Готові списки джерел за темами / Mavacamten

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Добірка наукової літератури з теми "Mavacamten"

Автор: Grafiati

Опубліковано: 10 березня 2023

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Статті в журналах з теми "Mavacamten"

Sparrow, Alexander J., Hugh Watkins, Matthew J. Daniels, Charles Redwood, and Paul Robinson. "Mavacamten rescues increased myofilament calcium sensitivity and dysregulation of Ca2+ flux caused by thin filament hypertrophic cardiomyopathy mutations." American Journal of Physiology-Heart and Circulatory Physiology 318, no. 3 (March 1, 2020): H715—H722. http://dx.doi.org/10.1152/ajpheart.00023.2020.

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Thin filament hypertrophic cardiomyopathy (HCM) mutations increase myofilament Ca2+ sensitivity and alter Ca2+ handling and buffering. The myosin inhibitor mavacamten reverses the increased contractility caused by HCM thick filament mutations, and we here test its effect on HCM thin filament mutations where the mode of action is not known. Mavacamten (250 nM) partially reversed the increased Ca2+ sensitivity caused by HCM mutations Cardiac troponin T (cTnT) R92Q, and cardiac troponin I (cTnI) R145G in in vitro ATPase assays. The effect of mavacamten was also analyzed in cardiomyocyte models of cTnT R92Q and cTnI R145G containing cytoplasmic and myofilament specific Ca2+ sensors. While mavacamten rescued the hypercontracted basal sarcomere length, the reduced fractional shortening did not improve with mavacamten. Both mutations caused an increase in peak systolic Ca2+ detected at the myofilament, and this was completely rescued by 250 nM mavacamten. Systolic Ca2+ detected by the cytoplasmic sensor was also reduced by mavacamten treatment, although only R145G increased cytoplasmic Ca2+. There was also a reversal of Ca2+ decay time prolongation caused by both mutations at the myofilament but not in the cytoplasm. We thus show that mavacamten reverses some of the Ca2+-sensitive molecular and cellular changes caused by the HCM mutations, particularly altered Ca2+ flux at the myofilament. The reduction of peak systolic Ca2+ as a consequence of mavacamten treatment represents a novel mechanism by which the compound is able to reduce contractility, working synergistically with its direct effect on the myosin motor. NEW & NOTEWORTHY Mavacamten, a myosin inhibitor, is currently in phase-3 clinical trials as a pharmacotherapy for hypertrophic cardiomyopathy (HCM). Its efficacy in HCM caused by mutations in thin filament proteins is not known. We show in reductionist and cellular models that mavacamten can rescue the effects of thin filament mutations on calcium sensitivity and calcium handling although it only partially rescues the contractile cellular phenotype and, in some cases, exacerbates the effect of the mutation.

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Rohde, John A., Osha Roopnarine, David D. Thomas, and Joseph M. Muretta. "Mavacamten stabilizes an autoinhibited state of two-headed cardiac myosin." Proceedings of the National Academy of Sciences 115, no. 32 (July 17, 2018): E7486—E7494. http://dx.doi.org/10.1073/pnas.1720342115.

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We used transient biochemical and structural kinetics to elucidate the molecular mechanism of mavacamten, an allosteric cardiac myosin inhibitor and a prospective treatment for hypertrophic cardiomyopathy. We find that mavacamten stabilizes an autoinhibited state of two-headed cardiac myosin not found in the single-headed S1 myosin motor fragment. We determined this by measuring cardiac myosin actin-activated and actin-independent ATPase and single-ATP turnover kinetics. A two-headed myosin fragment exhibits distinct autoinhibited ATP turnover kinetics compared with a single-headed fragment. Mavacamten enhanced this autoinhibition. It also enhanced autoinhibition of ADP release. Furthermore, actin changes the structure of the autoinhibited state by forcing myosin lever-arm rotation. Mavacamten slows this rotation in two-headed myosin but does not prevent it. We conclude that cardiac myosin is regulated in solution by an interaction between its two heads and propose that mavacamten stabilizes this state.

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Maron, Martin S., Ethan J. Rowin, and Barry J. Maron. "Is surgical myectomy challenged by emergence of novel drug therapy with mavacamten?" Asian Cardiovascular and Thoracic Annals 30, no. 1 (January 2022): 11–18. http://dx.doi.org/10.1177/02184923221074414.

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For 60 years, surgical myectomy has been the definitive treatment for symptomatic obstructive hypertrophic cardiomyopathy (HCM). Myectomy provides the opportunity to reverse heart failure symptoms in the vast majority of patient with low risk when performed in experienced centers and associated with extended longevity. More recently, a novel class of negative inotropic drug therapy with mavacamten has emerged offering expanded treatment options for obstructive HCM. In the recently completed phase III clinical trial, the EXPLORER-HCM about one-third of patients on mavacamten achieved the primary end-point of subjective symptomatic improvement and increased functional capacity assessed by peak VO2. Of note, outflow gradients persistent in 43% of patients on mavacamten and 50% with symptoms consistent with NYHA class II or greater. A subset of patients also experienced significant reversible systolic dysfunction. Therefore, it is timely to place into perspective the potential role of mavacamten in context of the established low risk: high benefit of surgical myectomy for treatment of heart failure.

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Sewanan, Lorenzo R., Shi Shen, and Stuart G. Campbell. "Mavacamten preserves length-dependent contractility and improves diastolic function in human engineered heart tissue." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 3 (March 1, 2021): H1112—H1123. http://dx.doi.org/10.1152/ajpheart.00325.2020.

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We applied innovative methods to comprehensively characterize the length and load-dependent behaviors of engineered human cardiac muscle when treated with the cardiac β-myosin specific inhibitor mavacamten, a drug on the verge of clinical implementation for hypertrophic cardiomyopathy. We find mechanistic support for the role of mavacamten in improving diastolic function of cardiac tissue and note novel effects on work and power.

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Reyes, Klevin Roger L., Gizem Bilgili, and Florian Rader. "Mavacamten: A First-in-class Oral Modulator of Cardiac Myosin for the Treatment of Symptomatic Hypertrophic Obstructive Cardiomyopathy." Heart International 16, no. 2 (2022): 91. http://dx.doi.org/10.17925/hi.2022.16.2.91.

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Hypertrophic cardiomyopathy is the most common monogenic cardiovascular disease that is caused by sarcomeric protein gene mutations. A hallmark of the most common form of the disease is outflow obstruction secondary to systolic narrowing of the left ventricular outflow tract from septal hypertrophy, mitral valve abnormalities and, most importantly, hyperdynamic contractility. Recent mechanistic studies have identified excessive myosin adenosine triphosphatase activation and actin–myosin cross-bridging as major underlying causes. These studies have led to the development of mavacamten, a first-in-class myosin adenosine triphosphatase inhibitor and the first specific therapy for hypertrophic obstructive cardiomyopathy. Preclinical and subsequent pivotal clinical studies have demonstrated the efficacy and safety of mavacamten. A remarkable improvement among treated patients in peak oxygen consumption, functional capacity, symptom relief and post-exercise left ventricular outflow tract gradient, along with dramatic reductions in heart failure biomarkers, suggests that this new medication will be transformative for the symptom management of hypertrophic obstructive cardiomyopathy. There is also hope and early evidence that mavacamten may delay or obviate the need for invasive septal reduction therapies. In this article, we review the current evidence for the efficacy and safety of mavacamten and highlight important considerations for its clinical use.

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Quintana, Eduard, Pietro Bajona, and Patrick O. Myers. "Mavacamten for hypertrophic obstructive cardiomyopathy." Lancet 397, no. 10272 (January 2021): 369. http://dx.doi.org/10.1016/s0140-6736(20)32384-9.

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Heitner, Stephen B., Daniel Jacoby, Steven J. Lester, Anjali Owens, Andrew Wang, David Zhang, Joseph Lambing, June Lee, Marc Semigran, and Amy J. Sehnert. "Mavacamten Treatment for Obstructive Hypertrophic Cardiomyopathy." Annals of Internal Medicine 170, no. 11 (April 30, 2019): 741. http://dx.doi.org/10.7326/m18-3016.

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Papadakis, Michael, Joyee Basu, and Sanjay Sharma. "Mavacamten: treatment aspirations in hypertrophic cardiomyopathy." Lancet 396, no. 10253 (September 2020): 736–37. http://dx.doi.org/10.1016/s0140-6736(20)31793-1.

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Jacoby, Daniel, Carolyn Y. Ho, Steven J. Lester, Andrew Wang, and Iacopo Olivotto. "Mavacamten for hypertrophic obstructive cardiomyopathy – Authors' reply." Lancet 397, no. 10272 (January 2021): 369–70. http://dx.doi.org/10.1016/s0140-6736(20)32391-6.

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Beinfeld, Molly, Jason H. Wasfy, Surrey Walton, Jyotirmoy Sarker, Emily Nhan, David M. Rind, and Steven D. Pearson. "Mavacamten for hypertrophic cardiomyopathy: effectiveness and value." Journal of Managed Care & Specialty Pharmacy 28, no. 3 (March 2022): 369–75. http://dx.doi.org/10.18553/jmcp.2022.28.3.369.

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Більше джерел

Дисертації з теми "Mavacamten"

Aguiar, Tiago Filipe Sá Lopes Ribeiro. "Mavacamten, uma nova terapia revolucionária na HOCM: uma revisão de literatura." Master's thesis, 2021. https://hdl.handle.net/10216/134544.

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A miocardiopatia hipertrófica (MCH) é uma das doenças cardíacas genéticas mais frequentes, sendo definida por um espessamento da parede ventricular esquerda ≥15 mm, na ausência de outras causas de sobrecarga ventricular. Um dos principais problemas associados a esta doença é a obstrução do trato de saída do ventrículo esquerdo, presente em até ¾ dos doentes, designando-se nesta circunstância por miocardiopatia hipertrófica obstrutiva. Atualmente, os principais objetivos da terapêutica destes doentes são a redução sintomática e a redução da progressão da doença. Este objetivo é atingido através de terapia farmacológica empírica, intervenção cirúrgica, ablação septal por álcool e/ou introdução de dispositivos cardíacos. O Mavacamten é o primeiro inibidor alostérico da miosina cardíaca, que vem permitir uma terapia mais dirigida para estes doentes. O objetivo desta revisão é fornecer uma visão geral da atual abordagem diagnóstica e de tratamento da MCH, bem como integrar todo o conhecimento atual sobre o Mavacamten, antecipando uma futura mudança no algoritmo de tratamento de doentes com MCH.
Hypertrophic cardiomyopathy (HCM) is one of the most common inherited cardiac diseases, defined as a left ventricular wall thickness of ≥15 mm, in the absence of other causes of abnormal ventricular loading. A major hallmark of this disease is the presence of left ventricular outflow tract obstruction, which develops in up to ¾ of the patients, referred to as obstructive hypertrophic cardiomyopathy. Current treatment is offered to symptomatic patients, based on the presence of documented left ventricular obstruction, aimed at reducing symptoms and disease progression. This is achieved through pharmacological empirical therapy, surgery, alcohol ablation and/or pacing. Mavacamten is a first-in-class allosteric inhibitor of cardiac myosin that promises to provide clinicians with targeted therapy for these patients. The aim of this review is to provide a general overview of the modern approach in diagnosis and management of HCM, as well as to integrate all the current knowledge on Mavacamten, anticipating a future change in the treatment algorithm of patients with HCM.

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Aguiar, Tiago Filipe Sá Lopes Ribeiro. "Mavacamten, uma nova terapia revolucionária na HOCM: uma revisão de literatura." Dissertação, 2021. https://hdl.handle.net/10216/134544.

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Scellini, Beatrice, Nicoletta Piroddi, Marica Dente, Giulia Vitale, Josè Manuel Pioner, Raffaele Coppini, Cecilia Ferrantini, Corrado Poggesi, and Chiara Tesi. "EFFECTS OF MAVACAMTEN, A FIRST-IN-CLASS INHIBITOR OF SARCOMERIC MYOSINS, ON THE MECHANICS OF ATRIAL AND VENTRICULAR MAMMALIAN MYOCARDIUM AND FAST SKELETAL MUSCLE." Doctoral thesis, 2022. http://hdl.handle.net/2158/1275439.

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Mavacamten (MYK-461) is a small molecule allosteric inhibitor of sarcomeric myosins being used in preclinical/clinical trials for Hypertrophic Cardiomyopathy treatment. Despite the advancing of clinical studies, very little is known of Mavacamtem action on the mechanics of contraction of mammalian myocardium and fast skeletal muscle, especially in the human cardiac model. To date no information is available regarding the effect of the drug in the human atrium. Moreover, a better understanding of the impact of Mavacamten on force generation in intact or skinned striated muscle preparations, especially for human cardiac muscle, has been hindered by diffusional barriers. These limitations have been overcome by mechanical experiments using myofibrils subjected to perturbations of the contractile environment by sudden solution changes. Here we characterize the action of Mavacamten in atrial myofibrils from human and rat compared to ventricular myofibrils from human donor and fast skeletal myofibrils from rabbit psoas. Mavacamten had a fast, fully reversible, and dose dependent negative effect on maximal Ca2+-activated isometric force at 15º, which can be explained by a sudden decrease in the number of heads functionally available for interaction with actin. Mavacamten strongly depressed the kinetics of force generation of human and rat atrial myofibrils similarly to what had been observed in fast skeletal muscle myofibrils while it had no effect in human ventricular myofibrils. Mavacamten did not alter force relaxation of fast skeletal myofibrils, but it significantly accelerated the relaxation of human ventricular and atrial myofibrils. Mavacamten had no effect on resting tension but inhibited the ADP-stimulated force in the absence of Ca2+. Altogether, these effects outline a motor isoform-specific dependence of the inhibitory effect of Mavacamten on force generation, which is mediated by a reduction in the availability of strongly actin binding heads. Mavacamten may thus alter the interplay between thick and thin filament regulation mechanisms of contraction in association with the widely documented drug effect of stabilizing myosin motor heads into auto-inhibited states. In conclusion, although very promising, Mavacamten as well as the entire class of small molecules acting as inhibitors of sarcomeric myosins, can globally depress cardiac muscle contractility with potential detrimental consequences on the overall cardiac output. The characterization of the effect of Mavacamten described in this work is of great interest for clinical studies assessing the suitability of small molecules for the therapy of Hypertrophic Cardiomyopathy and for the development of new therapeutic approaches.

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Частини книг з теми "Mavacamten"

Affas, Ziad, Ghaid Touza, Rowaid Touza, Saif Affas, Zain Azzo, and Ali Shakir. "Mavacamten a Novel DiseaseSpecific Treatment for Hypertrophic Obstructive Cardiomyopathy: A Meta-Analysis and Systematic Review." In Current Innovations in Medicine and Medical Science Vol. 2, 114–28. Book Publisher International (a part of SCIENCEDOMAIN International), 2022. http://dx.doi.org/10.9734/bpi/cimms/v2/3922a.

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Тези доповідей конференцій з теми "Mavacamten"

Rader, Florian, and Rachel Giles. "Symptomatic obstructive hypertrophic cardiomyopathy: long-term mavacamten control." In 71st ACC Scientific Session, edited by Marc Bonaca. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/a6a40ff2.

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Desai, Milind, and Rachel Giles. "Replacing septal reduction therapy with mavacamten for HCM." In 71st ACC Scientific Session, edited by Marc Bonaca. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/75909ba6.

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Forouzandehmehr, "Mohamadamin, Michelangelo Paci, Jussi T. Koivumäki, and Jari A. Hyttinen." "Mutation-specific Hypertrophic Cardiomyopathy and Mavacamten: a Mechano-energetic In Silico Study." In 2022 Computing in Cardiology Conference. Computing in Cardiology, 2022. http://dx.doi.org/10.22489/cinc.2022.202.

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Vara, Sarina, Jason Dungu, Henry Oluwasefunmi Savage, and Brian Li. "32 Mavacamten eligibility in patients with hypertrophic cardiomyopathy attending cardiology clinic in essex, uk." In British Cardiovascular Society Annual Conference, ‘100 years of Cardiology’, 6–8 June 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-bcs.32.

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Margara, Francesca, Blanca Rodriguez, Christopher N. Toepfer, and Alfonso Bueno-Orovio. "Mavacamten Efficacy in Mutation-specific Hypertrophic Cardiomyopathy: an In Silico Approach to Inform Precision Medicine." In 2021 Computing in Cardiology (CinC). IEEE, 2021. http://dx.doi.org/10.23919/cinc53138.2021.9662736.

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