A derivative of benzodiazepine that acts on the cholecystokinin A (CCKA) receptor to antagonize CCK-8's (SINCALIDE) physiological and behavioral effects, such as pancreatic stimulation and inhibition of feeding.
Benzodiazepinones are a class of psychoactive drugs that bind to the GABA-A receptor and enhance its inhibitory effects, producing anxiolytic, sedative, hypnotic, anticonvulsant, and muscle relaxant properties.
Cell surface proteins that bind cholecystokinin (CCK) with high affinity and trigger intracellular changes influencing the behavior of cells. Cholecystokinin receptors are activated by GASTRIN as well as by CCK-4; CCK-8; and CCK-33. Activation of these receptors evokes secretion of AMYLASE by pancreatic acinar cells, acid and PEPSIN by stomach mucosal cells, and contraction of the PYLORUS and GALLBLADDER. The role of the widespread CCK receptors in the central nervous system is not well understood.
A subtype of cholecystokinin receptor found primarily in the PANCREAS; STOMACH; INTESTINE; and GALLBLADDER. It plays a role in regulating digestive functions such as gallbladder contraction, pancreatic enzyme secretion and absorption in the GASTROINTESTINAL TRACT.
A peptide, of about 33 amino acids, secreted by the upper INTESTINAL MUCOSA and also found in the central nervous system. It causes gallbladder contraction, release of pancreatic exocrine (or digestive) enzymes, and affects other gastrointestinal functions. Cholecystokinin may be the mediator of satiety.
An octapeptide hormone present in the intestine and brain. When secreted from the gastric mucosa, it stimulates the release of bile from the gallbladder and digestive enzymes from the pancreas.
Chemical substances which inhibit the function of the endocrine glands, the biosynthesis of their secreted hormones, or the action of hormones upon their specific sites.
A drug that exerts an inhibitory effect on gastric secretion and reduces gastrointestinal motility. It is used clinically in the drug therapy of gastrointestinal ulcers.
L-Tryptophyl-L-methionyl-L-aspartyl-L-phenylalaninamide. The C-terminal tetrapeptide of gastrin. It is the smallest peptide fragment of gastrin which has the same physiological and pharmacological activity as gastrin.
1-Deoxy-1-(methylamino)-D-glucitol. A derivative of sorbitol in which the hydroxyl group in position 1 is replaced by a methylamino group. Often used in conjunction with iodinated organic compounds as contrast medium.
The lack or loss of APPETITE accompanied by an aversion to food and the inability to eat. It is the defining characteristic of the disorder ANOREXIA NERVOSA.
A subtype of cholecystokinin receptor found primarily in the CENTRAL NERVOUS SYSTEM and the GASTRIC MUCOSA. It may play a role as a neuromodulator of dopaminergic neurotransmission the regulation of GASTRIC ACID secretion from GASTRIC PARIETAL CELLS.
Compounds that include the amino-N-phenylamide structure.

Proliferative effects of cholecystokinin in GH3 pituitary cells mediated by CCK2 receptors and potentiated by insulin. (1/106)

1. Proliferative effects of CCK peptides have been examined in rat anterior pituitary GH3 cells, which express CCK2 receptors. 2. CCK-8s, gastrin(1-17) and its glycine-extended precursor G(1-17)-Gly, previously reported to cause proliferation via putative novel sites on AR4-2J and Swiss 3T3 cells, elicited significant dose dependent increases of similar magnitude in [3H]thymidine incorporation over 3 days in serum-free medium of 39 +/- 10% (P < 0.01, n = 20), 37 +/- 8% (P < 0.01, n = 27) and 41 +/- 6% (P < 0.01, n = 36) respectively. 3. CCK-8s and gastrin potentially stimulated mitogenesis (EC50 values 0.12 nM and 3.0 nM respectively), whilst G-Gly displayed similar efficacy but markedly lower potency. L-365,260 consistently blocked each peptide. The CCK2 receptor affinity of G-Gly in GH3 cells was 1.09 microM (1.01;1.17, n = 6) and 5.53 microM (3.71;5.99, n = 4) in guinea-pig cortex. 4. 1 microM G-Gly weakly stimulated Ca2+ increase, eliciting a 104 +/- 21% increase over basal Ca2+ levels, and was blocked by 1 microM L-365,260 whilst CCK-8s (100 nM) produced a much larger Ca2+ response (331 +/- 14%). 5. Insulin dose dependently enhanced proliferative effects of CCK-8s with a maximal leftwards shift of the CCK-8s curve at 100 ng ml(-1) (17 nM) (EC50 decreased 500 fold, from 0.1 nM to 0.2 pM; P < 0.0001). 10 microg ml(-1) insulin was supramaximal reducing the EC50 to 5 pM (P = 0.027) whilst 1 ng ml(-1) insulin was ineffective. Insulin weakly displaced [125I]BHCCK binding to GH3 CCK2 receptors (IC50 3.6 microM). 6. Results are consistent with mediation of G-Gly effects via CCK2 receptors in GH3 cells and reinforce the role of CCK2 receptors in control of cell growth. Effects of insulin in enhancing CCK proliferative potency may suggest that CCK2 and insulin receptors converge on common intracellular targets and indicates that mitogenic stimuli are influenced by the combination of extracellular factors present.  (+info)

SR146131: a new potent, orally active, and selective nonpeptide cholecystokinin subtype 1 receptor agonist. I. In vitro studies. (2/106)

SR146131 inhibited the binding of [125I]-Bolton Hunter (BH)-sulfated cholecystokinin octapeptide (CCK-8S) for the human recombinant cholecystokinin subtype 1 (CCK1) receptor (IC50 = 0.56 nM) with high (300-fold) selectivity to the CCK2 receptor. The biological activity of SR146131 was characterized in vitro in a NIH-3T3 cell line expressing the human recombinant CCK1 receptor (3T3-hCCK1). Measuring intracellular calcium release, SR146131 behaved as a full agonist with an efficacy comparable with that of CCK-8S (EC50 = 1.38 +/- 0.06 nM). On individual cells, SR146131 induced, like CCK-8S, Ca2+ oscillations at subnanomolar concentrations and sustained responses at higher concentrations. Like CCK-8S, SR146131 also fully stimulated inositol monophosphate formation (EC50 = 18 +/- 4 nM). SR146131 partially activated mitogen-activated protein kinase and enhanced the expression of the immediate early gene krox 24. In the human CHP212 and IMR32 neuroblastoma cell lines, which constitutively express the CCK1 receptor, SR146131 behaved as a partial agonist on intracellular calcium release and inositol monophosphate formation. All of these effects of SR146131 were inhibited by the CCK1 receptor antagonists SR27897B and devazepide, suggesting that the effects of SR146131 were entirely mediated by the CCK1 receptor. In contrast, high concentrations (>1 microM) of SR146131 had only minimal effects on CCK-8S-stimulated and unstimulated Chinese hamster ovary (CHO) cells expressing the human CCK2 receptor, indicating that SR146131 is functionally inactive on the CCK2 receptor. In conclusion, these in vitro experiments show that SR146131 is a highly potent and selective agonist of the CCK1 receptor.  (+info)

CCK receptor dysfunction in muscle membranes from human gallbladders with cholesterol stones. (3/106)

Human gallbladders with cholesterol stones exhibit impaired muscle contraction induced by agonists that act on transmembrane receptors, increased membrane cholesterol content, and abnormal cholesterol-to-phospholipid ratio compared with those with pigment stones. The present study was designed to investigate the functions of the CCK receptor of gallbladder muscle membranes by radioreceptor assay and cross-linking. 125I-labeled CCK-8 binding was time-dependent, competitive, and specific. Scatchard analysis showed that the maximum specific binding (Bmax) was significantly decreased in cholesterol compared with pigment stone gallbladders (0.18 +/- 0. 07 vs. 0.38 +/- 0.05 pmol/mg protein, P < 0.05). In contrast, the affinity for CCK was higher in cholesterol than pigment stone gallbladders (0.18 +/- 0.06 vs. 1.2 +/- 0.23 nM). Similar results were observed in binding studies with the CCK-A receptor antagonist [3H]L-364,718. Cross-linking and saturation binding studies also showed significantly less CCK binding in gallbladders with cholesterol stones. These abnormalities were reversible after incubation with cholesterol-free liposomes. The Bmax increased (P < 0.01) and the dissociation constant decreased (P < 0.001) after incubation with cholesterol-free liposomes. In conclusion, human gallbladders with cholesterol stones have impaired CCK receptor binding compared with those with pigment stones. These changes are reversed by removal of the excess membrane cholesterol. These receptor alterations may contribute to the defective contractility of the gallbladder muscle in patients with cholesterol stones.  (+info)

Role of cholecystokinin in the anorexia produced by duodenal delivery of peptone in rats. (4/106)

We used the cholecystokinin receptor antagonist devazepide to assess the importance of CCK in mediating the anorexia produced by 2-h duodenal infusions of peptone, a protein digest, at dark onset in nonfasted rats. Peptone alone (0.14-2.24 g/h) suppressed food intake dose dependently by 18-96%, with an approximate half-maximal dose of 1 g/h. Peptone-induced reductions in caloric ingestion were comparable to the caloric loads infused. Devazepide alone (30-1,000 microgram/kg) stimulated food intake dose dependently by 30-73%, with a minimal effective dose of 100 micrograms/kg. Devazepide appeared to reverse the anorexic response to peptone (1.1 g/h) dose dependently by 29-65%, with a minimal effective dose of 30 micrograms/kg. The magnitudes of these devazepide-induced effects were similar to, and in some cases were larger than, those produced when the same doses of devazepide were administered alone. Coadministration of devazepide (1,000 micrograms/kg) and a lower peptone dose (0.8 g/h) produced similar results. These results suggest that an essential CCK mechanism plays a significant role in mediating the satiety response to duodenal delivery of protein.  (+info)

Small synthetic ligands of the cholecystokinin-B/gastrin receptor can mimic the function of endogenous peptide hormones. (5/106)

The gastric cholecystokinin-B/gastrin receptor (CCK-BR) is a key regulator of enterochromaffin-like cell function and proliferation. Over the last decade, a number of small non-peptide CCK-BR "antagonists" have been discovered. Here, we demonstrate that some of these non-peptide ligands in fact possess significant ability to activate the human CCK-BR, and are, therefore, more properly categorized as partial agonists. When tested in COS-7 cells transiently expressing the recombinant human CCK-BR, saturating concentrations of the small "peptoid" ligands PD 135,158 and PD 136,450 stimulated inositol phosphate formation to 23 and 43 percent, respectively, of the maximum response induced by a considerably larger endogenous peptide agonist, cholecystokinin octapeptide. In contrast, the benzodiazepine-derived CCK-BR ligand, YM022, acted as a "true" high-affinity antagonist of cholecystokinin-induced inositol phosphate formation (pA2 = 9.69). Consistent with recent findings in animal experiments, our data reveal that small synthetic ligands have the potential to function as either CCK-BR agonists or antagonists. These dual properties of synthetic molecules must be considered when evaluating candidate drugs for human disease.  (+info)

Duodenal loading with glucose induces fos expression in rat brain: selective blockade by devazepide. (6/106)

The role of CCK in mediating neuronal activity in the brain in response to dietary carbohydrate was measured by detecting Fos immunoreactivity in response to duodenal glucose load in rats after administration of the CCK-A receptor antagonist devazepide. In adult, male Sprague-Dawley rats, infusion for 30 min of 545 mg (2.18 kcal) dextrose through a duodenal cannula induced Fos expression in the nucleus of the solitary tract (NTS), area postrema (AP), lateral division of the central nucleus of the amygdala (CeAL), and the external subnucleus of the lateral parabrachial nucleus (LPBE). Devazepide treatment (1 mg/kg) attenuated Fos expression in the NTS and AP by 81 and 78%, respectively, but not in the CeAL or LPBE. These results indicate that central neuronal activation is elicited by dietary glucose in the intestinal lumen and that activation of neurons in the NTS and AP is mediated by CCK-A receptors.  (+info)

Effects of spinal cholecystokinin receptor antagonists on morphine antinociception in a model of visceral pain in the rat. (7/106)

The objective of the present study was to determine the effects of spinal cholecystokinin (CCK) receptor antagonists on morphine antinociception in a model of visceral nociception, colorectal distension, in rats with chronic colonic inflammation and vehicle-treated controls. Three to five days after intracolonic instillation of 2,4,6-trinitrobenzenesulfonic acid (TNBS), an enhanced visceromotor response to all pressures of colorectal distension (10-80 mm Hg) was evident. The ED(50) of intrathecal morphine (0.93 microgram) in vehicle-treated rats produced significantly greater antinociception in TNBS-treated rats. Intrathecal proglumide, a nonselective CCK receptor antagonist, dose dependently enhanced the antinociceptive effect of morphine in vehicle-treated rats, but not in TNBS-treated rats. Similarly, L-365, 260, a specific CCK(B) receptor antagonist, dose dependently increased morphine's antinociceptive effects in vehicle-treated rats but had no effect in rats with TNBS-induced colonic inflammation. L-364,718, a specific CCK(A) receptor antagonist, had no effect on morphine antinociception in either vehicle-treated or TNBS-treated rats. These data indicate that CCK, acting at the CCK(B) receptor, is involved in modulating morphine antinociception following a noxious visceral stimulus. However, CCK receptor antagonists no longer enhance morphine antinociception after instillation of intracolonic TNBS, suggesting that visceral inflammation may lead to a reduction in spinal CCK release.  (+info)

Devazepide reversed effect of sincalide against morphine on rat jejunal activities. (8/106)

AIM: To study the antagonism of sincalide to the effect of morphine and its mechanism. METHODS: The electrophysiologic and mechanic activities of rat jejunum in vitro were recorded. RESULTS: Acetylcholine (ACh, 150 nmol.L-1) increased the spike potential amplitude (SPA) and the number (SPN) of rat jejunum in vitro, followed by an increase of jejunal contraction amplitudes (CA), showing a positive correlation. Morphine 330 nmol.L-1 inhibited the potentiation of ACh, showing a negative correlation. Sincalide 0.7 nmol.L-1 antagonized the effects of morphine, i.e., the SPA and SPN were increased again, followed by an increase of CA. CCK-A receptor antagonist devazepide (10 nmol.L-1) reversed the antagonism of sincalide to the effect of morphine. CONCLUSION: Sincalide antagonized the effect of morphine which inhibited the potentiation of ACh on jejunal activities in vitro. The antagonistic effect of sincalide on morphine was mainly mediated by CCK-A receptor.  (+info)

Devazepide is not a medical term, but it is a pharmaceutical compound. It is a selective and competitive antagonist of the benzodiazepine site on GABA(A) receptors. This means that devazepide blocks the effects of benzodiazepines by binding to the same site on the GABA(A) receptor without activating it.

Devazepide has been studied in research settings as a potential treatment for alcohol use disorder and anxiety disorders, but it is not currently approved for medical use in any country.

Therefore, there is no official medical definition for 'Devazepide'.

Benzodiazepines are a class of psychoactive drugs that possess anxiolytic, anticonvulsant, amnesic, sedative, hypnotic, and muscle relaxant properties. Benzodiazepinones are a subclass of benzodiazepines that share a specific chemical structure, characterized by a 1,4-benzodiazepine ring with an additional nitrogen-containing ring attached at the 2-position of the benzodiazepine ring.

Examples of benzodiazepinones include clonazepam (Klonopin), diazepam (Valium), and flurazepam (Dalmane). These medications are commonly used in the treatment of anxiety disorders, insomnia, seizures, and muscle spasms. However, they can also cause physical dependence and withdrawal symptoms, so they should be prescribed with caution and under medical supervision.

Cholecystokinin (CCK) receptors are a type of G protein-coupled receptor that bind to and are activated by the hormone cholecystokinin. CCK is a peptide hormone that is released by cells in the duodenum in response to the presence of nutrients, particularly fat and protein. It has several physiological roles, including stimulating the release of digestive enzymes from the pancreas, promoting the contraction of the gallbladder and relaxation of the sphincter of Oddi (which controls the flow of bile and pancreatic juice into the duodenum), and inhibiting gastric emptying.

There are two main types of CCK receptors, known as CCK-A and CCK-B receptors. CCK-A receptors are found in the pancreas, gallbladder, and gastrointestinal tract, where they mediate the effects of CCK on digestive enzyme secretion, gallbladder contraction, and gastric emptying. CCK-B receptors are found primarily in the brain, where they play a role in regulating appetite and satiety.

CCK receptors have been studied as potential targets for the development of drugs to treat various gastrointestinal disorders, such as pancreatitis, gallstones, and obesity. However, more research is needed to fully understand their roles and therapeutic potential.

Cholecystokinin A (CCK-A) receptor is a type of G protein-coupled receptor that binds the hormone cholecystokinin (CCK). CCK is a peptide hormone that is released by cells in the duodenum in response to food intake, particularly fat and protein. The binding of CCK to the CCK-A receptor triggers several physiological responses, including contraction of the gallbladder and relaxation of the sphincter of Oddi, which controls the flow of bile from the gallbladder into the small intestine.

The CCK-A receptor is also found in the central nervous system, where it plays a role in regulating satiety and feeding behavior. Activation of the CCK-A receptor in the brain can lead to a decrease in food intake, making it a potential target for the development of anti-obesity drugs.

In summary, the Cholecystokinin A (CCK-A) receptor is a type of G protein-coupled receptor that binds the hormone cholecystokinin (CCK), and plays a role in regulating several physiological responses including gallbladder contraction, relaxation of the sphincter of Oddi, satiety and feeding behavior.

Cholecystokinin (CCK) is a hormone that is produced in the duodenum (the first part of the small intestine) and in the brain. It is released into the bloodstream in response to food, particularly fatty foods, and plays several roles in the digestive process.

In the digestive system, CCK stimulates the contraction of the gallbladder, which releases bile into the small intestine to help digest fats. It also inhibits the release of acid from the stomach and slows down the movement of food through the intestines.

In the brain, CCK acts as a neurotransmitter and has been shown to have effects on appetite regulation, mood, and memory. It may play a role in the feeling of fullness or satiety after eating, and may also be involved in anxiety and panic disorders.

CCK is sometimes referred to as "gallbladder-stimulating hormone" or "pancreozymin," although these terms are less commonly used than "cholecystokinin."

Sincalide is a synthetic hormone that stimulates the contraction of the gallbladder and the release of digestive enzymes from the pancreas. It is used in diagnostic procedures to help diagnose conditions such as gallstones or obstructions of the bile ducts.

Sincalide is a synthetic form of cholecystokinin (CCK), a hormone that is naturally produced in the body and stimulates the contraction of the gallbladder and the release of digestive enzymes from the pancreas. When sincalide is administered, it mimics the effects of CCK and causes the gallbladder to contract and release bile into the small intestine. This can help doctors see if there are any obstructions or abnormalities in the bile ducts or gallbladder.

Sincalide is usually given as an injection, and its effects can be monitored through imaging tests such as ultrasound or CT scans. It is important to note that sincalide should only be used under the supervision of a healthcare professional, as it can cause side effects such as abdominal pain, nausea, and vomiting.

Hormone antagonists are substances or drugs that block the action of hormones by binding to their receptors without activating them, thereby preventing the hormones from exerting their effects. They can be classified into two types: receptor antagonists and enzyme inhibitors. Receptor antagonists bind directly to hormone receptors and prevent the hormone from binding, while enzyme inhibitors block the production or breakdown of hormones by inhibiting specific enzymes involved in their metabolism. Hormone antagonists are used in the treatment of various medical conditions, such as cancer, hormonal disorders, and cardiovascular diseases.

Proglumide is not a medication that has a widely accepted or commonly used medical definition in current clinical practice. However, historically, it has been described as a synthetic benzamide derivative with antidomaminergic and gastrointestinal properties. It was initially investigated as a potential treatment for various gastrointestinal disorders, such as gastric ulcers, due to its ability to inhibit gastric acid secretion.

Proglumide has been found to act as an antagonist at certain dopamine receptors (D2 and D3) and serotonin receptors (5-HT3), which may contribute to its effects on gastrointestinal motility and gastric acid secretion. However, due to the development of more effective treatments and some uncertainty regarding its efficacy, proglumide is not widely used in modern medical practice.

It is important to note that this information might not be comprehensive or entirely up-to-date, as the use and understanding of proglumide have evolved over time. Always consult a reliable medical source or healthcare professional for the most accurate and current information.

Tetragastrin is not a medical condition but a synthetic peptide hormone that is used in medical research and diagnostic tests. It is composed of four amino acids (glutamic acid, proline, tryptophan, and methionine) and is similar to the natural hormone gastrin, which is produced by the stomach and helps regulate digestion.

Tetragastrin is used in medical research to study the function of the stomach and intestines, and it is also used in diagnostic tests to stimulate the release of gastric acid from the stomach. This can help diagnose conditions such as pernicious anemia, a condition in which the body cannot absorb vitamin B12 due to a lack of intrinsic factor, a protein produced by the stomach.

In summary, Tetragastrin is a synthetic hormone that mimics the function of natural gastrin and is used for research and diagnostic purposes related to the digestive system.

Meglumine is not a medical condition but a medication. It is an anticholinergic drug that is used as a diagnostic aid in the form of meglumine iodide, which is used to test for kidney function and to visualize the urinary tract. Meglumine is an amino sugar that is used as a counterion to combine with iodine to make meglumine iodide. It works by increasing the excretion of iodine through the kidneys, which helps to enhance the visibility of the urinary tract during imaging studies.

Anorexia is a medical condition defined as a loss of appetite or aversion to food, leading to significant weight loss. It can be a symptom of various underlying causes, such as mental health disorders (most commonly an eating disorder called anorexia nervosa), gastrointestinal issues, cancer, infections, or side effects of medication. In this definition, we are primarily referring to anorexia as a symptom rather than the specific eating disorder anorexia nervosa.

Anorexia nervosa is a psychological eating disorder characterized by:

1. Restriction of energy intake leading to significantly low body weight (in context of age, sex, developmental trajectory, and physical health)
2. Intense fear of gaining weight or becoming fat, or persistent behavior that interferes with weight gain
3. Disturbed body image, such as overvaluation of self-worth regarding shape or weight, or denial of the seriousness of low body weight

Anorexia nervosa has two subtypes: restricting type and binge eating/purging type. The restricting type involves limiting food intake without engaging in binge eating or purging behaviors (such as self-induced vomiting or misuse of laxatives, diuretics, or enemas). In contrast, the binge eating/purging type includes recurrent episodes of binge eating and compensatory behaviors to prevent weight gain.

It is essential to differentiate between anorexia as a symptom and anorexia nervosa as a distinct psychological disorder when discussing medical definitions.

Cholecystokinin B (CCK-B) receptor is a type of G protein-coupled receptor that binds the hormone cholecystokinin (CCK). CCK is a peptide hormone that is released by cells in the duodenum in response to food intake, particularly fat and protein. The binding of CCK to the CCK-B receptor triggers several physiological responses, including contraction of the gallbladder and relaxation of the sphincter of Oddi, which controls the flow of bile and pancreatic juices into the duodenum.

The CCK-B receptor is primarily found in the gastrointestinal tract, particularly in the smooth muscle cells of the gallbladder and the sphincter of Oddi. It is also expressed in the central nervous system (CNS), where it plays a role in regulating appetite and satiety.

The activation of CCK-B receptors in the CNS has been shown to reduce food intake, making it a potential target for the development of anti-obesity drugs. However, the use of CCK-B receptor agonists as therapeutic agents is limited by their side effects, which include nausea and abdominal pain.

Phenylurea compounds are a class of chemical compounds that contain a phenyl group (a functional group consisting of a six-membered aromatic ring with a hydrogen atom and a single bond to a carbon atom or other group) linked to a urea moiety. Urea is an organic compound that contains a carbonyl functional group connected to two amine groups.

Phenylurea compounds are commonly used as herbicides, fungicides, and insecticides in agriculture due to their ability to inhibit certain enzymes and disrupt plant growth processes. Some examples of phenylurea compounds include chlorotoluron, diuron, linuron, and monuron.

It is important to note that some phenylurea compounds have been found to be toxic to non-target organisms, including mammals, birds, and fish, and can pose environmental risks if not used properly. Therefore, it is essential to follow the recommended guidelines for their use and disposal to minimize potential health and ecological impacts.

... (L-364,718, MK-329) is benzodiazepine drug, but with quite different actions from most benzodiazepines, lacking ... Devazepide is synthesised in a similar manner to other benzodiazepines. Benzodiazepine Cholecystokinin antagonist US 4820834, ... EP 1492540, Jackson, Karen, "The use of devazepide as analgesic agent", published 2005-01-05, assigned to ML Laboratories plc ( ...
Cokelaere MM, Busselen P, Flo G, Daenens P, Decuypere E, Kühn E, Van Boven M (December 1995). "Devazepide reverses the anorexic ...
3-bromocamphor-8-sulfonic acid was used in the synthesis of enantiopure devazepide. Camphorsulfonic acid is also being used for ...
Josselyn, S. A.; Franco, V. P.; Vaccarino, F. J. (1996-01-01). "Devazepide, a CCKA receptor antagonist, impairs the acquisition ...
Antibodies Eptinezumab Erenumab Fremanezumab Galcanezumab Agonists Cholecystokinin Antagonists Amiglumide Asperlicin Devazepide ...
... devazepide MeSH D03.438.079.080.070.216 - diazepam MeSH D03.438.079.080.070.216.500 - nordazepam MeSH D03.438.079.080.070.305 ...
Selective CCKA receptor antagonists such as lorglumide and devazepide have been developed both for their anti-ulcer effects and ...
CAS# 130408-77-4 Proglumide Lorglumide Devazepide Dexloxiglumide Asperlicin SR-27897 IQM-95333 JNJ-17156516 Cholecystokinin ...
... and despite older selective CCKA antagonists such as lorglumide and devazepide having had only limited success in trials and ...
... such as devazepide and tifluadom, however these have not been included in the list below. 2,3-benzodiazepines such as tofisopam ...
... devazepide (INN) Dexacen-4 Dexacidin Dexacort Dexair dexamethasone acefurate (INN) dexamethasone cipecilate (INN) dexamethasone ...
Devazepide (L-364,718, MK-329) is benzodiazepine drug, but with quite different actions from most benzodiazepines, lacking ... Devazepide is synthesised in a similar manner to other benzodiazepines. Benzodiazepine Cholecystokinin antagonist US 4820834, ... EP 1492540, Jackson, Karen, "The use of devazepide as analgesic agent", published 2005-01-05, assigned to ML Laboratories plc ( ...
Counterbalanced devazepide (1 mg/kg; i.p.) or vehicle injections began 40-50 min after lights off, and food was immediately ... Devazepide (Tocris Bioscience), an antagonist of CCK-A receptors, was first dissolved in dimethylsulfoxide (DMSO), then further ... Injections were repeated every 72 h, each animal being tested for devazepide or vehicle at least twice. Values for each animal ... 4B; p , 0.05; determined using Bonferroni post-test). Devazepide treatment abolished this difference between genotypes (p , ...
Theres been a significant rise in benzodiazepine use despite the risk of side effects and addiction. Heres a look at whos using them and why.
DEVAZEPIDE. DEVAZEPIDA. DEVAZEPIDA. DEXFENFLURAMINE. DEXFENFLURAMINA. DEXFENFLURAMINA. DICHELOBACTER NODOSUS. DICHELOBACTER ...
DEVAZEPIDE. DEVAZEPIDA. DEXFENFLURAMINA. DEXFENFLURAMINE. DEXFENFLURAMINA. DICHELOBACTER NODOSUS. DICHELOBACTER NODOSUS. ...
DEVAZEPIDE. DEVAZEPIDA. DEXFENFLURAMINA. DEXFENFLURAMINE. DEXFENFLURAMINA. DICHELOBACTER NODOSUS. DICHELOBACTER NODOSUS. ...
DEVAZEPIDE. DEVAZEPIDA. DEVAZEPIDA. DEXFENFLURAMINE. DEXFENFLURAMINA. DEXFENFLURAMINA. DICHELOBACTER NODOSUS. DICHELOBACTER ...
DEVAZEPIDE. DEVAZEPIDA. DEVAZEPIDA. DEXFENFLURAMINE. DEXFENFLURAMINA. DEXFENFLURAMINA. DICHELOBACTER NODOSUS. DICHELOBACTER ...
DEVAZEPIDE. DEVAZEPIDA. DEXFENFLURAMINA. DEXFENFLURAMINE. DEXFENFLURAMINA. DICHELOBACTER NODOSUS. DICHELOBACTER NODOSUS. ...
DEVAZEPIDE. DEVAZEPIDA. DEVAZEPIDA. DEXFENFLURAMINE. DEXFENFLURAMINA. DEXFENFLURAMINA. DICHELOBACTER NODOSUS. DICHELOBACTER ...
DEVAZEPIDE. DEVAZEPIDA. DEXFENFLURAMINA. DEXFENFLURAMINE. DEXFENFLURAMINA. DICHELOBACTER NODOSUS. DICHELOBACTER NODOSUS. ...
DEVAZEPIDE. DEVAZEPIDA. DEXFENFLURAMINA. DEXFENFLURAMINE. DEXFENFLURAMINA. DICHELOBACTER NODOSUS. DICHELOBACTER NODOSUS. ...
DEVAZEPIDE. DEVAZEPIDA. DEXFENFLURAMINA. DEXFENFLURAMINE. DEXFENFLURAMINA. DICHELOBACTER NODOSUS. DICHELOBACTER NODOSUS. ...
DEVAZEPIDE. DEVAZEPIDA. DEVAZEPIDA. DEXFENFLURAMINE. DEXFENFLURAMINA. DEXFENFLURAMINA. DICHELOBACTER NODOSUS. DICHELOBACTER ...
DEVAZEPIDE. DEVAZEPIDA. DEVAZEPIDA. DEXFENFLURAMINE. DEXFENFLURAMINA. DEXFENFLURAMINA. DICHELOBACTER NODOSUS. DICHELOBACTER ...
Devazepide - No affinity for GABAa, selective CCKa antagonist.. :Lorglumide - Selective CCKa antagonist for treatment of ... Devazepide - No affinity for GABAa, selective CCKa antagonist.. Lorglumide - Selective CCKa antagonist for treatment of ...
DEVAZEPIDE - Antagonist chembl_ligand pubchem ENDOGENOUS LIGANDS. CCK-8, CCK-33, CCK-4, CCK-39, gastrin-17, CCK-58, desulfated ...
Inhibitory Effects of Devazepide on the Pancreatic Exocrine Function of Ginseng Saponin in Rats ... The amylase activity was significantly increased by acute TS treatment, but this increase was inhibited by devazepide ... However, the volume of pancreaticobiliary juice was significantly increased by devazepide treatment. The amylase activity was ... We studied the effects of ginseng saponins and devazepide, cholecys-tokinin receptor antagonist, on pancreaticobiliary ...
Inflammation is the first innate immune response to infection or irritation resulting from leukocyte (neutrophils, mast cells, etc.) accumulation and their secretion of inflammatory, biogenic chemicals such as histamine, prostaglandin, and pro-inflammatory cytokines. As cited, it has recently been discovered that resistin also participates in the inflammatory response.[12][13][14][15] In further support of its inflammatory profile, resistin has been shown to increase transcriptional events, leading to an increased expression of several pro-inflammatory cytokines including (but not limited to) interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-12 (IL-12), and tumor necrosis factor-α (TNF-α) in an NF-κB-mediated (nuclear factor kappa-light-chain-enhancer of activated B cells-mediated) fashion.[16][17] It has also been demonstrated that resistin upregulates intercellular adhesion molecule-1 (ICAM1) vascular cell-adhesion molecule-1 (VCAM1) and chemokine (C-C motif) ligand 2 (CCL2), all of ...
Caeruleins effect on PPI was blocked by pretreatment with a CCKA antagonist (devazepide) but not a CCKB antagonist (L-365,260 ...
Cokelaere MM, Busselen P, Flo G, Daenens P, Decuypere E, Kühn E, Van Boven M. Devazepide reverses the anorexic effect of ...
Bentazepam • Devazepide • Ketazolam • Razobazam • Tifluadom. Retrieved from "http://www.drugwiki.net/drugs/Sulazepam" ...
Devazepide D3.438.79.80.70.200 D3.633.100.79.80.70.200 Dexamethasone D4.808.745.432.769.344 D4.210.500.745.432.769.344 D4.808. ...
... devazepide British Journal of Pharmacology 118(2): 400-406 ...
ProIAPP has been linked to Type 2 diabetes and the loss of islet β-cells.[20] Islet amyloid formation, initiated by the aggregation of proIAPP, may contribute to this progressive loss of islet β-cells. It is thought that proIAPP forms the first granules that allow for IAPP to aggregate and form amyloid which may lead to amyloid-induced apoptosis of β-cells. IAPP is cosecreted with insulin. Insulin resistance in Type 2 diabetes produces a greater demand for insulin production which results in the secretion of proinsulin.[21] ProIAPP is secreted simultaneously, however, the enzymes that convert these precursor molecules into insulin and IAPP, respectively, are not able to keep up with the high levels of secretion, ultimately leading to the accumulation of proIAPP. In particular, the impaired processing of proIAPP that occurs at the N-terminal cleavage site is a key factor in the initiation of amyloid.[21] Post-translational modification of proIAPP occurs at both the carboxy terminus and the ...
Inflammation is the first innate immune response to infection or irritation resulting from leukocyte (neutrophils, mast cells, etc.) accumulation and their secretion of inflammatory, biogenic chemicals such as histamine, prostaglandin, and pro-inflammatory cytokines. As cited, it has recently been discovered that resistin also participates in the inflammatory response.[12][13][14][15] In further support of its inflammatory profile, resistin has been shown to increase transcriptional events, leading to an increased expression of several pro-inflammatory cytokines including (but not limited to) interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-12 (IL-12), and tumor necrosis factor-α (TNF-α) in an NF-κB-mediated (nuclear factor kappa-light-chain-enhancer of activated B cells-mediated) fashion.[16][17] It has also been demonstrated that resistin upregulates intercellular adhesion molecule-1 (ICAM1) vascular cell-adhesion molecule-1 (VCAM1) and chemokine (C-C motif) ligand 2 (CCL2), all of ...
Eledoisin is an undecapeptide of mollusk origin, belonging to the tachykinin family of neuropeptides. It was first isolated from the posterior salivary glands of two mollusk species Eledone muschata and Eledone aldovandi, which belong to the octopod order of Cephalopoda. [1] Other tachykinins from nonmammalian sources include kassinin and physalaemin. The mammalian tachykinins substance P, NKA, and NKB have similar effects as tachykinins of nonmammals and have been more widely studied and characterized. These peptides exhibit a wide and complex spectrum of pharmacological and physiological activities such as vasodilation, hypertension, and stimulation of extravascular smooth muscle.[2] Eledoisin has the amino acid sequence pGlu-Pro-Ser-Lys-Asp-Ala-Phe-Ile-Gly-Leu-Met-NH. Like all tachykinin peptides, Eledoisin shares the same consensus C-terminal sequence, that is, Phe-Xxx-Gly-Leu-Met-NH. The invariant "Phe7" residue is probably required for receptor binding. "Xxx" is either an aromatic ...
  • Devazepide (L-364,718, MK-329) is benzodiazepine drug, but with quite different actions from most benzodiazepines, lacking affinity for GABAA receptors and instead acting as an CCKA receptor antagonist. (wikipedia.org)
  • Devazepide is synthesised in a similar manner to other benzodiazepines. (wikipedia.org)