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Artigos de revistas sobre o tema "Bqcap"

Autor: Grafiati

Publicado: 15 de fevereiro de 2025

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1

Ma, Lei, Matthew A. Seager, Marion Wittmann, Marlene Jacobson, Denise Bickel, Maryann Burno, Keith Jones et al. "Selective activation of the M1 muscarinic acetylcholine receptor achieved by allosteric potentiation". Proceedings of the National Academy of Sciences 106, n.º 37 (26 de agosto de 2009): 15950–55. http://dx.doi.org/10.1073/pnas.0900903106.

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The forebrain cholinergic system promotes higher brain function in part by signaling through the M1 muscarinic acetylcholine receptor (mAChR). During Alzheimer's disease (AD), these cholinergic neurons degenerate, therefore selectively activating M1 receptors could improve cognitive function in these patients while avoiding unwanted peripheral responses associated with non-selective muscarinic agonists. We describe here benzyl quinolone carboxylic acid (BQCA), a highly selective allosteric potentiator of the M1 mAChR. BQCA reduces the concentration of ACh required to activate M1 up to 129-fold with an inflection point value of 845 nM. No potentiation, agonism, or antagonism activity on other mAChRs is observed up to 100 μM. Furthermore studies in M1−/− mice demonstrates that BQCA requires M1 to promote inositol phosphate turnover in primary neurons and to increase c-fos and arc RNA expression and ERK phosphorylation in the brain. Radioligand-binding assays, molecular modeling, and site-directed mutagenesis experiments indicate that BQCA acts at an allosteric site involving residues Y179 and W400. BQCA reverses scopolamine-induced memory deficits in contextual fear conditioning, increases blood flow to the cerebral cortex, and increases wakefulness while reducing delta sleep. In contrast to M1 allosteric agonists, which do not improve memory in scopolamine-challenged mice in contextual fear conditioning, BQCA induces β-arrestin recruitment to M1, suggesting a role for this signal transduction mechanism in the cholinergic modulation of memory. In summary, BQCA exploits an allosteric potentiation mechanism to provide selectivity for the M1 receptor and represents a promising therapeutic strategy for cognitive disorders.

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2

Pavlov, Valentin, Mahendar Ochani, Meghan Dancho, Yousef Al-Abed, Neil Nathanson e Kevin Tracey. "Positive allosteric modulation of M1 muscarinic acetylcholine receptors suppresses lethal peripheral inflammation (P5082)". Journal of Immunology 190, n.º 1_Supplement (1 de maio de 2013): 180.24. http://dx.doi.org/10.4049/jimmunol.190.supp.180.24.

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Abstract Peripheral inflammation can be regulated by activation of brain muscarinic acetylcholine receptor (mAChR)-dependent signaling functionally associated with a vagus-nerve mediated anti-inflammatory circuit (Proc Natl Acad Sci USA, 2006, 5219; Brain Behav Immun, 2009, 23:41). Here, we studied the specific role of the M1 mAChR subtype in this regulation by utilizing BQCA, a highly specific allosteric M1 mAChR activator that crosses the blood-brain barrier. Single drug (5,10 or 20 mg/kg, i.p) administration in mice 1h prior to endotoxin (8 mg/kg, i.p.) dose-dependently reduced serum and splenic TNF levels and significantly improved survival in mice as compared to vehicle-treated controls. Pharmacological blockade of brain mAChRs significantly abolished BQCA anti-inflammatory effects. Furthermore, BQCA (20 mg/kg, i.p.) significantly reduced serum and splenic TNF levels in wild type mice, but failed to alter TNF levels in M1 KO mice. Together these results indicate the anti-inflammatory role of increased functional activity of endogenous acetylcholine on the M1 mAChR by selective allosteric receptor activation. Our findings are of interest for further development of BQCA and other centrally-acting allosteric activators of the M1 mAChR as a novel class of experimental anti-inflammatory therapeutics.

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3

Khatwal, Rizwan Basha, Anil Dubala, Jayasankar Kosaraju, Santhivardhan Chinni, Manjunatha Narayanappa, Shashank Mulukutla, Satish Kumar Muthureddy Nataraj e Malay Kumar Samanta. "Pharmacokinetics and tissue distribution of a M1 muscarinic acetylcholine receptor positive allosteric potentiator, benzyl quinolone carboxylic acid". Anal. Methods 6, n.º 8 (2014): 2672–78. http://dx.doi.org/10.1039/c4ay00102h.

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4

Avila, Olga Beatriz, Liliana Ester Contini e Stefanía D´Iorio. "RENDIMIENTO ACADÉMICO EN ESTADÍSTICA, ¿CÓMO IMPACTAN EN ÉL LAS DISTINTAS ESTRATEGIAS DE ENSEÑANZA SEGÚN LOS PLANES DE ESTUDIO?" Revista Binacional Brasil-Argentina: Diálogo entre as ciências 11, n.º 02 (4 de dezembro de 2022): 82–97. http://dx.doi.org/10.22481/rbba.v11i02.11582.

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Durante los últimos cinco años, en la Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Santa Fe-Argentina, un equipo de docentes investigadores ha trabajado en la implementación, de la estrategia “Enseñanza por proyectos” en Estadística en las carreras de Licenciatura en Nutrición (LN) , Licenciatura en Biotecnología (LB) y Bioquímica (Bqca). En este trabajo se muestra la evolución del rendimiento de los alumnos desde el año 2016 (dictado convencional con clases de teoría y práctica) hasta el año 2021 donde se fue poniendo en práctica de manera paulatina (incluido los años de pandemia, de cursado virtual), la estrategia didáctica mencionada. A partir de los resultados obtenidos se muestra que su aplicación tendría una acción favorable en el proceso de enseñanza y aprendizaje de los conceptos estudiados, reflejado en los porcentajes de estudiantes que regularizaron, más perceptible para LN, tanto si se compara en relación a los regulares de Bqca y LB, como cuando se compara el porcentaje de regulares antes y después de la implementación de la estrategia de enseñanza por proyectos.

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5

Tichenor, MT(ASCP), Patricia H., Barbara M. Eiland, MT(ASCP), Cari E. Reed, MT(ASCP), Brian K. Adler, MD, Brian D. Ragland, MD, Christine L. Hudson, MT(ASCP), George A. Fritsma, MT(ASCP) e Marisa B. Marques, MD. "The Effect of Lupus Anticoagulant in the Second-Generation Assay for Activated Protein C Resistance". American Journal of Clinical Pathology 119, n.º 1 (1 de janeiro de 2003): 66–71. http://dx.doi.org/10.1309/1gn6-ntm7-bqap-8vkx.

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6

Ma, Lei, Marlene A. Jacobson, Constantine Kreatsoulas, Krista L. Getty, Guy R. Seabrook e William J. Ray. "P4-322: Exploring the pharmacology of BQCA, a highly selective allosteric M1 potentiator". Alzheimer's & Dementia 4 (julho de 2008): T767. http://dx.doi.org/10.1016/j.jalz.2008.05.2392.

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7

Chintamaneni, Pavan Kumar, Praveen Thaggikuppe Krishnamurthy e Sai Kiran S. S. Pindiprolu. "Polysorbate-80 surface modified nano-stearylamine BQCA conjugate for the management of Alzheimer's disease". RSC Advances 11, n.º 10 (2021): 5325–34. http://dx.doi.org/10.1039/d1ra00049g.

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8

Niklas, Beata, Bruno Lapied e Wieslaw Nowak. "In Search of Synergistic Insect Repellents: Modeling of Muscarinic GPCR Interactions with Classical and Bitopic Photoactive Ligands". Molecules 27, n.º 10 (20 de maio de 2022): 3280. http://dx.doi.org/10.3390/molecules27103280.

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Insect vector-borne diseases pose serious health problems, so there is a high demand for efficient molecules that could reduce transmission. Using molecular docking and molecular dynamics (MD) simulation, we studied a series of compounds acting on human and insect muscarinic acetylcholine receptors (mAChRs), a novel target of synergistic agents in pest control. We characterized early conformational changes of human M1 and fruit fly type-A mAChR G protein-coupled receptors (GPCRs) in response to DEET, IR3535, and muscarine binding based on the MD analysis of the activation microswitches known to form the signal transduction pathway in class A GPCRs. We indicated groups of microswitches that are the most affected by the presence of a ligand. Moreover, to increase selectivity towards insects, we proposed a new, bitopic, photoswitchable mAChR ligand—BQCA-azo-IR353 and studied its interactions with both receptors. Modeling data showed that using a bitopic ligand may be a promising strategy in the search for better insect control.

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9

Wakeham, Matthew C. L., Briana J. Davie, David K. Chalmers, Arthur Christopoulos, Ben Capuano, Celine Valant e Peter J. Scammells. "Structural Features of Iperoxo–BQCA Muscarinic Acetylcholine Receptor Hybrid Ligands Determining Subtype Selectivity and Efficacy". ACS Chemical Neuroscience 13, n.º 1 (14 de dezembro de 2021): 97–111. http://dx.doi.org/10.1021/acschemneuro.1c00572.

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10

Wittmann, Marion, Guangping Xu, Michelle Pearson, Susan Garson, Scott Doran, John J. Renger, Andrew Danziger, Christopher P. Regan, Guy R. Seabrook e William J. Ray. "P4-332: In vivo pharmacodynamic effects of BQCA, a novel selective allosteric M1 receptor modulator". Alzheimer's & Dementia 4 (julho de 2008): T770. http://dx.doi.org/10.1016/j.jalz.2008.05.2402.

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11

Schramm, Simon, Luca Agnetta, Marcel Bermudez, Hubert Gerwe, Matthias Irmen, Janine Holze, Timo Littmann, Gerhard Wolber, Christian Tränkle e Michael Decker. "Novel BQCA‐ and TBPB‐Derived M 1 Receptor Hybrid Ligands: Orthosteric Carbachol Differentially Regulates Partial Agonism". ChemMedChem 14, n.º 14 (3 de julho de 2019): 1349–58. http://dx.doi.org/10.1002/cmdc.201900283.

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12

Dean, Brian, Shaun Hopper, P. Jeffrey Conn e Elizabeth Scarr. "Changes in BQCA Allosteric Modulation of [3H]NMS Binding to Human Cortex within Schizophrenia and by Divalent Cations". Neuropsychopharmacology 41, n.º 6 (29 de outubro de 2015): 1620–28. http://dx.doi.org/10.1038/npp.2015.330.

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13

Hepnarova, V., J. Korabecny, L. Matouskova, P. Jost, L. Muckova, M. Hrabinova, N. Vykoukalova et al. "The concept of hybrid molecules of tacrine and benzyl quinolone carboxylic acid (BQCA) as multifunctional agents for Alzheimer's disease". European Journal of Medicinal Chemistry 150 (abril de 2018): 292–306. http://dx.doi.org/10.1016/j.ejmech.2018.02.083.

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14

Mistry, Shailesh N., Celine Valant, Patrick M. Sexton, Ben Capuano, Arthur Christopoulos e Peter J. Scammells. "Synthesis and Pharmacological Profiling of Analogues of Benzyl Quinolone Carboxylic Acid (BQCA) as Allosteric Modulators of the M1 Muscarinic Receptor". Journal of Medicinal Chemistry 56, n.º 12 (17 de junho de 2013): 5151–72. http://dx.doi.org/10.1021/jm400540b.

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15

Gore, Babasaheb Sopan, Chein Chung Lee, Jessica Lee e Jeh‐Jeng Wang. "Copper‐Catalyzed Synthesis of Substituted 4‐Quinolones using Water as a Benign Reaction Media: Application for the Construction of Oxolinic Acid and BQCA". Advanced Synthesis & Catalysis 361, n.º 14 (14 de maio de 2019): 3373–86. http://dx.doi.org/10.1002/adsc.201900286.

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16

Nicolle, Michelle M., Mona L. Watson, Joseph A. McQuail, Kumar Sambamurti, Ashley E. Brady, Carrie Jones, P. Jeffrey Conn e Craig W. Lindsey. "P3-276: Acute administration of a novel M1 receptor allosteric potentiator (BQCA) restores reversal learning in a transgenic mouse model of Alzheimer's disease (Tg2576)". Alzheimer's & Dementia 5, n.º 4S_Part_14 (julho de 2009): P424. http://dx.doi.org/10.1016/j.jalz.2009.04.947.

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17

Davie, Briana J., Celine Valant, Jonathan M. White, Patrick M. Sexton, Ben Capuano, Arthur Christopoulos e Peter J. Scammells. "Synthesis and Pharmacological Evaluation of Analogues of Benzyl Quinolone Carboxylic Acid (BQCA) Designed to Bind Irreversibly to an Allosteric Site of the M1Muscarinic Acetylcholine Receptor". Journal of Medicinal Chemistry 57, n.º 12 (5 de junho de 2014): 5405–18. http://dx.doi.org/10.1021/jm500556a.

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18

Mir, M. Amin. "Preparation, Computational and Spectroscopic Analysis of an Efficient Medicinal Molecule: 4-Bromoquinoline-2-carboxaldehyde". Current Organocatalysis 12 (7 de janeiro de 2025). https://doi.org/10.2174/0122133372362996241228014644.

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Introduction: This paper presents the synthesis, spectroscopic characterization, and computational modeling of 4-Bromoquinoline-2-carboxaldehyde (4-BQCA), an effective therapeutic compound. 4-BQCA, a quinoline derivative, has drawn interest because of its distinct chemical structure and its medical uses. Method: The chemical was produced with excellent yield and purity using a simple, repeatable reaction route. Density functional theory (DFT) studies were carried out to learn more about the compound's molecular characteristics, including its electronic structure, bonding, and stability. The structure and functional groups found in 4-BQCA were verified by spectroscopic investigation, which included UV-Vis, FT-IR, NMR, and mass spectrometry. Result: The compound's stability and advantageous electrical characteristics are highlighted by the results of both computational and experimental methods, indicating that it may find application in medication design and development. Conclusion: These results offer a starting point for further investigations into the biological activity and therapeutic effectiveness of 4-BQCA, indicating that it is a viable option for more study in pharmaceutical applications.

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19

Ellis, John, e Gwendolynne Elmslie. "Benzyl quinolone carboxylic acid (BQCA) elicits positive allosteric modulation at M₂‐M₅ muscarinic receptors with specific mutations". FASEB Journal 30, S1 (abril de 2016). http://dx.doi.org/10.1096/fasebj.30.1_supplement.lb519.

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The muscarinic acetylcholine receptors (mAChRs) comprise a family of G‐protein‐coupled receptors, all of which are expressed in the CNS. Physiological, behavioral, and knock‐out mouse studies all suggest that these receptors play crucial roles in many CNS functions and disorders. Unfortunately, the structures of the five subtypes of mAChRs are very highly conserved in the transmembrane regions where ACh binds; this has hampered the development of subtype‐selective agonists and antagonists. Additionally, the mAChRs also play essential roles in the autonomic system; this means that non‐selective muscarinic agents have serious dose‐limiting side effects. One approach to developing ligands with sufficient selectivity has been to target allosteric sites on the receptors, which are typically much less conserved than the orthosteric site. BQCA is a premier example of a positive allosteric modulator that is highly selective for the M1 mAChR, which is a subtype whose enhancement is likely to benefit cognitive deficits, including those of Alzheimer's Disease. BQCA enhances the potency of ACh by 100‐fold or more at M1, while having no effect at the other subtypes. Such selectivity can be due either to highly selective affinity for M1 or to neutral cooperativities at the other subtypes, and it is of significant interest to determine which mechanism is at work for this prototypical agent. We have used mutagenesis to identify residues that are key to the selective PAM activity. In agreement with others, we found that the aromatic nature of M1Y5.29 is essential (superscript numerals refer to the system of Ballesteros and Weinstein); Y=>A mutation abolishes activity, while Y=>F preserves it. Of the five subtypes, only M5 lacks Y or F at this site. We found that the M5Q=>Y5.29 mutant displays modest PAM activity. Additionally, the PAM activity of the double mutant M1E=>A7.32, E=>A7.36 is markedly attenuated, whereas the M5Y5.29E7.32E7.36 mutant has PAM activity equal to M1. Unlike the case with M5, the M2E7.32E7.36, M3E7.32E7.36, and M4E7.32E7.36 mutants exhibit only moderate PAM activity, despite the Y or F present at position 5.29. Finally, the interactions between BQCA and ACh in inhibiting the binding of the labeled orthosteric antagonist [3H]N‐methylscopolamine to M1 vs M1A7.32A7.36 and M5Y5.29 vs M5Y5.29E7.32E7.36 were evaluated using a mathematical allosteric model. The mutations were found to exert marked changes in the cooperativity between BQCA and ACh, but not to alter the affinity of BQCA for the receptor. This indicates that the region near the top of TM7 that contains E7.32 and E7.36 is not part of the binding site. In agreement with this, BQCA was not found to be competitive with the allosteric modulator W84, which has previously been shown to bind within this region.Support or Funding InformationThis project is funded, in part, under a grant with the Pennsylvania Department of Health using Tobacco CURE Funds. The Department specifically disclaims responsibility for any analyses, interpretations, or conclusions. Also supported by the National Institute on Aging [Grant R01AG005214] and by funds from the Department of Psychiatry, Penn State University College of Medicine

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20

Pavlov, Valentin A., Kurt R. Lehner, Sangeeta S. Chavan, Vania F. Prado, Marco A. M. Prado e Kevin J. Tracey. "Cholinergic signaling in the forebrain regulates peripheral inflammation". FASEB Journal 31, S1 (abril de 2017). http://dx.doi.org/10.1096/fasebj.31.1_supplement.lb798.

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The brain regulates physiological functions integral to survival. Relatively little is known about the brain neuronal regulation of peripheral immune function. Brain cholinergic signals have been implicated in controlling peripheral inflammation, but specific insight is lacking. Here, utilizing neuron‐and receptor‐specific approaches, we studied the role of forebrain cholinergic signaling and the M1 muscarinic acetylcholine receptor (M1 mAChR) in the regulation of peripheral inflammation. Forebrain‐specific Cre‐loxP‐based ablation of the vesicular acetylcholine transporter (required for synaptic acetylcholine release) and vagotomy abolished the suppression of serum TNF by the centrally‐acting cholinergic drug galantamine in murine endotoxemia. Basal forebrain cholinergic neurons innervate areas with abundant M1 mAChR localization. Enhancement of acetylcholine action on the brain M1 mAChR with the selective positive allosteric modulator benzyl quinolone carboxylic acid (BQCA) suppressed serum TNF levels in endotoxemia. Peripheral administration of the centrally‐acting BQCA also suppressed TNF levels and improved survival in endotoxemia, effects abolished in M1 mAChR KO mice. Optogenetic stimulation of basal forebrain cholinergic neurons in the medial septum reduced serum TNF in endotoxemic mice as compared to sham stimulation. These findings provide novel insights into brain regulation of peripheral inflammation and are of interest for developing new brain‐based treatments for inflammatory conditions.Support or Funding InformationThis work was supported by the following grants from the National Institute of General Medical Sciences, NIH: RO1GM089807 (to VAP and KJT) and RO1GM057226 (to KJT).

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21

Gerwe, Hubert, Eva Schaller, Rosalba Sortino, Ekin Opar, Joaquin Martínez -Tambella, Marcel Bermudez, J. Robert Lane, Pau Gorostiza e Michael Decker. "Photo‐BQCA: Positive Allosteric Modulators Enabling Optical Control of the M1 Receptor". Angewandte Chemie, 13 de agosto de 2024. http://dx.doi.org/10.1002/ange.202411438.

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The field of G protein‐coupled receptor (GPCR) research has greatly benefited from the spatiotemporal resolution provided by light controllable, photoswitchable agents. Most of the developed tools have targeted the Rhodopsin‐like family (Class A), the largest family of GPCRs. However, to date, all such Class A photoswitchable ligands were designed to act at the orthosteric binding site of these receptors. Herein, we report the development of the first photoswitchable allosteric modulators of Class A GPCRs, designed to target the M1 muscarinic acetylcholine receptor. The presented benzyl quinolone carboxylic acid (BQCA) derivatives, photo‐BQCisA and photo‐BQCtrAns, exhibit complementary photopharmacological behavior and allow reversible control over the receptor using light as an external stimulus. This makes them valuable tools to further investigate M1 receptor signaling and a proof of concept for photoswitchable allosteric modulators at Class A receptors.

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22

Gerwe, Hubert, Eva Schaller, Rosalba Sortino, Ekin Opar, Joaquin Martínez -Tambella, Marcel Bermudez, J. Robert Lane, Pau Gorostiza e Michael Decker. "Photo‐BQCA: Positive Allosteric Modulators Enabling Optical Control of the M1 Receptor". Angewandte Chemie International Edition, 13 de agosto de 2024. http://dx.doi.org/10.1002/anie.202411438.

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The field of G protein‐coupled receptor (GPCR) research has greatly benefited from the spatiotemporal resolution provided by light controllable, photoswitchable agents. Most of the developed tools have targeted the Rhodopsin‐like family (Class A), the largest family of GPCRs. However, to date, all such Class A photoswitchable ligands were designed to act at the orthosteric binding site of these receptors. Herein, we report the development of the first photoswitchable allosteric modulators of Class A GPCRs, designed to target the M1 muscarinic acetylcholine receptor. The presented benzyl quinolone carboxylic acid (BQCA) derivatives, photo‐BQCisA and photo‐BQCtrAns, exhibit complementary photopharmacological behavior and allow reversible control over the receptor using light as an external stimulus. This makes them valuable tools to further investigate M1 receptor signaling and a proof of concept for photoswitchable allosteric modulators at Class A receptors.

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23

Chintamaneni, Pavan Kumar, Praveen Thaggikuppe Krishnamurthy, Saikiran S. S. Pindiprolu e NandhaKumar Sathyamoorthy. "Quantum Dot loaded BQCA‐Octadecylamine conjugate nanosystems for theranostic applications in Alzheimer’s Disease." Alzheimer's & Dementia 18, S10 (dezembro de 2022). http://dx.doi.org/10.1002/alz.067578.

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Gerwe, Hubert, Eva Schaller, Rosalba Sortino, Ekin Opar, Joaquín Martínez‐Tambella, Marcel Bermudez, J. Robert Lane, Pau Gorostiza e Michael Decker. "Inside Back Cover: Photo‐BQCA: Positive Allosteric Modulators Enabling Optical Control of the M1 Receptor". Angewandte Chemie, 2 de outubro de 2024. http://dx.doi.org/10.1002/ange.202417162.

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Gerwe, Hubert, Eva Schaller, Rosalba Sortino, Ekin Opar, Joaquín Martínez‐Tambella, Marcel Bermudez, J. Robert Lane, Pau Gorostiza e Michael Decker. "Inside Back Cover: Photo‐BQCA: Positive Allosteric Modulators Enabling Optical Control of the M1 Receptor". Angewandte Chemie International Edition, 2 de outubro de 2024. http://dx.doi.org/10.1002/anie.202417162.

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26

"PM484. BQCA Allosteric Modulation of [3H]NMS Binding to Human Cortex is Reduced in a Subgroup of Schizophrenia and Modulation by Divalent Cations". International Journal of Neuropsychopharmacology 19, Suppl_1 (27 de maio de 2016): 76. http://dx.doi.org/10.1093/ijnp/pyw041.484.

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