카르펜타닐

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.

Carfentanil and other fentanyl-related compounds are a serious danger to public safety, first responder, medical, treatment, and laboratory personnel. ... If encountered, responding personnel should do the following based on the specific situation: Exercise extreme caution. Only properly trained and outfitted law enforcement professionals should handle any substance suspected to contain fentanyl or a fentanyl-related compound. If encountered, contact the appropriate officials within your agency. Be aware of any sign of exposure. Symptoms include: respiratory depression or arrest, drowsiness, disorientation, sedation, pinpoint pupils, and clammy skin. The onset of these symptoms usually occurs within minutes of exposure. Seek IMMEDIATE medical attention. Carfentanil and other fentanyl-related substances can work very quickly, so in cases of suspected exposure, it is important to call EMS immediately. ...

Using a crossover study design, the pharmacokinetics of carfentanil and naltrexone after i.v., i.m., and s.c. administration were determined in eight domestic goats (Capra hircus). Serial blood samples were taken up to 120 hr after carfentanil administration, and the plasma drug concentrations were determined using liquid chromatography and mass spectroscopy. All goats were immobilized with 40 ug/kg carfentanil i.m., although the resulting neurologic effects varied considerably. Plasma profiles showed rapid carfentanil absorption and a simple biphasic decline for 12-48 hr. Naltrexone given at 100 mg naltrexone/mg carfentanil 30 min after carfentanil administration produced rapid reversal of immobilization after all routes of administration. Variable fluctuations in the naltrexone plasma concentrations during the first 2.5-3.5 hr were observed, followed by a more consistent biphasic decline. The time to standing was significantly shorter after i.v. compared with s.c. naltrexone, although the time difference (1 min) had little clinical relevance. No statistically significant differences between the naltrexone pharmacokinetic parameters measured for the three routes of naltrexone administration were identified, although the recoveries after i.m. administration were, subjectively, the smoothest. The carfentanil half-life did not differ significantly in the goats given naltrexone by different routes. Although it is currently recommended that the naltrexone dose be divided into s.c. and i.v. portions, this practice does not appear to offer any benefit.

With the use of a crossover study design, we investigated the respiratory and cardiovascular effects of naloxone administration in eight healthy Rocky Mountain wapiti (Cervus elaphus nelsoni) anesthetized with carfentanil (10 ug/kg i.m.) and xylazine (0.1 mg/kg). Anesthetized animals showed profound hypoxemia with mild hypercapnia, tachycardia, hypertension, and acidosis prior to naloxone administration. After monitoring equipment was placed, animals were administered either naloxone (2 ug/ug carfentanil i.v.) or an equivalent volume of normal saline. Mean values for PaO2, PaCO2, heart rate, and respiratory rate were significantly different between naloxone- and saline-treated groups, but mean blood pressure, hematocrit, and serum electrolyte concentrations were not. Mean PaO2 was 23.0 +/- 4.1 mm Hg prior to administration of naloxone or saline and increased to 50.2 +/- 7.3 mm Hg after naloxone administration. Mean PaO2 of saline-treated animals did not change significantly. Electrocardiograms of three saline-treated animals suggested myocardial hypoxia. Hypoxemia appeared to be caused by respiratory depression, hemodynamic alterations, and lateral recumbency. All but one animal remained anesthetized after naloxone administration. Anesthesia in all animals was reversed in < or = 4 min with naltrexone (100 mg/mg carfentanil i.v. s.c.) and yohimbine (0.1 mg/kg i.v.). One bolus of naloxone improved oxygenation in carfentanil-xylazine-anesthetized wapiti.

Reversing the respiratory depression induced by carfentanil involves intravenous administration of naloxone or naltrexone, but this treatment has disadvantages. Hence, finding a more appropriate treatment to counter the depressive actions of carfentanil is needed. In the present study, with the naloxone as a control, we investigated the efficacy of nalmefene for countering the depressive actions of carfentanil. Rats were treated successively with carfentanil (10 ug/kg, i.v.) and nalmefene (9.4-150.0 ug/kg, i.m.), and the duration of loss of righting reflex (LORR) recorded. Respiratory parameters were measured in free-moving rats using a whole-body plethysmograph after rats were administered carfentanil (20 ug/kg, i.v.) and nalmefene (9.4-150.0 ug/kg, i.m.) sequentially. The parameters of arterial blood gases were also examined. Nalmefene (9.4-150.0 ug/kg, i.m.) treatment dose-dependently decreased the duration of carfentanil-induced LORR. The respiratory rate after 60 min of nalmefene (150.0 ug/kg, i.m.) treatment increased from 34.3 +/- 5.3 bursts/min to 117.8 +/- 18.9 bursts/min, and enhanced pause decreased from 1.1 +/- 0.1 to 0.4 +/- 0.1, and was close to those of normal rats. Furthermore, nalmefene (37.5-150.0 ug/kg) treatment could enable the PaO2, SaO2 and PaCO2 to approach normal levels 10 min (15 min after carfentanil injection) or 30 min (25 min after carfentanil injection) after injection. While, a single injection of naloxone (150.0 ug/kg, i.m.) only achieved partial remission of respiratory depression. These data suggest that nalmefene more effectively counters the depressive actions induced by carfentanil and is a more appropriate treatment to antagonize carfentanil toxicity compared with naloxone.

We evaluated efficacy and safety of naltrexone for antagonizing carfentanil immobilization in 12 captive Rocky Mountain elk (Cervus elaphus nelsoni) using a randomized incomplete block experiment. In three replicate trials, elk were hand-injected with 10 micrograms carfentanil citrate/kg body weight intramuscularly. Fifteen min after each elk became recumbent, we administered naltrexone HCl (25% of dose intravenously, 75% subcutaneously) dosed at 0 (control), 25, 50, or 100 mg/mg carfentanil; after an additional 15 min of immobilization, controls received 500 mg naltrexone HCl/mg carfentanil. Elk were immobilized in 34 of 36 attempts; the mean (+/-SE) induction time was 3.1 +/- 0.2 min. Regardless of dose, all elk stood < 9 min after receiving naltrexone; controls remained immobilized until they received antagonist. Mean recovery times did not differ with increasing naltrexone dose (P = 0.31) or among individuals (P = 0.16). None of the elk receiving 100 or 500 mg naltrexone/mg carfentanil renarcotized, but three of eight and seven of nine elk receiving 50 and 25 mg naltrexone/mg carfentanil, respectively, showed signs of mild renarcotization 8 to 24 hr later (P = 0.0002). We observed no adverse clinical effects in elk receiving < or = 500 mg naltrexone/mg carfentanil. Based on these data, we recommend 100 mg/mg carfentanil as a minimum effective dose for rapidly antagonizing immobilization and preventing renarcotization.

For more Interactions (Complete) data for Carfentanil (8 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 18,000(SRC), determined from a structure estimation method(2), indicates that carfentanil is expected to be immobile in soil(SRC). The estimated pKa of carfentanil is 8.05(3), 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(4). Volatilization of the cation form from moist soil is not expected because cations do not volatilize(SRC). Volatilization of neutral carfentanil from moist soil surfaces is not expected(SRC) given an estimated Henry's Law constant of 4.4X10-13 atm-cu m/mole(SRC), using a fragment constant estimation method(2). Carfentanil is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2X10-10 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2017).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 18,000(SRC), determined from a structure estimation method(2), indicates that carfentanil is expected to adsorb to suspended solids and sediment(SRC). An estimated pKa of 8.05(3) indicates carfentanil will exist partially in the cation form at pH values of 5 to 9 and, therefore, volatilization of the cation from water surfaces is not expected to be an important fate process(SRC). Volatilization from water surfaces of neutral carfentanil is not expected(4) based upon an estimated Henry's Law constant of 4.4X10-13 atm-cu m/mole(SRC), developed using a fragment constant estimation method(2). The estimated hydrolysis half-life of carfentanil at pH values of 7 and 8 was calculated as 35 and 3.5 years, respectively(2). According to a classification scheme(5), an estimated BCF of 80(SRC), from an estimated log Kow of 3.39(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is moderate. Biodegradation data in water were not available(SRC, 2017).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), carfentanil, which has an estimated vapor pressure of 2X10-10 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 carfentanil may be removed from the air by wet and dry deposition(SRC). Carfentanil contains chromophores that absorb at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

IDENTIFICATION AND USE: Carfentanil is a Schedule II controlled substance. It is a large animal immobilizing agent use in Cervidae (deer, elk, moose), and veterinary anesthetic used for zoo animals. Carfentanil is an ultra-potent synthetic opioid. These substances can come in several forms, including powder, blotter paper, tablets, and spray - they can be absorbed through the skin or accidental inhalation of airborne powder. HUMAN STUDIES: Carfentanil has been discovered in postmortem and antemortem cases throughout the United States in the heroin supply either alone or mixed with heroin and/or other fentanyl analogs. The potency of carfentanil is approximately 10,000 times greater than morphine and 100 times greater than fentanyl. In some cases, carfentanil was identified and ruled to be the cause of death, either alone or in combination with other drugs. In October 2002, the Russian military used a mysterious "gas" to incapacitate Chechen rebels at a Moscow theater. The available evidence strongly suggests that a combination of a potent aerosolized fentanyl derivative, such as carfentanil, and an inhalational anesthetic, such as halothane, was used in this case. Other study suggested that aerosol comprised a mixture of two anaesthetics -carfentanil and remifentanil. ANIMAL STUDIES: After carfentanil citrate administration, 3 horses developed severe tachycardia and hypertension, which resulted in the death of 1 horse from pulmonary edema. Intramuscularly administered etorphine and carfentanil induce hypertension, bradycardia, and bradypnea in goats. The mean dose of carfentanil used in wood bison was 7.0 ug/kg. Narcotic antagonists used were naltrexone, naloxone and M5050.

Using a structure estimation method based on molecular connectivity indices(1), the Koc of carfentanil can be estimated to be 18,000(SRC). According to a classification scheme(2), this estimated Koc value suggests that carfentanil is expected to be immobile in soil. The estimated pKa of carfentanil is 8.05(3), 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(4).

/CASE REPORTS/ Recreational use of potent fentanyl derivatives is increasing and poses a serious threat to health and public safety. The fentanyl derivative carfentanil, a large animal tranquilizer, is one of the most potent opioids known (10,000 times more potent than morphine) and can lead to severe or fatal intoxications even among opioid-tolerant users. Naloxone can be lifesaving in acute intoxications. The substance should be handled with utmost caution, as even inhalation, dermal or mucosal exposure can lead to intoxication. We report a case of confirmed acute carfentanil intoxication in Switzerland in order to contribute to the scarce knowledge of its toxicodynamic properties in humans. Case report: A 16-year-old male was admitted to the intensive care unit after sudden collapse, reportedly following the intake of an unknown drug via an unknown route. His regular medications were atomoxetine and mirtazapine. The patient was found unconscious (Glasgow Coma Scale 3/15), hypotensive (71/58 mmHg), tachycardic (126 beats per minute), apneic and cyanotic with peripheral oxygen saturation of 70%. Temperature and pupil findings were normal. After intubation, he was airlifted to the emergency department, where, after intravenous naloxone and flumazenil, he rapidly regained consciousness, becoming agitated and hypertensive. Other investigations including focused sonography, electrocardiogram, head computed tomography and laboratory analyses were normal except for mild respiratory acidosis. Urine drug screening immunoassay was negative twice. When a white powder along with a snorting tube were found in the patient's belongings, cocaine intoxication was suspected, but gas chromatography-mass spectrometry (GC-MS) and liquid chromatography combined with high resolution tandem mass spectrometry (LC-MS/MS) both identified the powder as carfentanil. Traces of carfentanil were also detected in blood using LC-MS/ MS. According to the caretaking institution, the patient was known for online substance acquisitions for self-experimenting and trafficking. He was discharged the day after the event. Conclusion: Recreational use of carfentanil caused sudden deep coma, hypotension and respiratory arrest responsive to naloxone.

/CASE REPORTS/ Carfentanil is a fentanyl analog frequently used in large animal veterinary medicine. Recently, carfentanil has been discovered in postmortem and antemortem cases throughout the United States in the heroin supply either alone or mixed with heroin and/or other fentanyl analogs. The potency of carfentanil is approximately 10,000 times greater than morphine and 100 times greater than fentanyl. In two recent cases, carfentanil was identified and ruled to be the cause of death, either alone or in combination with other drugs. Case 1 involved a known heroin user. He was discovered slumped over in a running van blocking the bays of a carwash. Two syringes, a spoon with cotton and residue and a yellow baggie of powder were found in the van. Case 2 involved a man living in a tent in a park with his mother. He was last heard from by a sister via phone who stated he sounded very intoxicated and by his mother who noted him to be "itching all over" and upset over his girlfriend. When the mother returned from work, she discovered him unresponsive with a small baggie of brown powder next to him. Routine drug and volatile screening tests were performed on heart blood using headspace gas chromatography, immunoassay and gas chromatography mass spectrometry methods. Results from initial testing on both cases did not have any significant toxicological findings. However, due to the history, scene photos, toxicological findings in blood and urine and analysis of the drug paraphernalia on one of the cases which identified carfentanil and furanyl fentanyl, fentanyl analogues were suspected. Heart blood was sent to a reference laboratory for carfentanil and furanyl fentanyl analysis. Case 1 had a carfentanil concentration of 1.3 ng/mL and a furanyl fentanyl concentration of 0.34 ng/mL. Case 2 had a carfentanil concentration of 0.12 ng/mL.

Carfentanil's production and use as a radiotracer in positron emission tomography (PET)(1) and a large animal tranquilizer(2) may result in its release to the environment through various waste streams(SRC). It is a Schedule II controlled substance(3).[(1) Pecina M, Zubieta JK; Mol Psychiatry 20: 416-23 (2015) (2) Daughton CG; Rev Environ Contam Toxicol 210: 59-110 (2011) (3) DEA; Title 21 Code Fed Reg. Part 1308 - Schedules of Controlled Substances. Schedules. Sec 1308.12 Schedule II.

An estimated BCF of 80 was calculated in fish for carfentanil(SRC), using an estimated log Kow of 3.39(1) and a regression-derived equation(1). According to a classification scheme(2), this BCF suggests the potential for bioconcentration in aquatic organisms is moderate.

An estimated pKa of 8.05(1) indicates carfentanil will exist partially in the cation form at pH values of 5 to 9 and, therefore, volatilization of the cation from water and moist soil surfaces is not expected to be an important fate process(SRC). The Henry's Law constant for carfentanil is estimated as 4.4X10-13 atm-cu m/mole(SRC) using a fragment constant estimation method(2). This Henry's Law constant indicates that neutral carfentanil is expected to be essentially nonvolatile from water and moist soil surfaces(3). Carfentanil is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2X10-10 mm Hg(SRC), determined from a fragment constant method(2).

/LABORATORY ANIMALS: Acute Exposure/ This study examined the real-time exposure-response effects of aerosolized carfentanil (CRF) on opioid-induced toxicity, respiratory dynamics and cardiac function in mice. Unrestrained, conscious male CD-1 mice (25-30 g) were exposed to 0.4 or 4.0 mg/cu m of aerosolized CRF for 15 min (Ct = 6 or 60 mg min/cu m) in a whole-body plethysmograph chamber. Minute volume (MV), core body temperature (Tc), mean arterial blood pressure (MAP) and heart rate (HR) were evaluated in animals exposed to CRF or sterile H2O. Loss of consciousness and Straub tail were observed in before 1 min following initiation of exposure to 6 or 60 mg min/cu m of CRF. Clinical signs of opioid-induced toxicity were observed in a dose-dependent manner. Exposure to 6 or 60 mg min/cu m of CRF resulted in significant decrease in MV as compared to the controls. MAP, HR and Tc decreased 24 hr in animals exposed to either 6 or 60 mg min/cu m of CRF as compared to the controls. Post-exposure administration of naloxone (NX, 0.05 mg/kg, i.m.) did not increase the MV of animals exposed to CRF to control levels within 24 hr, but decreased clinical signs of opioid-induced toxicity and the duration of respiratory depression. This is the first study to evaluate real-time respiratory dynamics and cardiac function during exposure and up to 24 hr post-exposure to CRF. The evaluation of toxicological signs and respiratory dynamics following exposure to CRF will be useful in the development of therapeutic strategies to counteract the ongoing threat of abuse and overuse of opioids and their synthetic variants.

/VETERINARY CASE REPORTS/ Ten black bears (Ursus americanus) were immobilized with orally administered carfentanil citrate. The total carfentanil dose was mixed with 5 to 20 mL honey and given incrementally to captive bears. The bears ranged in weight from 80 (estimated) to 233 kg. Total carfentanil doses ranged from 0.7 to 3.0 mg, resulting in dosages of 6.8 to 18.8 ug carfentanil/kg. Mean (+/- SD) times from estimated 80% mixture consumption to sternal recumbency, and first safe human contact were 7.7 +/- 2.3 min and 19.7 +/- 5.6 min, respectively. Undesired side effects of immobilization were muscle rigidity, bradypnea, and oxygen desaturation. All bears received diazepam to alleviate muscle rigidity and were insufflated with oxygen during immobilization. Nine immobilizations were considered satisfactory or good. The bear receiving 6.8 ug carfentanil/kg, the lowest dosage used, was very excited during induction and required intravenous (IV) ketamine to permit safe examination. Immobilization was reversed with 100 mg naltrexone/mg carfentanil administered (75% subcutaneous, 25% IV). Bears recovered to full mobility in 6.3 +/- 1.9 min. Five bears vomited post-recovery but no episodes of renarcotization were observed.

/VETERINARY CASE REPORTS/ /The purpose of this study was/ to determine comparative cardiopulmonary effects of IM administered etorphine and carfentanil in goats. Seven clinically normal adult female goats ... received at least 9 drug treatments (etorphine HCl, 5 [twice], 10, 20, and 40 and carfentanil citrate, 5, 10, 20 and 40 ug/kg of body weight), with a minimal 2-day interval between trials. Although drug dosages were randomized, etorphine and carfentanil treatments were alternated. To assess for drug tolerance, the first and last treatments always were etorphine (5 ug/kg). All goats were instrumented for long-term cardiopulmonary variable data collection. Both drugs induced rapid catatonic immobilization, characterized by limb and neck hyperextension, with occasional vocalization and bruxation. Etorphine elicited transient violent struggling and vocalization immediately. Time to immobilization appeared dose-dependent, and was more rapid with carfentanil (< or = 5 minutes) than etorphine (5 to 10 minutes) at all dosages. Recovery to standing occurred earlier for etorphine (1 to 2 hours) than carfentanil (> 2 hours) at all dosages. Both drugs at all dosages significantly (P < or = 0.05) increased systemic and left ventricular (LV) end-diastolic pressures, LV peak negative dP/dt, total peripheral resistance (TPR), hemoglobin concentration, and left atrial (LA) and pulmonary O2 contents. They also significantly decreased heart and respiration rates, and TPR. A significant increase was observed at some dosages for LV stroke volume and index, LV peak positive dP/dt, mean pulmonary artery pressure, PaO2, pulmonary artery oxygen partial pressure, PaCO2, pulmonary mixed venous carbon dioxide partial pressure, LA hemoglobin saturation, LA transport index, and body temperature. Pulmonary and systemic mixed venous carbon dioxide and oxygen contents were significantly decreased at some dosages. Intramuscularly administered etorphine and carfentanil induce hypertension, bradycardia, and bradypnea in goats. The hypertension appears attributable to an increase in TPR. Although the cardiopulmonary effects of carfentanil occurred more rapidly, these effects were similar in magnitude for etorphine and carfentanil over the evaluated dosage range.

A base-catalyzed second-order hydrolysis rate constant of 0.0062 L/mole-sec(SRC) was estimated for carfentanil using a structure estimation method(1); this corresponds to half-lives of 35 and 3.5 years at pH values of 7 and 8, respectively(1). Carfentanil contains chromophores that absorb at wavelengths >290 nm(2) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

Occupational exposure to carfentanil may occur through dermal contact with this compound at workplaces where carfentanil is produced or administered. Exposure to carfentanil among the general population may be limited to its use as a positron emission tomography (PET) imaging compound and as an illicit drug. (SRC)

Carfentanil's production and use as a radiotracer in positron emission tomography(PET) and a large animal tranquilizer may result in its release to the environment through various waste streams. If released to air, an estimated vapor pressure of 2X10-10 mm Hg at 25 °C indicates carfentanil will exist solely in the particulate phase in the atmosphere. Particulate-phase carfentanil will be removed from the atmosphere by wet and dry deposition. Carfentanil contains chromophores that absorb at wavelengths >290 nm and, therefore, may be susceptible to direct photolysis by sunlight. If released to soil, carfentanil is expected to have no mobility based upon an estimated Koc of 18,000. The estimated pKa of carfentanil is 8.05, 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. Volatilization from moist soil surfaces is not expected to be an important fate process based upon the estimated pKa and an estimated Henry's Law constant of 4.4X10-13 atm-cu m/mole. Carfentanil is not expected to volatilize from dry soil surfaces based upon its estimated vapor pressure. Biodegradation data in soil or water were not available. If released into water, carfentanil is expected to adsorb to suspended solids and sediment based upon the estimated Koc. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's estimated pKa and Henry's Law constant. An estimated BCF of 80 suggests the potential for bioconcentration in aquatic organisms is moderate. Estimated hydrolysis half-lives are 35 and 3.5 years at pH values of 7 and 8, respectively. Occupational exposure to carfentanil may occur through dermal contact with this compound at workplaces where carfentanil is produced or administered. Exposure to carfentanil among the general population may be limited to its use as a PET imaging compound and as an illicit drug. (SRC)

Implantation or injectable dosage form new animal drugs. Carfentanil. ... Indications for use. For immobilizing free ranging and confined members of the family Cervidae (deer, elk, and moose). ... Limitations. Do not use in domestic animals intended for food. Do not use 30 days before or during hunting season. Federal law restricts this drug to use by or on the order of a licensed veterinarian. The licensed veterinarian shall be a veterinarian engaged in zoo and exotic animal practice, wildlife management programs, or research.

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. Carfentanil citrate is included on this list. /Carfentanil citrate/

Schedule II shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. ... Opiates. Unless specifically excepted or unless in another schedule any of the following opiates, including its isomers, esters, ethers, salts and salts of isomers, esters and ethers whenever the existence of such isomers, esters, ethers, and salts is possible within the specific chemical designation, dextrorphan and levopropoxyphene excepted:. Carfentanil (DEA Code Number: 9743) is included on this list.

(11)C-Carfentanil has been widely used in positron emission tomography (PET) studies for measuring micro-opioid receptor binding in humans . ...

MEDICATION (VET)

Carfentanil (DEA Code Number: 9743) is a Schedule II controlled substance.

Schedule II Controlled Substance: (A) The drug or other substance has a high potential for abuse; (B) The drug or other substance has a currently accepted medical use in treatment in the United States or a currently accepted medical use with severe restrictions; and (C) Abuse of the drug or other substances may lead to severe psychological or physical dependence.

For more Uses (Complete) data for Carfentanil (6 total), please visit the HSDB record page.