An antimuscarinic agent that inhibits gastric secretion at lower doses than are required to affect gastrointestinal motility, salivary, central nervous system, cardiovascular, ocular, and urinary function. It promotes the healing of duodenal ulcers and due to its cytoprotective action is beneficial in the prevention of duodenal ulcer recurrence. It also potentiates the effect of other antiulcer agents such as CIMETIDINE and RANITIDINE. It is generally well tolerated by patients.
A PEPTIC ULCER located in the DUODENUM.
A histamine congener, it competitively inhibits HISTAMINE binding to HISTAMINE H2 RECEPTORS. Cimetidine has a range of pharmacological actions. It inhibits GASTRIC ACID secretion, as well as PEPSIN and GASTRIN output.
A non-imidazole blocker of those histamine receptors that mediate gastric secretion (H2 receptors). It is used to treat gastrointestinal ulcers.
Drugs that bind to but do not activate MUSCARINIC RECEPTORS, thereby blocking the actions of endogenous ACETYLCHOLINE or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system.
Ulceration of the GASTRIC MUCOSA due to contact with GASTRIC JUICE. It is often associated with HELICOBACTER PYLORI infection or consumption of nonsteroidal anti-inflammatory drugs (NSAIDS).
Various agents with different action mechanisms used to treat or ameliorate PEPTIC ULCER or irritation of the gastrointestinal tract. This has included ANTIBIOTICS to treat HELICOBACTER INFECTIONS; HISTAMINE H2 ANTAGONISTS to reduce GASTRIC ACID secretion; and ANTACIDS for symptomatic relief.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
Ketonic amines prepared from the condensation of a ketone with formaldehyde and ammonia or a primary or secondary amine. A Mannich base can act as the equivalent of an alpha,beta unsaturated ketone in synthesis or can be reduced to form physiologically active amino alcohols.
A technology, in which sets of reactions for solution or solid-phase synthesis, is used to create molecular libraries for analysis of compounds on a large scale.
A group of compounds derived from ammonia by substituting organic radicals for the hydrogens. (From Grant & Hackh's Chemical Dictionary, 5th ed)
Substances that destroy fungi by suppressing their ability to grow or reproduce. They differ from FUNGICIDES, INDUSTRIAL because they defend against fungi present in human or animal tissues.
Possesses an unusual and selective cytotoxicity for VASCULAR SMOOTH MUSCLE cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial fibrosis or cardiac decompensation.
A benzodiazepine derivative used as an anticonvulsant and hypnotic.
An epileptic syndrome characterized by the triad of infantile spasms, hypsarrhythmia, and arrest of psychomotor development at seizure onset. The majority present between 3-12 months of age, with spasms consisting of combinations of brief flexor or extensor movements of the head, trunk, and limbs. The condition is divided into two forms: cryptogenic (idiopathic) and symptomatic (secondary to a known disease process such as intrauterine infections; nervous system abnormalities; BRAIN DISEASES, METABOLIC, INBORN; prematurity; perinatal asphyxia; TUBEROUS SCLEROSIS; etc.). (From Menkes, Textbook of Child Neurology, 5th ed, pp744-8)
An anticonvulsant used for several types of seizures, including myotonic or atonic seizures, photosensitive epilepsy, and absence seizures, although tolerance may develop. It is seldom effective in generalized tonic-clonic or partial seizures. The mechanism of action appears to involve the enhancement of GAMMA-AMINOBUTYRIC ACID receptor responses.
Drugs used to prevent SEIZURES or reduce their severity.
Drugs used to induce drowsiness or sleep or to reduce psychological excitement or anxiety.
A heterogeneous group of drugs used to produce muscle relaxation, excepting the neuromuscular blocking agents. They have their primary clinical and therapeutic uses in the treatment of muscle spasm and immobility associated with strains, sprains, and injuries of the back and, to a lesser degree, injuries to the neck. They have been used also for the treatment of a variety of clinical conditions that have in common only the presence of skeletal muscle hyperactivity, for example, the muscle spasms that can occur in MULTIPLE SCLEROSIS. (From Smith and Reynard, Textbook of Pharmacology, 1991, p358)
Compounds or factors that act on a specific enzyme to increase its activity.
Mutant mice exhibiting a marked obesity coupled with overeating, hyperglycemia, hyperinsulinemia, marked insulin resistance, and infertility when in a homozygous state. They may be inbred or hybrid.
Biosynthesis of GLUCOSE from nonhexose or non-carbohydrate precursors, such as LACTATE; PYRUVATE; ALANINE; and GLYCEROL.
Consumption of excessive DIETARY FATS.
The chemical reactions involved in the production and utilization of various forms of energy in cells.
A status with BODY WEIGHT that is grossly above the acceptable or desirable weight, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).
The processes whereby the internal environment of an organism tends to remain balanced and stable.
Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).
A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.
A publication issued at stated, more or less regular, intervals.
"The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.
The premier bibliographic database of the NATIONAL LIBRARY OF MEDICINE. MEDLINE® (MEDLARS Online) is the primary subset of PUBMED and can be searched on NLM's Web site in PubMed or the NLM Gateway. MEDLINE references are indexed with MEDICAL SUBJECT HEADINGS (MeSH).
Publications in any medium issued in successive parts bearing numerical or chronological designations and intended to be continued indefinitely. (ALA Glossary of Library and Information Science, 1983, p203)
An order of gram-positive, primarily aerobic BACTERIA that tend to form branching filaments.
Polyacenes with four ortho-fused benzene rings in a straight linear arrangement. This group is best known for the subclass called TETRACYCLINES.
Substances that reduce the growth or reproduction of BACTERIA.
A mass of organic or inorganic solid fragmented material, or the solid fragment itself, that comes from the weathering of rock and is carried by, suspended in, or dropped by air, water, or ice. It refers also to a mass that is accumulated by any other natural agent and that forms in layers on the earth's surface, such as sand, gravel, silt, mud, fill, or loess. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p1689)
A strain of Staphylococcus aureus that is non-susceptible to the action of METHICILLIN. The mechanism of resistance usually involves modification of normal or the presence of acquired PENICILLIN BINDING PROTEINS.
The functional hereditary units of a microorganism.
Any tests that demonstrate the relative efficacy of different chemotherapeutic agents against specific microorganisms (i.e., bacteria, fungi, viruses).

Proliferative effects of cholecystokinin in GH3 pituitary cells mediated by CCK2 receptors and potentiated by insulin. (1/379)

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)

Benzodiazepine receptor agonists modulate thymocyte apoptosis through reduction of the mitochondrial transmembrane potential. (2/379)

Peripheral-type benzodiazepines have been shown to exert immunological effects. In this study, we examined the effects of the peripheral-type benzodiazepines on murine thymocytes. Murine thymocytes that were incubated with the peripheral-type benzodiazepines underwent apoptosis associated with the collapse of mitochondrial transmembrane potential (delta psi(m)). The drugs stimulated dexamethasone- and etoposide-induced apoptosis with the enhanced collapse of delta psi(m). The central-type benzodiazepines had no effect on either the delta psi(m) or apoptosis. The reduction of delta psi(m) depended on protein synthesis and protein phosphorylation. These results suggest that the immunomodulating effect of benzodiazepines is in part due to the modulation of thymocyte apoptosis associated with the collapse of delta psi(m).  (+info)

Analysis of the behaviour of selected CCKB/gastrin receptor antagonists in radioligand binding assays performed in mouse and rat cerebral cortex. (3/379)

1. The previously described complex behaviour of the CCKB/gastrin receptor antagonist, L-365,260, in radioligand binding assays could be explained by a variable population of two binding sites. We have investigated whether other CCKB/gastrin receptor ligands (PD134,308, PD140,376, YM022 and JB93182) can distinguish between these sites. 2. In the mouse cortex assay, Hill slopes were not different from unity and the ligand pKI values did not differ when either [125I]-BH-CCK-8S or [3H]-PD140,376 was used as label as expected for a single site (G2). 3. In the rat cortex, where previous analysis of replicate (n=48) L-365,260 data indicated the presence of two CCKB/gastrin sites (G1 and G2), the competition data for PD134,308, PD140,376, YM022 and JB93182 could be explained by a homogeneous population of CCKB/gastrin sites because the Hill slope estimates were not significantly different from unity. However, the estimated affinity values for JB93182 and YM022 were significantly higher and that for PD134,308 was significantly lower than those obtained in the mouse cortex when the same radioligand was used. In view of our previous data obtained with L-365,260, the rat cortex data were also interpreted using a two-site model. In this analysis, SR27897 expressed approximately 9 fold, PD134,308 approximately 13 fold and PD140,376 approximately 11 fold selectivity for the G2 site. In contrast, JB93182 expressed approximately 23 fold and YM022 approximately 4 fold selectivity for the G1 site. If the two-site interpretation of the data is valid then, because of its reverse selectivity to L-365,260, JB93182 has been identified as a compound which if radiolabelled could provide a test of this receptor subdivision.  (+info)

Characterization of the binding of a novel radioligand to CCKB/gastrin receptors in membranes from rat cerebral cortex. (4/379)

1. We have investigated the binding of a novel radiolabelled CCKB/gastrin receptor ligand, [3H]-JB93182 (5[[[(1S)-[[(3,5-dicarboxyphenyl)amino]carbonyl]-2-phenylethyla mino]-carbonyl]-6-[[(1-adamantylmethyl) amino]carbonyl]-indole), to sites in rat cortex membranes. 2. The [3H]-JB93182 was 97% radiochemically pure as assessed by reverse-phase HPLC (RP-HPLC) and was not degraded by incubation (150 min) with rat cortex membranes. 3. Saturation analysis indicated that [3H]-JB93182 labelled a homogeneous population of receptors in rat cortex membranes (pKD=9.48+/-0.08, Bmax=3.61+/-0.65 pmol g(-1) tissue, nH=0.97+/-0.02, n=5). The pKD was not significantly different when estimated by association-dissociation analysis (pKD=9.73+/-0.11; n=10). 4. In competition studies, the low affinity of the CCKA receptor antagonists, L-364,718; SR27897 and 2-NAP, suggest that, under the assay conditions employed, [3H]-JB93182 (0.3 nM) does not label CCKA receptors in the rat cortex. 5. The affinity estimates obtained for reference CCKB/gastrin receptor antagonists were indistinguishable from one of the affinity values obtained when a two site model was used to interpret [125I]-BH-CCK8S competition curves obtained in the same tissue (Harper et al., 1999). 6. This study provides further evidence for the existence of two CCKB/gastrin sites in rat cortex. [3H]-JB93182 appears to label selectively sites previously designated as gastrin-G1 and therefore it may be a useful compound for the further discrimination and characterization of these putative receptor subtypes.  (+info)

L-365,260 inhibits in vitro acid secretion by interacting with a PKA pathway. (5/379)

The aim of this study was to analyse the antisecretory mechanism of L-365,260 in vitro in isolated rabbit gastric glands. We showed that compound L-365,260, described as a non-peptide specific competitive CCK-B receptor antagonist, was able to dose-dependently inhibit [14C]-aminopyrine accumulation induced by histamine (10(-4) M), carbachol (5x10(-5) M), 3-isobutyl-1-methyl-xanthine (IBMX) (5x10(-6) M) and forskolin (5x10(-7) M) with similar IC50 values respectively of 1.1+/-0.6x10(-7) M, 1.9+/-1.2x10(-7) M, 4.2+/-2.0x10(-7) M and 4.0+/-2.8x10(-7) M. We showed that L-365,260 acted beyond receptor activation and production of intracellular second messengers and that it had no action on the H+/K+ -ATPase. We found that L-365,260 inhibited cyclic AMP-induced [14C]-aminopyrine accumulation in digitonin-permeabilized rabbit gastric glands, suggesting that this compound acted, at least in part, as an inhibitor of the cyclic AMP-dependent protein kinase (PKA) pathway.  (+info)

Central and peripheral benzodiazepine ligands prevent mitochondrial damage induced by noise exposure in the rat myocardium: an ultrastructural study. (6/379)

Noise represents an environmental stress factor affecting several organs and apparatuses, including the cardiovascular system. In experimental animals undergoing noise exposure, subcellular myocardial changes have been reported, especially at the mitochondrial level. In previous studies we found that diazepam, acting at both central and peripheral benzodiazepine receptors, prevented the onset of this myocardial damage. In the present study, we investigated the specific role played by central and/or peripheral benzodiazepine receptors in preventing noise-induced myocardial alterations. In particular, the effect of clonazepam as a selective ligand for central sites, in comparison with the efficacy of ligands selective for peripheral sites, such as Ro 5-4864 and PK-11195, was evaluated. Rats were pretreated with the test drugs 30 min before exposure to noise for 6 or 12 hr and then sacrificed. After fixing, samples of right atrium and ventricle were taken and processed for either transmission or scanning electron microscopy. After 6 hr of noise exposure, only the atrium exhibited significant mitochondrial alterations, whereas after 12 hr both atrium and ventricle were damaged. As expected, diazepam prevented noise-induced mitochondrial injury at both 6 and 12 hr. By contrast, clonazepam was effective only after 6 hr. The peripheral ligand PK-11195 attenuated mitochondrial damage at both 6 and 12 hr, whereas Ro 5-4864 was effective only after 12 hr. In the present study, we confirm that noise exposure induces mitochondrial damage in the rat myocardium. Drugs acting at both central and peripheral benzodiazepine receptors significantly prevent this damage. Differences in the amount and in the duration of the protective effect might depend on variability in the potency and in the pharmacokinetics of the specific drugs.  (+info)

Rat hippocampal neurons are critically involved in physiological improvement of memory processes induced by cholecystokinin-B receptor stimulation. (7/379)

The involvement in memory processes of the neuropeptide cholecystokinin (CCK) through its interaction with the CCK-B receptors was studied. The two-trial recognition memory task was used. Control animals showed recognition memory after a 2 hr time interval but not after a 6 hr time interval between the two trials. The improving effect of a selective CCK-B agonist, BC 264, intraperitoneally administered (0.3 microgram/kg) in the retrieval phase of the task (6 hr time interval), was also observed after its injection (1 pmol/0.5 microliter) in the dorsal subiculum/CA1 of the hippocampus but not in the caudate/putamen nucleus or in the prefrontal cortex of rats. The CCK-B antagonist L-365,260 injected (10 ng/0.5 microliter) into this region of the hippocampus abolished the improving effect of BC 264 injected intraperitoneally. Furthermore, L-365,260 injected in the hippocampus suppressed the recognition of the novel arm normally found in the controls (2 hr time interval) when it was injected before the acquisition or the retrieval phase of the task. In addition, an increase of the extracellular levels of CCK-like immunoreactivity in the hippocampus of rats during the acquisition and retention phase of the task was observed. Finally, CCK-B receptor-deficient mice have an impairment of performance in the memory task (2 hr time interval). Together, these results support the physiological involvement of the CCKergic system through its interaction with CCK-B receptors in the hippocampus to improve performance of rodents in the spatial recognition memory test.  (+info)

Apparent pA2 values of benzodiazepine antagonists and partial agonists in monkeys. (8/379)

Drugs that bind to benzodiazepine recognition sites of gamma-aminobutyric acid type A receptor complexes may function as agonists in some behavioral assays and as antagonists in other behavioral assays. The present studies compared the effects of the benzodiazepines midazolam, flumazenil, bretazenil, Ro 41-7812, and Ro 42-8773 and the beta-carboline, beta-carboline-3-carboxylate-t-butyl ester (beta-CCt) under two different types of schedule-controlled responding in squirrel monkeys. One group of monkeys responded under a fixed-ratio schedule of stimulus-shock termination, and a second group of monkeys responded under a multiple fixed-ratio schedule of food presentation involving suppressed and nonsuppressed behavior. Under the schedule of stimulus-shock termination, midazolam produced dose-related decreases in response rate, and these effects were surmountably antagonized by flumazenil, bretazenil, Ro 41-7812, Ro 42-8773, and beta-CCt. Schild plot analysis of these data revealed the following mean pA(2) values: flumazenil, 7.18; bretazenil, 7.62; Ro 41-7812, 7. 06; Ro 42-8773, 6.95. Apparent pA(2) values were not calculated for beta-CCt because the CL of the slope of the Schild plot included positive values. Under the multiple schedule, midazolam, bretazenil, and Ro 42-8773 dose-dependently increased rates of suppressed responding, whereas flumazenil, Ro 41-7812, and beta-CCt had no significant rate-altering effects. Flumazenil antagonized the antisuppressant effects of midazolam and bretazenil; however, individual variability in these effects prohibited the determination of apparent pA(2) values. These results indicate that in vivo pA(2) values may be determined for benzodiazepine-site ligands. These results further demonstrate that some benzodiazepine-site ligands, e. g., bretazenil and Ro 42-8773, may function as both agonists and as competitive antagonists in vivo.  (+info)

TY - JOUR. T1 - Mitochondrial peripheral-type benzodiazepine receptor expression: correlation with gonadotropin-releasing hormone (GnRH) agonist-induced apoptosis in the corpus luteum. AU - Papadopoulos, V.. AU - Dharmarajan, Arunasalam. AU - Li, H.. AU - Culty, M.. AU - Lemay, M.. AU - Sridaran, R.. PY - 1999. Y1 - 1999. U2 - 10.1016/S0006-2952(99)00215-4. DO - 10.1016/S0006-2952(99)00215-4. M3 - Article. VL - 58. SP - 1389. EP - 1393. JO - Journal of Biochemical Pharmacology. JF - Journal of Biochemical Pharmacology. SN - 0006-2952. ER - ...
The present invention relates in particular to a combination product comprising at least one compound with affinity for the mitochondrial benzodiazepine receptor, and to at least one apoptosis-inducing agent for simultaneous or separate use or for use spread out over time, which is intended for the treatment of cancer. Another aspect of the present invention relates to the use of the said compound and/or of the said combination product for the manufacture of a medicinal product intended to facilitate the induction of apoptosis.
Ro5-4864 (4-chlorodiazepam) is a drug which is a benzodiazepine derivative of diazepam. However unlike most benzodiazepine derivatives, Ro5-4864 lacks affinity for GABAA receptors and lacks typical benzodiazepine effects, instead being sedative yet also convulsant and anxiogenic in effects. Ro5-4864 was found to be a potent ligand for the peripheral benzodiazepine receptor, later renamed to mitochondrial translocator protein 18kDa (TSPO). Despite its convulsant effects, at lower doses Ro5-4864 has proved to be neuroprotective and has become widely used for research into the role of the TSPO protein in neurotoxicity. In vitro studies and rodent models also suggest the possibility of analgesic, antidepressant, cardioprotective, and anti-cancer effects.[non-primary source needed] Diclazepam (2-chlorodiazepam) PK-11195 US 3136815 Patel J, Marangos PJ (May 1982). Differential effects of GABA on peripheral and central type benzodiazepine binding sites in brain. Neuroscience Letters. 30 (2): ...
Just recently researchers were able to unveil the crystallized structure of translocator protein. It has long been thought that various polymorphisms of
N-benzyl-N-ethyl-2-(7,8-dihydro-7-methyl-8-oxo-2-phenyl-9H-purin-9-yl)acetamide: mitochondrial benzodiazepine receptor ligand with anti-anxiety and antidepressant-like effects; structure in first source
You are viewing an interactive 3D depiction of the molecule 2-[2-(hexahydro-1h-pyrrolo[1,2-a][1,4]diazepin-2(3h)-yl)ethyl]guanidine (C11H23N5) from the PQR.
(3S)-7-Chloro-3-(1H-indol-3-ylmethyl)-5-phenyl-1,3-dihydro-1,4-benzodiazepin-2-one/ACM50691946 can be provided in Alfa Chemistry. We are dedicated to provide our customers the best products and services.
Structure, properties, spectra, suppliers and links for: 7-Nitro-5-(|sup>2|/sup>H|sub>5|/sub>)phenyl-1,3-dihydro-2H-1,4-benzodiazepin-2-one, 136765-45-2.
4,5-dihydro-6H-pyrrolo[1,2-a][1,4]benzodiazepin-6-one - chemical structural formula, chemical names, chemical properties, synthesis references
258849-92-2 - SCGYOQRKXLNHMV-JTQLQIEISA-N - 2H-1,4-Benzodiazepin-2-one, 7-chloro-1,3,4,5-tetrahydro-3-methyl-4-(1H-pyrrol-2-ylmethyl)-, (3S)- - Similar structures search, synonyms, formulas, resource links, and other chemical information.
65647-14-5 - DUKOQRXNBYNJED-UHFFFAOYSA-N - 5H-1,4-Benzodiazepin-5-one, 1,2,3,4-tetrahydro-4-(2-diethylaminoethyl)-1-phenyl- - Similar structures search, synonyms, formulas, resource links, and other chemical information.
TY - JOUR. T1 - Involvement of peripheral-type benzodiazepine receptors in the proconvulsant actions of pyrethroid insecticides. AU - Devaud, L. L.. AU - Murray, Thomas F.. PY - 1988. Y1 - 1988. N2 - It has been demonstrated previously that select Type II pyrethroids are potent proconvulsants in the rat and that the proconvulsant actions of deltamethrin are blocked by administration of PK 11195, an antagonist of the peripheral-type benzodiazepine receptor (PTBR). The present investigation has extended these findings to include various Type I pyrethroids as proconvulsants. Additionally, the proconvulsant activity of cismethrin was reversed by administration of PK 11195. Pyrethroid displacement of specific [3H]Ro5-4864 binding to rat brain membranes was investigated to further define the interaction of pyrethroids with the PTBR. Both Type I and Type II pyrethroids potently inhibited [3H]Ro5-4864 binding with affinities ranging from nanomolar to micromolar. The ED50 values for the proconvulsant ...
Title: Peripheral Benzodiazepine Receptor (PBR) New Insight in Cell Proliferation and Cell Differentiation Review. VOLUME: 3 ISSUE: 1. Author(s):Lorenzo Corsi, Elisa Geminiani and Mario Baraldi. Affiliation:Department of Biomedical Sciences, University of Modena and Reggio Emilia, 41100 Modena, Italy.. Keywords:Cell proliferation, tumour, PBR, translocator protein, cell survival, PK11195. Abstract: The peripheral benzodiazepine receptor (PBR), is an 18 kDa protein of the mammalian mitochondrial membrane and is a highly conserved protein among the mammalian. PBR is involved in numerous biological functions, including steroid biosynthesis, mitochondrial oxidative phosporylation and cell proliferation. The presence of PBR at the nuclear subcellular level has been demonstrated in aggressive breast cancer cell line and human glioma cells, where it seems to be involved in cell proliferation. In our previous studies we investigated the presence of nuclear PBR in different hepatic tumour cell lines with ...
TY - JOUR. T1 - The peripheral benzodiazepine receptor modulates Ca2+ transport through the VDAC in rat heart mitochondria. AU - Tamse, C. T.. AU - Lu, X.. AU - Mortel, E. G.. AU - Cabrales, E.. AU - Feng, W.. AU - Schaefer, Saul. PY - 2008. Y1 - 2008. N2 - The voltage-dependent anion channel (VDAC) is a key mitochondrial protein involved in the transport of calcium. Its function is, in part, regulated by associated proteins such as the 18 kD peripheral benzodiazepine receptor (PBR). We tested the hypothesis that an endogenous ligand of the PBR, hemin, could modulate calcium transport by modifying VDAC conductance. In isolated rat cardiac mitochondria, hemin (0-10 μM) exhibited multiple, time-dependent effects. Initially, hemin reduced the calcium uptake rate in a dose-dependent manner, an effect independent of the mitochondrial permeability transition (MPT) as it was not altered by cyclosporine A (CsA). However, subsequent to this inhibitory effect on calcium influx, hemin facilitated MPT as ...
BioAssay record AID 389903 submitted by ChEMBL: Displacement of [3H]PK11195 from peripheral benzodiazepine receptor in Sprague-Dawley rat cerebral cortex membrane by liquid scintillation counting.
Drugs that bound to the peripheral-type or mitochondrial benzodiazepine receptors in rat kidney mitochondria produced several effects on mitochondrial respiration with succinate and malate/pyruvate as substrates. These drugs increased state IV and decreased state III respiration rates, which resulted in a significant decrease in the respiratory control ratio. ADP: O ratios were not affected. The receptor binding affinities of a set of 10 compounds (Ro5-4864, PK11195, diazepam, mesoporphyrin IX, flunitrazepam, deuteroporphyrin IX, dipyridamole, dibutylphthalate, cyclosporin A, and CL259,763) correlated over a concentration range of almost 4 orders of magnitude with their potencies at inhibiting respiratory control (r = 0.95). The anxiolytic benzodiazepine clonazepam had no effect on mitochondrial respiratory control and bound with negligible affinity to the receptor. The magnitude of the effect of Ro5-4865 on respiration increased in parallel with the density of mitochondrial benzodiazepine ...
In the present study, our aim was to analyze molecularly the inhibitory effect of BDZs on MC activity by comparison of the effects of the two BDZs Ro5-4864 and clonazepam. The two drugs differ markedly in their affinities for the archetypical BDZ recognition sites, i.e., the GABAA receptor and the TSPO, previously termed peripheral-type BDZ receptor. Ro5-4864 is an agonist at TSPO and has only low affinity to the GABAA receptor [39], whereas clonazepam is a high-affinity GABAA receptor agonist, but has only low affinity for TSPO [12]. Ro5-4864 concentration-dependently inhibited Ag-triggered degranulation in BMMCs and PMCs, whereas clonazepam was essentially ineffective in this respect. In accordance with this observation, Ro5-4864 suppressed Ca2+ mobilization, production of ROS and activation of the PI3K pathway (as measured by phosphorylation of Akt at Ser473), which are all important signaling events in the positive regulation of the secretory response [26, 27]. These data suggest that ...
The IUPHAR/BPS Guide to Pharmacology. bretazenil ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
A broad-spectrum spectrum antineoplastic antibiotic isolated from Streptomyces refuineus var. thermotolerans. It has low toxicity, some activity against Trichomonas and Endamoeba, and inhibits RNA and DNA synthesis. It binds irreversibly to DNA ...
0011] In yet another embodiment the Quinazolinone linked pyrrolo[2,1-c][1,4]benzodiazepine hybrids is represented by the group of the following compounds: [0012] 7-methoxy-8{-2-[4-(2-methyl-4-oxo-3,4-dihydro-3-quinazolinyl)phenoxy]etho- xy}-(11aS)-1,2,3,11a-tetrahydrO-5H-pyrrolo[2,1-c][1,4]benzodiazepine-5-one- (5a); [0013] 7-methoxy-8{-3-[4-(2-methyl-4-oxo-3,4-dihydro-3-quinazolinyl)phenoxy]prop- oxy}-(11aS)-1,2,3,11a-tetrahydro-5H-pyrrolo[2,1-c][1,4]benzodiazepine-5-on- e(5b); [0014] 7-methoxy-8{-4-[4-(2-methyl-4-oxo-3,4-dihydro-3-quinazolinyl)phenoxy]buto- xy-}-(11aS)-1,2,3,11a-tetrahydro-5H-pyrrolo[2,1-c][1,4]benzodiazepine-5-on- e(5c); [0015] 7-methoxy-8-{5-[4-(2-methyl-4-oxo-3,4-dihydro-3-quinazolinyl)phenoxy]pent- yloxy-}-(11aS)-1,2,3,11a-tetrahydro-5H-pyrrolo[2,1-c][1,4]benzodiazepine-5- -one(5d); [0016] 7-methoxy-8{-6-[4-(2-methyl-4-oxo-3,4-dihydro-3-quinazolinyl)phenoxy]hexy- loxy}-(11aS)-1,2,3,11a-tetrahydro-5H-pyrrolo[2,1-c][1,4]benzodiazepine-5-o- ne(5e); [0017] ...
Abramets, I. I., & Komissarov, I. V. (1985). [Effect of fenibut on the GABA B receptors of the spinal motor neurons]. Biulleten Eksperimentalnoi Biologii i Meditsiny, 99(6), 698-700. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/2861865. Ahuja, T., Mgbako, O., Katzman, C., & Grossman, A. (2018). Phenibut ( β -Phenyl- γ -aminobutyric Acid) Dependence and Management of Withdrawal: Emerging Nootropics of Abuse. Case Reports in Psychiatry, 2018, 1-3. https://doi.org/10.1155/2018/9864285. Allan, R. D., Bates, M. C., Drew, C. A., Duke, R. K., Hambley, T. W., Johnston, G. A. R., … Spence, I. (1990). A new synthesis resolution and in vitro activities of (R)- and (S)-β-Phenyl-Gaba. Tetrahedron, 46(7), 2511-2524. https://doi.org/10.1016/S0040-4020(01)82032-9. Allikmets, L. H., & Rägo, L. K. (1983). The action of benzodiazepine antagonist Ro 15-1788 on the effects of GABA-ergic drugs. Naunyn-Schmiedebergs Archives of Pharmacology, 324(3), 235-7. Retrieved from ...
Suppliers List, E-mail/RFQ Form, Molecular Structure, Weight, Formula, IUPAC, Synonyms for ACETIC ACID (4-CHLOROPHENOXY)-,2-(HEXAHYDRO-4-METHYL-1H-1,4-DIAZEPIN-1-YL)ETHYL ESTER,(Z)-2-BUTENEDIOATE (1:1) (CAS No. 87575-98-2)
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Buy PK 11195 - an affordable, high quality Peripheral benzodiazepine receptor (PBR) Antagonist from Hello Bio, a trusted supplier for life science researchers worldwide
[email protected] Biomarkers Consortiums PET Radioligand Project, completed in December 2012, developed improved, more sensitive PET radioligands with higher binding to the peripheral benzodiazepine receptor. Findings from this study suggest that the [11C]PBR38 ligand, in particular, may be useful in detecting progression from mild cognitive impairment or treatment response in Alzheimers Disease.. ...
[email protected] Biomarkers Consortiums PET Radioligand Project, completed in December 2012, developed improved, more sensitive PET radioligands with higher binding to the peripheral benzodiazepine receptor. Findings from this study suggest that the [11C]PBR38 ligand, in particular, may be useful in detecting progression from mild cognitive impairment or treatment response in Alzheimers Disease.. ...
Drugs may be covered by multiple patents or regulatory protections. All trademarks and applicant names are the property of their respective owners or licensors. Although great care is taken in the proper and correct provision of this service, thinkBiotech LLC does not accept any responsibility for possible consequences of errors or omissions in the provided data. The data presented herein is for information purposes only. There is no warranty that the data contained herein is error free. thinkBiotech performs no independent verifification of facts as provided by public sources nor are attempts made to provide legal or investing advice. Any reliance on data provided herein is done solely at the discretion of the user. Users of this service are advised to seek professional advice and independent confirmation before considering acting on any of the provided information. thinkBiotech LLC reserves the right to amend, extend or withdraw any part or all of the offered service without notice. ...
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Bhakta, Sanjib and Guzman, Juan David and Evangelopoulos, Dimitrios and Munshi, Tulika and Mcmahon, Eleanor (2016) DNA sequence-selective C8-linked pyrrolobenzodiazepine(PBD)-heterocyclic polyamide conjugates show anti-tubercular specific activities. The Journal of Antibiotics 69 , pp. 843-849. ISSN 0021-8820. Brucoli, F. and Guzman, Juan David and Basher, M.A. and Evangelopoulos, Dimitrios and Mcmahon, Eleanor and Munshi, Tulika and McHugh, T.D. and Fox, K.R. and Bhakta, Sanjib (2016) DNA sequence-selective C8-linked pyrrolobenzodiazepine-heterocyclic polyamide conjugates show anti-tubercular-specific activities. The Journal of Antibiotics 69 , pp. 843-849. ISSN 0021-8820. Guzman, Juan D. and Pesnot, T. and Barrera, D.A. and Davies, H.M. and McMahon, E. and Evangelopoulos, Dimitrios and Mortazavi, Parisa Nakhostin and Munshi, Tulika and Maitra, Arundhati and Lamming, E.D. and Angell, R. and Gershater, M.C. and Redmond, J.M. and Needham, D. and Ward, J.M. and Cuca, L.E. and Hailes, H.C. and ...
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Tonkiha N.; Rižanova K.; Petrova M.; Strakovs A. 10-Alkil- un 10-acil-11-aril-3,3-dimetil-1,2,3,4,10,11-heksahidro-5H-dibenzo[b,e][1,4]diazepīn-1-oni = 10-Alkyl- and 10-acyl-11-aryl-3,3-dimethyl-1,2,3,4,10,11-hexahydro-5H-dibenzo[b,e][1,4]diazepin-1-one. Programme , RTU 43.Starptautiskā Zinātniskā Konference = RTU 43rd International Scientific Conference: RTU 140 (1862-2002); October 10-14: Rīga, Latvija, 2002; 41 ...
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Compounds which bind with high affinity to peripheral benzodiazepine receptors are useful as antiinflammatory agents. Such compounds include isoquinoline and benzodiazepine derivatives, such as PK 111
ABSTRACT Background: The Peripheral Benzodiazepine Receptor (PBR) can be classified as a distinct receptor from the central benzodiazepine receptor. The PBR gene has been located to chromosome 22q13.31 in humans and has been found to consist of four exons, with the first and half of the fourth exon being untranslated to form the PBR protein. PBR is involved in numerous biological conditions including the regulation of cellular proliferation and apoptosis, steroidogenesis, heme biosynthesis, anion and porphyrin transport and mitochondrial functions such as oxidative phosphorylation and translocation of cholesterol from the outer to the inner mitochondrial membrane. Recent studies showed that the expression of PBR correlated with tumour malignancy and patient survival. Aim: The objectives of this research were to determine the expression pattern and level of PBR mRNA in various types of human normal and cancer tissues and to isolate the PBR protein ...
Objective. Inflammation in the vascular wall plays an important role in the pathophysiology of atherosclerosis, including development of plaque, plaque destabilization and rupture. Clinical and basic scientific data demonstrate the importance of peripheral white blood cells in this process. Therefore, a noninvasive method to detect inflammatory activity in atherosclerosis may be of great value to help determine prognosis, direct therapy and perhaps assess novel therapies for stabilization of atherosclerotic plaque.. The peripheral benzodiazepine receptor (PBR) is distinct from central benzodiazepine receptors associated with GABAA receptors and has been associated with immune function. PBR is expressed in macrophages, therefore, they may be a clinically useful marker to detect inflammation. Our preliminary autoradiographic data demonstrate specific PBR binding in carotid atherosclerosis samples. Though PBR has been imaged in vivo with positron emission tomography (PET) using ...
Objective:. Abnormal immune responses and inflammatory mechanisms have been implicated in the pathogenesis of certain neurodegenerative diseases. Frontotemporal dementia (FTD) is a neurodegenerative disease characterized by focal atrophy of the frontal and temporal lobes. Evidence supports the presence of inflammation in FTD; however, the relationship between inflammation and FTD pathogenesis is poorly understood. In addition, there is evidence of inflammation in temporal lobe epilepsy (TLE), a condition characterized by seizures originating from the mesial temporal lobe.. In response to brain inflammation, microglia are activated and over-express the peripheral benzodiazepine receptor (PBR). In normal conditions, PBR is expressed in low numbers. Measuring PBR density can identify areas of brain inflammation, because activated microglial cells in these areas express more PBR than microglial cells in resting conditions. Positron emission tomography (PET) imaging can quantify PBR density in vivo ...
Reviews the interaction between anxiety and the immune system and modulating effects of benzodiazepines. Research indicates that anxiety induces immune-inflammatory changes pointing toward the complex regulatory responses in interleukin-6 signalling, decreased anti-inflammatory capacity of the serum, and interactions with T cell and monocytic activation. Experimental and clinical studies suggest that the central and peripheral benzodiazepine receptors together with their ligands form a network Show moreReviews the interaction between anxiety and the immune system and modulating effects of benzodiazepines. Research indicates that anxiety induces immune-inflammatory changes pointing toward the complex regulatory responses in interleukin-6 signalling, decreased anti-inflammatory capacity of the serum, and interactions with T cell and monocytic activation. Experimental and clinical studies suggest that the central and peripheral benzodiazepine receptors together with their ligands form a network ...
Title:Structural and Functional Evolution of the Translocator Protein (18 kDa). VOLUME: 12 ISSUE: 4. Author(s):J. Fan, P. Lindemann, M. G.J. Feuilloley and V. Papadopoulos. Affiliation:Research Institute of the McGill University Health Centre, Montreal General Hospital, 1650 Cedar Avenue, Room C10-148, Montreal, Quebec H3G 1A4, Canada.. Keywords:Cholesterol transport/binding, evolutionary origin, gene family, oxygen sensor, peripheral benzodiazepine receptor, steroidogenesis, translocator protein (18 kDa). Abstract:Translocator proteins (TSPO) are the products of a family of genes that is evolutionarily conserved from bacteria to humans and expressed in most mammalian tissues and cells. Human TSPO (18 kDa) is expressed at high levels in steroid synthesizing endocrine tissues where it localizes to mitochondria and functions in the first step of steroid formation, the transport of cholesterol into the mitochondria. TSPO expression is elevated in cancerous tissues and during tissue injury, which ...
A. Chapalain, S. Chevalier, A. Dagorn, C. Poc, N. Orange, et al.. Eukaryotic benzodiazepine receptors ligands are sensed by Pseudomonas.. 3rd Congress of European Microbiologists, Jun 2009, GOTEBORG, Sweden. ⟨hal-02537348⟩ ...
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Tetrahydro-imidazo[4,5,1-jk][1,4]-benzodiazepin-2(1H)-one and -thione (TIBO) derivatives were shown to specifically block human immunodeficiency virus type 1 (HIV-1) replication through a unique interaction with the HIV-1 reverse transcriptase (RT). Through further modification of the lead compounds …
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... formation of novel benzodiazepinones". Organic Letters. 13 (3): 486-489. doi:10.1021/ol102824k. PMID 21175141.. ...
... and benzodiazepinones, are efficiently prepared. Lactamization reactions are commonly employed to form the heterocycles, ...
US patent 3121076, Keller O, "Benzodiazepinones and Processes", published 11 February 1964, assigned to Hoffmann-La Roche ...
... benzodiazepinones MeSH D03.438.079.080.070.050 - anthramycin MeSH D03.438.079.080.070.110 - bromazepam MeSH D03.438.079.080. ...
The National Center for Biomedical Ontology was founded as one of the National Centers for Biomedical Computing, supported by the NHGRI, the NHLBI, and the NIH Common Fund under grant U54-HG004028 ...
Benzodiazepinones / pharmacology * Cathepsin B / metabolism * Ceruletide / pharmacology * Cholecystokinin / antagonists & ...
Binding levels of [3H]Ro5-4864, a ligand selective for peripheral-type benzodiazepine receptors, are substantially higher in homogenates of the olfactory bulb than in the rest of the brain. Among peripheral tissues evaluated, high levels of [3H]Ro5-4864 binding are found in the nasal epithelium. Dru …
Benzodiazepinones*Pirenzepine: 484*otenzepad: 30. *telenzepine: 25. *AFDX 384: 9. *LS 75: 2 ...
Scheme 73: Benzodiazepinones synthesized via the post-condensation Ugi/ Staudinger-Aza-Wittig cyclization. ...
Benzodiazepinones and processes US3121075A (en) 1964-02-11. Aminobenzodiazepines KR20000022297A (en) 2000-04-25. Tricyclic ...
... formation of novel benzodiazepinones". Organic Letters. 13 (3): 486-489. doi:10.1021/ol102824k. PMID 21175141.. ...
Other small molecules have been developed, such as calchones, benzodiazepinones and spiro-oxindoles. Most of the small molecule ...
of functionalized anilines ; aminobenzoic acids and benzodiazepinones via regioselective metalation/electrophilic substitution ... of functionalized anilines, aminobenzoic acids and benzodiazepinones via regioselective metalation/electrophilic substitution ... of functionalized anilines, aminobenzoic acids and benzodiazepinones via regioselective metalation/electrophilic substitution ... of functionalized anilines, aminobenzoic acids and benzodiazepinones via regioselective metalation/electrophilic substitution ...
US patent 3121076, Keller O, "Benzodiazepinones and Processes", published 11 February 1964, assigned to Hoffmann-La Roche ...
Animals; Animals, Genetically Modified; Benzodiazepinones/pharmacology; Drug Design; Fasting/metabolism (all 20) Animals; ... Animals, Genetically Modified; Benzodiazepinones/pharmacology; Drug Design; Fasting/metabolism; Food Deprivation*; ...
A computational chemistry study has been performed on a series of tetrahydroimidazo-benzodiazepinones as HIV-1-NNRT inhibitors ...
... and benzodiazepinones, are efficiently prepared. Lactamization reactions are commonly employed to form the heterocycles, ...
Benzodiazepinones / pharmacology. Cell Line, Tumor. Daunorubicin / pharmacology. Dexamethasone / pharmacology. Down-Regulation ... Benzodiazepinones; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; EC ...
Advances in the synthesis of benzimidazolones via rearrangements of benzodiazepinones and quinalin(on)es. Mendeleev Commun., ...
Benzodiazepinones/pharmacology. *Cell Cycle/drug effects. *Cell Differentiation/drug effects. *Cell Division/drug effects ...
Benzodiazepinones/chemistry. *Corpus Striatum/metabolism. *Humans. *Kidney/metabolism. *Leucine-Rich Repeat Serine-Threonine ...
Benzodiazepinones. Trending Feeds. COVID-19. Coronaviruses encompass a large family of viruses that cause the common cold as ...
Substances mentioned in the article: Anticonvulsants; Benzodiazepinones; Receptors, Serotonin; Serotonin; Hydroxyindoleacetic ... Mesh terms: Animals; Anticonvulsants; Benzodiazepinones/pharmacology; Clonazepam/pharmacology; DDT/pharmacology; ...
Benzodiazepinones Descriptor Spanish: Benzodiazepinonas Descriptor Portuguese: Benzodiazepinonas Descriptor French: ...
Benzodiazepinones Cell Line, Tumor Data Mining Drug Resistance, Bacterial Enterococcus faecalis Fermentation Genomics Humans ...
The highly aggressive pediatric sarcomas are characterized by high levels of matrix metalloproteinase (MMP)-2 and MMP-9, which play crucial roles in tumor invasion and metastasis by degradation of the extracellular membrane leading to cancer cell spread to distal organs. We examined the effects of cytokines, mitogens, inducers and inhibitors on MMP-2 and -9 expression in osteosarcoma (U2OS) and rhabdomyosarcoma (RD). The selected compounds included natural cytokines and growth factors, as well as chemical compounds applied in therapy of sarcoma and natural compounds that have demonstrated anticancer therapeutic potential. These cell lines were cultured in their respective media to near confluence and the cells were washed with PBS and incubated in serum-free medium with various concentrations of several cytokines, mitogens and inhibitors. After 24 h the media were removed and analyzed for MMP-2 and -9 by gelatinase zymography and quantitated by densitometry. Osteosarcoma and rhabdomyosarcoma ...
Benzodiazepinones (1974). Pyrroles (1972-1974). Public MeSH Note:. 91; was see under BENZODIAZEPINONES 1975-90. ...
Mesh terms: Animals; Benzodiazepinones/metabolism; Binding, Competitive; Brain/metabolism; Clonazepam/metabolism; Convulsants/ ... Substances mentioned in the article: Benzodiazepinones; Convulsants; Receptors, GABA-A; Muscimol; 4-chlorodiazepam; Clonazepam ...
Humans , Female , Aged , Benzodiazepinones/metabolism , Benzodiazepinones/pharmacology , Benzodiazepinones/therapeutic use , ... Benzodiazepinones/administration & dosage , Benzodiazepinones/therapeutic use , Carbamazepine/administration & dosage , ... Benzodiazepinones , Chemistry , Pharmacology , Cell Line, Tumor , HIV Long Terminal Repeat , Genetics , HIV-1 , Genetics , ... Benzodiazepinones , Pharmacology , Blotting, Western , Cell Line, Tumor , Colonic Neoplasms , Genetics , Metabolism , Pathology ...
Index: LILACS (Americas) Main subject: Anxiety / Benzodiazepinones Limits: Adolescent / Adult / Female / Humans / Male Language ... Index: LILACS (Americas) Main subject: Anxiety / Benzodiazepinones Limits: Adolescent / Adult / Female / Humans / Male Language ... Adolescent , Adult , Middle Aged , Humans , Male , Female , Anxiety/drug therapy , Benzodiazepinones/therapeutic use , ...
Benzodiazepinones - administration & dosage , Drug Stability , Crystallization , Solubility , Benzodiazepinones - chemistry , ... Benzodiazepinones - pharmacokinetics , Dogs , Hydrophobic and Hydrophilic Interactions , Index Medicus ...
D03.633.100.079.080.070 Benzodiazepinones .. D03.633.100.079.080.070.216 Diazepam .. D12 Amino Acids, Peptides, and Proteins . ...
D03.633.100.079.080.070 Benzodiazepinones .. D03.633.100.079.080.070.750 Pirenzepine .. D03.633.100.103 Benzimidazoles .. ...
  • Iridium Catalyzed Asymmetric Hydrogenation of Cyclic Imines of Benzodiazepinones and Benzodiazepines. (dicp.ac.cn)
  • A computational chemistry study has been performed on a series of tetrahydroimidazo-benzodiazepinones as HIV-1-NNRT inhibitors. (scialert.net)