in pulmonary arterial pressure) and reduce the incidence of epinephrine-induced arrhythmias; however, droperidol's activity against other arrhythmias has not been observed.

Droperidol produces the inhibition of K+ channels in cardiac myocytes. However, the effects of droperidol on K+ channels have not been studied in blood vessels. Therefore, /investigators/ designed the present study to determine whether droperidol modulates the activity of adenosine triphosphate (ATP)-sensitive K+ channels in vascular smooth muscle cells. Rat aortic rings without endothelium were suspended or used for isometric force and membrane potential recordings, respectively. Vasorelaxation and hyperpolarization induced by levcromakalim (10(-8) to 10(-5) M or 10(-5) M, respectively) were completely abolished by the ATP-sensitive K+ channel antagonist glibenclamide (10(-5) M). Droperidol (10(-7) M) and an alpha-adrenergic receptor antagonist phentolamine (3 x 10(-9) M) caused a similar vasodilator effect (approximately 20% of vasorelaxation compared with maximal vasorelaxation induced by papaverine 3 x 10(-4) M, whereas glibenclamide did not alter vasorelaxation induced by droperidol. Droperidol (3 x 10(-8) M to 10(-7) M) augmented vasorelaxation and hyperpolarization produced by levcromakalim, whereas phentolamine (3 x 10(-9) M) did not alter this vasorelaxation. Glibenclamide (10(-5) M) abolished the vasodilating and hyperpolarizing effects of levcromakalim in the aorta treated with droperidol (10(-7) M). These results suggest that droperidol augments vasodilator activity via ATP-sensitive K+ channels. However, it is unlikely that this augmentation is mediated by the inhibition of alpha-adrenergic receptors in vascular smooth muscles.

... An inhibitory dopaminergic receptor has been described that modulates catecholamine release from adrenal medulla. It has also been reported that low doses of droperidol increase arterial pressure in some patients with pheochromocytoma. The authors investigated whether an effect of droperidol on such a receptor could be one of the mechanisms involved in the hypertensive response. Isolated cat adrenal glands were perfused with Krebs-bicarbonate solution, and the catecholamine release was measured in the effluent. Then, the glands were stimulated by activation of the nicotinic receptor (nicotine, 5 uM), and the effect of low and high doses of droperidol and/or apomorphine on the catecholamine secretory responses evoked by nicotine was investigated. Low concentrations of droperidol (0.05 uM) (a dopaminergic antagonist) markedly increased the secretory response induced by nicotine whereas higher concentrations (50 uM) decreased it. Apomorphine (1 uM) (a dopaminergic agonist) inhibits the catecholamine release produced by nicotine, and this inhibitory effect was completely reversed by the lowest concentration of droperidol but not by the highest. In fact, the high concentration of droperidol further inhibited the catecholamine release induced by nicotine. The results suggest that the hypertensive responses evoked by low doses of droperidol in some patients with pheochromocytoma could be due to the inactivation of a dopaminergic inhibitory system present in the adrenal medulla that, under physiologic conditions, limits the amount of catecholamines released by the gland. Such as an inhibitory mechanism could operate in an exaggerated manner in patients with pheochromocytoma.

For more Mechanism of Action (Complete) data for DROPERIDOL (6 total), please visit the HSDB record page.

Biphasic distribution. The rapid distribution phase is 1.4 &plusmn; 0.5 minutes and the slower distribution phase is 14.3 &plusmn; 6.5 minutes. Elimination half-life in adults is 134 &plusmn; 13 minutes and may be increased in geriatric patients. In children, it is 101.5 &plusmn; 26.4 minutes.

...Droperidol is rapidly absorbed after im injections, and plasma-level profiles of unchanged drug obey 2-compartment model kinetics. Plasma t1/2 is about 130 min...

Extensively metabolized.

Although the exact metabolic fate of droperidol is not clearly established, the drug is metabolized in the liver. The butyrophenone moiety of droperidol is metabolized to p-fluorophenylacetic acid, which is then conjugated with glycine. The nitrogenous moiety of droperidol appears to be metabolized to benzimidazolone and p-hydroxypiperidine.

O9U0F09D5X

DROPERIDOL

Mechanisms of Action [MoA] - Dopamine D2 Antagonists

Established Pharmacologic Class [EPC] - Dopamine-2 Receptor Antagonist

Droperidol is a Dopamine-2 Receptor Antagonist. The mechanism of action of droperidol is as a Dopamine D2 Antagonist.

DROPERIDOL

Agents that are administered in association with anesthetics to increase effectiveness, improve delivery, or decrease required dosage.

Drugs used to prevent NAUSEA or VOMITING.

Agents that control agitated psychotic behavior, alleviate acute psychotic states, reduce psychotic symptoms, and exert a quieting effect. They are used in SCHIZOPHRENIA; senile dementia; transient psychosis following surgery; or MYOCARDIAL INFARCTION; etc. These drugs are often referred to as neuroleptics alluding to the tendency to produce neurological side effects, but not all antipsychotics are likely to produce such effects. Many of these drugs may also be effective against nausea, emesis, and pruritus.

Compounds and drugs that bind to and inhibit or block the activation of DOPAMINE D2 RECEPTORS.

Completely absorbed following intramuscular administration.

Following im or iv administration, the onset of pharmacologic action of droperidol occurs within 3-10 minutes, but peak pharmacologic effects may not be apparent until 30 minutes. The sedative and tranquilizing effects of droperidol generally persist for 2-4 hours following im or iv administration of a single dose; alteration of consciousness may persist for up to 12 hours.

Droperidol reportedly crosses the blood-brain barrier and is distributed into the CSF.

Droperidol drug reportedly crosses the placenta, but data are limited.

It is not known if droperidol is distributed into milk.

For more Absorption, Distribution and Excretion (Complete) data for DROPERIDOL (7 total), please visit the HSDB record page.

MEDICATION

MEDICATION (VET)

Ingredient of Thalamonal, Innovar

Table: Droperidol Preparations [Table#4529]

Animal Drugs -> FDA Approved Animal Drug Products (Green Book) -> Active Ingredients

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