BENZOIC ACID amides.
Rhodium. A hard and rare metal of the platinum group, atomic number 45, atomic weight 102.905, symbol Rh. (Dorland, 28th ed)
An opioid antagonist with properties similar to those of NALOXONE; in addition it also possesses some agonist properties. It should be used cautiously; levallorphan reverses severe opioid-induced respiratory depression but may exacerbate respiratory depression such as that induced by alcohol or other non-opioid central depressants. (From Martindale, The Extra Pharmacopoeia, 30th ed, p683)
An antipsychotic agent that is specific for dopamine D2 receptors. It has been shown to be effective in the treatment of schizophrenia.
The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.
The location of the atoms, groups or ions relative to one another in a molecule, as well as the number, type and location of covalent bonds.
It is a form of protection provided by law. In the United States this protection is granted to authors of original works of authorship, including literary, dramatic, musical, artistic, and certain other intellectual works. This protection is available to both published and unpublished works. (from Circular of the United States Copyright Office, 6/30/2008)
Works about lists of drugs or collections of recipes, formulas, and prescriptions for the compounding of medicinal preparations. Formularies differ from PHARMACOPOEIAS in that they are less complete, lacking full descriptions of the drugs, their formulations, analytic composition, chemical properties, etc. In hospitals, formularies list all drugs commonly stocked in the hospital pharmacy.
Economic aspects of the fields of pharmacy and pharmacology as they apply to the development and study of medical economics in rational drug therapy and the impact of pharmaceuticals on the cost of medical care. Pharmaceutical economics also includes the economic considerations of the pharmaceutical care delivery system and in drug prescribing, particularly of cost-benefit values. (From J Res Pharm Econ 1989;1(1); PharmacoEcon 1992;1(1))
That segment of commercial enterprise devoted to the design, development, and manufacture of chemical products for use in the diagnosis and treatment of disease, disability, or other dysfunction, or to improve function.
Organizations representing specialized fields which are accepted as authoritative; may be non-governmental, university or an independent research organization, e.g., National Academy of Sciences, Brookings Institution, etc.
Informed consent given by a parent on behalf of a minor or otherwise incompetent child.
Exclusive legal rights or privileges applied to inventions, plants, etc.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
An enzyme formed from PROTHROMBIN that converts FIBRINOGEN to FIBRIN.
The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.
Formation and development of a thrombus or blood clot in the blood vessel.
A novel composition, device, or process, independently conceived de novo or derived from a pre-existing model.
Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.
A family of hexahydropyridines.
A condition in which the FORAMEN OVALE in the ATRIAL SEPTUM fails to close shortly after birth. This results in abnormal communications between the two upper chambers of the heart. An isolated patent ovale foramen without other structural heart defects is usually of no hemodynamic significance.
Diseases in any segment of the GASTROINTESTINAL TRACT from ESOPHAGUS to RECTUM.
The profession of writing. Also the identity of the writer as the creator of a literary production.
Collections of facts, assumptions, beliefs, and heuristics that are used in combination with databases to achieve desired results, such as a diagnosis, an interpretation, or a solution to a problem (From McGraw Hill Dictionary of Scientific and Technical Terms, 6th ed).
The guidelines and policy statements set forth by the editor(s) or editorial board of a publication.
Intentional falsification of scientific data by presentation of fraudulent or incomplete or uncorroborated findings as scientific fact.
"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.
A polynucleotide formed from the ADP-RIBOSE moiety of nicotinamide-adenine dinucleotide (NAD) by POLY(ADP-RIBOSE) POLYMERASES.
Inorganic compounds that contain nitrogen as an integral part of the molecule.
Inorganic compounds that contain oxygen as an integral part of the molecule.
Organic compounds containing the carboxy group (-COOH). This group of compounds includes amino acids and fatty acids. Carboxylic acids can be saturated, unsaturated, or aromatic.
Inorganic or organic compounds that contain sulfur as an integral part of the molecule.
One of the Liliaceae used as a spice (SPICES) and traditional remedy. It contains alliin lyase and alliin, which is converted by alliin lyase to allicin, the pungent ingredient responsible for the aroma of fresh cut garlic.
A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.
An adrenocortical steroid that has modest but significant activities as a mineralocorticoid and a glucocorticoid. (From Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p1437)
A large group of structurally diverse cell surface receptors that mediate endocytic uptake of modified LIPOPROTEINS. Scavenger receptors are expressed by MYELOID CELLS and some ENDOTHELIAL CELLS, and were originally characterized based on their ability to bind acetylated LOW-DENSITY LIPOPROTEINS. They can also bind a variety of other polyanionic ligand. Certain scavenger receptors can internalize micro-organisms as well as apoptotic cells.
Cell surface proteins that bind lipoproteins with high affinity. Lipoprotein receptors in the liver and peripheral tissues mediate the regulation of plasma and cellular cholesterol metabolism and concentration. The receptors generally recognize the apolipoproteins of the lipoprotein complex, and binding is often a trigger for endocytosis.
Leukocyte differentiation antigens and major platelet membrane glycoproteins present on MONOCYTES; ENDOTHELIAL CELLS; PLATELETS; and mammary EPITHELIAL CELLS. They play major roles in CELL ADHESION; SIGNAL TRANSDUCTION; and regulation of angiogenesis. CD36 is a receptor for THROMBOSPONDINS and can act as a scavenger receptor that recognizes and transports oxidized LIPOPROTEINS and FATTY ACIDS.
A pair of glands located at the cranial pole of each of the two KIDNEYS. Each adrenal gland is composed of two distinct endocrine tissues with separate embryonic origins, the ADRENAL CORTEX producing STEROIDS and the ADRENAL MEDULLA producing NEUROTRANSMITTERS.
Device constructed of either synthetic or biological material that is used for the repair of injured or diseased blood vessels.
Generating tissue in vitro for clinical applications, such as replacing wounded tissues or impaired organs. The use of TISSUE SCAFFOLDING enables the generation of complex multi-layered tissues and tissue structures.
Surgical insertion of BLOOD VESSEL PROSTHESES, or transplanted BLOOD VESSELS, or other biological material to repair injured or diseased blood vessels.
Cell growth support structures composed of BIOCOMPATIBLE MATERIALS. They are specially designed solid support matrices for cell attachment in TISSUE ENGINEERING and GUIDED TISSUE REGENERATION uses.
Stretch receptors found in the bronchi and bronchioles. Pulmonary stretch receptors are sensors for a reflex which stops inspiration. In humans, the reflex is protective and is probably not activated during normal respiration.

Activation of c-Abl tyrosine kinase requires caspase activation and is not involved in JNK/SAPK activation during apoptosis of human monocytic leukemia U937 cells. (1/4453)

Genotoxic stress triggers the activation of several sensor molecules, such as p53, JNK1/SAPK and c-Abl, and occasionally promotes the cells to apoptosis. We previously reported that JNK1/SAPK regulates genotoxic stress-induced apoptosis in p53-negative U937 cells by activating caspases. c-Abl is expected to act upstream of JNK1/SAPK activation upon treatment with genotoxic stressors, but its involvement in apoptosis development is still unclear. We herein investigated the kinase activities of c-Abl and JNK1/SAPK during apoptosis elicited by genotoxic anticancer drugs and tumor necrosis factor (TNF) in U937 cells and their apoptosis-resistant variant UK711 cells. We found that the activation of JNK1/SAPK and c-Abl correlated well with apoptosis development in these cell lines. Unexpectedly, however, the JNK1/SAPK activation preceded the c-Abl activation. Moreover, the caspase inhibitor Z-Asp suppressed c-Abl activation and the onset of apoptosis but not the JNK1/SAPK activation. Interestingly, c-Abl tyrosine kinase inhibition by CGP 57148 reduced apoptosis without interfering with JNK1/SAPK activation. These results indicate that c-Abl acts not upstream of JNK1/ SAPK but downstream of caspases during the development of p53-independent apoptosis and is possibly involved in accelerating execution of the cell death pathway.  (+info)

Meta-analysis of the reversible inhibitors of monoamine oxidase type A moclobemide and brofaromine for the treatment of depression. (2/4453)

The reversible inhibitors of monoamine oxidase type A (RIMAs) are a newer group of antidepressants that have had much less impact on clinical psychopharmacology than another contemporary class of medications, the selective serotonin reuptake-inhibitors (SSRIs). The RIMAs agents are distinguished from the older monoamine oxidase inhibitors (MAOIs) by their selectivity and reversibility. As a result, dietary restrictions are not required during RIMA therapy, and hypertensive crises are quite rare. In this article, we describe a series of meta-analyses of studies of the two most widely researched RIMAs, moclobemide (MOC; Aurorex) and brofaromine (BRO). Our findings confirm that both BRO and MOC are as effective as the tricyclic antidepressants, and they are better tolerated. However, BRO is not being studied at present for reasons unrelated to efficacy or side effects. MOC, which is available throughout much of the world (but not the United States), is significantly more effective than placebo and, at the least, comparable to the SSRIs in both efficacy and tolerability. For MOC, higher dosages may enhance efficacy for more severe depressions. We also found evidence that supports clinical impressions that MOC is somewhat less effective, albeit better tolerated, than older MAOIs, such as phenelzine or tranylcypromine. Little evidence has yet emerged to suggest that the RIMAs share older MAOIs' utility for treatment of depressions characterized by prominent reverse neurovegetative features. Based on available evidence, the RIMAs appear to have a limited, but useful, role in the differential therapeutics of the depressive disorders.  (+info)

The geranylgeranyltransferase I inhibitor GGTI-298 induces hypophosphorylation of retinoblastoma and partner switching of cyclin-dependent kinase inhibitors. A potential mechanism for GGTI-298 antitumor activity. (3/4453)

The geranylgeranyltransferase I inhibitor GGTI-298 has recently been shown to arrest human tumor cells in the G1 phase of the cell cycle, induce apoptosis, and inhibit tumor growth in nude mice. In the present manuscript, we provide a possible mechanism by which GGTI-298 mediates its tumor growth arrest. Treatment of the human lung carcinoma cell line Calu-1 with GGTI-298 results in inhibition of the phosphorylation of retinoblastoma protein, a critical step for G1/S transition. The kinase activities of two G1/S cyclin-dependent kinases, CDK2 and CDK4, are inhibited in Calu-1 cells treated with GGTI-298. Furthermore, GGTI-298 has little effect on the expression levels of CDK2, CDK4, CDK6, cyclins D1 and E, but decreases the levels of cyclin A. GGTI-298 increases the levels of the cyclin-dependent kinase inhibitors p21 and p15 and had little effect on those of p27 and p16. Most interesting is the ability of GGTI-298 to induce partner switching for several CDK inhibitors. GGTI-298 promotes binding of p21 and p27 to CDK2 while decreasing their binding to CDK6. Reversal of partner switching and G1 block was observed after removal of GGTI-298. Furthermore, GGTI-298 treatment results in an increased binding of p15 to CDK4, which is paralleled with decreased binding to p27. The results demonstrate that the GGTI-298-mediated G1 block in Calu-1 cells involves increased expression and partner switching of CDK inhibitors resulting in inhibition of CDK2 and CDK4, and retinoblastoma protein phosphorylation.  (+info)

Vasoconstriction in human isolated middle meningeal arteries: determining the contribution of 5-HT1B- and 5-HT1F-receptor activation. (4/4453)

AIMS: Sumatriptan is a 5-HT1B/1D-receptor agonist which also has affinity for 5-HT1F-receptors. The vasoconstrictor effects of sumatriptan are thought to be 5-HT1B-receptor mediated and these receptors have been shown to be expressed in human cranial blood vessels. However, in the same tissue mRNA coding for 5-HT1F-receptors has also been identified and this study addresses the possibility of whether 5-HT1F-receptor activation contributes to vasoconstriction. METHODS: The ability of two selective 5-HT1B/1D-receptor antagonists (GR125,743 and GR127,935) with no affinity for 5-HT1F-receptors, to inhibit sumatriptan evoked contractions in human isolated middle meningeal artery was investigated. Using a series of 5-HT1B/1D-receptor agonists (sumatriptan, zolmitriptan, CP122,288, L-741,519 and L-741,604), some with high affinity for 5-HTIF-receptors and the non-selective 5-HT-receptor agonists 5-HT and 5-CT, we compared the vasoconstrictor potency of these drugs in human isolated middle meningeal artery with their affinities at cloned human 5-HT1B-, 5-HT1D-and 5-HT1F-receptors expressed in CHO cell lines. RESULTS: GR125,743 antagonized sumatriptan evoked contractions in a competitive manner (apparent pA2 9.1) and GR127,935 antagonized sumatriptan-induced responses in a non-competitive manner (reducing the maximum contraction to 27%). There was a significant correlation between vasoconstrictor potency and 5-HT1B-receptor affinity (r=0.93, P=0.002) but not with 5-HT1D- or 5-HT1F-receptor affinity (r=0.74, P=0.06; r= 0.31, P= 0.49, respectively). CONCLUSIONS: These experiments show that in human middle meningeal artery vasoconstriction to sumatriptan-like agents is 5-HT1B-receptor mediated with little if any contribution from 5-HT1F-receptor activation.  (+info)

Involvement of tachykinin receptors in sensitisation to cow's milk proteins in guinea pigs. (5/4453)

BACKGROUND: There is growing evidence for a pivotal role for tachykinins in gut neuroimmune interactions. AIMS: To determine whether NK1, NK2, and NK3 tachykinin receptors are involved in milk protein induced allergic sensitisation. METHODS: Eight groups of 12 Dunkin-Hartley guinea pigs (250-300 g) were used. Four groups were sensitised to milk proteins for three weeks. During this period, these animals were injected intraperitoneally each day with NK1 (SR 140333; 0.3 mg/kg), NK2 (SR 48968; 5 mg/kg), or NK3 (SR 142801; 5 mg/kg) receptor antagonist or vehicle. The fifth group had water available instead of milk and was used as a non-sensitised control. The three other groups received the NK receptor antagonists for three weeks but were not sensitised to milk proteins. RESULTS: Sensitised animals treated with NK1 and NK3 receptor antagonists had both lower IgE and IgG serum titres, evaluated by passive cutaneous anaphylaxis, and lower specific IgG serum titres, determined by enzyme linked immunosorbent assay (ELISA), than vehicle treated animals. Sensitisation induced an increase in intestinal mast cell number which was abolished by treatment with the NK1 receptor antagonist. Antigenic challenge-induced jejunal hypersecretion was also blocked by treatment with the NK1 receptor antagonist. CONCLUSION: In guinea pigs, NK1 and NK3 but not NK2 receptors are involved in sensitisation to cow's milk. However, NK1 but not NK3 receptor antagonists abolish both the hypermastocytosis induced by food allergy and the hypersecretion induced by antigenic challenge, suggesting different roles for NK1 and NK3 receptors in the mechanisms of sensitisation to beta-lactoglobulin.  (+info)

Neurogenic plasma leakage in mouse airways. (6/4453)

1. This study sought to determine whether neurogenic inflammation occurs in the airways by examining the effects of capsaicin or substance P on microvascular plasma leakage in the trachea and lungs of male pathogen-free C57BL/6 mice. 2. Single bolus intravenous injections of capsaicin (0.5 and 1 micromol kg(-1), i.v.) or substance P (1, 10 and 37 nmol kg(-10, i.v.) failed to induce significant leakage in the trachea, assessed as extravasation of Evans blue dye, but did induce leakage in the urinary bladder and skin. 3. Pretreatment with captopril (2.5 mg kg(-1), i.v.), a selective inhibitor of angiotensin converting enzyme (ACE), either alone or in combination with phosphoramidon (2.5 mg kg(-1), i.v.), a selective inhibitor of neutral endopeptidase (NEP), increased baseline leakage of Evans blue in the absence of any exogenous inflammatory mediator. The increase was reversed by the bradykinin B2 receptor antagonist Hoe 140 (0.1 mg kg(-1), i.v.). 4. After pretreatment with phosphoramidon and captopril, capsaicin increased the Evans blue leakage above the baseline in the trachea, but not in the lung. This increase was reversed by the tachykinin (NK1) receptor antagonist SR 140333 (0.7 mg kg(-1), i.v.), but not by the NK2 receptor antagonist SR 48968 (1 mg kg(-1), i.v.). 5. Experiments using Monastral blue pigment as a tracer localized the leakage to postcapillary venules in the trachea and intrapulmonary bronchi, although the labelled vessels were less numerous in mice than in comparably treated rats. Blood vessels of the pulmonary circulation were not labelled. 6. We conclude that neurogenic inflammation can occur in airways of pathogen-free mice, but only after the inhibition of enzymes that normally degrade inflammatory peptides. Neurogenic inflammation does not involve the pulmonary microvasculature.  (+info)

A synthetic inhibitor of histone deacetylase, MS-27-275, with marked in vivo antitumor activity against human tumors. (7/4453)

Synthetic benzamide derivatives were investigated for their ability to inhibit histone deacetylase (HDA). In this study, one of the most active benzamide derivatives, MS-27-275, was examined with regard to its biological properties and antitumor efficacy. MS-27-275 inhibited partially purified human HDA and caused hyperacetylation of nuclear histones in various tumor cell lines. It behaved in a manner similar to other HDA inhibitors, such as sodium butyrate and trichostatin A; MS-27-275 induced p21(WAF1/CIP1) and gelsolin and changed the cell cycle distribution, decrease of S-phase cells, and increase of G1-phase cells. The in vitro sensitivity spectrum of MS-27-275 against various human tumor cell lines showed a pattern different than that of a commonly used antitumor agent, 5-fluorouracil, and, of interest, the accumulation of p21(WAF1/CIP1) tended to be faster and greater in the cell lines sensitive to MS-27-275. MS-27-275 administered orally strongly inhibited the growth in seven of eight tumor lines implanted into nude mice, although most of these did not respond to 5-fluorouracil. A structurally analogous compound to MS-27-275 without HDA-inhibiting activity showed neither the biological effects in cell culture nor the in vivo therapeutic efficacy. These results suggest that MS-27-275 acts as an antitumor agent through HDA inhibition and may provide a novel chemotherapeutic strategy for cancers insensitive to traditional antitumor agents.  (+info)

Selective induction of apoptosis in Philadelphia chromosome-positive chronic myelogenous leukemia cells by an inhibitor of BCR - ABL tyrosine kinase, CGP 57148. (8/4453)

The BCR - ABL tyrosine kinase has been implicated as the cause of Philadelphia chromosome (Ph1)-positive leukemias. We report herein that CGP 57148, a selective inhibitor of the ABL tyrosine kinase, caused apoptosis specifically in bcr - abl-positive chronic myelogenous leukemia (CML) cells, K562 and KYO-1. Upon treatment with CGP 57148, CRKL, a specific substrate for BCR - ABL that propagates signals via phosphatidylinositol-3' kinase (PI3K), was dephosphorylated, indicating inhibition of BCR - ABL tyrosine kinase at the cellular level. Likewise, MAPK/ERK, a downstream mediator of Ras, was also dephosphorylated. Caspase activation and cleavage of retinoblastoma protein (pRB) accompanied the development of CGP 57148-induced apoptosis. Inhibition of caspase suppressed apoptosis and the cleavage of pRB, and in turn arrested cells in the G1 phase. These results indicate that CGP 57148 shows apoptogenic and anti-proliferative effects on bcr - abl-positive cells by blocking BCR - ABL-initiated signaling pathways.  (+info)

TY - JOUR. T1 - Favorable long-term follow-up results over 6 years for response, survival, and safety with imatinib mesylate therapy in chronic-phase chronic myeloid leukemia after failure of interferon-α treatment. AU - Hochhaus, Andreas. AU - Druker, Brian. AU - Sawyers, Charles. AU - Guilhot, Francois. AU - Schiffer, Charles A.. AU - Cortes, Jorge. AU - Niederwieser, Dietger W.. AU - Gambacorti, Carlo. AU - Stone, Richard M.. AU - Goldman, John. AU - Fischer, Thomas. AU - OBrien, Stephen G.. AU - Reiffers, Jose J.. AU - Mone, Manisha. AU - Krahnke, Tillmann. AU - Talpaz, Moshe. AU - Kantarjian, Hagop M.. PY - 2008. Y1 - 2008. N2 - Imatinib mesylate, a targeted inhibitor of BCR-ABL tyrosine kinase, is the standard of care for chronic myeloid leukemia (CML). A phase 2 trial of imatinib in late chronic-phase (CP) CML after interferon-α (IFNα) failure enrolled 532 patients, 454 with a confirmed diagnosis of CP CML. Median time from diagnosis was 34 months; median duration of imatinib ...
TY - JOUR. T1 - Nilotinib. T2 - A novel Bcr-Abl tyrosine kinase inhibitor for the treatment of leukemias. AU - Jabbour, Elias. AU - El Ahdab, Samih. AU - Cortes, Jorge. AU - Kantarjian, Hagop. PY - 2008/7/1. Y1 - 2008/7/1. N2 - The successful introduction of the tyrosine kinase inhibitors has initiated a new era in the management of chronic myeloid leukemia (CML). Imatinib mesilate therapy has significantly improved the prognosis of CML. A minority of patients in chronic-phase CML - and more patients in advanced phases - are resistant to imatinib, or develop resistance during treatment. This is attributed, in 40 - 50% of cases, to the development of mutations in the Bcr-Abl tyrosine kinase domain that impair imatinib binding. Nilotinib (Tasigna®) is a novel potent selective oral kinase inhibitor. Preclinical and clinical investigations demonstrate nilotinib effectively overcomes imatinib resistance, and has induced high rates of hematologic and cytogenetic responses in CML post imatinib ...
OUTLINE: This is a multicenter, dose-escalation study of imatinib mesylate and cytarabine.. Patients receive oral imatinib mesylate alone once daily on days 1-21. Patients then receive oral imatinib mesylate once daily and cytarabine IV over 1-3 hours on days 1-7. Combination therapy repeats every 28-42 days for 2 courses. Patients then receive maintenance oral imatinib mesylate once daily. Treatment continues in the absence of disease progression or unacceptable toxicity.. Cohorts of 5-20 patients receive escalating doses of imatinib mesylate and cytarabine until the maximum tolerated dose (MTD) is determined. The MTD is defined as the dose preceding that at which at least 5/5, 5/10, or 5/20 patients experience dose-limiting toxicity.. Patients are followed every 6 months.. PROJECTED ACCRUAL: A total of 30-60 patients will be accrued for this study within 2 years. ...
A highly mono-selective ortho-methylthiolation of benzamides was achieved via Co-catalyzed coupling of benzamides with DMSO. The reaction employs an 8-aminoquinoline group as the bidentate directing group and DMSO as the methylthiolation source. Instead of a mixture of mono- and di-alkylthio-substituted prod
TY - JOUR. T1 - Recent advances in Philadelphia chromosome-positive malignancies. T2 - the potential role of arsenic trioxide.. AU - ODwyer, Michael E.. AU - La Rosée, Paul. AU - Nimmanapalli, Ramedivi. AU - Bhalla, Kapil N.. AU - Druker, Brian. PY - 2002/4. Y1 - 2002/4. N2 - Chronic myelogenous leukemia (CML) is characterized by the presence of the Bcr-Abl fusion gene, which encodes a constitutively active tyrosine kinase that has been strongly implicated as the sole oncogenic abnormality in early-stage CML. Treatment with the specific tyrosine kinase inhibitor imatinib mesylate has achieved excellent results in CML, at all stages of the disease. However, limitations to the successful use of imatinib mesylate as a single agent include the problem of resistance, seen chiefly in patients with advanced-phase disease. This review summarizes the clinical results to date with imatinib mesylate and briefly discusses the problem of resistance before describing potential strategies, including the use ...
Elevated serum glucocorticoid levels contribute to the progression of many diseases, including depression, Alzheimers disease, hypertension, and acquired immunodeficiency syndrome. Here we show that the benzamide derivative N-[2-(4-cyclopropanecarbonyl-3-methyl-piperazin-1-yl)-1-(tert-butyl-1H-indol-3-yl-methyl)-2-oxo-ethyl]-4-nitrobenzamide (SP-10) inhibits dibutyryl cyclic AMP (dbcAMP)-induced corticosteroid synthesis in a dose-dependent manner in Y-1 adrenal cortical mouse tumor cells, without affecting basal steroid synthesis and reduced stress-induced corticosterone increases in rats without affecting the physiological levels of the steroid in blood. SP-10 did not affect cholesterol transport and metabolism by the mitochondria but was unexpectedly found to increase 3-hydroxy-3-methylglutaryl-coenzyme A, low density lipoprotein receptor, and scavenger receptor class B type I (SR-BI) expression. However, it also markedly reduced dbcAMP-induced NBD-cholesterol uptake, suggesting that this is a
A compound which functions to inhibit capsaicin receptor VR1 activation and is useful as a therapeutic agent for, e.g., various pains including inflammatory pain and neurogenic pain, migraine, cluster headache, and bladder diseases including overactive bladder. It is a benzamide derivative or salt thereof, the derivative being characterized by comprising: a benzene ring; a ring D (a mono- or dicyclic hydrocarbon ring or mono- or dicyclic heteroaromatic ring) bonded to the benzene ring through an amide bond; a ring E (a mono- or dicyclic hydrocarbon ring or mono- or dicyclic heteroaromatic ring) directly bonded to the benzene ring; and A (an amino moiety or a mono- or dicyclic heteroring) bonded to the benzene ring through L (a lower alkylene).
An Open-Label Randomized Phase III Study of Dasatinib vs. High-Dose (600 mg) Imatinib Mesylate in the Treatment of Subjects With Chronic Phase Philadelphia Chromosome-Positive Chronic Myeloid Leukemia Who Are Imatinib Failures or Who Have Had a Suboptimal Response After 3-18 Months of Therapy With 400 mg ...
TY - JOUR. T1 - Cardiovascular toxicity in patients with chronic myeloid leukemia treated with second-generation tyrosine kinase inhibitors in the real-life practice. T2 - Identification of risk factors and the role of prophylaxis. AU - Caocci, Giovanni. AU - Mulas, Olga. AU - Annunziata, Mario. AU - Luciano, Luigiana. AU - Bonifacio, Massimiliano. AU - Orlandi, Ester Maria. AU - Pregno, Patrizia. AU - Galimberti, Sara. AU - Russo Rossi, Antonella. AU - Abruzzese, Elisabetta. AU - Iurlo, Alessandra. AU - Martino, Bruno. AU - Sgherza, Nicola. AU - Binotto, Gianni. AU - Castagnetti, Fausto. AU - Gozzini, Antonella. AU - Fozza, Claudio. AU - Bocchia, Monica. AU - Sicuranza, Anna. AU - Stagno, Fabio. AU - Efficace, Fabio. AU - Usala, Emilio. AU - De Gregorio, Fiorenza. AU - Scaffidi, Luigi. AU - Elena, Chiara. AU - Pirillo, Francesca. AU - Baratè, Claudia. AU - Trawinska, Malgorzata Monika. AU - Cattaneo, Daniele. AU - Labate, Claudia. AU - Gugliotta, Gabriele. AU - Molica, Matteo. AU - Specchia, ...
Novartis (es); Novartis (hu); Novartis (eu); Novartis (ms); Novartis (de-ch); Novartis (de); Novartis (en-gb); Новартис (sr-ec); Новартис (bg); Novartis (da); Novartis (ro); ノバルティス (ja); Novartis (sv); נוברטיס (he); 諾華公司 (zh-hant); Novartis (gsw); 노바티스 (ko); Новартис (kk); Novartis (en-ca); Novartis (cs); நோவார்ட்டீசு (ta); Novartis (it); Novartis (fr); Novartis (tr); 诺华公司 (zh-hans); Novartis (sr-el); Novartis (en); Novartis (pt); Novartis (vi); Novartis (ru); نوارتیس (fa); โนวาร์ติส (th); Новартис (sr); Novartis (nl); 诺华公司 (zh); Novartis (pt-br); Novartis (pl); Novartis (id); Novartis (nn); Novartis (nb); Novartis (sh); Novartis (fi); 諾華公司 (zh-hk); ნოვარტისი (ka); Novartis (uk); Novartis (gl); نوفارتس (ar); Novartis (el); Novartis (ca) Empresa farmacéutica multinacional (es); スイスの製薬・バイオテクノロジー企業 ...
Fingerprint Dive into the research topics of Multicenter Phase II trial assessing effectiveness of imatinib mesylate on relapsed or refractory KIT-positive or PDGFR-positive sarcoma. Together they form a unique fingerprint. ...
The t(9;22) translocation is seen in cases of chronic myeloid leukemia (CML), a subset of acute lymphocytic leukemia (ALL) and rarely in acute myeloid leukemia (AML). The resulting BCR-ABL fusion gene is transcribed and translated into a 210 kD (p210, major transcript) or 190 kD (p190, minor transcript) BCR-ABL fusion product with dysregulated (significantly enhanced) tyrosine kinase activity. Detection of the BCR/ABL1 fusion gene transcript is a critical determinant in diagnosis. The BCR/ABL1 fusion gene product is the cause of disease and growth of leukemic cells and expression levels of the transcript are directly related to disease severity. The use of new drugs for treatment such as the tyrosine kinase inhibitor imatinib mesylate (Gleevec) reduces the amount of leukemic cells below the level of cytogenetic detection and therefore makes molecular determination in the detection of minimal residual disease desirable. A consensus treatment goal is the achievement of major molecular response, ...
In the presence of imatinib mesylate, both age groups displayed little change in spontaneous slow-wave activity with the exception of the highest concentration (Fig. 2ii). A major difference between the two age groups occurred in the amplitude of contractile activity at all concentrations of imatinib mesylate. In the ageing guinea-pig prostate, a concentration-dependent inhibition was seen where low concentrations of imatinib mesylate produced the most inhibition whereas high concentrations produced less inhibition of contractile activity.. In contrast, contractile amplitude was generally reduced to 26-40% across all concentrations in the younger guinea-pig prostate. This difference between age groups may parallel the reduction in pacemaker potential activity and increase in spike potential activity with age, which was previously observed by Dey et al. [14]. Like the guinea-pig bladder [16], the guinea-pig prostate generates nifedipine-sensitive spike potentials, as well as slow-wave activity. ...
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Novel N-(3-hydroxy-4-pipridinyl)benzamides and derivatives thereof, said compounds being used as stimulators of the motility of the gastro-intestinal system.
BACKROUND: The selective tyrosine kinase inhibitor imatinib inhibits growth of bcr/abl positive cells and, thus, has become a novel therapeutic option for the treatment of Ph+ leukaemic patients. Various mutations within the abl sequence have been described that prevent adequate imatinib binding to bcr/abl resulting in cellular resistance of CML cells. METHODS: We investigated 69 CML patients under treatment with imatinib as part of an ongoing clinical trial. At recruitment 37 patients were in chronic phase, 21 patients in accelerated phase and 11 patients in blast crisis. Bcr/abl, WT1, MDR1and AGP RNA transcripts were quantified in peripheral leucocytes by real time PCR. AGP protein levels in plasma were measured by turbidimetric analysis. By combining peptide nucleic acid (PNA) based DNA clamping with a fluorescence hybridisation probe assay we developed a new and highly sensitive technique for the detection of known mutations within the bcr/abl kinase domain. RESULTS: 1. Our results ...
BACKGROUND: The cause of chronic myeloid leukemia (CML) is a constitutively active BCR-ABL tyrosine kinase. Imatinib inhibits this kinase, and in a short-term study was superior to interferon alfa plus cytarabine for newly diagnosed CML in the chronic phase. For 5 years, we followed patients with CML who received imatinib as initial therapy. METHODS: We randomly assigned 553 patients to receive imatinib and 553 to receive interferon alfa plus cytarabine and then evaluated them for overall and event-free survival; progression to accelerated-phase CML or blast crisis; hematologic, cytogenetic, and molecular responses; and adverse events. RESULTS: The median follow-up was 60 months. Kaplan-Meier estimates of cumulative best rates of complete cytogenetic response among patients receiving imatinib were 69% by 12 months and 87% by 60 months. An estimated 7% of patients progressed to accelerated-phase CML or blast crisis, and the estimated overall survival of patients who received imatinib as initial ...
The clinical success of the ABL tyrosine kinase inhibitor imatinib in chronic myeloid leukaemia (CML) serves as a model for molecularly targeted therapy of cancer, but at least two critical questions remain. Can imatinib eradicate leukaemic stem cells? What are the dynamics of relapse due to imatinib resistance, which is caused by mutations in the ABL kinase domain? The precise understanding of how imatinib exerts its therapeutic effect in CML and the ability to measure disease burden by quantitative polymerase chain reaction provide an opportunity to develop a mathematical approach. We find that a four-compartment model, based on the known biology of haematopoietic differentiation, can explain the kinetics of the molecular response to imatinib in a 169-patient data set. Successful therapy leads to a biphasic exponential decline of leukaemic cells. The first slope of 0.05 per day represents the turnover rate of differentiated leukaemic cells, while the second slope of 0.008 per day represents ...
Celecoxib is a selective COX-2 inhibitor and its anti-tumor effect has been reported in various cancers [7-9]. In this paper, we demonstrated that the anti-tumor activities of celecoxib included cell cycle arrest, necrosis, apoptosis and autophagy suppression in KBM5 and KBM5-T315I cells. KBM5-T315I cell is a mutation line of KBM5 with a threonine to isoleucine mutation at position 315 in the Abl fragment of the Bcr-Abl kinase domain. This leads to an alteration of the enzymes active site and makes these cells resistant to the first and second generation of TKI [35]. Results showed that celecoxib caused cytotoxic effect in the two CML cell lines which was dose and time-dependent. When extending the celecoxib incubation time, the inhibition effect was stronger in KBM5-T315I cells than in KBM5 cells (Fig. 1), indicating that celecoxib might be used as a new therapeutic agents in imatinib-resistant CML. In accordance with other reports [19, 21], our findings also confirmed that the anti-tumor ...
Imatinib (STI571 or Gleevec) is a small-molecule inhibitor of the BCR-ABL tyrosine kinase that produces clinical remissions in chronic myeloid leukemia (CML) patients with minimal toxicity (1, 2). Imatinib is now frontline therapy for CML, but resistance is increasingly encountered. Clinical resistance is primarily mediated by mutations within the kinase domain of BCR-ABL and, to a lesser extent, by amplification of the BCR-ABL genomic locus (3). Crystallographic studies revealed that imatinib binds to the adenosine triphosphate (ATP)-binding site of ABL only when the activation loop of the kinase is closed and thus stabilizes the protein in this inactive conformation (4). In addition, the normally smooth contour of the phosphate-binding loop of ABL is distorted by imatinib binding, adding further to the unique conformational requirements for optimal kinase inhibition. These conformation-specific binding requirements contribute to imatinibs selectivity, particularly with regard to the closely ...
Abstract. Imatinib has become the treatment of choice for most with CML. The standard dose (SD) for CP CML is 400 mg daily, but pre-clinical and clinical observ
BACKGROUND AND OBJECTIVES: Imatinib mesylate inhibits ABL tyrosine kinase. This protein serves a complex role in cell cycling and is important in lymphopoiesis. We describe the immunologic findings in patients with chronic myeloid leukemia resistant to or intolerant of interferon (IFN) a who were treated with imatinib. This aspect could be of interest since patients with these characteristics may be exposed to this treatment for long periods. DESIGN AND METHODS: Immunologic and hematologic evaluation (including immunoglobulin levels and parameters of autoimmunity), immunophenotyping analysis of peripheral blood and bone marrow, and cytogenetic bone marrow analysis were performed at sequential time points of the treatment (0, 3, 6, and 9 and 12 months). The relationships among immunologic variables, and between the immunologic findings and response, were investigated. RESULTS: Hypogammaglobulinemia IgG, IgA and IgM developed in 28%, 14% and 22% of the patients, respectively. Lymphocyte counts ...
Study 200 (NCT00261846), a single-arm, open-label, multicenter study in patients with CML who were resistant or intolerant to prior therapy was conducted to evaluate the efficacy and safety of BOSULIF 500 mg once daily in patients with imatinib-resistant or -intolerant CML with separate cohorts for CP, AP, and BP disease previously treated with 1 prior TKI (imatinib) or more than 1 TKI (imatinib followed by dasatinib and/or nilotinib). The definition of imatinib resistance included (1) failure to achieve or maintain any hematologic improvement within 4 weeks; (2) failure to achieve a CHR by 3 months, cytogenetic response by 6 months or major cytogenetic response (MCyR) by 12 months; (3) progression of disease after a previous cytogenetic or hematologic response; or (4) presence of a genetic mutation in the BCR-ABL gene associated with imatinib resistance. Imatinib intolerance was defined as inability to tolerate imatinib due to toxicity, or progression on imatinib and inability to receive a ...
Imatinib mesylate is a specific tyrosine kinase inhibitor that may block the platelet-derived growth factor and transforming growth factor pathways. These pathways are known to provoke fibroblast activation. We evaluated whether imatinib, by inhibiting these pathways, prevents diastolic dysfunction and attenuates myocardial remodeling using spontaneously hypertensive rats (SHRs). Eight-week-old male SHRs were randomly assigned to either imatinib treatment group (30 mg/kg per day; n=10; SHR-I) or hypertensive control group (distilled water, n=10; SHR-C). Wistar-Kyoto rats were used as normal controls (n=10). At 16 weeks, all rats underwent hemodynamic studies and Doppler echocardiography and then were euthanized. Their hearts were extracted for histopathologic, immunoblotting, and quantitative reverse transcriptase polymerase chain reaction analyses. Although imatinib did not affect blood pressure, it markedly reduced perivascular and interstitial fibrosis in the hearts of SHR. Echocardiogram ...
An Open Label, Multi-center Imatinib Roll-over Protocol for Patients Who Have Completed a Previous Novartis-sponsored Imatinib Study and Are Judged by the Investigator to Benefit From Continued Imatinib Treatment
Imatinib has shown remarkable clinical benefit for treatment of Bcr/Abl+ leukemia, especially CML patients in early chronic phase. However, it has become clear that rare clones with mutations that confer resistance to imatinib (e.g., mutations in bcr-abl that prevent imatinib binding) can survive, and this resistance can lead to relapse and limits the effects for patients with advanced disease (1). Because the inhibition of cell proliferation by the blockade of Bcr/Abl with imatinib is not sufficient for eradicating Bcr/Abl+ leukemic clones, a better understanding of the mechanisms by which imatinib kills cells and how this killing can be augmented may lead to improved therapeutic strategies.. Although, our study confirmed that Bcl-2 or Bcl-xL overexpression (7) or RNAi-mediated reduction of Bim (8, 9) inhibits imatinib-induced apoptosis in K562 cells, we found that it is the combination of Bim and Bad that accounts for the killing activity of imatinib. Imatinib caused a marked reduction in ...
TY - JOUR. T1 - Clinical Strategies to Achieve an Early and Successful Response to Tyrosine Kinase Inhibitor Therapy. AU - Hughes, Timothy. AU - Hochhaus, Andreas. PY - 2009/1/1. Y1 - 2009/1/1. N2 - Imatinib is the standard of care for previously untreated chronic myeloid leukemia (CML), with high response rates that lead to improved event-free and overall survival compared with interferon alfa. Imatinib dose is one important factor affecting response, and early clinical studies showed promising molecular response rates with high-dose therapy. Large, randomized trials are now ongoing to test this potential benefit and establish whether a starting dose of 800 mg/d improves long-term clinical outcomes compared with the current standard dose of 400 mg/d. Low plasma imatinib levels are associated with a decreased chance of response. The importance of imatinib dosing and plasma levels is likely due to their impact on intracellular concentrations of the drug. Cellular influx of imatinib is mediated by ...
1. Stoler D.L. , Chen N. , Basik M. et al. The onset and extent of genomic instability in sporadic colorectal tumor progression . Proc Natl Acad Sci U S A . 1999 ; 96 : 15121 - 15126 . 2. Hahn W.C. , Weinberg R.A. Modelling the molecular circuitry of cancer . Nat Rev Cancer . 2002 ; 2 : 331 - 341 . 3. La Rosee P. , ODwyer M.E. , Druker B.J. Insights from pre-clinical studies for new combination treatment regimens with the Bcr-Abl kinase inhibitor imatinib mesylate (Gleevec/Glivec) in chronic myelogenous leukemia: a translational perspective . Leukemia . 2002 ; 16 : 1213 - 1219 . 4. Kitano H. Cancer robustness: tumour tactics . Nature . 2003 ; 426 : 125 . 5. Hetz C. , Soto C. Protein misfolding and disease: the case of prion disorders . Cell Mol Life Sci . 2003 ; 60 : 133 - 143 . 6. Nardai G. , Vegh E.M. , Prohaszka Z. , Csermely P. Chaperone-related immune dysfunction: an emergent property of distorted chaperone networks . Trends Immunol . 2006 ; 27 : 74 - 79 . 7. Zhao R. , Davey M. , Hsu Y.C. ...
OBJECTIVE: Despite the efficacy of the BCR-ABL tyrosine kinase inhibitor imatinib, the development of resistance against imatinib has been observed. The most important mechanisms known to cause resistance are point mutations in the ABL tyrosine kinase and the ATP domain. This study describes the use of denaturing high performance liquid chromatography (dHPLC) as a method to screen for mutations of the ABL gene.METHODS: We used the dHPLC based assay for the screening of ABL point mutations. Forty chronic myeloid leukemia (CML) patients who showed resistance to imatinib were screened in parallel by dHPLC and direct sequencing.RESULTS: Nine of the 40 patients (23%) had mutations. CONCLUSION: dHPLC can be a useful method for pre-screening. Analyzing the mutations and monitoring (high-risk) patients can improve their prognosis and survival rate. dHPLC can potentially become a valuable tool for regular testing of patients in the future ...
C07D213/60-Heterocyclic compounds containing six-membered rings, not condensed with other rings, with one nitrogen atom as the only ring hetero atom and three or more double bonds between ring members or between ring members and non-ring members having three double bonds between ring members or between ring members and non-ring members having no bond between the ring nitrogen atom and a non-ring member or having only hydrogen or carbon atoms directly attached to the ring nitrogen atom with heteroatoms or with carbon atoms having three bonds to hetero atoms, with at the most one to halogen, e.g. ester or nitrile radicals, directly attached to ring carbon atoms ...
Glivec leukaemia drug binding to its target, the enzyme Bcr-Abl tyrosine kinase. This enzyme is produced by a genetic mutation, the swapping of parts of two chromosomes, leading to the formation of the oncogene (cancer-causing gene) Bcr-Abl, which produces a constantly-active version of normal Abl tyrosine kinase. This causes chronic myelogenous leukaemia (CML), a cancer of white blood cells. The drug Glivec (Imatinib) works by binding to the active site of the Bcr-Abl enzyme, producing a change in shape that prevents the enzyme from functioning. This causes the death of cancerous cells expressing the enzyme. Glivec, the first such tyrosine kinase inhibitor to be produced, is marketed by Novartis. - Stock Video Clip K003/2147
This extension II study will allow for further follow-up of the disease under treatment with imatinib mesylate and allow the patients to continue to receive imatinib mesylate.
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RAD51 is a key protein in the homologous recombination (HR) pathway of DNA double-strand break repair, and HR represents a novel target for cancer therapy. Because imatinib (Gleevec) has been reported to reduce RAD51 protein levels, we tested the clonogenic survival for RT112, H1299, PANC1, and PC3 tumor cell lines of varying p53 status and normal GM05757 normal fibroblasts after exposure to single agent imatinib (0-20 micromol/L; 0-72 hours). We also combined imatinib with DNA damaging agents that are toxic to RAD51-deficient cells, including ionizing radiation, gemcitabine, and mitomycin C. We observed decreased nuclear expression and chromatin binding of RAD51 protein following imatinib treatment. Imatinib also resulted in decreased error-free HR as determined by a flow cytometry-based integrated direct repeat-green fusion protein reporter system; this correlated to reduced RAD51 expression. Clonogenic survival experiments revealed increased cell kill for imatinib-treated cells in combination with
RAD51 is a key protein in the homologous recombination (HR) pathway of DNA double-strand break repair, and HR represents a novel target for cancer therapy. Because imatinib (Gleevec) has been reported to reduce RAD51 protein levels, we tested the clonogenic survival for RT112, H1299, PANC1, and PC3 tumor cell lines of varying p53 status and normal GM05757 normal fibroblasts after exposure to single agent imatinib (0-20 micromol/L; 0-72 hours). We also combined imatinib with DNA damaging agents that are toxic to RAD51-deficient cells, including ionizing radiation, gemcitabine, and mitomycin C. We observed decreased nuclear expression and chromatin binding of RAD51 protein following imatinib treatment. Imatinib also resulted in decreased error-free HR as determined by a flow cytometry-based integrated direct repeat-green fusion protein reporter system; this correlated to reduced RAD51 expression. Clonogenic survival experiments revealed increased cell kill for imatinib-treated cells in combination with
It has been clearly established that response is the most important prognostic factor for long-term outcome in CML.17⇓-19 The depth and time of response obtained by patients with CML during TKI therapy are critical from a prognostic standpoint.17⇓-19 Patients who achieved a CCyR at 12, 18, or 24 months in the IRIS study had improved progression-free survival compared with those who obtained only a partial cytogenetic response at each of those time points.3 Moreover, patients who do not achieve optimal response at 12 months of imatinib therapy had a higher risk of progression and poorer outcome compared with patients who achieved a 12-month CCyR, thus making the 12-month CCyR, the most relevant endpoint.17⇓-19. Our study of homogeneous patients with early CML-CP treated with TKI has confirmed that second-generation TKI used in the frontline setting is highly efficacious and induced higher rates of CCyR early. In addition, our study has confirmed that an early achievement of CCyR remains a ...
Breast cancer accounts for 29% of malignant tumors. It is an heterogenous disease covering a spectrum of different molecular subtypes. Epigenetic aberrations may affect gene expression through DNA and histone proteins modifications thus promoting tumor progression and resistance to anti- tumor treatment. Area covered: This article explores the potential role of entinostat in the treatment of breast cancer. The clinical trials evaluating entinostat are discussed, highlighting preclinical data and early-phase clinical studies results. The emerging activity of entinostat in several clinical settings is evaluated by focusing on endocrine-resistant, HER2 positive and triple-negative breast cancer with promising activity in boosting the immune-system. Expert opinion: Entinostat, a synthetic benzamide derivative class I histone deacetylases (HDACs) inhibitor, inhibits cell proliferation and promotes apoptosis in breast cancer. Several results from clinical trials demonstrate that the addition of an ...
Discussion. The concept of achieving deeper molecular responses with first generation TKIs for a sufficient period of time has been the basis for considering TKI withdrawal, looking for a possible cure in CML. This was defined as a 4-log reduction of BCR-ABL1 transcripts [molecular response (MR)4.0] for more than two years in the Stop Imatinib (STIM) trial as the criteria for imatinib withdrawal. However, the results have shown that 60% of patients had molecular relapse necessitating the reintroduction of TKIs. Hence, deep molecular response does not equate with a cure.7. This same concept was tried in a different setting in a few cases where there was initial imatinib failure due to TKD mutations but deep molecular responses were obtained with the 2nd generation TKI dasatinib. Dasatinib cessation was tried in these cases as well, with no relapse. The presence of BCR-ABL positive cells in the blood of a patient in a stable drug-free CMR appears to indicate that eradication of the leukemic clone ...
Gleevec Gleevec - description, side Effects of Gleevec Gleevec, dosage (Gleevec Gleevec), proper use of Gleevec Gleevec. Drugs review.
Hentschel J, Rubio I, Eberhart M, Hipler C, Schiefner J, Schubert K, Loncarevic IF, Wittig U, Baniahmad A, von Eggeling F. Int J Oncol. 2011 Sep Although the BCR-ABL tyrosine kinase inhibitor Imatinib has undoubtedly revolutionized the therapy of chronic … Continue reading →. ...
Degradation mechanisms of chemicals in sediment must be known in order to permit more accurate assessment of aquatic pollutants. One possible degradation mechanism -- abiotic transformation -- has received little attention, however. In this study, the abiotic transformation of para- substituted benzonitriles in an extract prepared by protein extraction from sediment was compared with that in raw sediment and in water.. In water, the benzonitriles were hydrolyzed to benzoic acid through benzamides at elevated temperature. In anaerobic river sediment, the benzonitriles were transformed to the corresponding benzoic acids, except for iodo- and methoxy-derivatives. In the sediment extract, the benzonitriles, including iodo- and methoxy-derivatives, were transformed to benzoic acids. Benzonitrile transformation did not produce benzamides as intermediates in the latter two media. Transformation in sediment and in sediment extract must have been mediated by an enzyme whose activity is similar to that of ...
The present invention of compounds of formula (I) ##STR00001## a stereochemically isomeric form thereof, an N-oxide form thereof or a pharmaceutically acceptable acid addition salt thereof. Processes for preparing said products, formulations comprising said products and their use as a medicine are disclosed, in particular for treating conditions which are related to impairment of gastric emptying.
Duncan DR, Chen PY, Patterson JT, Lee YU, Hibino N, Cleary M, Naito Y, Yi T, Gilliland T, Kurobe H, Church SN, Shinoka T, Fahmy TM, Simons M, Breuer CK. TGFßR1 inhibition blocks the formation of stenosis in tissue-engineered vascular grafts. J Am Coll Cardiol. 2015 Feb 10; 65(5):512-4 ...
Gouty arthritis is caused by the deposition of monosodium urate (MSU) crystals in joints. Despite many treatment options for gout, there is a substantial need for alternative treatments for patients unresponsive to current therapies. Tyrosine kinase inhibitors have demonstrated therapeutic benefit in experimental models of antibody-dependent arthritis and in rheumatoid arthritis in humans, but to date, the potential effects of such inhibitors on gouty arthritis has not been evaluated. Here we demonstrate that treatment with the tyrosine kinase inhibitor imatinib mesylate (imatinib) can suppress inflammation induced by injection of MSU crystals into subcutaneous air pouches or into the ankle joint of wild type mice. Moreover, imatinib treatment also largely abolished the lower levels of inflammation which developed in IL-1R1-/- or KitW-sh/W-sh mice, indicating that this drug can inhibit IL-1-independent pathways, as well as mast cell-independent pathways, contributing to pathology in this model. ...
TY - JOUR. T1 - Impact of rechallenge with imatinib in patients with advanced gastrointestinal stromal tumor after failure of imatinib and sunitinib. AU - Sawaki, Akira. AU - Kanda, Tatsuo. AU - Komatsu, Yoshito. AU - Nishida, Toshirou. PY - 2014. Y1 - 2014. N2 - Purpose. This retrospective, nonrandomized study investigated the effect of imatinib rechallenge plus best supportive care (BSC) on overall survival after imatinib and sunitinib treatment for patients with locally advanced or metastatic gastrointestinal stromal tumor (GIST). Methods. Twenty-six patients who had previously been exposed to both imatinib and sunitinib were enrolled in this study. The treatment regimen was BSC with or without imatinib, based on the patients choice after discussion with his or her physician. The primary endpoint was overall survival, and secondary endpoints were time to treatment failure, clinical response rate assessed by Choi criteria, and safety. Results. Fourteen patients were treated with imatinib plus ...
TY - JOUR. T1 - Phase II study of motesanib in Japanese patients with advanced gastrointestinal stromal tumors with prior exposure to imatinib mesylate. AU - Sawaki, Akira. AU - Yamada, Yasuhide. AU - Komatsu, Yoshito. AU - Kanda, Tatsuo. AU - Doi, Toshihiko. AU - Koseki, Masato. AU - Baba, Hideo. AU - Sun, Yu Nien. AU - Murakami, Koji. AU - Nishida, Toshirou. PY - 2010/4/1. Y1 - 2010/4/1. N2 - Purpose: Motesanib (AMG 706) is a multitargeted anticancer agent with an inhibitory action on the human vascular endothelial growth factor receptor, the platelet-derived growth factor receptor, and the cellular stem-cell factor receptor (KIT). The aim of this single-arm phase II clinical study was to assess the efficacy and safety of single-agent motesanib in Japanese patients with advanced gastrointestinal stromal tumors with prior exposure to imatinib mesylate. Methods: All patients had experienced progression or relapse while undergoing with imatinib as 400 mg/day or higher. The patients were ...
The added value of 2nd generation tyrosine kinase inhibitors (TKIs) is currently perhaps the most-discussed issue in chronic myeloid leukemia (CML) research and treatment. Therefore, with their recently published article Second-generation tyrosine kinase inhibitors improve the survival of patients with chronic myeloid leukemia in whom imatinib therapy has failed, Ibrahim et al.1 focussed on an important topic. However, in our opinion, the methodological approach used in this paper is not always appropriate.. The choice of the historical control group treated with interferon-alfa seems not to be optimal. Even before the imatinib era, progress had been made in the treatment of CML as the results of the consecutive German studies and of the French CML-study group show.2-4 We doubt that the results of the 20-year old MRC trial represent an appropriate comparator group for the results achieved by the use of 2nd generation tyrosine kinase inhibitors. Furthermore, the authors use two different ...
Imatinib mesylate (Gleevec, STI571) is a kinase inhibitor selective for Bcr-Abl, activated c-Kit kinases, and platelet-derived growth factor receptor tyrosine kinase. Imatinib mesylate, similar to many other tyrosine kinase inhibitors (TKIs), such as members of the 4-anilinoquinazoline class, competes for ATP binding. Previously, 4-anilinoquinazoline TKIs have been shown to inhibit the function of the breast cancer resistance-associated drug transporter (ABCG2), reversing resistance to camptothecin derivatives topotecan and SN-38. However, the potential to inhibit ABCG2 for the 2-phenylamino-pyrimidine class of TKIs, exemplified by imatinib mesylate, has not been examined. Here, we show that imatinib mesylate potently reverses ABCG2-mediated resistance to topotecan and SN-38 and significantly increases accumulation of topotecan only in cells expressing functional ABCG2. However, overexpression of ABCG2 does not confer resistance to imatinib mesylate. Furthermore, accumulation and efflux of ...
This trial will investigate the efficacy and tolerability of palbociclib in patients with advanced gastrointestinal stromal tumours refractory to imatinib and
Imatinib is a small molecule kinase inhibitor used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN). It is occasionally referred to as CGP57148B or STI571 (especially in older publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies. It is the first member of a new class of agents that act by inhibiting particular tyrosine kinase enzymes, instead of non-specifically inhibiting rapidly dividing cells ...
TY - JOUR. T1 - Chronic myeloid leukemia following therapy with imatinib mesylate (Gleevec). T2 - Bone marrow histopathology and correlation with genetic status. AU - Frater, John L.. AU - Tallman, Martin S.. AU - Variakojis, Daina. AU - Druker, Brian J.. AU - Resta, Debra. AU - Riley, Mary Beth. AU - Hrisinko, Mary Ann. AU - Peterson, Lo Ann C.. N1 - Copyright: Copyright 2018 Elsevier B.V., All rights reserved.. PY - 2003/6/1. Y1 - 2003/6/1. N2 - We evaluated bone marrow pathologic features and cytogenetic and molecular genetic status of 13 patients with interferon- resistant, chronic-phase chronic myeloid leukemia (CML), treated with imatinib mesylate (Gleevec). All had morphologic evidence of CML in the blood and bone marrow and were positive for bcr-abl by reverse transcriptase-polymerase chain reaction, fluorescence in situ hybridization (FISH), or both. Follow-up marrow biopsies, interphase FISH for bcr-abl, and conventional cytogenetics were performed at 3-month intervals (up to 24 ...
TY - JOUR. T1 - Tyrosine kinase inhibitor therapy can cure chronic myeloid leukemia without hitting leukemic stem cells. AU - Lenaerts, Tom. AU - Pacheco, Jorge M.. AU - Traulsen, Arne. AU - Dingli, David M. PY - 2010/6. Y1 - 2010/6. N2 - Background: Tyrosine kinase inhibitors, such as imatinib, are not considered curative for chronic myeloid leukemia - regardless of the significant reduction of disease burden during treatment - since they do not affect the leukemic stem cells. However, the stochastic nature of hematopoiesis and recent clinical observations suggest that this view must be revisited. Design and Methods: We studied the natural history of a large cohort of virtual patients with chronic myeloid leukemia under tyrosine kinase inhibitor therapy using a computational model of hematopoiesis and chronic myeloid leukemia that takes into account stochastic dynamics within the hematopoietic stem and early progenitor cell pool. Results: We found that in the overwhelming majority of patients ...
Targeted molecular agents are a landmark achievement in cancer treatment. In particular, the tyrosine kinase inhibitor imatinib mesylate targets mutant KIT prot...
The significance of molecular response depth is not well defined in patients with chronic phase chronic myeloid leukemia (CP-CML) under imatinib treatment. We retrospectively evaluated clinical records of 178 patients with CP-CML. Eighty-eight patients achieved complete molecular response during long term follow-up. Our results implicate that deeper molecular response is associated with improvement in disease outcome and a slight prolongation in progression-free survival. ...
Read about the report that tyrosine kinase inhibitors therapy is relatively safe for kidney function in chronic myeloid leukemia patients.
After 10 months of imatinib therapy, the patient was referred to our department owing to elevated aminotransferase level without any specific symptoms for several months. He denied any causal alcohol consumption or medication. His physical examination was normal. The laboratory tests revealed the following values: white blood cell count, 4,770/µL; eosinophil count, 467/µL (range, ,500/µL); hemoglobin, 13.8 g/µL; platelet count, 184 K/µL; total protein, 6.34 g/dL; albumin, g/dL, total bilirubin (TB), 1.59 mg/dL; direct bilirubin, 0.31 mg/dL; aspartate aminotransferase (AST), 239 IU/L; alanine aminotransferase (ALT), 393 IU/L; alkaline phosphatase, 194 IU/L (range, 30-120 IU/L); gamma glutamyl transferase, 52 IU/L (range, ,50 IU/L); blood urea nitrogen, 12 mg/dL; creatinine, 1 mg/dL; and international normalized ratio, 1.06. Serologic markers for viral hepatitis, including hepatitis A virus, hepatitis B virus, and hepatitis C virus, were negative. There was no evidence of acute viral ...
PURPOSE Imatinib mesylate is a targeted agent that may be used against Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL), one of the highest risk pediatric ALL groups. PATIENTS AND METHODS We evaluated whether imatinib (340 mg/m(2)/d) with an intensive chemotherapy regimen improved outcome in children ages 1 to 21 years with Ph+ ALL (N = 92) and compared toxicities to Ph- ALL patients (N = 65) given the same chemotherapy without imatinib. Exposure to imatinib was increased progressively in five patient cohorts that received imatinib from 42 (cohort 1; n = 7) to 280 continuous days (cohort 5; n = 50) before maintenance therapy. Patients with human leukocyte antigen (HLA) -identical sibling donors underwent blood and marrow transplantation (BMT) with imatinib given for 6 months following BMT. RESULTS Continuous imatinib exposure improved outcome in cohort 5 patients with a 3-year event-free survival (EFS) of 80% +/- 11% (95% CI, 64% to 90%), more than twice historical controls
The KIT-inhibitor imatinib mesylate (IM) has greatly improved the treatment of metastatic gastrointestinal stromal tumors (GIST). IM exhibits strong antiproliferative effects but fails to induce sufficient levels of apoptosis resulting in low pathologic complete remission rates and a high rate of secondary progression in the metastatic setting. Upregulation of p53 by MDM2 inhibitors has been shown to induce apoptosis in p53 wildtype tumors. Analyzing a series of 62 mostly untreated, localized and metastatic GIST we detected a low rate (3%) of inactivating p53 mutations, thus providing a rationale for further exploration of p53-directed therapeutic strategies. To this end, we studied nutlin-3, an inhibitor of the p53 antagonist MDM2, and RITA, a putative p53 activator, in GIST cell lines. Nutlin-3 effectively induced p53 at therapeutically relevant levels, which resulted in moderate antiproliferative effects and cell cycle arrest in p53 wildtype GIST cell lines GIST430, GIST48 and GIST48B. P53
TY - JOUR. T1 - A prospective, multicenter, phase 2 study of imatinib mesylate in Korean patients with metastatic or unresectable gastrointestinal stromal tumor. AU - Ryu, Min Hee. AU - Kang, Won Ki. AU - Bang, Yung Jue. AU - Lee, Kyung Hee. AU - Shin, Dong Bok. AU - Ryoo, Baek Yeol. AU - Roh, Jae Kyung. AU - Kang, Jin Hyoung. AU - Lee, Hyoungnam. AU - Kim, Tae Won. AU - Chang, Heung Moon. AU - Park, Joon Oh. AU - Park, Young Suk. AU - Kim, Taeyou. AU - Kim, Min Kyoung. AU - Lee, Woon Kee. AU - Kang, Hye Jin. AU - Kang, Yoon Koo. PY - 2009/4/1. Y1 - 2009/4/1. N2 - Objectives: This prospective, multicenter, phase 2 study evaluated the efficacy and safety of imatinib mesylate and assessed KIT and PDGFRA gene mutation status in Korean patients with gastrointestinal stromal tumors (GISTs). Methods: Forty-seven patients with pathologically proven KIT-positive metastatic or unresectable GISTs were accrued from eight institutions in Korea. Imatinib was administered orally at 400 mg once daily. In case ...
Currently available medicines in the BCR-ABL TKIs class of drugs include Gleevec and Iclusig, as well as Tasigna, Bosulif, and Sprycel.. These BCR-ABL tyrosine kinase inhibitors (TKIs) are used for the treatment of specific types of blood cancers, including Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML) and Ph+ acute lymphoblastic leukemia (ALL), and less commonly, other types of cancers.. In May 2016 Health Canada issued a safety warning, BCR-ABL Tyrosine Kinase Inhibitors [GLEEVEC (imatinib mesylate), TASIGNA (nilotinib), BOSULIF (bosutinib), SPRYCEL (dasatinib), ICLUSIG (ponatinib hydrochloride)] - Risk of Hepatitis B Reactivation, which did not receive much public attention in the US.. From that May 2016 Health Canada document, we get the following detailed safety information about these drugs:. ...
The DREAM complex in antitumor activity of imatinib mesylate in gastrointestinal stromal tumors. Curr Opin Oncol. 2014 Jul; 26(4):415-21 ...
TY - JOUR. T1 - Phase II, open-label, single-arm trial of imatinib mesylate in patients with metastatic melanoma harboring c-Kit mutation or amplification. AU - Guo, Jun. AU - Si, Lu. AU - Kong, Yan. AU - Flaherty, Keith T.. AU - Xu, Xiaowei. AU - Zhu, Yanyan. AU - Corless, Christopher L.. AU - Li, Li. AU - Li, Haifu. AU - Sheng, Xinan. AU - Cui, Chuanliang. AU - Chi, Zhihong. AU - Li, Siming. AU - Han, Mei. AU - Mao, Lili. AU - Lin, Xuede. AU - Du, Nan. AU - Zhang, Xiaoshi. AU - Li, Junling. AU - Wang, Baocheng. AU - Qin, Shukui. N1 - Copyright: Copyright 2011 Elsevier B.V., All rights reserved.. PY - 2011/7/20. Y1 - 2011/7/20. N2 - Purpose: Melanomas harbor aberrations in the c-Kit gene. We tested the efficiency of the tyrosine kinase inhibitor imatinib in selected patients with metastatic melanoma harboring c-Kit mutations or amplifications. Patients and Methods: Forty-three patients with metastatic melanoma harboring c-Kit aberrations were enrolled on this phase II trial. Each patient ...
The FDA has approved bosutinib (Bosulif) to treat chronic myelogenous leukemia (CML). The drug is intended for patients with chronic, accelerated, or blast phase Philadelphia chromosome-positive CML who are resistant to or who cannot tolerate other therapies, including imatinib (Gleevec).. The safety and effectiveness of Bosulif was evaluated in a single clinical trial that enrolled 546 adult patients with chronic, accelerated, or blast phase CML. All patients had disease that progressed after treatment with imatinib or imatinib followed by dasatinib (Sprycel) and/or nilotinib (Tasigna), or who could not tolerate the side effects of prior therapy.. Results showed 34% of patients with chronic phase CML who had been previously treated with imatinib achieved a major cytogenetic response after 24 weeks. Of the patients who achieved a major cytogenetic response at any time, 52.8% had their response last at least 18 months. Among patients previously treated with imatinib followed by dasatinib and/or ...
For hematologic toxicity, treatment should be withheld for an absolute neutrophil count , 1,000 × 106/L or platelets , 50,000 × 106/L until levels increase above these thresholds. Treatment can be resumed at the same dose if recovery occurs within 2 weeks and at a dose reduced by 100 mg if recovery takes , 2 weeks. If cytopenia recurs, the dose should be reduced by an additional 100 mg when restarting treatment after recovery.. Concomitant use of bosutinib with strong CYP3A inhibitors (eg, ketoconazole, itraconazole, clarithromycin), moderate CYP3A inhibitors (eg, erythromycin, fluconazole, diltiazem), or strong CYP3A inducers (eg, rifampin, carbamazepine, phenytoin) should be avoided. Short-acting antacids or H2 blockers should be used as an alternative to proton pump inhibitors.. Safety Profile IN THE TOTAL population of the phase III trial, the most common adverse events of any grade in the bosutinib group were diarrhea (70% vs 34% in imatinib group), nausea (35% vs 38%), thrombocytopenia ...
The development of Imatinib Mesylate (IM), the first specific inhibitor of BCR-ABL1, has had a major impact in patients with Chronic Myeloid Leukemia (CML), establishing IM as the standard therapy for CML.. Despite the clinical success obtained with the use of IM, primary resistance to IM and molecular evidence of persistent disease has been observed in 20-25% of IM treated patients. The existence of second generation TK inhibitors, which are effective in patients with IM resistance, makes identification of predictors of resistance to IM an important goal in CML.. In this study, we have identified a group of 19 miRNAs that may predict clinical resistance to IM in patients with newly diagnosed CML.. CITATION Mol Cancer. 2009 Sep 1;8:69. ...
This work presents the synthesis and spectroscopic characterization of novel methoxy and hydroxy derivates of amidino substituted benzimidazoles and benzamides. Novel compounds were prepared by classical reactions of organic chemistry. Hydroxy derivates of amidino substituted benzimidazoles 13-18 were prepared by the condensation reaction from 4-amidino substituted 1,2-phenylenediamine hydrochlorides 8 and 9 with aromatic aldehydes. In the condensation of corresponding methoxy substituted benzoyl-chlorides 19-21 with p-cyanoaniline methoxy substituted N-(4-cyanophenyl)benzamides 26-28 were prepared. Hydroxy substituted benzamide derivates 29-31 were prepared removing methoxy protection groups using reagents BCl3 and BBr3. Amidino substituted benzamide derivates 33-36 were prepared in the acidic Pinner reaction from the corresponding cyano substituted benzamides 29-30. The Pinner reaction was monitored with IR spectroscopy while the structures of all newly prepared compounds were confirmed by ...
Clinical trial for Chronic myeloid leukemia , Nilotinib Treatment-free Remission Study in CML (Chronic Myeloid Leukemia) Patients
The long-term outcome of imatinib treatment for metastatic GIST has emerged from several large trials. Approximately 45% of patients with metastatic GIST have a measurable response after administration of imatinib, whereas ∼30% will have at least stable disease (15). Although the 2-year survival of patients with metastatic GIST treated with imatinib approximates 72%, half of the patients develop disease progression by 2 years (3). Other investigators (1, 2), with follow-up periods between 24 and 40 weeks, have reported similar rates of progression and resistance to imatinib therapy. In only a minority of cases, patients are insensitive to the drug, a so-called primary resistance.. Most of the above studies have defined clinical response based on imaging methods using the Response Evaluation Criteria in Solid Tumors for solid tumor response to therapy. Few studies have correlated the clinical response with the pathologic response of the tumor. Scaife et al. (16) compared the radiologic and ...
Imatinib mesylate is currently the drug of choice to treat chronic myeloid leukemia. However, patient resistance and cytotoxicity make secondary lines of treatment, such as omacetaxine mepesuccinate, a necessity. Given that drug cytotoxicity represents a major problem during treatment, it is essential to understand the biological pathways affected to better predict poor drug response and prioritize a treatment regime. We conducted cell viability and gene expression assays to determine heritability and gene expression changes associated with imatinib and omacetaxine treatment of 55 non-cancerous lymphoblastoid cell lines, derived from 17 pedigrees. In total, 48,803 transcripts derived from Illumina Human WG-6 BeadChips were analyzed for each sample using SOLAR, whilst correcting for kinship structure. Cytotoxicity within cell lines was highly heritable following imatinib treatment (h2 = 0.60-0.73), but not omacetaxine treatment. Cell lines treated with an IC20 dose of imatinib or omacetaxine showed
Currently available medicines in the BCR-ABL TKIs class of drugs include Gleevec and Iclusig, as well as Tasigna, Bosulif, and Sprycel.. These BCR-ABL tyrosine kinase inhibitors (TKIs) are used for the treatment of specific types of blood cancers, including Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML) and Ph+ acute lymphoblastic leukemia (ALL), and less commonly, other types of cancers.. In May 2016 Health Canada issued a safety warning, BCR-ABL Tyrosine Kinase Inhibitors [GLEEVEC (imatinib mesylate), TASIGNA (nilotinib), BOSULIF (bosutinib), SPRYCEL (dasatinib), ICLUSIG (ponatinib hydrochloride)] - Risk of Hepatitis B Reactivation, which did not receive much public attention in the US.. From that May 2016 Health Canada document, we get the following detailed safety information about these drugs:. ...
Background Tyrosine kinase inhibitors have been shown to have marked clinical efficacy in patients with unresectable or metastatic gastrointestinal stromal tumors (GIST). We performed a comparative...
53 NCCN Guidelines for Patients ® : Chronic Myeloid Leukemia, 2018 Acronyms Acronyms ALL acute lymphoblastic leukemia AML acute myeloid leukemia CAM complementary and alternative medicine CBC complete blood count CCyR complete cytogenetic response CBC complete blood count CML chronic myeloid leukemia CMR complete molecular response DLI donor lymphocyte infusion DNA deoxyribonucleic acid EMR early molecular response FDA Food and Drug Administration FISH fluorescence in situ hybridization GVL graft-versus-leukemia HCT hematopoietic cell transplant HLA human leukocyte antigen IS International Scale NCCN National Comprehensive Cancer Network MMR major molecular response MPN myeloproliferative neoplasm QPCR quantitative reverse transcriptase-polymerase chain reaction TKI tyrosine kinase inhibitor ...
Kronik myeloid l semi tedavisinde kullan lan imatinib mesilat ayn zamanda k k h cre fakt r n de inhibe etmektedir. Imatinib mesilat n baz polistemia veral hastalarda otonom eritroid koloni geli imini inhibe etti i ve flebotomi ihtiyac n azaltt da g sterilmi tir. Bu al mada, imatinib mesilat varl nda, polistemia veral hasta ile sa l kl d rt kontrolden elde edilen periferik kan eritroid nc l h creleri zerine yar -kat ortamda ins lin benzeri b y me fakt r -l (IGF-l), k k h cre fakt r (SCF) ve eritropoietin (EPO) ile interl kin-3 (IL-3), gran losit-koloni stimule edici fakt r n (GM-CSF) ve gran losit-koloni stimule edici fakt r n n (G-CSF) etkisi ara t r ld . Sa l kl kontrollerden elde edilen hematopoietik nc h crelerden eritroid koloni geli imi sadece t m sitokinlerin varl nda g zlendi. Bununla birlikte eritroid kolonilerin say s polistemia veral hastalardan elde edilen say lara ula amad . Imatinib mesilat n eritroid koloni geli imi zerindeki inhibe edici etkisi belirgindi. Polistemia veral ...
The long-term analysis, completed in 2005, continues to demonstrate promising results. Eighty-four percent of the 147 GIST study participants on Gleevec showed clinical improvement during the study period, meaning that their disease stabilized or went into remission. Two of those experienced complete remission. However, some subjects developed resistance to the drug and some experienced a relapse of their cancer ...
The so-called Philadelphia (Ph) chromosome is present in more than 90% of chronic myeloid leukemia (CML) cases. It results in juxtaposition of the 5′ part of the BCR gene on chromosome 22 to the 3′ part of the ABL gene on chromosome 9. Since the majority of CML cases are currently treated with Imatinib, variant rearrangements in general have no specific prognostic significance, although the mechanisms involved in resistance to therapy have yet to be investigated. The T315I mutation within the abl-gene is the most frequent one associated with resistance to tyrosine kinase inhibitors. This study evaluated a Ph chromosome positive CML case resistant to imatinib mesylate. A dic(17;18), loss of TP53 gene, co-expression of b2a2 and b3a2 fusions transcript and a T315I mutation were found. We reported here a novel case of a Ph chromosome positive CML with a secondary abnormality [dic(17;18)], resulting to Glivec resistance but good response to nilotinib. The dic(17;18) might be a marker for poor prognosis
... cytotoxic benzamides from Streptomyces sp. DGC1". The Journal of Antibiotics. 65 (12): 615-22. doi:10.1038/ja.2012.81. PMC ...
A derivative of benzamide, tiapride is chemically and functionally similar to other benzamide antipsychotics such as sulpiride ... Benzamide and its derivatives are highly water-soluble, and because of their polarity are believed to cross the blood-brain ... Härtter S, Hüwel S, Lohmann T, Abou El Ela A, Langguth P, Hiemke C, Galla HJ (November 2003). "How does the benzamide ... Bischoff S, Bittiger H, Delini-Stula A, Ortmann R (April 1982). "Septo-hippocampal system: target for substituted benzamides". ...
Jacob Szmuszkovicz (4 July 1978). "Patent US4098904 - Analgesic N-(2-aminocycloaliphatic)benzamides". The Upjohn Company. Hayes ... benzamides at the primary morphine receptor". Journal of Medicinal Chemistry. 28 (12): 1853-64. doi:10.1021/jm00150a017. PMID ...
... benzamides". Cheney BV, Szmuszkovicz J, Lahti RA, Zichi DA (December 1985). "Factors affecting binding of trans-N-[2-( ... 2-Diaminocyclohexane Benzamide Series". Heterocycles. 52 (1): 325-332. doi:10.3987/com-99-s27. Loew G, Lawson J, Toll L, ... benzamides as water diuretic drugs". Casy AF, Parfitt RT (1986). Miscellaneous Groups of Analgesics. Opioid Analgesics. ... methylamino)cyclohexyl]benzamides at the primary morphine receptor". Journal of Medicinal Chemistry. 28 (12): 1853-64. doi: ...
Mukherjee J, Yang ZY, Das MK, Brown T (April 1995). "Fluorinated benzamide neuroleptics--III. Development of (S)-N-[(1-allyl-2- ...
This work led on from an earlier series of sulfamoyl benzamide derivatives for which a patent was filed in 2004. The quinolin-8 ... May 2008). "Sulfamoyl benzamides as novel CB2 cannabinoid receptor ligands". Bioorganic & Medicinal Chemistry Letters. 18 (9): ... US application 7297796, Roland E. Dolle, Karin Worm, Q. Jean Zhou, "Sulfamoyl benzamide derivatives and methods of their use", ... January 2010). "Novel sulfamoyl benzamides as selective CB(2) agonists with improved in vitro metabolic stability". Bioorganic ...
... is a benzamide. It is an off-white powder and has the chemical formula C7H8N2O. 3-Aminobenzamide can be ...
... is a substituted benzamide; cisapride and mosapride are structurally related. Metoclopramide was first described ...
It is structurally related to metoclopramide and other benzamides. Ballatori E, Roila F (September 2003). "Impact of nausea and ...
In Bulgaria and other countries of East Europe itopride (50 mg) is sold by Zentiva under the brand name Zirid Benzamides " ... Itopride belongs to the same benzamide group as cisapride, a drug found to affect QT interval and possibly predispose those ... Moreover, itopride has no affinity for the 5-HT4 receptors, unlike other benzamides such as cisapride and mosapride, which are ... Itopride (INN) (brand name Ganaton) is a prokinetic benzamide derivative. These drugs inhibit dopamine and acetylcholine ...
Analgesic potency and acute toxicity of substituted anilides and benzamides. Toxicology and Applied Pharmacology 1971;19(1):20- ...
"2-Phenylpyrroles as conformationally restricted benzamide analogues. A new class of potential antipsychotics. 1". Journal of ...
It reacts with amines to afford N-substituted benzamides after hydrolysis. It is a precursor to Diphenylketimine Ph 2C=NH (b.p ... 3 H 2O In the laboratory it can be prepared by the dehydration of benzamide or by the Rosenmund-von Braun reaction using ...
... and the benzamides : entinostat (MS-275), tacedinaline (CI994), and mocetinostat (MGCD0103). The sirtuin Class III HDACs are ... benzamides, electrophilic ketones, and the aliphatic acid compounds such as phenylbutyrate and valproic acid. "Second- ... "Distinct pharmacological properties of second generation HDAC inhibitors with the benzamide or hydroxamate head group". ...
... benzamides, CP339818, progesterone and the anti-lepromatous drug clofazimine). The Kv1.3 blocker clofazimine has been reported ... "Benzamide derivatives as blockers of Kv1.3 ion channel". Bioorganic & Medicinal Chemistry Letters. 13 (6): 1161-4. doi:10.1016/ ...
Typical antipsychotic Benzamide Carranza-Lira S (September 2010). "Actual status of veralipride use". Clinical Interventions in ... Veralipride (Agreal, Agradil) is a benzamide neuroleptic medicine indicated in the treatment of vasomotor symptoms associated ...
The resulting imidic acid tautomerizes to the benzamide. The compound acts as a strong oxidizing agent and can cause skin ...
... , sold under the brand name Neoprad is a substituted benzamide antipsychotic, reported to be a selective ... Other benzamide derivatives include metoclopramide, tiapride, and sultopride. "Levosulpiride - S-(-)-Sulpiride". Generon. ... Sulpiride is a substituted benzamide derivative and a selective dopamine D2 antagonist with antipsychotic and antidepressant ...
Valsborg, J.; Sorensen, L.; Foged, C. (2001). "Organoiridium catalysed hydrogen isotope exchange of benzamide derivatives". ...
The founding case of fibrous vs rhombic benzamide illustrates the case. Another example is provided by two polymorphs of ... Present-day analysis identifies three polymorphs for benzamide: the least stable one, formed by flash cooling is the ... Thun, Jürgen (2007). "Polymorphism in Benzamide: Solving a 175-Year-Old Riddle". Angewandte Chemie International Edition. 46 ( ... They observed that the silky needles of freshly crystallized benzamide slowly converted to rhombic crystals. ...
... is a substituted benzamide, closely related to metoclopramide. It is identical to metoclopramide except for the ...
... as well as related benzamides LY-344,864 (N-[(3R)-3-(Dimethylamino)-2,3,4,9-tetrahydro-1H-carbazol-6-yl]-4-fluorobenzamide) ... synthesis and evaluation of bicyclic benzamides as novel 5-HT1F receptor agonists". Bioorganic & Medicinal Chemistry Letters. ...
Another key identifying feature is its ability to split benzamide. M. hassiacum can also split urea, nicotinamide, and ...
Chemically, it is a substituted benzamide, closely related to metoclopramide. A small Spanish study found that more adverse ...
Kuş C, Özer E, Korkmaz Y, Yurtcu E, Dağalp R (2018). "Benzamide and Benzamidine Compounds as New Inhibitors of Urokinasetype ...
Benzamide Gastroprokinetic agent Robert M, Salvà M, Segarra R, et al. (July 2007). "The prokinetic cinitapride has no ... Cinitapride (trade names Cintapro, Pemix) is a gastroprokinetic agent and antiemetic agent of the benzamide class which is ...
Dose M, Lange HW (January 2000). "The benzamide tiapride: treatment of extrapyramidal motor and other clinical syndromes". ...
"Discovery and structure-activity relationship of quinuclidine benzamides as agonists of alpha7 nicotinic acetylcholine ...
Based Group 9 Metal-Catalyzed Direct C-H Amination of Benzamides". Organometallics. 33 (15): 4076-4085. doi:10.1021/om5005868 ...
Benzamide is a white solid with the chemical formula of C6H5C(O)NH2. It is the simplest amide derivative of benzoic acid. It is ... A number of substituted benzamides are commercial drugs: sulpiride, remoxipride, amisulpride, tiapride, sultopride, veralipride ... aminohippuric acid, cisapride, imatinib, and procainamide ATC code N05AL Benzamides Nomenclature of Organic Chemistry : IUPAC ...
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Benzamide derivatives as thrombin inhibitors. WO1997036580A1. Mar 27, 1997. Oct 9, 1997. 3-Dimensional Pharmaceuticals, Inc.. ... The present invention is directed to a novel class of benzamide and sulfonamide derivatives having Formula I: ... Benzamide and sulfonamide substituted aminoguanidines and alkoxyguanidines as protease inhibitors. US 6344486 B1 ... Benzamide and sulfonamide substituted aminoguanidines and alkoxyguanidines as protease inhibitors. ...
... benzamides and derivatives thereof, said compounds being used as stimulators of the motility of the gastro-intestinal system. ... Benzamide derivatives. US9771348. Jul 11, 2014. Sep 26, 2017. Dong-A St Co., Ltd. Method for preparing benzamide derivative, ... Novel benzamide derivatives. WO2015012515A1. Jul 11, 2014. Jan 29, 2015. 돜아엔슞티 죿신횊삪. Method for preparing benzamide derivative ... benzamide. The mother-liquor was evaporated, yielding 70 parts of cis-N-[3-(phenylmethoxy)-4-piperidinyl]benzamide as an oily ...
Aromatic polyimides are distinguished as high performance polymers owing to excellent thermal, mechanical, and chemical properties (Yang et al., 1999, More et al., 2010). They are not only used as beneficial substitutes for metals or ceramics in presently used goods but also as new materials in novel technological applications (Litvinov et al., 2010). Nevertheless, infusibility and insolubility are some of the shortcomings due to the highly regular and rigid polymer backbones and the formation of intermolecular hydrogen bonding, causing deterioration in processability and applications (Sheng et al., 2009, Choi et al., 1992). In order to improve upon these drawbacks, recent research has aimed at improving their processability and solubility without an intense loss in the chemical, thermal, and mechanical properties. For this, improvement of solubility is targeted through diminishing the cohesive energy by lowering the interchain interactions. To achieve this, designing and synthesizing new ...
... benzamide; find Sigma-Aldrich-ALD01832 MSDS, related peer-reviewed papers, technical documents, similar products & more at ...
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice ...
High impact information on benzamide. *Changes in the phenylcarboxamide side chain or in C-methylation in the linking chain had ... Analytical, diagnostic and therapeutic context of benzamide. *Moreover, use of the traditional cell labels BrdU and BBZ may ... and bis benzamide (BBZ) prior to transplantation into the adult hippocampus or striatum [2]. ...
Benzamides , Antipsychotics , Psycholeptics Brokerage service for pharmaceutical and parapharmaceutical products active ...
Two series of benzamides compounds bearing piperidine groups were synthesized and the Gli-luc luciferase activity was screened ... Keywords: benzamide; hedgehog signaling; Gli-luc luciferase activity benzamide; hedgehog signaling; Gli-luc luciferase activity ... Ding H, Chen K, Song B, Deng C, Li W, Niu L, Bai M, Song H, Zhang L. Synthesis and Smo Activity of Some Novel Benzamide ... Two series of benzamides compounds bearing piperidine groups were synthesized and the Gli-luc luciferase activity was screened ...
In connection with on-going studies into N-substituted benzamides (Saeed et al., 2011a,b), we recently determined the crystal ... For background to the biological activity of N-substituted benzamides, their use in synthesis and for related structures, see: ... For background to the biological activity of N-substituted benzamides, their use in synthesis and for related structures, see: ... structure of 3,5-dinitro-N-(1,3-thiazol-2-yl)-benzamide monohydrate (Saeed et al., 2011a). In this paper we present the crystal ...
... benzamide hydrochloride; CAS Number: 1193389-02-4; find Enamine-ENA238712780 MSDS, related peer-reviewed papers, technical ...
Benzamide, N-[2-(2-pyridinylcarbonyl)phenyl] / Benzamide, N-[2-(2-pyridinylcarbonyl)phenyl] / 91025-05-7 ... Benzamide, N-[2-(2-piridinilcarbonil)fenil]. CAS names 1 IUPAC names 2 Trade names 1 Other identifiers 1 ...
Mentions de prudence: P261-P264b-P271-P280-P302+P352-P304+P340-P305+P351+P338-P312-P332+P313-P337+P313-P362-P501c Avoid breathing dust/fume/gas/mist/vapours/spray. Wash face, hands and any exposed skin thoroughly after handling Use only outdoors or in a well-ventilated area. Wear protective gloves/protective clothing/eye protection/face protection. IF ON SKIN: Wash with plenty of soap and water. IF INHALED: Remove to fresh air and keep at rest in a position comfortable for breathing. IF IN EYES: Rinse cautiously with water for several minutes. Remove contact lenses, if present and easy to do. Continue rinsing. Call a POISON CENTER or doctor/physician if you feel unwell. If skin irritation occurs: Get medical advice/attention. If eye irritation persists: Take off contaminated clothing and wash before reuse. Dispose of contents/ container to an approved waste disposal plant ...
... is a benzamides (CHEBI: ... CHEBI:94373 - 4-amino-5-chloro-2-ethoxy-N-[[4-[(4-fluorophenyl)methyl]-2-morpholinyl]methyl]benzamide. Main. ChEBI Ontology. ... 4-amino-5-chloro-2-ethoxy-N-[[4-[(4-fluorophenyl)methyl]-2-morpholinyl]methyl]benzamide. ...
N-(4-aminobiphenyl-3-yl)benzamide. C19 H16 N2 O. ZWLFHHHQRUYIBT-UHFFFAOYSA-N. Ligand Interaction. ... Exploration of the HDAC2 foot pocket: Synthesis and SAR of substituted N-(2-aminophenyl)benzamides.. Bressi, J.C., Jennings, A. ... A series of N-(2-amino-5-substituted phenyl)benzamides (3-21) were designed, synthesized and evaluated for their inhibition of ... A series of N-(2-amino-5-substituted phenyl)benzamides (3-21) were designed, synthesized and evaluated for their inhibition of ...
These are compounds containing a benzamide moiety that is N-linked to a benzyl group.. Kingdom. Organic compounds. Super Class ... N-(2-Flouro-Benzyl)-4-Sulfamoyl-Benzamide. Accession Number. DB02069 (EXPT01497) Type. Small Molecule. Groups. Experimental. ...
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N-(Morpholin-4-ylmethyl)benzamide (1) [11, 12]. Benzamide (0.001 M) was dissolved in ethanol. To this morpholine (0.001 M) and ... N-(Piperazine-1-ylmethyl)benzamide (2) [13]. Benzamide (0.001 M) was dissolved in ethanol. To this piperazine (0.001 M) and ( ... N-Phenyl-aminomethyl-benzamide (4). Benzamide (0.001 M) was dissolved in ethanol. To this aniline (0.001 M) and (0.015 M) ... N-[(4-Bromo-phenylamino)-methyl]-benzamide (3). Benzamide (0.001 M) was dissolved in ethanol. To this 4-bromoaniline (0.001 M) ...
4-(AMINOSULFONYL)-N-[(4-FLUOROPHENYL)METHYL]-BENZAMIDE. C14 H13 F N2 O3 S. IXDVPACDZDRCTN-UHFFFAOYSA-N. Ligand Interaction. ... CARBONIC ANHYDRASE II (F131V) COMPLEXED WITH 4-(AMINOSULFONYL)-N-[(4-FLUOROPHENYL)METHYL]-BENZAMIDE. *DOI: 10.2210/pdb1I9L/pdb ...
Here we show that the benzamide derivative N-[2-(4-cyclopropanecarbonyl-3-methyl-piperazin-1-yl)-1-(tert-butyl-1H-indol-3-yl- ... Identification of a Benzamide Derivative that Inhibits Stress-Induced Adrenal Corticosteroid Synthesis. Jing Xu 1. ... Here we show that the benzamide derivative N-[2-(4-cyclopropanecarbonyl-3-methyl-piperazin-1-yl)-1-(tert-butyl-1H-indol-3-yl- ... "Identification of a Benzamide Derivative that Inhibits Stress-Induced Adrenal Corticosteroid Synthesis." Molecules 14, no. 9: ...
Methoxylated benzamides and 2-aryl-2-oxazolines are important intermediates in the synthesis of natural products which possess ... The following procedure illustrates the general method used for preparation of benzamides (3a,b) and 2-aryl-2-oxazolines (4a,b ... The introduction of a methoxyl group in the aromatic ring, decreased the degree of conversion of benzamide to oxazoline [23]. ... The control of the power applied and the reaction time allowed adequate conditions for preferential formation of benzamides and ...
... benzamide , C17H24N2O4S , CID 1119029 - structure, chemical names, physical and chemical properties, classification, patents, ...
"Benzamides" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... This graph shows the total number of publications written about "Benzamides" by people in this website by year, and whether " ... Below are the most recent publications written about "Benzamides" by people in Profiles. ...
Benzamide. Description. Benzamide is an intermediate in the Benzoate degradation via CoA ligation. Benzamides are a class of ... Showing metabocard for Benzamide (HMDB0004461). IdentificationTaxonomyOntologyPhysical propertiesSpectraBiological properties ... Chiba R, Ogasawara A, Kubo T, Yamazaki H, Umino M, Ishizuka Y: Direct determination of benzamides in serum by column-switching ... This compound belongs to the class of organic compounds known as benzamides. These are organic compounds containing a ...
Histone deacetylase inhibitors FK228, N-(2-aminophenyl)-4-[N-(pyridin-3-yl-methoxycarbonyl)amino- methyl]benzamide and m- ...
  • 5. A compound according to claim 1 wherein the compound is cis-4-amino-5-chloro-2-methoxy-N-[3-methoxy-1-pyridinylmethyl)-4-piperidinyl]benzamide. (google.com)
  • 10. The pharmaceutical composition of claim 6 wherein the compound is cis-4-amino-5-chloro-2-methoxy-N-[3-methoxy-1-(2-pyridinylmethyl)-4-piperidinyl]benzamide. (google.com)
  • A series of N-(2-amino-5-substituted phenyl)benzamides (3-21) were designed, synthesized and evaluated for their inhibition of HDAC2 and their cytotoxicity in HCT116 cancer cells. (rcsb.org)
  • Histone deacetylase inhibitors FK228, N-(2-aminophenyl)-4-[N-(pyridin-3-yl-methoxycarbonyl)amino- methyl]benzamide and m-carboxycinnamic acid bis-h. (nih.gov)
  • Histone deacetylase inhibitors FK228, N-(2-aminophenyl)-4-[N-(pyridin-3-yl-methoxycarbonyl)amino- methyl]benzamide and m-carboxycinnamic acid bis-hydroxamide augment radiation-induced cell death in gastrointestinal adenocarcinoma cells. (nih.gov)
  • The compounds 1 treatment with amino benzyl amine and amino benzamide in boiling benzene or toluene gave the corresponding pyrazole-3-carboxamides 6,7 as main products. (thefreedictionary.com)
  • In this study, we used biochemical enzyme assays and a cellular target biomarker assay to define PF-4950834 [ N- methyl-3-{[(4-pyridin-4-ylbenzoyl)amino]methyl}benzamide] as an ATP-competitive, selective Rho kinase inhibitor. (aspetjournals.org)
  • Novel N-(3-hydroxy-4-pipridinyl)benzamides and derivatives thereof, said compounds being used as stimulators of the motility of the gastro-intestinal system. (google.com)
  • Two series of benzamides compounds bearing piperidine groups were synthesized and the Gli-luc luciferase activity was screened by Gys-luc luciferase gene detection method. (mdpi.com)
  • These are compounds containing a benzamide moiety that is N-linked to a benzyl group. (drugbank.ca)
  • Benzamides are a class of chemical compounds derived from Benzamid, the carbonic acid amide of benzoic acid. (hmdb.ca)
  • This compound belongs to the class of organic compounds known as benzamides. (hmdb.ca)
  • The aromatic compounds used were 4-nitrophenol, 2aminobenzoic acid, benzamide , 4-aminobenzoic acid, resorcinol, o-bromonitrobenzene and 2-nitroaniline as coupling partners (Scheme I and II). (thefreedictionary.com)
  • 5 wt% triglycidyl isocyanurate in the presence of catalytically acting amines or salts [28], and a variety of N,N-diglycidyl substituted benzamide , aniline, diimide or imidazolone compounds [29]. (thefreedictionary.com)
  • 7. Synthesis and antidopaminergic properties of the atypical highly potent (S)-5-bromo-2,3-dimethoxy-N-[(1-ethyl-2pyrrolidinyl)methyl]benzamide and related compounds. (springer.com)
  • Control of neurodegenerative diseases with benzothiazole-benzamide derivatives CSIC has developed a group of heterocyclic compounds derived from a privileged structural nucleus with the capacity to inhibit the LRRK2 enzyme. (innoget.com)
  • The clinical development of FtsZ-targeting benzamide compounds like PC190723 has been limited by poor drug-like and pharmacokinetic properties. (asm.org)
  • 60/570,669, entitled " Substituted N-Aryl Benzamides and Related Compounds for Treatment of Amyloid Diseases and Synucleinopathies" to Snow et al. (allindianpatents.com)
  • filed May 12, 2004 and 60/629,525, entitled " Substituted N-Aryl Benzamides and Related Compounds for Treatment of Amyloid Diseases and Synuoleinopathies" to Snow et al, filed November 18, 2004. (allindianpatents.com)
  • Provided herein are substituted N-aryl benzamides and related compounds, pharmaceutical compositions and methods for treatment of amyloid diseases, including beta-amyloid protein (Aβ), such as observed in Alzheimer's disease and Down's syndrome, islet amyloid polypeptide (IAPP), such as observed in type 2 diabetes, and alpha-synuclein, such as observed in Parkinson's disease. (allindianpatents.com)
  • The present invention includes compound compositions and methods of making compounds that include an oligo-benzamide compound having at least two optionally substituted benzamides. (patentsencyclopedia.com)
  • We provide independent and unbiased information on manufacturers, prices, production news and consumers for the global and regional (North America, Asia and Europe) market of N-[4-bromo-2-(2-pyridylcarbonyl)phenyl]benzamide. (reportsnreports.com)
  • Xu J, Lecanu L, Tan M, Greeson J, Papadopoulos V. Identification of a Benzamide Derivative that Inhibits Stress-Induced Adrenal Corticosteroid Synthesis. (mdpi.com)
  • This paper presents a simple, rapid and efficient green synthesis of aryl methoxylated benzamides and 2-oxazolines from renewable Eucalyptus biomass - tar derivatives. (degruyter.com)
  • However, benzamide did not affect DNA and RNA syntheses except for one period: 24 to 30 h after the start of culture, RNA synthesis was stimulated. (biologists.org)
  • Phosphazene Superbase-mediated Regio- and Stereoselective Iodoaminocyclization of 2-(1-Alkynyl)benzamides for the Synthesis of Isoindolin-1-ones. (bioportfolio.com)
  • N-(3-Guanidino-4-methylphenyl)-4-(methylpiperazine-1-yl-methyl)benzamide Dihydrochloride is a compound useful in organic synthesis. (trc-canada.com)
  • Chemical derivatives of benzamide are used in a wide range of therapeutics including analgesics (e.g., salicylamide), antiemetics (e.g., metoclopramide), antipsychotics (e.g., sultopride) and other agents. (thefreedictionary.com)
  • Differentiation of MDA-MB468 breast cancer cells is induced by benzamide and hydroxamate analogs. (nih.gov)
  • We conclude that despite a different HDAC isoenzyme inhibition profile, hydroxamate and benzamide analogs as studied display similar cellular profiles. (nih.gov)
  • D.O. Kiesewetter, R. Kawai, M. Chelliah, E. Owens, C. Mclellan and R.G. Blasberg: Preparation and biological evaluation of 18F-labeled benzamide analogs as potential dopamine D2 receptor ligands, Nucl Med Biol 17: 347-356 (1990). (springer.com)
  • Remoxipride (Figure 1), a substituted benzamide analog of sulpiride, was developed as a potential antipsychotic agent on the assumption that the poor bioavailability of sulpiride was due to hydrolysis of the amide bond. (springer.com)
  • Trabucchi, M. / Sulpiride and other benzamides as specific antagonists at the D2 dopamine receptor . (elsevier.com)
  • The structure-affinity correlations of a series of benzamides for dopamine D 2 receptor imaging agents have been studied with SYBYL 6.4 software on SGI O 2 workstation. (pku.edu.cn)
  • This study aimed at comparing the pharmacological properties of selected second generation HDAC inhibitors with the hydroxamate and benzamide head group, namely SAHA, LAQ824/LBH589, CI994, MS275 and MGCD0103. (nih.gov)
  • The present invention provides a more efficient industrial method for producing a pyrazol-3-yl-benzamide derivative expressed by a formula useful as medicine: ##STR00001## wherein R 2 , R 3 and R 4 each independently represent a lower alkyl group. (patentsencyclopedia.com)
  • [0001] The present invention relates to a more efficient and new production method for a pyrazol-3-yl-benzamide derivative useful as medical products. (patentsencyclopedia.com)
  • Further, it also relates to an intermediate for producing the pyrazol-3-yl-benzamide derivative efficiently. (patentsencyclopedia.com)
  • And it relates to crystalline of pyrazol-3-yl-benzamide derivative which is useful as medicine. (patentsencyclopedia.com)
  • An efficient strategy for the oxidative carbonylation of benzamides via C-H/N-H activation to form phthalimides has been developed. (princeton.edu)
  • Du, Y, Hyster, TK & Rovis, T 2011, ' Rhodium-catalyzed oxidative carbonylation of benzamides with CO under mild conditions ', ACS National Meeting Book of Abstracts . (princeton.edu)
  • The oxidative cycloaddition of benzamides and alkynes has been developed. (princeton.edu)
  • Hyster, TK & Rovis, T 2010, ' Rhodium-catalyzed oxidative cycloaddition of benzamides and alkynes via C-H/N-H activation ', Journal of the American Chemical Society , vol. 132, no. 30, pp. 10565-10569. (princeton.edu)
  • In contrast, the benzamides CI994, MS275 and MGCD0103 are more selective, potent inhibitors of at least HDAC1 and HDAC3. (nih.gov)
  • These 4-(aminomethyl)benzamide-based inhibitors are also effective against Marburg virus. (cdc.gov)
  • These 4-(aminomethyl)benzamides are suitable for further optimization as inhibitors of filovirus entry, with the potential to be developed as therapeutic agents for the treatment and control of Ebola virus infections. (cdc.gov)
  • Division was recently validated as an important target for antibiotics by the demonstration that low-molecular-weight inhibitors of FtsZ, called benzamides, can cure mice infected with Staphylococcus aureus. (ncl.ac.uk)
  • In psychiatry some substituted benzamides are therapeutically used as neuroleptics and/or antipsychotics (wikipedia). (hmdb.ca)
  • J. Mukherjee, B.D. Perry, M. Cooper: Fluorinated benzamide neuroleptics. (springer.com)
  • Herein we report detailed investigation into the anticancer activity of sulfamoyl benz(sulfon)amides (1a-1g, 2a-2k) and 1H-pyrazol-4-yl benzamides (3a-3j) against three cancer cell lines, breast cancer cells (MCF-7), bone-marrow cancer cells (K-562) and cervical cancer cells (HeLa). (ovid.com)
  • Sun, Haifeng , Page, Michael I. , Atherton, John H. and Hall, Alan (2014) Kinetics of the conversion of methyl benzoate to benzamide by the alumina catalysed reaction with liquid ammonia at 120 °C. Catalysis Science & Technology, 4 (11). (hud.ac.uk)
  • Benzamide is less easily hydrolysed than methyl benzoate. (chemzipper.com)
  • Therefore, magnitude of positive charge on carbonyl carbon in benzamide is less than in methyl benzoate. (chemzipper.com)
  • K.A. Neve, R.A. Henningsen, J.M. Kinzie, T. de Paulis, D.E. Schmidt, R.M. Kessler and A. Janowsky: Sodium-dependent isomerization of dopamine D-2 receptors characterized using [125I]epidepride, a high-affinity substituted benzamide ligand, J Pharm Exp Ther 252: 1108-1116 (1990). (springer.com)
  • C.-T. Chen, C. Ortega, R.N. Beck and M. Cooper: Dopamine D-2 receptors imaged by PET in Cebus apella using [18F]benzamide neuroleptic, Eur J Pharm 175: 363-364 (1990). (springer.com)
  • Coplanar Effect Studies on the Benzamides of Dopamine D 2 Receptor Imaging Agents[J].Acta Phys. (pku.edu.cn)
  • Benzamide is a white solid with the chemical formula of C6H5C(O)NH2. (wikipedia.org)
  • Here, the disulfide-based conjugation was performed using a new coupling reagent, maleimidoethyl 3-(trimethylstannyl)benzamide (MSB), and evaluated for chemical stability in vitro. (chalmers.se)
  • Coyne et al (31) transplanted marrow stromal cells (MSCs) double-labelled with BrdU and bis- benzamide (BBZ) into the adult hippocampus or striatum noticed that BrdU labelling was colocalized to host phagocytes, astrocytes, and neurons in both regions. (thefreedictionary.com)
  • New N-(benzyl carbamothioyl)-2-hydroxy substituted benzamides 13 , 20 , and 21 were synthesized using sodium bicarbonate and benzyl amine with 2-thioxo-substituted-1,3-benzoxazines 6, 10a, b, 11c , and 12a-n . (hindawi.com)
  • Products 15a, b, e, f , and g were also synthesized by boiling the corresponding N-(benzyl carbamothioyl)-2-hydroxy substituted benzamides 13a, b, f, l , and m in acetic acid. (hindawi.com)
  • The N-(benzyl carbamoyl)-2-hydroxy substituted benzamide 23 was synthesized from the reaction of 2-oxo-substituted-1,3-benzoxazine 22 with benzylamine. (hindawi.com)
  • Using a bulky catalyst/cocatalyst system allows reactions between benzamides and alkenes to afford the corresponding para-alkylated products. (bvsalud.org)
  • A highly mono-selective ortho -methylthiolation of benzamides was achieved via Co-catalyzed coupling of benzamides with DMSO. (rsc.org)
  • para-Selective Alkylation of Benzamides and Aromatic Ketones by Cooperative Nickel/Aluminum Catalysis. (bvsalud.org)
  • We report a method that ensures the selective alkylation of benzamides and aromatic ketones at the para-position via cooperative nickel / aluminum catalysis . (bvsalud.org)
  • the incorporation of 35 SO 4 2− into the trichloroacetic-acid-insoluble constituents of cell masses as well as the formation of cartilage nodules (Nishio, Nakanishi, Doull & Uyeki, 1983) occurred about 24h earlier than in untreated cultures and continued to be enhanced in benzamide-treated cultures of stage 23- to 24-chick limb bud cells. (biologists.org)
  • Cisapride is a substituted benzamide compound that stimulates motor activity in all segments of the gastrointestinal tract by enhancing the release of acetylcholine from the enteric nervous system Actions at enteric neuronal serotonin (5-hydroxytryptamine-[5-HT]) receptors have been implied in the prokinetic effects of cisapride. (thefreedictionary.com)
  • Benzamides" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (umassmed.edu)
  • In vitro, the benzamides strongly promote the polymerization of FtsZ, into hyperstable polymers, which are highly curved. (ncl.ac.uk)
  • The results of conformational analysis and PM3 calculation have demonstrated that the coplanar effect of benzamides is one of the most important requirements for activity in vitro. (pku.edu.cn)
  • The kinetics are complex, mainly because inhibition by the product benzamide is a significant factor. (hud.ac.uk)
  • 2,5-Dihydroxy-N-(2-hydroxyethyl) benzamide 1a, 2,4-dihydroxy-N-(2-hydroxyethyl) benzamide 1b (Aldrich) and other chemicals and solvents were used as received. (thefreedictionary.com)
  • On the other hand, the amide-directed C-N and C-O activation/coupling reactions are broadly applicable on benzamides and naphthamides. (queensu.ca)
  • An isomer grid of nine fluoro-N-(pyridyl)benzamides (Fxx) (x = para-/meta-/ortho-) has been examined to correlate structural relationships between the experimental crystal structure and ab initio calculations, based on the effect of fluorine (Fx) and pyridine N-atom (x) substitution patterns on molecular conformation. (dcu.ie)
  • Importantly, even at low concentrations, benzamides transform the structure of the Z ring, resulting in abnormal helical cell division events. (ncl.ac.uk)
  • Benzamide is an intermediate in the Benzoate degradation via CoA ligation. (hmdb.ca)