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Journal articles on the topic 'Mavacamten'

Author: Grafiati

Published: 10 March 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Hanchate, Shivani, Allison Perry, Karen McClean, Christopher M. Kramer, and Michael Ayers. "MAVACAMTEN IN HYPERTROPHIC CARDIOMYOPATHY: EFFECTIVE, BUT AFFORDABLE?" Journal of the American College of Cardiology 81, no. 8 (March 2023): 713. http://dx.doi.org/10.1016/s0735-1097(23)01157-9.

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12

Candelario, Isabel Rodriguez, Jose Roman-Ramos, and Francisco Tirado Polo. "MARVELOUS MAVACAMTEN: EXPLORING PHARMACOLOGICAL IMPROVEMENT OF HYPERTROPHIC CARDIOMYOPATHY." Journal of the American College of Cardiology 81, no. 8 (March 2023): 3189. http://dx.doi.org/10.1016/s0735-1097(23)03633-1.

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13

Langley, Paul C. "Concerns with Patient Reported Outcome Measurement and Value Claims for Therapy Response: The Case of Mavacamten and Symptomatic Hypertrophic Cardiomyopathy (SHCM)." INNOVATIONS in pharmacy 13, no. 2 (August 3, 2022): 16. http://dx.doi.org/10.24926/iip.v13i2.4861.

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Fundamental measurement is the basis for a rational assessment of patient reported outcome (PRO) value claims; both as response to therapy and the submission of credible and evaluable value claims to formulary committees and other health system decision makers. It is important to emphasize the importance of creating interval and ratio scales as opposed to nominal and ordinal scales to support value claims; a recognition that follows from acceptance of conjoint simultaneous measurement and the contribution of Rasch or modern measurement theory (RMT). Failure to appreciate the role of RMT has led thousands of researchers simply to apply numerals to events, inappropriately applying the techniques of classical statistical analysis, with the result that all that is produced are ordinal PRO scores. Instead, we should be aiming for interval and ratio scores based on a comprehensible latent trait and the application of the Rasch model. The purpose of this brief commentary is to review the measurement properties of PRO value claims for mavacamten (Camzyos; Bristol Myers Squibb) in symptomatic hypertrophic cardiomyopathy (SHCM) and to judge whether they have any validity when judged against the requirements of modern measurement theory. The assessment includes both the recent evidence report by the Institute for Clinical and Economic Review (ICER) for mavacamten as well as pivotal randomized trial (RCT) value claims that combine clinical endpoints with PROs that fail the standards of fundamental evidence. These include the Kansas City Cardiomyopathy Questionnaire (KCCQ), the New York Heart Association (NYHA) functional classification and the EuroQuol EQ-5D-5L multiattribute health related quality of life (HRQoL) preference instrument. The review concludes that apart from purely clinical claims based on the various pivotal trials, there are no PRO claims for mavacamten in SHCM that meet the required measurement standards.

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14

Manus, Jean-Marie. "Mavacamten, un nouveau traitement biologique de la cardiomyopathie hypertrophique." Revue Francophone des Laboratoires 2022, no. 544 (July 2022): 7. http://dx.doi.org/10.1016/s1773-035x(22)00224-6.

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15

Dvornikov, Alexey V., and Samantha P. Harris. "Myofibril relaxation with mavacamten is modified by cMyBP-c." Biophysical Journal 122, no. 3 (February 2023): 402a—403a. http://dx.doi.org/10.1016/j.bpj.2022.11.2193.

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16

Ho, Carolyn Y., Matthew E. Mealiffe, Richard G. Bach, Mondira Bhattacharya, Lubna Choudhury, Jay M. Edelberg, Sheila M. Hegde, et al. "Evaluation of Mavacamten in Symptomatic Patients With Nonobstructive Hypertrophic Cardiomyopathy." Journal of the American College of Cardiology 75, no. 21 (June 2020): 2649–60. http://dx.doi.org/10.1016/j.jacc.2020.03.064.

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17

Abella, Lina Maria Rayo, Britt Hofmann, Ulrich Gerds, and Joachim Neumann. "Effects of omecamtiv mecarbil and mavacamten 461 in isolated human atrium." Journal of Molecular and Cellular Cardiology 173 (December 2022): 135. http://dx.doi.org/10.1016/j.yjmcc.2022.08.265.

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18

Yusof, Liyana, Derek Yellon, and Sean Davidson. "Investigation into the role of mavacamten in myocardial ischaemia-reperfusion injury." Journal of Molecular and Cellular Cardiology 173 (December 2022): 2. http://dx.doi.org/10.1016/j.yjmcc.2022.08.008.

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19

Sewanan, Lorenzo, Shi Shen, and Stuart Campbell. "MAVACAMTEN PRESERVED LENGTH-DEPENDENT CONTRACTILITY AND IMPROVED DIASTOLIC FUNCTION IN HUMAN ENGINEERED MYOCARDIUM." Journal of the American College of Cardiology 77, no. 18 (May 2021): 536. http://dx.doi.org/10.1016/s0735-1097(21)01895-7.

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20

Hegde, Sheila M., Steven J. Lester, Scott D. Solomon, Michelle Michels, Perry M. Elliott, Sherif F. Nagueh, Lubna Choudhury, et al. "Effect of Mavacamten on Echocardiographic Features in Symptomatic Patients With Obstructive Hypertrophic Cardiomyopathy." Journal of the American College of Cardiology 78, no. 25 (December 2021): 2518–32. http://dx.doi.org/10.1016/j.jacc.2021.09.1381.

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21

Ferrantini, Cecilia, Beatrice Scellini, Giulia Vitale, J. Manuel Pioner, Silvia Querceto, Raffaele Coppini, Nicoletta Piroddi, Corrado Poggesi, and Chiara Tesi. "Mavacamten depresses human atrial contractility in the same EC50% range as human ventricle." Biophysical Journal 121, no. 3 (February 2022): 106a—107a. http://dx.doi.org/10.1016/j.bpj.2021.11.2179.

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22

Mathai, Susan, and Lynne Williams. "Left ventricular outflow tract obstruction in hypertrophic cardiomyopathy and the impact of mavacamten." Therapeutic Advances in Chronic Disease 13 (January 2022): 204062232211360. http://dx.doi.org/10.1177/20406223221136074.

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Hypertrophic cardiomyopathy (HCM) is a common genetic disorder characterised by unexplained left ventricular hypertrophy. Left ventricular outflow tract obstruction is an integral component of the disease, often resulting in significant symptoms, but also carrying a risk of progression to heart failure and death. Advancements in our understanding of the pathophysiology of HCM have led to the development of new therapies targeting the molecular basis of the disease at the level of the cardiac sarcomere, the basic contractile apparatus of the myocardium. Myosin modulators are a novel class of small molecules which target cardiac myosins directly to modulate cardiac contractility. The myosin inhibitors present the first advancement in pharmacological management of obstructive HCM in almost 35 years, with a growing body of evidence for the safety, tolerability and efficacy of mavacamten, and to a lesser extent aficamten. The aim of this review is to summarise the current management of patients with obstructive HCM and review the most recent available data from clinical trials pertaining to myosin inhibition.

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23

Hameed, Ishaque, Omer Mustafa Siddiqui, and Syed Abdus Samad. "MAVACAMTEN: A door that has opened in the treatment of Hyper-trophic Cardiomyopathy." Journal of the Pakistan Medical Association 73, no. 2 (February 15, 2023): 446–47. http://dx.doi.org/10.47391/jpma.7258.

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24

Ma, Weikang, Marcus Henze, Robert L. Anderson, Henry Gong, Fiona L. Wong, Carlos L. del Rio, and Thomas Irving. "The Super-Relaxed State and Length Dependent Activation in Porcine Myocardium." Circulation Research 129, no. 6 (September 3, 2021): 617–30. http://dx.doi.org/10.1161/circresaha.120.318647.

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Rationale: Myofilament length-dependent activation (LDA) is the key underlying mechanism of cardiac heterometric autoregulation, commonly referred as the Frank-Starling Law of the heart. Although alterations in LDA are common in cardiomyopathic states, the precise structural and biochemical mechanisms underlying LDA remain unknown. Objective: Here, we examine the role of structural changes in the thick filament during diastole, in particular changes in the availability of myosin heads, in determining both calcium sensitivity and maximum contractile force during systole in permeabilized porcine cardiac fibers. Methods and Results: Permeabilized porcine fibers from ventricular myocardium were studied under relaxing conditions at short and long sarcomere length using muscle mechanics, biochemical measurements, and X-ray diffraction. Upon stretch, the porcine myocardium showed the increased calcium sensitivity and maximum calcium-activated force characteristic of LDA. Stretch increased diastolic ATP turnover, recruiting reserve myosin heads from the super-relaxed state at longer sarcomere length. Structurally, X-ray diffraction studies in the relaxed-muscle confirmed a departure from the helical ordering of the thick filament upon stretch which occurred concomitantly with a displacement of myosin heads towards actin, facilitating cross-bridge formation upon systolic activation. Mavacamten, a selective myosin-motor inhibitor known to weaken the transition to actin-bound power-generating states and to enrich the ordered super-relaxed state myosin population, reversed the structural effects of stretch on the thick filament, blunting the mechanical consequences of stretch; mavacamten did not, however, prevent other structural changes associated with LDA in the sarcomere, such as decreased lattice spacing or troponin-displacement. Conclusions: Our findings strongly indicate that in ventricular muscle, LDA and its systolic consequences are dependent on the population of myosin heads competent to form cross bridges and involves the recruitment of myosin heads from the reserve super-relaxed state pool during diastole.

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25

Alsulami, Khulud, and Steven Marston. "Small Molecules Acting on Myofilaments as Treatments for Heart and Skeletal Muscle Diseases." International Journal of Molecular Sciences 21, no. 24 (December 16, 2020): 9599. http://dx.doi.org/10.3390/ijms21249599.

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Hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) are the most prevalent forms of the chronic and progressive pathological condition known as cardiomyopathy. These diseases have different aetiologies; however, they share the feature of haemodynamic abnormalities, which is mainly due to dysfunction in the contractile proteins that make up the contractile unit known as the sarcomere. To date, pharmacological treatment options are not disease-specific and rather focus on managing the symptoms, without addressing the disease mechanism. Earliest attempts at improving cardiac contractility by modulating the sarcomere indirectly (inotropes) resulted in unwanted effects. In contrast, targeting the sarcomere directly, aided by high-throughput screening systems, could identify small molecules with a superior therapeutic value in cardiac muscle disorders. Herein, an extensive literature review of 21 small molecules directed to five different targets was conducted. A simple scoring system was created to assess the suitability of small molecules for therapy by evaluating them in eight different criteria. Most of the compounds failed due to lack of target specificity or poor physicochemical properties. Six compounds stood out, showing a potential therapeutic value in HCM, DCM or heart failure (HF). Omecamtiv Mecarbil and Danicamtiv (myosin activators), Mavacamten, CK-274 and MYK-581 (myosin inhibitors) and AMG 594 (Ca2+-sensitiser) are all small molecules that allosterically modulate troponin or myosin. Omecamtiv Mecarbil showed limited efficacy in phase III GALACTIC-HF trial, while, results from phase III EXPLORER-HCM trial were recently published, indicating that Mavacamten reduced left ventricular outflow tract (LVOT) obstruction and diastolic dysfunction and improved the health status of patients with HCM. A novel category of small molecules known as “recouplers” was reported to target a phenomenon termed uncoupling commonly found in familial cardiomyopathies but has not progressed beyond preclinical work. In conclusion, the contractile apparatus is a promising target for new drug development.

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26

Argirò, Alessia, Mattia Zampieri, Martina Berteotti, Alberto Marchi, Luigi Tassetti, Chiara Zocchi, Luisa Iannone, et al. "Emerging Medical Treatment for Hypertrophic Cardiomyopathy." Journal of Clinical Medicine 10, no. 5 (March 1, 2021): 951. http://dx.doi.org/10.3390/jcm10050951.

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Hypertrophic cardiomyopathy (HCM) is a common myocardial disease characterized by otherwise unexplained left ventricular hypertrophy. The main cause of disabling symptoms in patients with HCM is left ventricular outflow tract (LVOT) obstruction. This phenomenon is multifactorial, determined both by anatomical and functional abnormalities: myocardial hypercontractility is believed to represent one of its major determinants. The anatomical anomalies are targeted by surgical interventions, whereas attenuating hypercontractility is the objective of old and new drugs including the novel class of allosteric myosin inhibitors. This review summarizes the current treatment modalities and discusses the emerging therapeutical opportunities focusing on the recently developed cardiac myosin ATPase inhibitors Mavacamten and CK-274. Novel surgical and interventional approaches are also discussed.

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27

Sarker, J., M. Joshi, JH Wasfy, M. Beinfeld, E. Nhan, M. Whittington, SD Pearson, DM Rind, and SM Walton. "EE457 Long-Term Cost Effectiveness of Mavacamten for Treatment of Hypertrophic Obstructive Cardiomyopathy (HOCM)." Value in Health 25, no. 7 (July 2022): S424. http://dx.doi.org/10.1016/j.jval.2022.04.705.

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28

Zakharyan, E. A., G. M. Salieva, and I. E. Terzeman. "Hypertrophic cardiomyopathy: A modern view on the diagnosis and management of patients (review)." Siberian Journal of Clinical and Experimental Medicine 37, no. 2 (July 14, 2022): 35–40. http://dx.doi.org/10.29001/2073-8552-2022-37-2-35-40.

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Hypertrophic cardiomyopathy (HCM) is a genetically determined disease with a high prevalence and manifestation at the age of 30–40 years. Currently available most effective treatments are extended myectomy and Morrow septal myectomy. However, the frequent occurrence of postoperative complications and restrictions to the use of these methods in certain groups of patients provides rationale for the improvement of the existing treatment methods and search for new pharmacological approaches. One of the most promising areas of conservative therapy is the study of a specific small-molecule allosteric inhibitor of myosinadenosine triphosphatase (mavacamten). Clinical studies of the efficacy and safety of this drug continue to this day, and if they are successfully completed, the drug may be included in the pharmacotherapy protocol for HCM.

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29

Taddei-Allen, Patty. "Considerations for managed care pharmacy in evaluating mavacamten, a novel agent for obstructive hypertrophic cardiomyopathy." Journal of Managed Care & Specialty Pharmacy 28, no. 3 (March 2022): 376–78. http://dx.doi.org/10.18553/jmcp.2022.28.3.376.

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30

Pysz, Piotr, Renata Rajtar-Salwa, Grzegorz Smolka, Iacopo Olivotto, Wojciech Wojakowski, and Paweł Petkow-Dimitrow. "Mavacamten — a new disease-specific option for pharmacological treatment of symptomatic patients with hypertrophic cardiomyopathy." Kardiologia Polska 79, no. 9 (September 30, 2021): 949–54. http://dx.doi.org/10.33963/kp.a2021.0064.

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31

Tower-Rader, Albree, Jay Ramchand, Steve E. Nissen, and Milind Y. Desai. "Mavacamten: a novel small molecule modulator of β-cardiac myosin for treatment of hypertrophic cardiomyopathy." Expert Opinion on Investigational Drugs 29, no. 11 (September 20, 2020): 1171–78. http://dx.doi.org/10.1080/13543784.2020.1821361.

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32

Ma, Weikang, Lin Qi, Momcilo Prodanovic, Henry M. Gong, Christopher Zambataro, Sampath K. Gollapudi, Srboljub M. Mijailovich, Carlos L. Del Rio, Suman Nag, and Thomas C. Irving. "Myosin in autoinhibited off state(s), stabilized by mavacamten, can be recruited via inotropic effectors." Biophysical Journal 122, no. 3 (February 2023): 122a. http://dx.doi.org/10.1016/j.bpj.2022.11.829.

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33

Reza, Nosheen, Amy B. Marzolf, Nicole Hornsby, Laura C. Vann, Alejandro de Feria, and Anjali Tiku Owens. "REAL WORLD EXPERIENCE OF THE USE OF MAVACAMTEN IN PATIENTS WITH SYMPTOMATIC OBSTRUCTIVE HYPERTROPHIC CARDIOMYOPATHY." Journal of the American College of Cardiology 81, no. 8 (March 2023): 322. http://dx.doi.org/10.1016/s0735-1097(23)00766-0.

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34

Musumeci, Monica, Chiara Palandri, Lorenzo Santini, Lucrezia Giammarino, Giulia Vitale, Marianna Langione, Cecilia Ferrantini, Manuel Jose Pioner, Raffaele Coppini, and Elisabetta Cerbai. "Effects of mavacamten in human myocardium from hypertrophic obstructive cardiomyopathy (HOCM) patients: A comparison with disopyramide." Vascular Pharmacology 146 (October 2022): 107061. http://dx.doi.org/10.1016/j.vph.2022.107061.

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35

Awinda, Peter O., Yemeserach Bishaw, Marissa Watanabe, Maya A. Guglin, Kenneth S. Campbell, and Bertrand C. W. Tanner. "Effects of mavacamten on Ca 2+ sensitivity of contraction as sarcomere length varied in human myocardium." British Journal of Pharmacology 177, no. 24 (October 21, 2020): 5609–21. http://dx.doi.org/10.1111/bph.15271.

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36

Scellini, Beatrice, Nicoletta Piroddi, Marica Dente, Cecilia Ferrantini, Raffaele Coppini, Corrado Poggesi, and Chiara Tesi. "Impact of Mavacamten on Force Generation in Single Myofibrils from Rabbit Psoas and Human Cardiac Muscle." Biophysical Journal 118, no. 3 (February 2020): 7a. http://dx.doi.org/10.1016/j.bpj.2019.11.231.

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37

Cuéllar Rodríguez, Santiago. "Novel Drugs Recently Authorized by EMA and FDA (Q2, 2022)." Anales de la Real Academia Nacional de Farmacia 88, no. 88(02) (June 30, 2022): 235–47. http://dx.doi.org/10.53519/analesranf.2022.88.02.07.

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EMA: Semaglutida (Wegovy®): obesidad. Voxelotor (Oxbryta®): anemia falciforme. Finerenona (Kerendia®): insuficiencia renal. Lonapegsomatropina (Lonapegsomatropina ascendis®): trastorno del crecimiento (déficit HG). Somatrogon (Ngenla®): trastorno del crecimiento (déficit HG). Nirmatrelvir/Ritonavir (Paxlovid®): covid-19. Tixagevimab/Cilgavimab (Evusheld®): covid-19. Tecovirimat (Tecovirimat Siga®): viruela. Sotorasib (Lumykras®): cáncer de pulmón. Tepotinib (Tepmetko®): cáncer de pulmón. Enfortumab vedotina (Padcev®): cáncer urotelial. Ciltacabtagene autoleucel (Carvykti®): mieloma múltiple. Mosunetuzumab (Lunsumio®): linfoma folicular. Avacopan (Tavneos®): granulomatosis. Inebilizumab (Uplizna®): neuromielitis óptica. Anifrolumab (Saphnelo®): lupus eritematoso sistémico. Eptinezumab (Vyepti®): migraña. Glucarpidasa (Voraxaze®): intoxicación por metotrexato. FDA: Tirzepatida (Mounjaro®): diabetes mellitus tipo 2. Vonoprazan (Voquezna®): infección por Helicobacter pylori. Mavacamten (Camzyos®): miocardiopatía hipertrófica. Tapinarof (Vtama®): psoriasis. Oteseconazol (Vivjoa®): candidiasis vulvovaginal. Relatlimag/Nivolumab (Opdualag ®): melanoma. Pacritinib (Vonjo®): mielofibrosis. Ganaxolona (Ztalmy®): epilepsia por déficit CDKL5. Lutecio (177Lu) Vipivotida Tetraxetano (Pluvicto®): cáncer de próstata (radioterapia).

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38

Anderson, Robert L., Darshan V. Trivedi, Saswata S. Sarkar, Marcus Henze, Weikang Ma, Henry Gong, Christopher S. Rogers, et al. "Deciphering the super relaxed state of human β-cardiac myosin and the mode of action of mavacamten from myosin molecules to muscle fibers." Proceedings of the National Academy of Sciences 115, no. 35 (August 13, 2018): E8143—E8152. http://dx.doi.org/10.1073/pnas.1809540115.

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Mutations in β-cardiac myosin, the predominant motor protein for human heart contraction, can alter power output and cause cardiomyopathy. However, measurements of the intrinsic force, velocity, and ATPase activity of myosin have not provided a consistent mechanism to link mutations to muscle pathology. An alternative model posits that mutations in myosin affect the stability of a sequestered, super relaxed state (SRX) of the protein with very slow ATP hydrolysis and thereby change the number of myosin heads accessible to actin. Here we show that purified human β-cardiac myosin exists partly in an SRX and may in part correspond to a folded-back conformation of myosin heads observed in muscle fibers around the thick filament backbone. Mutations that cause hypertrophic cardiomyopathy destabilize this state, while the small molecule mavacamten promotes it. These findings provide a biochemical and structural link between the genetics and physiology of cardiomyopathy with implications for therapeutic strategies.

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39

Gras, J. "Mavacamten. Allosteric modulator of cardiac myosin, Treatment of hypertrophic cardiomyopathy, Treatment of heart failure with preserved ejection fraction." Drugs of the Future 46, no. 6 (2021): 443. http://dx.doi.org/10.1358/dof.2021.46.6.3273821.

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Wheeler, Matthew Thomas, Iacopo Olivotto, Perry M. Elliott, Sara Saberi, Anjali Tiku Owens, Mathew S. Maurer, Ahmad Masri, et al. "THE EFFECT OF MAVACAMTEN ON CARDIOPULMONARY EXERCISE TESTING PERFORMANCE OF PATIENTS WITH OBSTRUCTIVE HYPERTROPHIC CARDIOMYOPATHY IN EXPLORER-HCM." Journal of the American College of Cardiology 79, no. 9 (March 2022): 237. http://dx.doi.org/10.1016/s0735-1097(22)01228-1.

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41

Ma, Weikang, Suman Nag, Srinivas Chakravarthy, Sampath Gollapudi, Na Sa, Ivan Tomasic, and Thomas C. Irving. "Effects of Mavacamten and Blebbistatin on the Small-Angle X-ray Scattering Structure of Human β-cardiac Myosin." Biophysical Journal 118, no. 3 (February 2020): 422a. http://dx.doi.org/10.1016/j.bpj.2019.11.2378.

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42

Cresci, Sharon, Richard G. Bach, Sara Saberi, Anjali Tiku Owens, Neal K. Lakdawala, Ester Kim Nilles, Daniel M. Wojdyla, Amy J. Sehnert, and Andrew Wang. "WOMEN IN EXPLORER-HCM HAD MORE SEVERE HEART FAILURE AT BASELINE BUT SIMILAR, OR GREATER, RESPONSE TO MAVACAMTEN." Journal of the American College of Cardiology 81, no. 8 (March 2023): 344. http://dx.doi.org/10.1016/s0735-1097(23)00788-x.

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43

Maron, Barry J., Ethan J. Rowin, and Martin S. Maron. "Is Regression of Left Ventricular Hypertrophy Really a Good Thing for Patients With Hypertrophic Cardiomyopathy?: The Emerging Mavacamten Story." American Journal of Cardiology 147 (May 2021): 145–46. http://dx.doi.org/10.1016/j.amjcard.2021.01.034.

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44

Tanner, Bertrand C. W., Peter O. Awinda, Yemeserach Bishaw, Marissa Watanabe, Katherine L. Thompson, Mindy S. Thompson, Emma J. Birks, and Kenneth S. Campbell. "Effects of mavacamten and sarcomere length on the Ca2+-sensitivity of permeabilized myocardial strips from patients with heart failure." Biophysical Journal 121, no. 3 (February 2022): 107a. http://dx.doi.org/10.1016/j.bpj.2021.11.2182.

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45

Gollapudi, Sampath K., Weikang Ma, Srinivas Chakravarthy, Ariana C. Combs, Na Sa, Stephen Langer, Thomas C. Irving, and Suman Nag. "Two Classes of Myosin Inhibitors, Para-nitroblebbistatin and Mavacamten, Stabilize β-Cardiac Myosin in Different Structural and Functional States." Journal of Molecular Biology 433, no. 23 (November 2021): 167295. http://dx.doi.org/10.1016/j.jmb.2021.167295.

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46

Jacoby, Daniel, Steven Lester, Anjali Owens, Andrew Wang, Don Young, Radhika Tripuraneni, Marc Semigran, and Stephen Heitner. "REDUCTION IN LEFT VENTRICULAR OUTFLOW TRACT GRADIENT WITH MAVACAMTEN (MYK-461) IN SYMPTOMATIC OBSTRUCTIVE HYPERTROPHIC CARDIOMYOPATHY PATIENTS (PIONEER-HCM)." Journal of the American College of Cardiology 71, no. 11 (March 2018): A644. http://dx.doi.org/10.1016/s0735-1097(18)31185-9.

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47

Olivotto, Iacopo, Artur Oreziak, Roberto Barriales-Villa, Theodore P. Abraham, Ahmad Masri, Pablo Garcia-Pavia, Sara Saberi, et al. "Mavacamten for treatment of symptomatic obstructive hypertrophic cardiomyopathy (EXPLORER-HCM): a randomised, double-blind, placebo-controlled, phase 3 trial." Lancet 396, no. 10253 (September 2020): 759–69. http://dx.doi.org/10.1016/s0140-6736(20)31792-x.

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Awinda, Peter O., Marissa Watanabe, Yemeserach Bishaw, Katarzyna Kazmierczak, Danuta Szczesna-Cordary, and Bertrand C. Tanner. "Mavacamten Decreases Maximal Force and Ca2+-Sensitivity of Contraction in Myocardial Strips From a Mouse Model for Hypertrophic Cardiomyopathy." Biophysical Journal 118, no. 3 (February 2020): 594a. http://dx.doi.org/10.1016/j.bpj.2019.11.3214.

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49

Tschöpe, Carsten, Ahmed Elsanhoury, Sonja Diekmann, and Uwe Kühl. "Hypertrophe Kardiomyopathien und die kardiale ATTR-Amyloidose – eine aktuelle Übersicht für den klinischen Alltag." DMW - Deutsche Medizinische Wochenschrift 147, no. 17 (August 28, 2022): 1127–34. http://dx.doi.org/10.1055/a-1744-3126.

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Was ist neu? Hypertrophe obstruktive Kardiomyopathie Mavacamten, der erste Myosin-Aktivator, konnte erfolgreich in dem EXPLORER-HCM-Studienprogramm getestet werden. Lebensqualität und linksventrikuläre Druckgradienten-Abnahme wurden optimiert. Ob damit jedoch auch die Überlebensrate und Prognose der betroffenen Patienten verbessert wird, kann bis heute noch nicht gesagt werden. Die europäischen Zulassungsbehörden sehen allerdings bisher die Ergebnisse als so bedeutsam an, dass mit einer Führung der Substanzklasse vielleicht schon in den nächsten 6–8 Monaten zu rechnen ist. In den USA ist die Substanz bereits seit April 2022 zugelassen. Der Einsatz der Substanz bei HCM-Patienten ohne Obstruktion wird ebenfalls zurzeit untersucht. Kardiale Transthyretin-Amyloidosen Kardiale Amyloidosen haben meist eine gute Ejektionsfraktion, jedoch sind auch EF mit 40 oder < 30 % möglich. Das Auftreten einer kardialen Amyloidose bei Patienten mit der Symptomatik einer Herzinsuffizienz mit erhaltener Ejektionsfraktion (HFpEF) ist in bis zu 15 % der Fälle nachzuweisen. Tafamidis ist die einzige zurzeit zugelassene erfolgreiche Therapiemöglichkeit bei Patienten mit kardialer ATTR-Amyloidose. Dies wurde auch durch weitere Beobachtungsregister der ATTR-ACT-Studie gezeigt. Für die Klinik ist zusätzlich wichtig, dass die Amyloidose auch die Aortenklappe befällt. Zahlreiche Patienten entwickeln somit auch eine Aortenstenose, die erkannt und meist interventionell zu behandeln ist.

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Daaboul, Yazan, Ethan Rowin, Martin Maron, and Carey Kimmelstiel. "TCT-355 Lifetime Costs of Septal Reduction Therapies are Substantially Lower Compared to Mavacamten in Patients With Obstructive Hypertrophic Cardiomyopathy." Journal of the American College of Cardiology 80, no. 12 (September 2022): B144. http://dx.doi.org/10.1016/j.jacc.2022.08.416.

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