Journal articles: 'Istaroxime'

1

Revill, P., N. Serradell, J. Bolós, and E. Rosa. "Istaroxime." Drugs of the Future 32, no. 7 (2007): 595. http://dx.doi.org/10.1358/dof.2007.032.07.1118134.

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Stagno, Matias Julian, Nefeli Zacharopoulou, Jonas Bochem, Anna Tsapara, Lisann Pelzl, Tamer al-Maghout, Galatea Kallergi, et al. "Istaroxime Inhibits Motility and Down-Regulates Orai1 Expression, SOCE and FAK Phosphorylation in Prostate Cancer Cells." Cellular Physiology and Biochemistry 42, no. 4 (2017): 1366–76. http://dx.doi.org/10.1159/000479200.

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Background/Aims: Istaroxime is a validated inotropic Na+/K+ ATPase inhibitor currently in development for the treatment of various cardiac conditions. Recent findings established that this steroidal drug exhibits potent apoptotic responses in prostate tumors in vitro and in vivo, by affecting key signaling orchestrating proliferation and apoptosis, such as c-Myc and caspase 3, Rho GTPases and actin cytoskeleton dynamics. In the present study we examined whether istaroxime is affecting cell motility and analyzed the underlying mechanism in prostate tumor cells. Methods: Migration was assessed by transwell and wound healing assays, Orai1 and Stim1 abundance by RT-PCR and confocal immunofluorescence microscopy, Fura-2 fluorescence was utilized to determine intracellular Ca2+ and Western blotting for FAK/pFAK measurements. Results: We observed strong inhibition of cell migration in istaroxime treated DU-145 prostate cancer cells. Istaroxime further decreased Orai1 and Stim1 transcript levels and downregulated Orai1 protein expression. Moreover, SOCE was significantly decreased upon istaroxime treatment. Furthermore, istaroxime strikingly diminished phosphorylated FAK levels. Interestingly, the efficacy of istaroxime on the inhibition of DU-145 cell migration was further enhanced by blocking Orai1 with 2-APB and FAK with the specific inhibitor PF-00562271. These results provide strong evidence that istaroxime prevents cell migration and motility of DU-145 prostate tumor cells, an effect at least partially attributed to Orai1 downregulation and FAK de-activation. Conclusion: Collectively our results indicate that this enzyme inhibitor, besides its pro-apoptotic action, affects motility of cancer cells, supporting its potential role as a strong candidate for further clinical cancer drug development.

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Dec, G. William. "Istaroxime in Heart Failure." Journal of the American College of Cardiology 51, no. 23 (June 2008): 2286–88. http://dx.doi.org/10.1016/j.jacc.2008.04.005.

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Forzano, Imma, Pasquale Mone, Gaetano Mottola, Urna Kansakar, Luigi Salemme, Antonio De Luca, Tullio Tesorio, Fahimeh Varzideh, and Gaetano Santulli. "Efficacy of the New Inotropic Agent Istaroxime in Acute Heart Failure." Journal of Clinical Medicine 11, no. 24 (December 18, 2022): 7503. http://dx.doi.org/10.3390/jcm11247503.

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Current therapeutic strategies for acute heart failure (AHF) are based on traditional inotropic agents that are often associated with untoward effects; therefore, finding new effective approaches with a safer profile is dramatically needed. Istaroxime is a novel compound, chemically unrelated to cardiac glycosides, that is currently being studied for the treatment of AHF. Its effects are essentially related to its inotropic and lusitropic positive properties exerted through a dual mechanism of action: activation of the sarcoplasmic reticulum Ca2+ ATPase isoform 2a (SERCA2a) and inhibition of the Na+/K+-ATPase (NKA) activity. The advantages of istaroxime over the available inotropic agents include its lower arrhythmogenic action combined with its capability of increasing systolic blood pressure without augmenting heart rate. However, it has a limited half-life (1 hour) and is associated with adverse effects including pain at the injection site and gastrointestinal issues. Herein, we describe the main mechanism of action of istaroxime and we present a systematic overview of both clinical and preclinical trials testing this drug, underlining the latest insights regarding its adoption in clinical practice for AHF.

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Liang, G. P., J. H. Guo, and R. W. Jiang. "Novel approach to the synthesis of istaroxime." Russian Journal of General Chemistry 87, no. 11 (November 2017): 2643–47. http://dx.doi.org/10.1134/s1070363217110196.

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&NA;. "Istaroxime: a new HF treatment on the HORIZON." Inpharma Weekly &NA;, no. 1633 (April 2008): 6. http://dx.doi.org/10.2165/00128413-200816330-00014.

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Torre, E., A. M. Lodrini, P. Barassi, M. Ferrandi, E. Boz, C. Bussadori, P. Ferrari, G. Bianchi, and M. Rocchetti. "Istaroxime improves diabetic diastolic dysfunction through SERCA stimulation." Archives of Cardiovascular Diseases Supplements 11, no. 2 (April 2019): 234–35. http://dx.doi.org/10.1016/j.acvdsp.2019.02.117.

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Aditya, Suruchi, and Aditya Rattan. "Istaroxime: A rising star in acute heart failure." Journal of Pharmacology and Pharmacotherapeutics 3, no. 4 (2012): 353. http://dx.doi.org/10.4103/0976-500x.103705.

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Farmakis, Dimitrios, and Gerasimos Filippatos. "Istaroxime: Is the Remedy Better than the Disease?" Cardiovascular Drugs and Therapy 25, no. 2 (April 2011): 115–17. http://dx.doi.org/10.1007/s10557-011-6295-7.

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Gonano, Luis Alberto, María Florencia Racciopi, Malena Morell, and Martín Vila Petroff. "Istaroxime, an emerging inotrope with less cardiotoxicity than digitalis." Journal of Molecular and Cellular Cardiology 140 (March 2020): 6. http://dx.doi.org/10.1016/j.yjmcc.2019.11.011.

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Mattera, Giovan Giuseppe, Pietro Lo Giudice, Francesca M. P. Loi, Emilio Vanoli, Jean-Pierre Gagnol, Franco Borsini, and Paolo Carminati. "Istaroxime: A New Luso-Inotropic Agent for Heart Failure." American Journal of Cardiology 99, no. 2 (January 2007): S33—S40. http://dx.doi.org/10.1016/j.amjcard.2006.09.004.

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Luciani, Paola, Maréva Fevre, and Jean-Christophe Leroux. "Development and physico-chemical characterization of a liposomal formulation of istaroxime." European Journal of Pharmaceutics and Biopharmaceutics 79, no. 2 (October 2011): 285–93. http://dx.doi.org/10.1016/j.ejpb.2011.04.013.

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Chioncel, Ovidiu, Sean P. Collins, and Javed Butler. "Istaroxime in acute heart failure: the holy grail is at HORIZON?" European Journal of Heart Failure 22, no. 9 (May 6, 2020): 1694–97. http://dx.doi.org/10.1002/ejhf.1843.

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Huang, Christopher L. H. "SERCA2a stimulation by istaroxime: a novel mechanism of action with translational implications." British Journal of Pharmacology 170, no. 3 (September 17, 2013): 486–88. http://dx.doi.org/10.1111/bph.12288.

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Lo Giudice, Pietro, Giovan Giuseppe Mattera, Jean-Pierre Gagnol, and Franco Borsini. "Chronic Istaroxime Improves Cardiac Function and Heart Rate Variability in Cardiomyopathic Hamsters." Cardiovascular Drugs and Therapy 25, no. 2 (February 3, 2011): 133–38. http://dx.doi.org/10.1007/s10557-011-6283-y.

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&NA;. "Istaroxime* is well tolerated in patients with systolic dysfunction and chronic heart failure." Inpharma Weekly &NA;, no. 1577 (March 2007): 9. http://dx.doi.org/10.2165/00128413-200715770-00021.

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Badone, Beatrice, Roel Spatjens, Cristina Altrocchi, Paul Volders, and Antonio Zaza. "Istaroxime Accelerates Calcium Transient Decay in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes." Biophysical Journal 114, no. 3 (February 2018): 306a. http://dx.doi.org/10.1016/j.bpj.2017.11.1738.

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Arici, Martina, Mara Ferrandi, Shih-Che Hsu, Eleonora Torre, Paolo Barassi, Andrea Luraghi, Carlotta Ronchi, et al. "Istaroxime metabolite PST3093 selectively stimulates SERCA2a and reverses disease-induced changes in cardiac function." Vascular Pharmacology 146 (October 2022): 107028. http://dx.doi.org/10.1016/j.vph.2022.107028.

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Ferrandi, Mara, Paolo Barassi, Francesco Tadini-Buoninsegni, Gianluca Bartolommei, Isabella Molinari, Maria Grazia Tripodi, Cristina Reina, Maria Rosa Moncelli, Giuseppe Bianchi, and Patrizia Ferrari. "Istaroxime stimulates SERCA2a and accelerates calcium cycling in heart failure by relieving phospholamban inhibition." British Journal of Pharmacology 169, no. 8 (July 26, 2013): 1849–61. http://dx.doi.org/10.1111/bph.12278.

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20

Gheorghiade, Mihai, John E. A. Blair, Gerasimos S. Filippatos, Cezar Macarie, Witold Ruzyllo, Jerzy Korewicki, Serban I. Bubenek-Turconi, et al. "Hemodynamic, Echocardiographic, and Neurohormonal Effects of Istaroxime, a Novel Intravenous Inotropic and Lusitropic Agent." Journal of the American College of Cardiology 51, no. 23 (June 2008): 2276–85. http://dx.doi.org/10.1016/j.jacc.2008.03.015.

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Avvisato, Roberta, Stanislovas S. Jankauskas, and Gaetano Santulli. "Istaroxime and Beyond: New Therapeutic Strategies to Specifically Activate SERCA and Treat Heart Failure." Journal of Pharmacology and Experimental Therapeutics 384, no. 1 (December 29, 2022): 227–30. http://dx.doi.org/10.1124/jpet.122.001446.

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Bossu, Alexandre, Amée Kostense, Henriette D. M. Beekman, Marien J. C. Houtman, Marcel A. G. van der Heyden, and Marc A. Vos. "Istaroxime, a positive inotropic agent devoid of proarrhythmic properties in sensitive chronic atrioventricular block dogs." Pharmacological Research 133 (July 2018): 132–40. http://dx.doi.org/10.1016/j.phrs.2018.05.001.

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23

Gobbini, Mauro, Silvia Armaroli, Leonardo Banfi, Alessandra Benicchio, Giulio Carzana, Giorgio Fedrizzi, Patrizia Ferrari, et al. "Novel Analogues of Istaroxime, a Potent Inhibitor of Na+,K+-ATPase: Synthesis and Structure−Activity Relationship†." Journal of Medicinal Chemistry 51, no. 15 (August 2008): 4601–8. http://dx.doi.org/10.1021/jm800257s.

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Kislitsina, Olga N., Jonathan D. Rich, Jane E. Wilcox, Duc T. Pham, Andrei Churyla, Esther B. Vorovich, Kambiz Ghafourian, and Clyde W. Yancy. "Shock – Classification and Pathophysiological Principles of Therapeutics." Current Cardiology Reviews 15, no. 2 (March 12, 2019): 102–13. http://dx.doi.org/10.2174/1573403x15666181212125024.

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The management of patients with shock is extremely challenging because of the myriad of possible clinical presentations in cardiogenic shock, septic shock and hypovolemic shock and the limitations of contemporary therapeutic options. The treatment of shock includes the administration of endogenous catecholamines (epinephrine, norepinephrine, and dopamine) as well as various vasopressor agents that have shown efficacy in the treatment of the various types of shock. In addition to the endogenous catecholamines, dobutamine, isoproterenol, phenylephrine, and milrinone have served as the mainstays of shock therapy for several decades. Recently, experimental studies have suggested that newer agents such as vasopressin, selepressin, calcium-sensitizing agents like levosimendan, cardiac-specific myosin activators like omecamtiv mecarbil (OM), istaroxime, and natriuretic peptides like nesiritide can enhance shock therapy, especially when shock presents a more complex clinical picture than normal. However, their ability to improve clinical outcomes remains to be proven. It is the purpose of this review to describe the mechanism of action, dosage requirements, advantages and disadvantages, and specific indications and contraindications for the use of each of these catecholamines and vasopressors, as well as to elucidate the most important clinical trials that serve as the basis of contemporary shock therapy.

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Wallner, Markus, Mounir Khafaga, Ewald Kolesnik, Aris Vafiadis, Gerold Schwantzer, Deborah M. Eaton, Pero Curcic, et al. "Istaroxime, a potential anticancer drug in prostate cancer, exerts beneficial functional effects in healthy and diseased human myocardium." Oncotarget 8, no. 30 (April 30, 2017): 49264–74. http://dx.doi.org/10.18632/oncotarget.17540.

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26

Segal, Robert, Yuhui Zhang, Valentina Carubelli, Phillip Simmons, Steven Simonson, Giuseppe Bianchi, Marco Metra, and Jian Zhang. "EFFICACY OF 24-HOUR ISTAROXIME INFUSION IS SIMILAR BETWEEN CAUCASIAN AND ASIAN PATIENTS HOSPITALIZED FOR ACUTE HEART FAILURE." Journal of the American College of Cardiology 75, no. 11 (March 2020): 970. http://dx.doi.org/10.1016/s0735-1097(20)31597-7.

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27

Carubelli, Valentina, Yuhui Zhang, Marco Metra, Carlo Lombardi, G. Michael Felker, Gerasimos Filippatos, Christopher M. O'Connor, et al. "Treatment with 24 hour istaroxime infusion in patients hospitalised for acute heart failure: a randomised, placebo‐controlled trial." European Journal of Heart Failure 22, no. 9 (January 23, 2020): 1684–93. http://dx.doi.org/10.1002/ejhf.1743.

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28

Shah, Sanjiv J., John E. A. Blair, Gerasimos S. Filippatos, Cezar Macarie, Witold Ruzyllo, Jerzy Korewicki, Serban I. Bubenek-Turconi, et al. "Effects of istaroxime on diastolic stiffness in acute heart failure syndromes: Results from the Hemodynamic, Echocardiographic, and Neurohormonal Effects of Istaroxime, a Novel Intravenous Inotropic and Lusitropic Agent: a Randomized Controlled Trial in Patients Hospitalized with Heart Failure (HORIZON-HF) trial." American Heart Journal 157, no. 6 (June 2009): 1035–41. http://dx.doi.org/10.1016/j.ahj.2009.03.007.

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Mattera, Giovan G., Francesca M. P. Loi, Jean Pierre Gagnol, Emilio Vanoli, Franco Borsini, and Paolo Carminati. "A 24 h Infusion of Istaroxime Dose-Dependently Improves Cardiac Performance in Conscious, Free-Moving Dogs with Heart Failure." Journal of Cardiac Failure 12, no. 6 (August 2006): S85. http://dx.doi.org/10.1016/j.cardfail.2006.06.289.

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30

Micheletti, Rosella, Fiorentina Palazzo, Paolo Barassi, Giuseppe Giacalone, Mara Ferrandi, Antonio Schiavone, Barbara Moro, Oberdan Parodi, Patrizia Ferrari, and Giuseppe Bianchi. "Istaroxime, a Stimulator of Sarcoplasmic Reticulum Calcium Adenosine Triphosphatase Isoform 2a Activity, as a Novel Therapeutic Approach to Heart Failure." American Journal of Cardiology 99, no. 2 (January 2007): S24—S32. http://dx.doi.org/10.1016/j.amjcard.2006.09.003.

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31

Buttá, Carmelo, Marco Roberto, Antonino Tuttolomondo, Rossella Petrantoni, Giuseppe Miceli, Luca Zappia, and Antonio Pinto. "Old and New Drugs for Treatment of Advanced Heart Failure." Current Pharmaceutical Design 26, no. 14 (May 15, 2020): 1571–83. http://dx.doi.org/10.2174/1381612826666191226165402.

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Background: Advanced heart failure (HF) is a progressive disease with high mortality and limited medical therapeutic options. Long-term mechanical circulatory support and heart transplantation remain goldstandard treatments for these patients; however, access to these therapies is limited by the advanced age and multiple comorbidities of affected patients, as well as by the limited number of organs available. Methods: Traditional and new drugs available for the treatment of advanced HF have been researched. Results: To date, the cornerstone for the treatment of patients with advanced HF remains water restriction, intravenous loop diuretic therapy and inotropic support. However, many patients with advanced HF experience loop diuretics resistance and alternative therapeutic strategies to overcome this problem have been developed, including sequential nephron blockade or use of the hypertonic saline solution in combination with high-doses of furosemide. As classic inotropes augment myocardial oxygen consumption, new promising drugs have been introduced, including levosimendan, istaroxime and omecamtiv mecarbil. However, pharmacological agents still remain mainly short-term or palliative options in patients with acute decompensation or excluded from mechanical therapy. Conclusions: Traditional drugs, especially when administered in combination, and new medicaments represent important therapeutic options in advanced HF. However, their impact on prognosis remains unclear. Large trials are necessary to clarify their therapeutic potential and prognostic role in these fragile patients.

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Kanai, Ryuta, Flemming Cornelius, Haruo Ogawa, Kanna Motoyama, Bente Vilsen, and Chikashi Toyoshima. "Binding of cardiotonic steroids to Na+,K+-ATPase in the E2P state." Proceedings of the National Academy of Sciences 118, no. 1 (December 14, 2020): e2020438118. http://dx.doi.org/10.1073/pnas.2020438118.

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The sodium pump (Na+, K+-ATPase, NKA) is vital for animal cells, as it actively maintains Na+ and K+ electrochemical gradients across the cell membrane. It is a target of cardiotonic steroids (CTSs) such as ouabain and digoxin. As CTSs are almost unique strong inhibitors specific to NKA, a wide range of derivatives has been developed for potential therapeutic use. Several crystal structures have been published for NKA-CTS complexes, but they fail to explain the largely different inhibitory properties of the various CTSs. For instance, although CTSs are thought to inhibit ATPase activity by binding to NKA in the E2P state, we do not know if large conformational changes accompany binding, as no crystal structure is available for the E2P state free of CTS. Here, we describe crystal structures of the BeF3− complex of NKA representing the E2P ground state and then eight crystal structures of seven CTSs, including rostafuroxin and istaroxime, two new members under clinical trials, in complex with NKA in the E2P state. The conformations of NKA are virtually identical in all complexes with and without CTSs, showing that CTSs bind to a preformed cavity in NKA. By comparing the inhibitory potency of the CTSs measured under four different conditions, we elucidate how different structural features of the CTSs result in different inhibitory properties. The crystal structures also explain K+-antagonism and suggest a route to isoform specific CTSs.

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Cowart, Doug, Antonino Amato, Dan Zhang, Giovanni Valentini, Paolo Carminati, Philip B. Adamson, Mihai Gheorghiade, and Eric Brass. "The Use of Non-Invasive Impedance Cardiography (ICG) To Define the Active Dose Range for Invasive Right Heart Hemodynamic Studies – The Istaroxime Experience." Journal of Cardiac Failure 12, no. 6 (August 2006): S78. http://dx.doi.org/10.1016/j.cardfail.2006.06.265.

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Hohendanner, Felix, Senka Ljubojević, Niall MacQuaide, Michael Sacherer, Simon Sedej, Liesbeth Biesmans, Paulina Wakula, et al. "Intracellular Dyssynchrony of Diastolic Cytosolic [Ca 2+ ] Decay in Ventricular Cardiomyocytes in Cardiac Remodeling and Human Heart Failure." Circulation Research 113, no. 5 (August 16, 2013): 527–38. http://dx.doi.org/10.1161/circresaha.113.300895.

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Rationale : Synchronized release of Ca 2+ into the cytosol during each cardiac cycle determines cardiomyocyte contraction. Objective: We investigated synchrony of cytosolic [Ca 2+ ] decay during diastole and the impact of cardiac remodeling. Methods and Results: Local cytosolic [Ca 2+ ] transients (1-µm intervals) were recorded in murine, porcine, and human ventricular single cardiomyocytes. We identified intracellular regions of slow (slowCaR) and fast (fastCaR) [Ca 2+ ] decay based on the local time constants of decay (TAU local ). The SD of TAU local as a measure of dyssynchrony was not related to the amplitude or the timing of local Ca 2+ release. Stimulation of sarcoplasmic reticulum Ca 2+ ATPase with forskolin or istaroxime accelerated and its inhibition with cyclopiazonic acid slowed TAU local significantly more in slowCaR, thus altering the relationship between SD of TAU local and global [Ca 2+ ] decay (TAU global ). Na + /Ca 2+ exchanger inhibitor SEA0400 prolonged TAU local similarly in slowCaR and fastCaR. FastCaR were associated with increased mitochondrial density and were more sensitive to the mitochondrial Ca 2+ uniporter blocker Ru360. Variation in TAU local was higher in pig and human cardiomyocytes and higher with increased stimulation frequency (2 Hz). TAU local correlated with local sarcomere relengthening. In mice with myocardial hypertrophy after transverse aortic constriction, in pigs with chronic myocardial ischemia, and in end-stage human heart failure, variation in TAU local was increased and related to cardiomyocyte hypertrophy and increased mitochondrial density. Conclusions: In cardiomyocytes, cytosolic [Ca 2+ ] decay is regulated locally and related to local sarcomere relengthening. Dyssynchronous intracellular [Ca 2+ ] decay in cardiac remodeling and end-stage heart failure suggests a novel mechanism of cellular contractile dysfunction.

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Rocchetti, Marcella, Matteo Alemanni, Gaspare Mostacciuolo, Paolo Barassi, Claudia Altomare, Riccardo Chisci, Rosella Micheletti, Patrizia Ferrari, and Antonio Zaza. "Modulation of Sarcoplasmic Reticulum Function by PST2744 [Istaroxime; (E,Z)-3-((2-Aminoethoxy)imino) Androstane-6,17-dione Hydrochloride)] in a Pressure-Overload Heart Failure Model." Journal of Pharmacology and Experimental Therapeutics 326, no. 3 (June 6, 2008): 957–65. http://dx.doi.org/10.1124/jpet.108.138701.

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Khan, Hashim, Marco Metra, John E. A. Blair, Mark Vogel, Matthew E. Harinstein, Gerasimos S. Filippatos, Hani N. Sabbah, Herve Porchet, Giovanni Valentini, and Mihai Gheorghiade. "Istaroxime, a first in class new chemical entity exhibiting SERCA-2 activation and Na–K-ATPase inhibition: a new promising treatment for acute heart failure syndromes?" Heart Failure Reviews 14, no. 4 (February 24, 2009): 277–87. http://dx.doi.org/10.1007/s10741-009-9136-z.

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Gobbini, Mauro, Silvia Armaroli, Leonardo Banfi, Alessandra Benicchio, Giulio Carzana, Patrizia Ferrari, Giuseppe Giacalone, Giuseppe Marazzi, Barbara Moro, and Rosella Micheletti. "Novel analogues of Istaroxime, a potent inhibitor of Na+,K+-ATPase: Synthesis, structure–activity relationship and 3D-quantitative structure–activity relationship of derivatives at position 6 on the androstane scaffold." Bioorganic & Medicinal Chemistry 18, no. 12 (June 15, 2010): 4275–99. http://dx.doi.org/10.1016/j.bmc.2010.04.095.

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Alevizopoulos, Konstantinos, Konstantinos Dimas, Natalia Papadopoulou, Eva-Maria Schmidt, Anna Tsapara, Saad Alkahtani, Sabina Honisch, et al. "Functional characterization and anti-cancer action of the clinical phase II cardiac Na+/K+ ATPase inhibitor istaroxime: in vitro and in vivo properties and cross talk with the membrane androgen receptor." Oncotarget 7, no. 17 (March 24, 2016): 24415–28. http://dx.doi.org/10.18632/oncotarget.8329.

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Blair, John E. A., Cezar Macarie, Witold Ruzyllo, Antonella Bacchieri, Giovanni Valentini, Maria Bianchetti, Peter S. Pang, et al. "Rationale and Design of the Hemodynamic, Echocardiographic and Neurohormonal Effects of Istaroxime, a Novel Intravenous Inotropic and Lusitropic Agent: A Randomized Controlled Trial in Patients Hospitalized With Heart Failure (HORIZON-HF) Trial." American Journal of Therapeutics 15, no. 3 (May 2008): 231–40. http://dx.doi.org/10.1097/mjt.0b013e31816d9186.

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Ghali, Jalal K., William B. Smith, Guillermo Torre-Amione, William Haynos, Barry K. Rayburn, Antonino Amato, Dan Zhang, et al. "A Phase 1–2 Dose-Escalating Study Evaluating the Safety and Tolerability of Istaroxime and Specific Effects on Electrocardiographic and Hemodynamic Parameters in Patients with Chronic Heart Failure with Reduced Systolic Function." American Journal of Cardiology 99, no. 2 (January 2007): S47—S56. http://dx.doi.org/10.1016/j.amjcard.2006.09.006.

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Racioppi, María Florencia, Juan Ignacio Burgos, Malena Morell, Luis Alberto Gonano, and Martín Vila Petroff. "Cellular Mechanisms Underlying the Low Cardiotoxicity of Istaroxime." Journal of the American Heart Association 10, no. 14 (July 20, 2021). http://dx.doi.org/10.1161/jaha.120.018833.

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Background Istaroxime is an inhibitor of Na + /K + ATPase with proven efficacy to increase cardiac contractility and to accelerate relaxation attributable to a relief in phospholamban‐dependent inhibition of the sarcoplasmic reticulum Ca 2+ ATPase. We have previously shown that pharmacologic Na + /K + ATPase inhibition promotes calcium/calmodulin‐dependent kinase II activation, which mediates both cardiomyocyte death and arrhythmias. Here, we aim to compare the cardiotoxic effects promoted by classic pharmacologic Na + /K + ATPase inhibition versus istaroxime. Methods and Results Ventricular cardiomyocytes were treated with ouabain or istaroxime at previously tested equi‐inotropic concentrations to compare their impact on cell viability, apoptosis, and calcium/calmodulin‐dependent kinase II activation. In contrast to ouabain, istaroxime neither promoted calcium/calmodulin‐dependent kinase II activation nor cardiomyocyte death. In addition, we explored the differential behavior promoted by ouabain and istaroxime on spontaneous diastolic Ca 2+ release. In rat cardiomyocytes, istaroxime did not significantly increase Ca 2+ spark and wave frequency but increased the proportion of aborted Ca 2+ waves. Further insight was provided by studying cardiomyocytes from mice that do not express phospholamban. In this model, the lower Ca 2+ wave incidence observed with istaroxime remains present, suggesting that istaroxime‐dependent relief on phospholamban‐dependent sarcoplasmic reticulum Ca 2+ ATPase 2A inhibition is not the unique mechanism underlying the low arrhythmogenic profile of this drug. Conclusions Our results indicate that, different from ouabain, istaroxime can reach a significant inotropic effect without leading to calcium/calmodulin‐dependent kinase II–dependent cardiomyocyte death. Additionally, we provide novel insights regarding the low arrhythmogenic impact of istaroxime on cardiac Ca 2+ handling.

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Torre, Eleonora, Martina Arici, Alessandra Maria Lodrini, Mara Ferrandi, Paolo Barassi, Shih-Che Hsu, Gwo-Jyh Chang, et al. "SERCA2a stimulation by istaroxime improves intracellular Ca2+ handling and diastolic dysfunction in a model of diabetic cardiomyopathy." Cardiovascular Research, April 1, 2021. http://dx.doi.org/10.1093/cvr/cvab123.

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Abstract Aims Diabetic cardiomyopathy is a multifactorial disease characterized by an early onset of diastolic dysfunction (DD) that precedes the development of systolic impairment. Mechanisms that can restore cardiac relaxation improving intracellular Ca2+ dynamics represent a promising therapeutic approach for cardiovascular diseases associated to DD. Istaroxime has the dual properties to accelerate Ca2+ uptake into sarcoplasmic reticulum (SR) through the SR Ca2+ pump (SERCA2a) stimulation and to inhibit Na+/K+ ATPase (NKA). This project aims to characterize istaroxime effects at a concentration (100 nmol/L) marginally affecting NKA, in order to highlight its effects dependent on the stimulation of SERCA2a in an animal model of mild diabetes. Methods and results Streptozotocin (STZ) treated diabetic rats were studied at 9 weeks after STZ injection in comparison to controls (CTR). Istaroxime effects were evaluated in vivo and in left ventricular (LV) preparations. STZ animals showed (i) marked DD not associated to cardiac fibrosis, (ii) LV mass reduction associated to reduced LV cell dimension and T-tubules loss, (iii) reduced LV SERCA2 protein level and activity and (iv) slower SR Ca2+ uptake rate, (v) LV action potential (AP) prolongation and increased short-term variability (STV) of AP duration, (vi) increased diastolic Ca2+, and (vii) unaltered SR Ca2+ content and stability in intact cells. Acute istaroxime infusion (0.11 mg/kg/min for 15 min) reduced DD in STZ rats. Accordingly, in STZ myocytes istaroxime (100 nmol/L) stimulated SERCA2a activity and blunted STZ-induced abnormalities in LV Ca2+ dynamics. In CTR myocytes, istaroxime increased diastolic Ca2+ level due to NKA blockade albeit minimal, while its effects on SERCA2a were almost absent. Conclusions SERCA2a stimulation by istaroxime improved STZ-induced DD and intracellular Ca2+ handling anomalies. Thus, SERCA2a stimulation can be considered a promising therapeutic approach for DD treatment.

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Torre, E., M. Arici, AM Lodrini, M. Ferrandi, P. Barassi, SC Hsu, GJ Chang, et al. "SERCA2a stimulation by istaroxime improves intracellular Ca2+ handling and diastolic dysfunction in a model of diabetic cardiomyopathy." EP Europace 23, Supplement_3 (May 1, 2021). http://dx.doi.org/10.1093/europace/euab116.534.

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Abstract Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): This work was supported by CVie Therapeutics Limited (Taipei, Taiwan) and Windtree Therapeutics (Warrington, USA) Diabetic cardiomyopathy is a multifactorial disease characterized by an early onset of diastolic dysfunction (DD) that precedes the development of systolic impairment. Mechanisms that can restore cardiac relaxation improving intracellular Ca2+ dynamics represent a promising therapeutic approach for cardiovascular diseases associated to DD. Istaroxime has the double property to accelerate Ca2+ uptake into sarcoplasmic reticulum (SR) through the SR Ca2+ pump (SERCA2a) stimulation and to inhibit Na+/K+ ATPase (NKA). The project aims to characterize istaroxime effects at a concentration (100 nM) marginally affecting NKA, in order to highlight its effects dependent on the stimulation of SERCA2a in a model of mild diabetes. Streptozotocin (STZ) treated diabetic rats were studied at 9 weeks after STZ injection in comparison to controls (CTR). Istaroxime effects were evaluated in vivo and in left ventricular (LV) preparations. STZ animals showed 1) marked DD not associated to cardiac fibrosis, 2) LV mass reduction associated to reduced LV cell dimension and T-tubules loss, 3) reduced LV SERCA2 protein level and activity and 4) slower SR Ca2+ uptake rate, 5) LV action potential (AP) prolongation and increased short-term variability (STV) of AP duration, 6) increased diastolic Ca2+, 7) unaltered SR Ca2+ content and stability in intact cells. Acute istaroxime infusion (0.11 mg/kg/min for 15 min) reduced DD in STZ rats. Accordingly, in STZ myocytes istaroxime (100 nM) stimulated SERCA2a activity and blunted STZ-induced abnormalities in LV Ca2+ dynamics. In CTR myocytes, istaroxime increased diastolic Ca2+ level due to NKA blockade albeit minimal, while its effects on SERCA2a were almost absent. SERCA2a stimulation by istaroxime improved STZ-induced DD and intracellular Ca2+ handling anomalies. Thus, SERCA2a stimulation can be considered a promising therapeutic approach for DD treatment. Abstract Figure.

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"Istaroxime Stimulates SERCA2a Activity in Animal and Human Failing Heart Preparations." Journal of Cardiac Failure 11, no. 6 (August 2005): S154. http://dx.doi.org/10.1016/j.cardfail.2005.06.243.

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Kamel, S. M., C. J. M. van Opbergen, C. D. Koopman, A. O. Verkerk, B. J. D. Boukens, B. de Jonge, Y. L. Onderwater, et al. "Istaroxime treatment ameliorates calcium dysregulation in a zebrafish model of phospholamban R14del cardiomyopathy." Nature Communications 12, no. 1 (December 2021). http://dx.doi.org/10.1038/s41467-021-27461-8.

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AbstractThe heterozygous Phospholamban p.Arg14del mutation is found in patients with dilated or arrhythmogenic cardiomyopathy. This mutation triggers cardiac contractile dysfunction and arrhythmogenesis by affecting intracellular Ca2+ dynamics. Little is known about the physiological processes preceding induced cardiomyopathy, which is characterized by sub-epicardial accumulation of fibrofatty tissue, and a specific drug treatment is currently lacking. Here, we address these issues using a knock-in Phospholamban p.Arg14del zebrafish model. Hearts from adult zebrafish with this mutation display age-related remodeling with sub-epicardial inflammation and fibrosis. Echocardiography reveals contractile variations before overt structural changes occur, which correlates at the cellular level with action potential duration alternans. These functional alterations are preceded by diminished Ca2+ transient amplitudes in embryonic hearts as well as an increase in diastolic Ca2+ level, slower Ca2+ transient decay and longer Ca2+ transients in cells of adult hearts. We find that istaroxime treatment ameliorates the in vivo Ca2+ dysregulation, rescues the cellular action potential duration alternans, while it improves cardiac relaxation. Thus, we present insight into the pathophysiology of Phospholamban p.Arg14del cardiomyopathy.

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Kolesnik, E., M. Wallner, M. Khafaga, D. M. Eaton, G. Schwantzer, M. Koestenberger, I. Knez, and D. Von Lewinski. "P4482Anticancer drug istaroxime exerts strong positive inotropic effects in failing human ventricular myocardium." European Heart Journal 38, suppl_1 (August 1, 2017). http://dx.doi.org/10.1093/eurheartj/ehx504.p4482.

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"Intravenous Istaroxime Improves Left Ventricular Lusitropic Properties in Dogs with Advanced Heart Failure." Journal of Cardiac Failure 11, no. 6 (August 2005): S154. http://dx.doi.org/10.1016/j.cardfail.2005.06.240.

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"Istaroxime – A Novel Lusitropic and Inotropic Agent: Results of a Phase I-II Study." Journal of Cardiac Failure 11, no. 6 (August 2005): S152. http://dx.doi.org/10.1016/j.cardfail.2005.06.232.

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Arici, Martina, Mara Ferrandi, Paolo Barassi, Shih-Che Hsu, Eleonora Torre, Andrea Luraghi, Carlotta Ronchi, et al. "Istaroxime metabolite PST3093 selectively stimulates SERCA2a and reverses disease-induced changes in cardiac function." Journal of Pharmacology and Experimental Therapeutics, September 24, 2022, JPET—AR—2022–001335. http://dx.doi.org/10.1124/jpet.122.001335.

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"Intravenous Istaroxime Improves Left Ventricular Systolic Function in Dogs with Advanced Heart Failure without Increasing Myocardial Oxygen Consumption." Journal of Cardiac Failure 11, no. 6 (August 2005): S95. http://dx.doi.org/10.1016/j.cardfail.2005.06.019.

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Journal articles on the topic 'Istaroxime'

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