A kappa opioid receptor agonist. The compound has analgesic action and shows positive inotropic effects on the electrically stimulated left atrium. It also affects various types of behavior in mammals such as locomotion, rearing, and grooming.
An analgesic with mixed narcotic agonist-antagonist properties.
A semisynthetic analgesic used in the study of narcotic receptors.
Morphine derivatives of the methanobenzazocine family that act as potent analgesics.
A class of opioid receptors recognized by its pharmacological profile. Kappa opioid receptors bind dynorphins with a higher affinity than endorphins which are themselves preferred to enkephalins.
Cell membrane proteins that bind opioids and trigger intracellular changes which influence the behavior of cells. The endogenous ligands for opioid receptors in mammals include three families of peptides, the enkephalins, endorphins, and dynorphins. The receptor classes include mu, delta, and kappa receptors. Sigma receptors bind several psychoactive substances, including certain opioids, but their endogenous ligands are not known.
An opioid analgesic with actions and uses similar to MORPHINE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1095)
Compounds based on a partially saturated iminoethanophenanthrene, which can be described as ethylimino-bridged benzo-decahydronaphthalenes. They include some of the OPIOIDS found in PAPAVER that are used as ANALGESICS.
One of the three major families of endogenous opioid peptides. The enkephalins are pentapeptides that are widespread in the central and peripheral nervous systems and in the adrenal medulla.
A delta-selective opioid (ANALGESICS, OPIOID). It can cause transient depression of mean arterial blood pressure and heart rate.
A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.
Compounds based on benzeneacetamide, that are similar in structure to ACETANILIDES.
One of the three major groups of endogenous opioid peptides. They are large peptides derived from the PRO-OPIOMELANOCORTIN precursor. The known members of this group are alpha-, beta-, and gamma-endorphin. The term endorphin is also sometimes used to refer to all opioid peptides, but the narrower sense is used here; OPIOID PEPTIDES is used for the broader group.
One of the endogenous pentapeptides with morphine-like activity. It differs from MET-ENKEPHALIN in the LEUCINE at position 5. Its first four amino acid sequence is identical to the tetrapeptide sequence at the N-terminal of BETA-ENDORPHIN.
Pyrrolidines are saturated, heterocyclic organic compounds containing a five-membered ring with four carbon atoms and one nitrogen atom (NRCH2CH2), commonly found as structural components in various alkaloids and used in the synthesis of pharmaceuticals and other organic materials.
Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of NALOXONE. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence.
Agents inhibiting the effect of narcotics on the central nervous system.
A class of opioid receptors recognized by its pharmacological profile. Delta opioid receptors bind endorphins and enkephalins with approximately equal affinity and have less affinity for dynorphins.
A class of opioid receptors recognized by its pharmacological profile. Mu opioid receptors bind, in decreasing order of affinity, endorphins, dynorphins, met-enkephalin, and leu-enkephalin. They have also been shown to be molecular receptors for morphine.

kappa-Opioid receptor effects of butorphanol in rhesus monkeys. (1/38)

Butorphanol and nalbuphine have substantial affinity for mu and kappa-opioid receptor sites, yet their behavioral effects in monkeys are largely consistent with a mu receptor mechanism of action. Using ethylketocyclazocine (EKC) discrimination and diuresis assays in rhesus monkeys (Macaca mulatta), the purpose of the current investigation was to characterize the in vivo kappa-opioid activity of these compounds through the use of an insurmountable mu-opioid receptor antagonist, clocinnamox. Alone, butorphanol (0.001-0.032 mg/kg i.m.) failed to generalize to EKC, and pretreatment with the competitive opioid receptor antagonist quadazocine (0.1 or 0.32 mg/kg i.m.) did not alter this generalization. At 24 h after clocinnamox (0.1 mg/kg i.m.) administration, butorphanol fully generalized to EKC, and this generalization was maintained in two of three monkeys at 72 h. Parallel results were observed in diuresis: butorphanol alone and in the presence of quadazocine (1 mg/kg i.m.) did not alter urine output, and a marked diuretic effect was demonstrated 24 h to 2 weeks after clocinnamox administration. Clocinnamox did not alter the discriminative stimulus or diuretic effects of nalbuphine or of the kappa-opioid receptor agonists EKC or U69593. These results are consistent with an in vivo agonist activity of butorphanol at kappa-opioid receptors that can only be demonstrated when an insurmountable antagonist has substantially eliminated the dominant receptor population through which it exerts its action.  (+info)

GR89,696: a potent kappa-opioid agonist with subtype selectivity in rhesus monkeys. (2/38)

GR89,696 is a synthetic kappa-opioid receptor agonist, recently reported to have an agonist profile consistent with selectivity at the proposed "kappa(2)" subtype. The present studies evaluated the effects of GR89,696 in vitro (i.e., in radioligand binding and [(35)S]guanosine-5'-O-(3-thio)triphosphate assays) and in vivo in rhesus monkeys, in assays used to study kappa-opioid agonists (i.e., thermal antinociception, sedation and muscle relaxation, diuresis, and increases in serum prolactin levels, as well as ethylketocyclazocine and U69,593 discrimination). Furthermore, the sensitivity of GR89,696 to naltrexone and nor-binaltorphimine (nor-BNI) antagonism was compared with that of U50,488 and U69,593, ligands selective for the proposed "kappa(1)" subtype. Overall, GR89,696 displayed the profile of a highly potent kappa-opioid agonist, following parenteral administration in rhesus monkeys. GR89,696 was less sensitive than U50,488 and U69,593 to naltrexone or nor-BNI antagonism, consistent with an action through the proposed kappa(2) receptor subtype.  (+info)

Association of PI-3 kinase with PAK1 leads to actin phosphorylation and cytoskeletal reorganization. (3/38)

The family of p21-activated kinases (PAKs) have been implicated in the rearrangement of actin cytoskeleton by acting downstream of the small GTPases Rac and Cdc42. Here we report that even though Cdc42/Rac1 or Akt are not activated, phosphatidylinositol-3 (PI-3) kinase activation induces PAK1 kinase activity. Indeed, we demonstrate that PI-3 kinase associates with the N-terminal regulatory domain of PAK1 (amino acids 67-150) leading to PAK1 activation. The association of the PI-3 kinase with the Cdc42/Rac1 binding-deficient PAK1(H83,86L) confirms that the small GTPases are not involved in the PI-3 kinase-PAK1 interaction. Furthermore, PAK1 was activated in cells expressing the dominant-negative forms of Cdc42 or Rac1. Additionally, we show that PAK1 phosphorylates actin, resulting in the dissolution of stress fibers and redistribution of microfilaments. The phosphorylation of actin was inhibited by the kinase-dead PAK1(K299R) or the PAK1 autoinhibitory domain (PAK1(83-149)), indicating that PAK1 was responsible for actin phosphorylation. We conclude that the association of PI-3 kinase with PAK1 regulates PAK1 kinase activity through a Cdc42/Rac1-independent mechanism leading to actin phosphorylation and cytoskeletal reorganization.  (+info)

Pharmacological profile of various kappa-agonists at kappa-, mu- and delta-opioid receptors mediating presynaptic inhibition of neurotransmitter release in the rat brain. (4/38)

1. The potency, relative efficacy and selectivity of a series of kappa-opioid receptor agonists at the mu-, delta- and kappa-opioid receptors mediating inhibition of electrically-induced (radiolabelled) neurotransmitter release from superfused rat brain slices was determined. 2. With regard to their potencies at kappa-receptors mediating inhibition of striatal [3H]-dopamine release, the highest pD2 value (8.7) was found for bremazocine and the lowest (7.1) for U50488; the pD2 values for ethylketocyclazocine (EKC), tifluadom, U69593 and PD117302 were between 8.0 and 8.3. There were no marked differences between the relative efficacies of the kappa-agonists (maximum inhibition being 60-70%). In contrast to the other kappa-agonists, at a concentration of 1 microM, PD117302 caused a significant (25-40%) increase of the spontaneous efflux of tritium. 3. None of the kappa-agonists significantly affected striatal [14C]-acetylcholine (ACh) release, with the exception of a slight inhibitory effect of EKC. The delta-receptor-mediated inhibitory effect of [D-Ala2, D-Leu5]enkephalin (DADLE) on [14C]-ACh release was antagonized in a concentration-dependent manner by bremazocine (0.1 and 1.0 microM) and also partially by EKC (1 microM), but not by the other kappa-agonists. The pA2 value for bremazocine as an antagonist at the delta-receptors involved was 8.0, compared to 7.6 for naloxone. 4. None of the kappa-agonists significantly affected cortical [3H]-noradrenaline (NA) release, with the notable exception of tifluadom, which strongly inhibited release by activating mu-receptors. The mu-receptor-mediated inhibitory effect of Tyr-D-Ala-Gly-(NMe)Phe-Gly-ol (DAMGO) on [3H]-NA release was antagonized in a concentration-dependent manner by bremazocine and EKC, but not by the other K-agonists. The pA2 value for bremazocine as an antagonist at the mu-receptors involved was 8.2, compared to 8.6 for naloxone. 5. Thus, whereas U69593 and PD1 17302 display high potency and selectivity towards K-opioid receptors, the potent benzomorphan K-agonists bremazocine and EKC also appear to be strong mu-opioid receptor antagonists.  (+info)

Effects of kappa opioid agonists alone and in combination with cocaine on heart rate and blood pressure in conscious squirrel monkeys. (5/38)

As kappa agonists have been proposed as treatments for cocaine abuse, the cardiovascular effects of the kappa opioid receptor agonists ethylketocyclazocine (EKC) and enadoline were investigated in conscious squirrel monkeys. Both EKC and enadoline increased heart rate with little effect on blood pressure. This effect appeared to be specific for kappa receptors as the mu opioid agonist morphine did not mimic the effects of the kappa agonists. The opioid antagonist naltrexone, at a dose of 1.0 mg/kg, blocked the effect of EKC. An action at both central and peripheral receptors may be responsible for the heart rate increase following kappa agonist treatment. The ganglionic blocker chlorisondamine partially antagonized the effect of EKC on heart rate, suggesting central involvement, while the peripherally-acting agonist ICI 204,448 ((+/-)-1-[2,3- (Dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol hydrochloride) also increased heart rate, supporting a peripheral site of action. When given in combination with cocaine, EKC produced effects that were sub-additive, suggesting that the kappa agonists may be used safely as cocaine abuse treatments.  (+info)

Differential effects of opioid agonists on G protein expression in CHO cells expressing cloned human opioid receptors. (6/38)

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Opioid receptor ligands in the neonatal rat spinal cord: binding and in vitro depression of the nociceptive responses. (7/38)

1. Opioid receptors in the neonatal rat spinal cord have been characterized by measurements of ligand binding to crude membrane fractions and by functional tests on the nociceptive spinal response in a spinal cord-tail preparation in vitro. 2. There were high affinity binding sites for [3H]-[D-Ala2, MePhe4, Gly(ol)5]enkephalin (DAGOL), [3H]-U69593, and [3H]-ethylketocyclazocine (EKC) on spinal cord membranes from neonatal rats. Hill slopes for binding of [3H]-DAGOL and [3H]-U69593 were close to unity. The Hill slope for binding of [3H]-EKC was less than unity, even after its interactions at mu-receptors had been blocked with 100 nM unlabelled DAGOL. Binding sites for [3H]-[D-Pen2, D-Pen5]enkephalin (DPDPE) could not be detected. 3. In competition assays U50488 was as potent as PD117302 and U69593 in competition for either [3H]-U69593 or [3H]-EKC binding sites. Hill slopes for a range of competing ligands at [3H]-DAGOL or [3H]-U69593 sites were close to unity. Hill slopes for competition at [3H]-EKC sites were less than one. 4. In the spinal cord-tail preparation from neonatal rats, opioid receptor agonists depressed spinal nociceptive responses evoked by application of capsaicin or heat to the tail. The order of potency was DAGOL greater than U69593 = PD117302 greater than morphine greater than U50488 = [D-Pen2, L-Pen5]enkephalin (DPLPE). 5. The antagonist naloxone was about equally potent against DAGOL, morphine and DPLPE, and about ten times less potent against U69593 and PD117302. The effects of U50488 were much less sensitive to blockade by naloxone than the effects of PD11703 or U69593. The Kappa antagonist, nor-binaltorphimine was equipotent against all three Kappa agonists. 6. The absence of delta-binding sites, and the low potency and relatively high sensitivity to naloxone suggest that DPLPE could be working at mu-receptors in the neonatal rat spinal cord. 7. The binding assays show that U50488 has the same affinity as PD1 17302 and U69593 for Kappa-receptors, yet it was less effective in the depression of nociceptive responses. This may be because U50488 has a relatively low efficacy at Kappa-receptors. It is possible that at high concentrations U50488 activates receptors not affected by other Kappa-ligands. These additional receptors may be non-opioid receptors (hence the insensitivity to naloxone), or they could be a subtype of Kappa-opioid receptor.  (+info)

On the mechanism by which midazolam causes spinally mediated analgesia. (8/38)

The electrical current thresholds for pain (ECTP) in the skin of the neck and tail were measured in rats with chronically implanted lumbar subarachnoid catheters. The effects of a benzodiazepine antagonist and a gamma-aminobutyric acid (GABA) antagonist on the analgesic effects of equivalent doses of midazolam, fentanyl, and ketocyclazocine were studied. These were the minimum doses producing maximal segmental analgesia when given intrathecally (i.e., they all caused a significant and maximum increase in ECTP in the tail, which was similar for all three drugs, but no significant change in the ECTP in the neck). Flumazenil (Ro 15-1788) administration caused a parallel shift to the right of the dose-response curve for midazolam spinal analgesia. Segmental analgesia following midazolam was also significantly attenuated (P less than 0.05) when the selective GABA antagonist bicuculline was given intrathecally at the same time as midazolam. The highest dose of bicuculline used (50 pmol) caused no significant attenuation of the segmental analgesic effects of either ketocyclazocine or fentanyl. The authors concluded that the segmental analgesia produced by intrathecal midazolam is mediated by the benzodiazepine-GABA receptor complex that is involved in other benzodiazepine actions.  (+info)

Ethylketocyclazocine is a synthetic opioid drug that acts as a potent mixed agonist-antagonist at mu, kappa, and delta opioid receptors. It produces analgesic, sedative, and respiratory depressant effects, but its clinical use is limited due to its strong dysphoric and hallucinogenic properties. Ethylketocyclazocine is primarily used in research to study the pharmacology of opioid receptors and their roles in pain modulation, addiction, and other physiological processes.

Cyclazocine is a synthetic opioid drug that acts as a partial agonist at mu and kappa opioid receptors, and as an antagonist at delta opioid receptors. It has analgesic (pain-relieving) effects, but its use as an analgesic is limited due to its potential for abuse and the occurrence of unpleasant psychotomimetic side effects such as dysphoria, delusions, and hallucinations.

Cyclazocine was first synthesized in 1957 and has been studied for its potential use in the treatment of opioid addiction, but it is not currently approved for medical use in many countries, including the United States. It is classified as a Schedule I controlled substance in the US, indicating that it has a high potential for abuse and no accepted medical use.

Dihydromorphine is a semi-synthetic opioid agonist that is derived from morphine, which is a natural opiate alkaloid found in the poppy plant (Papaver somniferum). It is a potent analgesic drug used to treat moderate to severe pain. Dihydromorphine works by binding to and activating the mu-opioid receptors in the brain and spinal cord, which inhibits the transmission of pain signals and produces a subjective feeling of euphoria or pleasure.

Dihydromorphine is similar in structure and effects to other opioids such as heroin, oxycodone, and hydromorphone. It has a rapid onset of action and can produce strong analgesic effects, but it also carries a high risk of dependence, addiction, and respiratory depression, which can be fatal if not treated promptly.

Dihydromorphine is available in various forms, including tablets, injectable solutions, and suppositories. It is primarily used in Europe and Asia for the treatment of pain, although it has been largely replaced by other opioids such as morphine and fentanyl in many countries due to its higher abuse potential and narrower therapeutic index.

Benzomorphans are a class of opioid drugs that have a chemical structure similar to morphine. They are synthetic compounds, meaning they are made in a laboratory and do not occur naturally. Benzomorphans include drugs such as pentazocine and phenazocine, which are used for pain relief and cough suppression. These drugs work by binding to opioid receptors in the brain and spinal cord, which helps to reduce the perception of pain and suppress coughing.

Benzomorphans have a unique chemical structure that differs from other opioids such as morphine or fentanyl. They are classified as "mixed agonist-antagonists," meaning they can act as both an agonist (a substance that binds to a receptor and activates it) and an antagonist (a substance that binds to a receptor but does not activate it, and may block the effects of other substances that do activate the receptor). This property makes benzomorphans useful for pain relief in certain situations, as they can provide pain relief without causing some of the side effects associated with other opioids, such as respiratory depression.

However, like all opioid drugs, benzomorphans carry a risk of addiction and dependence, and can cause serious harm or even death if taken in large doses or mixed with other substances that depress the central nervous system. It is important to use these medications only as directed by a healthcare provider and to follow their instructions carefully.

Opioid receptors, also known as opiate receptors, are a type of G protein-coupled receptor found in the nervous system and other tissues. They are activated by endogenous opioid peptides, as well as exogenous opiates and opioids. There are several subtypes of opioid receptors, including mu, delta, and kappa.

Kappa opioid receptors (KORs) are a subtype of opioid receptor that are widely distributed throughout the body, including in the brain, spinal cord, and gastrointestinal tract. They are activated by endogenous opioid peptides such as dynorphins, as well as by synthetic and semi-synthetic opioids such as salvinorin A and U-69593.

KORs play a role in the modulation of pain, mood, and addictive behaviors. Activation of KORs has been shown to produce analgesic effects, but can also cause dysphoria, sedation, and hallucinations. KOR agonists have potential therapeutic uses for the treatment of pain, addiction, and other disorders, but their use is limited by their side effects.

It's important to note that opioid receptors and their ligands (drugs or endogenous substances that bind to them) are complex systems with many different actions and effects in the body. The specific effects of KOR activation depend on a variety of factors, including the location and density of the receptors, the presence of other receptors and signaling pathways, and the dose and duration of exposure to the ligand.

Opioid receptors are a type of G protein-coupled receptor (GPCR) found in the cell membranes of certain neurons in the central and peripheral nervous system. They bind to opioids, which are chemicals that can block pain signals and produce a sense of well-being. There are four main types of opioid receptors: mu, delta, kappa, and nociceptin. These receptors play a role in the regulation of pain, reward, addiction, and other physiological functions. Activation of opioid receptors can lead to both therapeutic effects (such as pain relief) and adverse effects (such as respiratory depression and constipation).

Phenazocine is a synthetic opioid analgesic, which is primarily used for the treatment of moderate to severe pain. It is a schedule II controlled substance in the United States due to its high potential for abuse and addiction. Phenazocine works by binding to the mu-opioid receptors in the brain and spinal cord, which are responsible for mediating pain perception, reward, and addictive behaviors.

The medical definition of Phenazocine is:

A potent opioid analgesic with a rapid onset of action and a duration of effect of 2-4 hours. It is approximately ten times more potent than morphine and has similar side effects, including respiratory depression, sedation, nausea, vomiting, and constipation. Phenazocine is used for the management of acute pain, cancer pain, and as an adjunct in anesthesia. It is available in oral and injectable forms and may be administered intravenously, intramuscularly, or subcutaneously.

It's important to note that Phenazocine should only be used under the supervision of a qualified medical professional due to its potential for addiction and abuse.

Morphinans are a class of organic compounds that share a common skeletal structure, which is based on the morphine molecule. The morphinan structure consists of a tetracyclic ring system made up of three six-membered benzene rings (A, C, and D) fused to a five-membered dihydrofuran ring (B).

Morphinans are important in medicinal chemistry because many opioid analgesics, such as morphine, hydromorphone, oxymorphone, and levorphanol, are derived from or structurally related to morphinans. These compounds exert their pharmacological effects by binding to opioid receptors in the brain and spinal cord, which are involved in pain perception, reward, and addictive behaviors.

It is worth noting that while all opiates (drugs derived from the opium poppy) are morphinans, not all morphinans are opiates. Some synthetic or semi-synthetic morphinans, such as fentanyl and methadone, do not have a natural origin but still share the same basic structure and pharmacological properties.

Enkephalins are naturally occurring opioid peptides that bind to opiate receptors in the brain and other organs, producing pain-relieving and other effects. They are derived from the precursor protein proenkephalin and consist of two main types: Leu-enkephalin and Met-enkephalin. Enkephalins play a role in pain modulation, stress response, mood regulation, and addictive behaviors. They are also involved in the body's reward system and have been implicated in various physiological processes such as respiration, gastrointestinal motility, and hormone release.

Enkephalins are naturally occurring opioid peptides in the body that bind to opiate receptors and help reduce pain and produce a sense of well-being. There are several different types of enkephalins, including Leu-enkephalin and Met-enkephalin, which differ based on their amino acid sequence.

Leucine-enkephalin (Leu-Enk) is a specific type of enkephalin that contains the amino acids tyrosine, glycine, glutamic acid, leucine, and methionine in its sequence. The Leucine-2-Alanine variant of Leu-Enk refers to a synthetic form of this peptide where the leucine at position 2 is replaced with alanine. This modification can affect the stability, activity, and pharmacological properties of the enkephalin molecule.

It's important to note that while Leu-Enk and its analogs have potential therapeutic applications in pain management, they are also subject to abuse and addiction due to their opioid properties. Therefore, their use is tightly regulated and requires careful medical supervision.

Naloxone is a medication used to reverse the effects of opioids, both illicit and prescription. It works by blocking the action of opioids on the brain and restoring breathing in cases where opioids have caused depressed respirations. Common brand names for naloxone include Narcan and Evzio.

Naloxone is an opioid antagonist, meaning that it binds to opioid receptors in the body without activating them, effectively blocking the effects of opioids already present at these sites. It has no effect in people who have not taken opioids and does not reverse the effects of other sedatives or substances.

Naloxone can be administered via intranasal, intramuscular, intravenous, or subcutaneous routes. The onset of action varies depending on the route of administration but generally ranges from 1 to 5 minutes when given intravenously and up to 10-15 minutes with other methods.

The duration of naloxone's effects is usually shorter than that of most opioids, so multiple doses or a continuous infusion may be necessary in severe cases to maintain reversal of opioid toxicity. Naloxone has been used successfully in emergency situations to treat opioid overdoses and has saved many lives.

It is important to note that naloxone does not reverse the effects of other substances or address the underlying causes of addiction, so it should be used as part of a comprehensive treatment plan for individuals struggling with opioid use disorders.

Benzeneacetamides are a class of organic compounds that consist of a benzene ring, which is a six-carbon cyclic structure with alternating double bonds, linked to an acetamide group. The acetamide group consists of an acetyl functional group (-COCH3) attached to an amide nitrogen (-NH-).

Benzeneacetamides have the general formula C8H9NO, and they can exist in various structural isomers depending on the position of the acetamide group relative to the benzene ring. These compounds are used in the synthesis of pharmaceuticals, dyes, and other chemical products.

In a medical context, some benzeneacetamides have been studied for their potential therapeutic effects. For example, certain derivatives of benzeneacetamide have shown anti-inflammatory, analgesic, and antipyretic properties, making them candidates for the development of new drugs to treat pain and inflammation. However, more research is needed to establish their safety and efficacy in clinical settings.

Endorphins are a type of neurotransmitter, which are chemicals that transmit signals in the nervous system and brain. The term "endorphin" comes from "endogenous morphine," reflecting the fact that these substances are produced naturally within the body and have effects similar to opiate drugs like morphine.

Endorphins are released in response to stress or pain, but they also occur naturally during exercise, excitement, laughter, love, and orgasm. They work by interacting with the opiate receptors in the brain to reduce the perception of pain and promote feelings of pleasure and well-being. Endorphins also play a role in regulating various physiological processes, including appetite, mood, and sleep.

In summary, endorphins are natural painkillers and mood elevators produced by the body in response to stress, pain, or enjoyable activities.

Enkephalins are naturally occurring opioid peptides in the body that bind to opiate receptors and help reduce pain and produce a sense of well-being. There are two major types of enkephalins: Met-enkephalin and Leu-enkephalin, which differ by only one amino acid at position 5 (Leucine or Methionine).

Leu-enkephalin, also known as YGGFL, is a type of enkephalin that contains the amino acids Tyrosine (Y), Glycine (G), Glycine (G), Phenylalanine (F), and Leucine (L) in its sequence. It is involved in pain regulation, mood, and other physiological processes.

Leu-enkephalin is synthesized from a larger precursor protein called proenkephalin and is stored in the secretory vesicles of neurons. When released into the synaptic cleft, Leu-enkephalin can bind to opioid receptors on neighboring cells, leading to various physiological responses.

Leu-enkephalin has a shorter half-life than Met-enkephalin due to its susceptibility to enzymatic degradation by peptidases. However, it still plays an essential role in modulating pain and other functions in the body.

Pyrrolidines are not a medical term per se, but they are a chemical compound that can be encountered in the field of medicine and pharmacology. Pyrrolidine is an organic compound with the molecular formula (CH2)4NH. It is a cyclic secondary amine, which means it contains a nitrogen atom surrounded by four carbon atoms in a ring structure.

Pyrrolidines can be found in certain natural substances and are also synthesized for use in pharmaceuticals and research. They have been used as building blocks in the synthesis of various drugs, including some muscle relaxants, antipsychotics, and antihistamines. Additionally, pyrrolidine derivatives can be found in certain plants and fungi, where they may contribute to biological activity or toxicity.

It is important to note that while pyrrolidines themselves are not a medical condition or diagnosis, understanding their chemical properties and uses can be relevant to the study and development of medications.

Naltrexone is a medication that is primarily used to manage alcohol dependence and opioid dependence. It works by blocking the effects of opioids and alcohol on the brain, reducing the euphoric feelings and cravings associated with their use. Naltrexone comes in the form of a tablet that is taken orally, and it has no potential for abuse or dependence.

Medically, naltrexone is classified as an opioid antagonist, which means that it binds to opioid receptors in the brain without activating them, thereby blocking the effects of opioids such as heroin, morphine, and oxycodone. It also reduces the rewarding effects of alcohol by blocking the release of endorphins, which are natural chemicals in the brain that produce feelings of pleasure.

Naltrexone is often used as part of a comprehensive treatment program for addiction, along with counseling, behavioral therapy, and support groups. It can help individuals maintain abstinence from opioids or alcohol by reducing cravings and preventing relapse. Naltrexone is generally safe and well-tolerated, but it may cause side effects such as nausea, headache, dizziness, and fatigue in some people.

It's important to note that naltrexone should only be used under the supervision of a healthcare provider, and it is not recommended for individuals who are currently taking opioids or who have recently stopped using them, as it can cause withdrawal symptoms. Additionally, naltrexone may interact with other medications, so it's important to inform your healthcare provider of all medications you are taking before starting naltrexone therapy.

Narcotic antagonists are a class of medications that block the effects of opioids, a type of narcotic pain reliever, by binding to opioid receptors in the brain and blocking the activation of these receptors by opioids. This results in the prevention or reversal of opioid-induced effects such as respiratory depression, sedation, and euphoria. Narcotic antagonists are used for a variety of medical purposes, including the treatment of opioid overdose, the management of opioid dependence, and the prevention of opioid-induced side effects in certain clinical situations. Examples of narcotic antagonists include naloxone, naltrexone, and methylnaltrexone.

Opioid delta receptors, also known as delta opioid receptors (DORs), are a type of G protein-coupled receptor found in the nervous system and other tissues throughout the body. They belong to the opioid receptor family, which includes mu, delta, and kappa receptors. These receptors play an essential role in pain modulation, reward processing, and addictive behaviors.

Delta opioid receptors are activated by endogenous opioid peptides such as enkephalins and exogenous opioids like synthetic drugs. Once activated, they trigger a series of intracellular signaling events that can lead to inhibition of neuronal excitability, reduced neurotransmitter release, and ultimately, pain relief.

Delta opioid receptors have also been implicated in various physiological processes, including immune function, respiratory regulation, and gastrointestinal motility. However, their clinical use as therapeutic targets has been limited due to the development of tolerance and potential adverse effects such as sedation and respiratory depression.

In summary, delta opioid receptors are a type of opioid receptor that plays an essential role in pain modulation and other physiological processes. They are activated by endogenous and exogenous opioids and trigger intracellular signaling events leading to various effects, including pain relief. However, their clinical use as therapeutic targets is limited due to potential adverse effects.

Opioid mu receptors, also known as mu-opioid receptors (MORs), are a type of G protein-coupled receptor that binds to opioids, a class of chemicals that include both natural and synthetic painkillers. These receptors are found in the brain, spinal cord, and gastrointestinal tract, and play a key role in mediating the effects of opioid drugs such as morphine, heroin, and oxycodone.

MORs are involved in pain modulation, reward processing, respiratory depression, and physical dependence. Activation of MORs can lead to feelings of euphoria, decreased perception of pain, and slowed breathing. Prolonged activation of these receptors can also result in tolerance, where higher doses of the drug are required to achieve the same effect, and dependence, where withdrawal symptoms occur when the drug is discontinued.

MORs have three main subtypes: MOR-1, MOR-2, and MOR-3, with MOR-1 being the most widely studied and clinically relevant. Selective agonists for MOR-1, such as fentanyl and sufentanil, are commonly used in anesthesia and pain management. However, the abuse potential and risk of overdose associated with these drugs make them a significant public health concern.

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Tam SW (February 1985). "(+)-[3H]SKF 10,047, (+)-[3H]ethylketocyclazocine, mu, kappa, delta and phencyclidine binding sites in ...
Tam SW (February 1985). "(+)-[3H]SKF 10,047, (+)-[3H]ethylketocyclazocine, mu, kappa, delta and phencyclidine binding sites in ...
Anazocine Bremazocine Butinazocine Carbazocine Cogazocine Cyclazocine Dezocine Eptazocine Etazocine Ethylketocyclazocine ...
... ethylketocyclazocine MeSH D03.383.113.767 - oxazocines MeSH D03.383.113.767.500 - nefopam MeSH D03.383.129.308 - imidazoles ... ethylketocyclazocine MeSH D03.605.497.150 - buprenorphine MeSH D03.605.497.165 - butorphanol MeSH D03.605.497.260 - dextrorphan ...
Explore the 1 paper that mention a possible interaction between Inosine and Ethylketocyclazocine. ...
Pasternak GW (June 1980). "Multiple opiate receptors: [3H]ethylketocyclazocine receptor binding and ketocyclazocine analgesia ...
Goedert, M., Lightman, S. L., Mantyh, P. W., Hunt, S. P. & Emson, P. C., Dec 9 1985, In: Brain Research. 358, 1-2, p. 59-69 11 p.. Research output: Contribution to journal › Article › peer-review ...
Young GA, Khazan N. "Self-administration of ketocyclazocine and ethylketocyclazocine by the rat." Pharmacol Biochem Behav. 1983 ...
The first characterisation of a k-receptor binding site in brain came from work using [3H]-ethylketocyclazocine (EKC).34 ...
Nalmefene antagonized the bindings of [3H]-dihydromorphine, [3H]-ethylketocyclazocine and [3H]-D-ala-D-leu enkephalin with ...
... ethylketocyclazocine] (EKC) together with the competing agents [D-Pro4]-morphiceptin and [D-Ser2, Thr6]-Leu-enkephalin, and an ...
However, the (-) isomers are only moderately more potent than the (+) isomers at displacing [3H]ethylketocyclazocine from κ ... However, the (-) isomers are only moderately more potent than the (+) isomers at displacing [3H]ethylketocyclazocine from κ ... However, the (-) isomers are only moderately more potent than the (+) isomers at displacing [3H]ethylketocyclazocine from κ ... However, the (-) isomers are only moderately more potent than the (+) isomers at displacing [3H]ethylketocyclazocine from κ ...
Specific binding of [3H]MERF was inhibited by DAMGO, Tyr-D-Arg-Phe-Sar(TAPS), bremazocine and ethylketocyclazocine (EKC), but ...
... or ethylketocyclazocine/or ethylmorphine/or etorphine/or fentanyl/or heroin/or hydrocodone/or hydromorphone/or levorphanol/or ... codeine or dihydrocodeine or dextromoramide or dextropropoxyphene or dihydromorphine or diphenoxylate or ethylketocyclazocine ...
The opioid agonist ethylketocyclazocine reverts the rapid, non-genomic effects of membrane testosterone receptors in the human ...
Ethylketocyclazocine Methanesulfonate Narrower Concept UI. M0024933. Registry Number. 0. Terms. Ethylketocyclazocine ... Ethylketocyclazocine Preferred Term Term UI T048661. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1991). ... Ethylketocyclazocine Preferred Concept UI. M0024932. Registry Number. 58640-84-9. Scope Note. A kappa opioid receptor agonist. ... Ethylketocyclazocine Methanesulfonate Win-35197-2 Pharm Action. Analgesics, Opioid. Registry Number. 58640-84-9. CAS Type 1 ...
Ethylketocyclazocine Methanesulfonate Narrower Concept UI. M0024933. Registry Number. 0. Terms. Ethylketocyclazocine ... Ethylketocyclazocine Preferred Term Term UI T048661. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1991). ... Ethylketocyclazocine Preferred Concept UI. M0024932. Registry Number. 58640-84-9. Scope Note. A kappa opioid receptor agonist. ... Ethylketocyclazocine Methanesulfonate Win-35197-2 Pharm Action. Analgesics, Opioid. Registry Number. 58640-84-9. CAS Type 1 ...
Goedert, M., Lightman, S. L., Mantyh, P. W., Hunt, S. P. & Emson, P. C., Dec 9 1985, In: Brain Research. 358, 1-2, p. 59-69 11 p.. Research output: Contribution to journal › Article › peer-review ...
N0000167066 Ethylenethiourea N0000006759 Ethylestrenol N0000179570 ethylhexyl palmitate N0000167219 Ethylketocyclazocine ...
OPIOID ETHYLKETOCYCLAZOCINE ANALGESICS, OPIOID ETHYLMORPHINE ANALGESICS, OPIOID ETORPHINE ANALGESICS, OPIOID FENTANYL ... ANALGESICS ETHYLKETOCYCLAZOCINE ANALGESICS ETHYLMORPHINE ANALGESICS ETODOLAC ANALGESICS ETORPHINE ANALGESICS FENOPROFEN ... CENTRAL NERVOUS SYSTEM AGENTS ETHYLKETOCYCLAZOCINE CENTRAL NERVOUS SYSTEM AGENTS ETHYLMORPHINE CENTRAL NERVOUS SYSTEM AGENTS ...
... ethylketocyclazocine, U50,488, U69,593, spiradoline, nor-binaltorphimine, naltrindole, DPDPE, [D-la2, glu4]deltorphin ...
Ethylketocyclazocine [D03.383.113.367.350] Ethylketocyclazocine * Oxazocines [D03.383.113.767] Oxazocines * CHEMICALS AND DRUGS ...
  • 15. The opioid agonist ethylketocyclazocine reverts the rapid, non-genomic effects of membrane testosterone receptors in the human prostate LNCaP cell line. (nih.gov)