55096-26-9C=C1CC[C@@]2(O)[C@H]3Cc4ccc(O)c5c4[C@@]2(CCN3CC2CC2)[C@H]1O5WJBLNOPPDWQMCH-MBPVOVBZSA-NNalmefene is a morphinane alkaloid.
55096-26-9DTXSID8023347CHEMBL982DEA NFLIS-Drug Category -> Narcotics
Pharmaceuticals -> Listed in ZINC15
Breast Feeding; Lactation; Milk, Human; Narcotic Antagonists
EMA approved medicines: Human medicine
7.6
pKa = 7.63 /Nalmefene hydrochloride/
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Warning
H315 (97.5%): Causes skin irritation [Warning Skin corrosion/irritation]
P261, P264, P264+P265, P271, P280, P302+P352, P304+P340, P305+P351+P338, P319, P321, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)
Aggregated GHS information provided per 40 reports by companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
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: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.
N07BB05
N - Nervous system
QN - Nervous system
Protein binding of nalmefene ranges from 30% to 45%. _In vitro_, 67% (CV 8.7%) of nalmefene was distributed into red blood cells and 39% (CV 6.4%) was distributed into plasma. The whole blood to plasma ratio was 1.3 (CV 6.6%) over the nominal concentration range in whole blood from 0.376 to 30 ng/mL.
Nalmefene is an opioid antagonist with no agonist activity. It works to prevent or reverse the effects of opioids, including respiratory depression, sedation, and hypotension. Nalmefene has a longer duration of action than [naloxone], another opioid antagonist used to reverse opioid overdose. In a study of brain receptor occupancy, a 1 mg dose of nalmefene blocked over 80% of brain opioid receptors within five minutes after administration. Nalmefene has no opioid agonist activity and it is not associated with drug tolerance, physical dependence, or abuse potential. Nalmefene is not known to produce respiratory depression, psychotomimetic effects, or pupillary constriction. No pharmacological activity was observed when nalmefene was administered in the absence of opioid agonists. However, as with all opioid antagonists, nalmefene can produce acute withdrawal symptoms in individuals with opioid dependence. These withdrawal symptoms should be managed with symptomatic and supportive treatment: the administration of large amounts of opioids to patients receiving opioid antagonists in an attempt to overcome a full blockade has resulted in adverse respiratory and circulatory reactions.
The opioid system consists of three opioid receptors - mu (μ), delta (δ), and kappa (κ) - that are G-protein coupled receptors. Opioid receptors are activated by endogenous opioid peptides and are expressed throughout the brain to play a critical role in mood regulation, pain, reward, addictive behaviours, and substance use disorders. Opioid receptors are involved in various brain signalling pathways, including the mesolimbic pathway, sometimes referred to as the reward pathway. The mesolimbic pathway plays an important role in the positive reinforcement of natural rewards like food and drugs of abuse like exogenous opioid drugs. Many abused drugs activate mu-opioid receptors, leading to positive reinforcing effects. Alcohol consumption can also cause the release of endogenous opioids, which bind to mu and delta receptors, thereby increasing the release of dopamine in the nucleus accumbens to induce reward and positive reinforcement effects. Nalmefene is an antagonist at the mu and delta-opioid receptors and a partial agonist at the kappa-opioid receptor. As an antagonist, nalmefene blocks ligands from binding to the opioid receptor. Animal studies suggest that kappa-opioid receptor signalling blocks acute reward and positive reinforcement effects of drugs with abusive potential by decreasing dopamine in the nucleus accumbens. _In vivo_ studies have demonstrated that nalmefene reduces alcohol consumption, possibly by modulating cortico-mesolimbic functions. Preclinical studies suggest that nalmefene restores alcohol-induced dysregulations of the MOR/endorphins and the KOR/dynorphin system.
Wird geladen…
CHEBI:7457Nalmefene is distributed in sealed ampuls which represent no known risk to health care workers. As with all parenterals, care should be taken to prevent the generation and inhalation of aerosols during preparation and use. Dermal absorption of spilled nalmefene should be prevented by prompt removal of contaminated clothing and rinsing the skin thoroughly with cool water.
Preclinical studies have shown that both flumazenil and nalmefene can induce seizures in animals. The coadministration of both flumazenil and nalmefene produced fewer seizures than expected in a study in rodents, based on the expected effects of each drug alone. Based on these data, an adverse interaction from the coadministration of the two drugs is not expected, but physicians should remain aware of the potential risk of seizures from agents in these classes.
Therapy with nalmefene has not been linked to serum enzyme elevations or to idiosyncratic acute, clinically apparent liver injury. Nalmefene is extensively metabolized in the liver, but largely by glucuronidation rather than transformation to a different metabolite. Patients with opioid overdose often have underlying chronic liver diseases such as alcoholic liver disease, hepatitis B or C, but treatment with nalmefene does not appear to exacerbate those conditions.
TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1.4X10+4(SRC), determined from a structure estimation method(2), indicates that nalmefene is expected to be immobile in soil(SRC). The pKa of nalmefene hydrochloride is 7.63(3), indicating that this compound will exist partially in 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 nalmefene from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.8X10-16 atm-cu m/mole(SRC), using a fragment constant estimation method(5). Nalmefene is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.7X10-14 mm Hg at 25 °C(6). Biodegradation data in soil were not available(SRC, 2009).
AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1.4X10+4(SRC), determined from a structure estimation method(2), indicates that nalmefene is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 1.8X10-16 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 27(SRC), from an estimated log Kow of 2.66(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data in water are not available(SRC, 2009).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), nalmefene, which has an estimated vapor pressure of 5.7X10-14 mm Hg at 25 °C(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase nalmefene may be removed from the air by wet or dry deposition(SRC). Nalmefene does not contain chromophores that absorb at wavelengths >290 nm(3) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).
Using a structure estimation method based on molecular connectivity indices(1), the Koc of nalmefene can be estimated to be 1.4X10+4(SRC). According to a classification scheme(2), this estimated Koc value suggests that nalmefene is expected to be immobile in soil. The pKa of nalmefene hydrochloride is 7.63(3), indicating that this compound will exist partially in cation form in the environment, and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).
/HUMAN EXPOSURE STUDIES/ A double blind randomized study of the pharmacology and abuse potential of nalmefene hydrochloride was conducted in 6 male volunteers (aged 28-43 yr) with histories of opiate abuse who received an oral capsule of 25, 50 and 100 mg oral nalmefene, an intramuscular injection of 15 and 30 mg morphine sulfate and placebo. Drowsiness or sleepiness was the most common drug effect reported after the administration of each treatment. Only morphine produced miosis and increased subject reported euphoria. Neither drug increased Addiction Research Inventory subscale scores measuring dysphoria or sedation or produced changes on the Profile of Mood States questionnaire. Adverse effects reported only after the administration of nalmefene included agitation/irritability and muscle tension. These effects did not appear to be dosage related. It was concluded that nalmefene did not produce typical morphine like effects and has no apparent abuse potential.
/SIGNS AND SYMPTOMS/ Intravenous doses of up to 24 mg of nalmefene, administered to healthy volunteers in the absence of opioid agonists, produced no serious adverse reactions, severe signs or symptoms, or clinically significant laboratory abnormalities. As with all opioid antagonists, use in patients physically dependent on opioids can result in precipitated withdrawal reactions that may result in symptoms that require medical attention. ... Administration of large amounts of opioids to patients receiving opioid antagonists in an attempt to overcome a full blockade has resulted in adverse respiratory and circulatory reactions.
/GENOTOXICITY/ nalmefene did exhibit a weak but significant clastogenic activity in the human lymphocyte metaphase assay in the absence but not in the presence of exogenous metabolic activation.
Drug-Induced Liver Injury Severity and Toxicity (DILIst)
Nalmefene
DILI Negative
Oral
DOI:10.1016/j.drudis.2019.09.022
An estimated BCF of 27 was calculated in fish for nalmefene(SRC), using an estimated log Kow of 2.66(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 nalmefene is estimated as 1.8X10-16 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that nalmefene is expected to be essentially nonvolatile from water surfaces(2). Nalmefene's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to occur(SRC). Nalmefene is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.7X10-14 mm Hg(3).
/LABORATORY ANIMALS: Acute Exposure/ The effects of the long-acting opioid antagonist, nalmefene [17-N-cyclopropylmethyl-3,14-beta-dihydroxy-4, 5-alpha-epoxy-6-methylene morphinan hydrochloride] on LH, T, and prolactin release in rhesus monkeys are unknown. The acute effects of nalmefene (0.01 and 0.10 mg/kg, IV) or placebo on LH, PRL, and T were studied, and samples were collected at 10-min intervals for 360 min to permit cluster analysis of pulsatile release patterns. LH increased significantly within 30 min after nalmefene, and remained significantly above baseline levels for 50 to 60 min (p < 0.05). Testosterone increased significantly within 70 to 80 min after nalmefene, and remained significantly above baseline for 60 min (p < 0.05). Although nalmefene antagonizes opioid agonists for 6-8 h, inhibitory feedback by testosterone appeared to limit the duration of its antagonism of endogenous opioid inhibition of LHRH and stimulation of LH. Nalmefene did not change LH or PRL pulse frequency or amplitude significantly in comparison to placebo administration.
/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Nalmefene is an orally available opioid receptor antagonist that has been shown to suppress appetite in humans, but its effects on chronic food intake and body weight remain unclear. Here, /investigators/ report that chronic (21-day) oral administration of nalmefene at 2 or 10 mg/kg/day in diet-induced obese (DIO) mice led to significant increases (9-11%) in cumulative food intake. Mice in the nalmefene-treated groups also gained body weight at a rate faster than the control. Body composition analysis showed that the extra body weight gains in the treated animals were mostly due to increased fat accumulation. Since acute nalmefene treatment showed a trend toward a decrease rather than an increase in food intake, it is possible that the orexigenic effect of chronic oral administration of nalmefene was caused by pharmacologically active metabolites rather than the drug itself. ...
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Reproduction studies have been performed in rats (up to 1200 mg/sq m/day) and rabbits (up to 2400 mg/sq m/day) by oral administration of nalmefene and in rabbits by intravenous administration up to 96 mg/sq m/day (114 times the human dose). There was no evidence of impaired fertility or harm to the fetus.
/GENOTOXICITY/ Nalmefene did not have mutagenic activity in the Ames test with five bacterial strains or the mouse lymphoma assay. Clastogenic activity was not observed in the mouse micronucleus test or in the cytogenic bone marrow assay in rats
Nalmefene is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(1). Nalmefene does not contain chromophores that absorb at wavelengths >290 nm(1) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).
Occupational exposure to nalmefene may occur through inhalation of dust during production, storage and transport, and dermal contact with this compound at workplaces where nalmefene is produced or used. Exposure to nalmefene among the general population may be limited to those administered the drug, an opioid antagonist. (SRC)
Nalmefene prevents or reverses the effects of opioids, including respiratory depression, sedation, and hypotension. Pharmacodynamic studies have shown that Nalmefene has a longer duration of action than naloxone at fully reversing doses. Nalmefene has no opioid agonist activity.
In humans, mu- and kappa-opioid receptor agonists lower tuberoinfundibular dopamine, which tonically inhibits prolactin release. Serum prolactin is, therefore, a useful biomarker for tuberoinfundibular dopamine. The current study evaluated the unexpected finding that the relative mu- and kappa-opioid receptor selective antagonist nalmefene increases serum prolactin, indicating possible kappa-opioid receptor agonist activity. In all, 33 healthy human volunteers (14 female) with no history of psychiatric or substance use disorders received placebo, nalmefene 3 mg, and nalmefene 10 mg in a double-blind manner. Drugs were administered between 0900 and 1000 on separate days via 2-min intravenous infusion. Serial blood specimens were analyzed for serum levels of prolactin. Additional in vitro studies of nalmefene binding to cloned human kappa-opioid receptors transfected into Chinese hamster ovary cells were performed. Compared to placebo, both doses of nalmefene caused significant elevations in serum prolactin (p<0.002 for nalmefene 3 mg and p<0.0005 for nalmefene 10 mg). There was no difference in prolactin response between the 3 and 10 mg doses. Binding assays confirmed nalmefene's affinity at kappa-opioid receptors and antagonism of mu-opioid receptors. [(35)S]GTPgammaS binding studies demonstrated that nalmefene is a full antagonist at mu-opioid receptors and has partial agonist properties at kappa-opioid receptors. Elevations in serum prolactin following nalmefene are consistent with this partial agonist effect at kappa-opioid receptors. As kappa-opioid receptor activation can lower dopamine in brain regions important to the persistence of alcohol and cocaine dependence, the partial kappa agonist effect of nalmefene may enhance its therapeutic efficacy in selected addictive diseases.
The terminal half-life is approximately 12.5 hours following oral administration. After intravenous administration of 1 mg nalmefene to healthy adult male subjects, plasma concentrations declined biexponentially with redistribution and a terminal elimination half-life of 41 ± 34 minutes and 10.8 ± 5.2 hours, respectively.
After intravenous administration of 1 mg nalmefene to normal males (ages 19-32), plasma concentrations declined biexponentially with a redistribution and a terminal elimination half-life of 41 +/- 34 minutes and 10.8 +/- 5.2 hours, respectively.
Elimination half-life increased from 10.2 +/- 2.2 hours to 11.9 +/- 2.0 hours in the hepatically impaired.
The elimination half-life was prolonged in ESRD patients from 10.2 +/- 2.2 hours in normals to 26.1 +/- 9.9 hours.
Half-life is 10.3 to 12.9 hr
Nalmefene is extensively metabolized by the liver, primarily by glucuronide conjugation mainly mediated by UGT2B7 and UGT1A3 and UGT1A8 to a lesser extent. The major metabolite is pharmacologically inactive nalmefene 3-O-glucuronide. Nalmefene is also metabolized to trace amounts of an N-dealkylated metabolite, which has minimal pharmacological activity. Nalmefene can undergo dealkylation mediated by CYP3A4/5 to form nornalmefene. Nornalmefene can be further converted to nornalmefene 3-O-glucuronide and nornalmefene 3-sulfate, which are generally inactive metabolites. Nalmefene can also undergo CYP3A4/5-mediated sulfation to form nalmefene 3-O-sulfate, which retains some pharmacological activity. However, nalmefene 3-O-sulfate is present in the circulation in less than 10% of that of nalmefene; thus, it is unlikely to be a major contributor to the pharmacological activity of nalmefene. The plasma concentration-time profile in some subjects suggests that nalmefene undergoes enterohepatic recycling.
Nalmefene is metabolized by the liver, primarily by glucuronide conjugation, and excreted in the urine. Nalmefene is also metabolized to trace amounts of an N-dealkylated metabolite. Nalmefene glucuronide is inactive and the N-dealkylated metabolite has minimal pharmacological activity. ... The plasma concentration-time profile in some subjects suggests that nalmefene undergoes enterohepatic recycling.
The disposition of nalmefene in rat and dog was studied using in vitro and in vivo methodology. In vitro metabolite profiles were obtained following incubation of nalmefene with liver microsomes and biological fluids were assayed to profile in vivo metabolites. Characterization of metabolites was accomplished using hplc, co-chromatography with synthetic standards, or LC/MS. In rat, tissue distribution and metabolite plasma concentration-time data were obtained following intravenous bolus dosing of nalmefene. The results indicate that the primary phase I metabolite of nalmefene from liver microsome incubations was the N-dealkylated metabolite, nornalmefene. Quantitative metabolite production was rat >> dog. In vivo, nornalmefene glucuronide was the major metabolite in rat urine, whereas nalmefene glucuronide(s) were predominant in dog urine. More than 90% of the radioactive dose was recovered in the rat excreta and tissues 24 hr after an intravenous bolus dose of 14C-nalmefene, with no apparent organ-specific retention of radioactivity. Pharmacokinetic analysis of the rat plasma metabolite data indicated that terminal half-lives for nalmefene and nornalmefene were comparable (approximately 1 hr). However, Cmax and AUC of nornalmefene were < or = 7% that of corresponding nalmefene values.
TOV02TDP9I
NALMEFENE
Established Pharmacologic Class [EPC] - Opioid Antagonist
Mechanisms of Action [MoA] - Opioid Antagonists
Nalmefene is an Opioid Antagonist. The mechanism of action of nalmefene is as an Opioid Antagonist.
Nalmefene is rapidly absorbed after a single oral administration of 18.06 mg with an absolute oral bioavailability of 41%. The Cmax was 16.5 ng/mL and Tmax was approximately 1.5 hours. The exposure (AUC) was 131 ng x h/mL. High-fat meal increased the AUC by 30% and Cmax by 50% and delayed Tmax by 30 min; however, this is unlikely of clinical significance. Nalmefene exhibits dose-proportional pharmacokinetics following intravenous administration of 0.5 mg to 2 mg. Tmax was 2.3 ± 1.1 hours following intramuscular administration and 1.5 ± 1.2 hours following subcutaneous administration. Therapeutic plasma concentrations are likely to be reached within 5 to 15 minutes after a 1 mg dose in an emergency. There is variability in the speed of absorption for intramuscular and subcutaneous dosing.
Renal excretion is the main route of elimination for nalmefene and its metabolites. About 54% of the total dose is excreted in the urine as nalmefene 3-O-glucuronide. Less than 3% of the dose is excreted as nalmefene or other metabolites. About 17% of the dose is excreted in the feces.
Following a 1 mg parenteral dose, nalmefene was rapidly distributed. The apparent volumes of distribution centrally (V<sub>c</sub>) and at steady-state (V<sub>dss</sub>) are 3.9 ± 1.1 L/kg and 8.6 ± 1.7 L/kg, respectively. Nalmefene readily crosses the blood-brain barrier.
The oral clearance of nalmefene (CL/F) was estimated as 169 L/h. Following intravenous administration of 1 mg nalmefene, the systemic clearance of nalmefene was 0.8 ± 0.2 L/hr/kg and the renal clearance was 0.08 ± 0.04 L/hr/kg.
Nalmefene was completely bioavailable following intramuscular or subcutaneous administration in 12 male volunteers relative to intravenous nalmefene. The relative bioavailabilities of intramuscular and subcutaneous routes of administration were 101.5% +/-8.1% (Mean +/- SD) and 99.7% +/-6.9%, respectively.
Nalmefene is administered primarily as an intravenous bolus, however, nalmefene can be given intra-muscularly (IM) or subcutaneously (SC) if venous access cannot be established. While the time to maximum plasma nalmefene concentration was 2.3 +/- 1.1 hours following intramuscular and 1.5 +/- 1.2 hours following subcutaneous administrations, therapeutic plasma concentrations are likely to be reached within 5-15 minutes after a 1 mg dose in an emergency. Because of the variability in the speed of absorption for im and sc dosing, and the inability to titrate to effect, great care should be taken if repeated doses must be given by these routes.
Is a pure opioid receptor antagonist ... used to reverse opioid intoxication and for the treatment of opioid dependence. The compound is in clinical development for the treatment of alcoholism, to support smoking cessation and to control pathological gambling.
Therapeutic Category: Narcotic antagonist
Therapeutic Category (Vet): Narcotic antagonist
MEDICATION
Nalmefene is synthesized by a Wittig reaction of naltrexone with triphenylmethylphosphonium bromide in DMSO under basic catalysis of NaH.
Preparation: J. Fishman, US 3814768 (1974 to M.J. Lewenstein)
Nalmetrene
REVEX
VerwendenA structural analog of Naltrexone (N285780) with opiate antagonist activity used in pharmaceutical treatment of alcoholism. Other pharmacological applications of this compound aim to reduce food cravings, drug abuse and pulmonary disease in affected individuals. Used as an opioid-induced tranquilizer on large animals in the veterinary industry. Narcotic antagonist.