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Human cardiomyocyte data predicting pro-arrhythmic risk
Peer-reviewed studies using adult human cardiomyocytes
This video protocol describes how to measure contractility in adult human primary cardiomyocytes from donor hearts with the MyoBLAZER system, a reliable platform for assessing drug-induced changes in contractility during preclinical development.
PUBLICATION: JoVE Journal (2022)
AUTHORS: Najah Abi Gerges, Alexa Stafford, Ky Truong, Yannick Miron, Bryce Winrow, Brian Krause, Guy Page and Andre Ghetti
Single-cell patch-clamp reverse transcriptase-quantitative polymerase chain reactions were used to clarify the composition of the iCell cardiomyocyte population to compare with atrial and ventricular cardiomyocytes. This comparison provided evidence that may hamper the interpretation of drug effects parameters depending on a combination of ionic currents, such as beat rate, and supports the evaluation of drug effects in a more realistic cardiomyocyte environment.Â
PUBLICATION: Cells (2021)
AUTHORS: Christina Schmid, Najah Abi-Gerges, Michael Georg Leitner, Dietmar Zellner and Georg Rast
This paper evaluates the pro-arrhythmia risk and inotropic effects of Hydroxychloroquine, Chloroquine and Azithromycin in the cardiomyocyte contractility-based model of the human heart due to their proposed repurposed use to treat COVID-19. The study conclusion has the potential to inform clinical studies evaluating repurposed therapies and demonstrates the translational value of human cardiomyocyte contractility-based model for novel COVID-19 therapies.
PUBLICATION: Society of Toxicology (2021)
AUTHORS: Pierre Jordaan, Berenge`re Dumotier, Martin Traebert, Paul E. Miller, Andre Ghetti, Laszlo Urban and Najah Abi-Gerges
To combat challenges in assessing drug effects on cardiac contractility, the development of an adult primary cardiomyocyte contractility model that has the potential to provide a predictive preclinical approach for simultaneously predicting drug-induced inotropic effect is needed. The contractility model used in this paper could accurately facilitate informed mechanistic-based decision making, risk management and discovery of molecules with the most desirable pharmacological profile for heart failure correction.
PUBLICATION: Scientific Reports (2020)
AUTHORS: Najah Abi-Gerges, Tim Indersmitten, KyTruong, William Nguyen, Phachareeya Ratchada, Nathalie Nguyen, Guy Page, Paul E. Miller & Andre Ghetti
The lack of selective sodium-calcium exchanger (NCX) inhibitors has hampered the exploration of physiological and pathophysiological roles of cardiac NCX 1.1. This paper aimed to discover more potent and selective drug like NCX 1.1 inhibitor. ORM-11372 was found to be a positive inotropic compound and potent inhibitor of human and rat NCX 1.1.
PUBLICATION: British Journal of Pharmacology (2020)
AUTHORS: Leena Otsomaa, Jouko Levijoki, Gerd Wohlfahrt, Hugh Chapman, Ari-Pekka Koivisto, Kaisa Syrjänen, Tuula Koskelainen, Saara-Elisa Peltokorpi, Piet Finckenberg, Aira Heikkilä, Najah AbiGerges, Andre Ghetti, Paul E. Miller, Guy Page, Eero Mervaala, Norbert Nagy, Zsófia Kohajda, Norbert Jost, László Virág, András Varró and Julius Gy. Papp
Computational cardiology currently stands at the threshold of clinical utility regarding risk stratification and treatment of patients at risk of sudden cardiac death. This white paper outlines a roadmap of what needs to be done to make a translational step using the relatively well-developed case of acquired or drug-induced long QT syndrome as an exemplar case.
PUBLICATION: Journal of Physiology (2016)
AUTHORS: Adam P. Hill, Matthew D. Perry, Najah Abi-Gerges, Jean-Philippe Couderc, Bernard Fermini, Jules C. Hancox, Bjorn C. Knollmann, Gary R. Mirams, Jon Skinner, Wojciech Zareba and Jamie I. Vandenberg
This paper describes the next steps for a human-based approach to disease supported by computational methodologies as described at a Workshop on Computational Cardiovascular Science. The main ideas outlined show a shift towards human-based methodologies spurred by advances in computational approaches to complement in vitro, in vivo and ex vivo experimental and clinical data as an integral part of pharmacology and medicine.
PUBLICATION: European Society of Cardiology (2017)
AUTHORS: Blanca Rodriguez, Annamaria Carusi, Najah Abi-Gerges, Rina Ariga, Oliver Britton, Gil Bub, Alfonso Bueno-Orovio, Rebecca A.B. Burton, Valentina Carapella, Louie Cardone-Noott, Matthew J. Daniels, Mark R. Davies, Sara Dutta, Andre Ghetti, Vicente Grau, Stephen Harmer, Ivan Kopljar, Pier Lambiase, Hua Rong Lu, Aurore Lyon, Ana Minchole, Anna Muszkiewicz, Julien Oster, Michelangelo Paci, Elisa Passini1, Stefano Severi, Peter Taggart, Andy Tinker, Jean-Pierre Valentin, Andras Varro, Mikael Wallman and Xin Zhou
A lack of human-specific data and appropriate model techniques have previously prevented quantitative comparison of drug effects between in silico models and recordings from human cardiac preparations. This paper compares changes in repolarization biomarkers caused by dofetilide, dl-sotalol, quinidine, and verapamil, between in silico populations of human ventricular cell models and ex vivo human ventricular trabeculae.
PUBLICATION: Frontiers in Physiology (2017)
AUTHORS: Oliver J. Britton, Najah Abi-Gerges, Guy Page, Andre Ghetti, Paul E. Miller and Blanca Rodriguez
This paper investigates if a human ex-vivo AP-based model could provide a more predictive approach for assessing pro-arrhythmic risk. The effects of dofetilide, dl-sotalol, quinidine, paracetamol, and verapamil on action potential (AP) duration and recognized pro-arrhythmia predictors, triangulation, and incidence of early afterdepolarizations were evaluated. The model provided an integrative translational assay assisting in shaping clinical development plans that could be used in conjunction with the new CiPA-proposed approach.
PUBLICATION: Journal of Pharmacological and Toxicological Methods (2016)
AUTHORS: Guy Page, Phachareeya Ratchada, Yannick Miron, Guido Steiner, Andre Ghetti, Paul E. Miller, Jack A. Reynolds, Ken Wang, Andrea Greiter-Wilke, Liudmila Polonchuk, Martin Traebert, Gary A. Gintant, Najah Abi-Gerges
Cardiac safety remains the leading cause of drug development discontinuation. AnaBios has developed a human cardiomyocyte-based model that has the potential to provide a predictive preclinical approach for simultaneously predicting drug-induced inotropic and pro-arrhythmia risk.
PUBLICATION: Frontiers in Physiology (2017)
AUTHORS: Nathalie Nguyen, William Nguyen, Brynna Nguyenton, Phachareeya Ratchada, Guy Page, Paul E. Miller, Andre Ghetti and Najah Abi-Gerges
The National Center for Toxicological Research of the US Food and Drug Administration (FDA) hosted a workshop to discuss current gaps and challenges in translating preclinical cardiovascular safety data to humans. This white paper summarizes the topics presented by speakers from academia, industry, and government intended to address the theme of improving cardiotoxicity assessment in drug development.
PUBLICATION: Circulation Research (2019)
AUTHORS: Li Pang, Philip Sager, Xi Yang, Hong Shi, Frederick Sannajust, Mathew Brock, Joseph C. Wu, Najah Abi-Gerges, Beverly Lyn-Cook, Brian R. Berridge, Norman Stockbridge
Cardiac Purkinje cells (PCs) are implicated in lethal arrhythmias caused by cardiac diseases, mutations, and drug action and are not entirely understood in humans. The aims of this study were to present novel human PCs electrophysiology biophysically detailed computational model, and to disentangle ionic mechanisms of human Purkinje-related electrophysiology, pacemaker activity and arrhythmogenicity. The model used unlocked further investigations into the role of cardiac Purkinje in ventricular arrhythmias through computer modelling and multiscale simulations.
PUBLICATION: Journal of Molecular and Cellular Cardiology (2020)
AUTHORS: Cristian Trovato, Elisa Passini, Norbert Nagy, Andras Varro, Najah Abi-Gerges, Stefano Severi and Blanca Rodriguez
AnaBios has established methodologies that consistently allow the procurement and experimental interrogation of human heart tissue preparations to provide a much-needed integrative preclinical model to reliably assess the toxicity risk of new drugs. These novel methodologies include scalable ex-vivo heart models from the isolation of adult human primary cardiomyocytes.
PUBLICATION: Journal of Pharmacological and Toxicological Methods (2017)
AUTHORS: Nathalie Nguyen, Yannick Miron, Phachareeya Ratchada, Guy Page, Paul E. Miller, Andre Ghetti and Najah Abi-Gerges
Third harmonic generation (THG) from atherosclerotic plaques revealed morphological details of cellular and extracellular lipid deposits. The THG signal adds an endogenous contrast mechanism with a practical degree of specificity for atherosclerotic plaques that complements current nonlinear optical methods for the investigation of cardiovascular disease. The use of the whole-mount tissue and backward scattered epi-detection suggests THG could potentially be used in the future as a clinical tool.
PUBLICATION: Biomedical Optics Express (2014)
AUTHORS: David M. Small, Jason S. Jones, Irwin I. Tendler, Paul E. Miller, Andre Ghetti and Nozomi Nishimurav
To assess drug-induced pro-arrhythmic risk, new models such as in-silico modeling of ventricular action potential (AP) and stem cell-derived cardiomyocytes (SC-CMs) have been proposed. The findings indicated that SC-CMs exhibited immature phenotype and had the propensity to generate false positives in predicting Torsades de Pointe (TdP) risk. Human ventricular trabeculae (hVT) were used to evaluate drugs to expand the knowledge base. The hVT AP-based model combined with the integrated analysis of pro-arrhythmic score was found to have a greater predictive performance when compared to human SC-CM models.
PUBLICATION: Frontiers in Physiology (2018)
AUTHORS: Yusheng Qu, Guy Page, Najah Abi-Gerges, Paul E. Miller, Andre Ghetti and Hugo M. Vargas
The adult human heart has long been considered incapable of self-repair, as mature cardiomyocytes lose the ability to divide. A new study challenges this by showing that a protein called Cyclin A2 (CCNA2) can reactivate cell division in adult human cardiomyocytes. Using a targeted gene delivery system, researchers introduced CCNA2 into cardiomyocytes isolated from adult human hearts, with live imaging confirming that cells underwent complete division while retaining structural integrity and calcium signaling in the resulting daughter cells. Advanced genomic analyses of mouse and human heart tissue revealed conserved genetic pathways that explain how CCNA2 drives these effects and identified a distinct cardiomyocyte subpopulation primed for proliferation and reprogramming — pointing to CCNA2 as a promising gene therapy strategy for cardiac regeneration in patients recovering from heart failure or injury.
PUBLICATION: BioRxiv  (2025)
AUTHORS: Najah Abi-Gerges, Hina Chaudhry, Andre Ghetti, Paul Miller, Amir Khan, et al.
Abnormal electrical activity in the heart — known as cardiac arrhythmia — remains a major therapeutic challenge, and the late sodium current (late INa) has emerged as a promising target for intervention. Using adult primary cardiomyocytes and tissue from donor hearts, researchers investigated the role of late INa in arrhythmia generation under both drug-induced and disease conditions. When late INa was artificially amplified, cells exhibited disrupted repolarization, impaired calcium handling, and increased arrhythmic activity — effects that were reversed by late INa inhibitors ranolazine and GS-967. Notably, atrial tissue from donor hearts with existing atrial fibrillation showed spontaneous arrhythmic behavior that was significantly reduced upon late INa inhibition. These findings establish late INa as a key driver of cardiac arrhythmias and support its inhibition as a viable therapeutic strategy, while also underscoring the value of human ex-vivo heart models in advancing cardiac research.
PUBLICATION: Scientific Reports  (2021)
AUTHORS: Najah Abi-Gerges, Ahn-Tuan Ton, William Nguyen, Andre Ghetti, Paul Miller, Alexa Stafford, Katrina Sweat, Tiara Wong, et al.
Reliable in vitro models that accurately replicate the heart’s physiological environment are essential for meaningful drug testing, yet existing systems have fallen short. Researchers developed a cardiac tissue culture model (CTCM) capable of applying physiological mechanical stretch to living heart slices throughout the cardiac cycle, mimicking the natural contraction and relaxation of the heart. While electro-mechanical stimulation alone improved tissue viability, full structural preservation required the addition of two small molecules — tri-iodothyronine (T3) and dexamethasone — to the culture media. With this combined approach, heart slices maintained their structural integrity, transcriptional profile, viability, and metabolic activity for 12 days at levels comparable to fresh tissue. The system also demonstrated the ability to model disease states, as deliberate overstretching of the tissue triggered cardiac hypertrophic signaling — a hallmark of heart disease. Together, these findings establish the CTCM as a robust platform for emulating both normal and pathological cardiac physiology over extended periods, offering a more reliable foundation for preclinical drug screening.
PUBLICATION: Communications Biology  (2022)
AUTHORS: Najah Abi-Gerges, Tamer Mohamed, Jessica Miller, Moustafa Meki, Ahmed Elnakib, Cindy Lin, Fahmi Khalifa, et al.
Damage or genetic mutations affecting the left ventricle (LV) — the heart’s primary pumping chamber — are a leading cause of severe and often fatal cardiovascular disease, making LV cardiomyocytes an important therapeutic target. A key obstacle in studying and treating these conditions has been the inability to produce human stem cell-derived cardiomyocytes that are sufficiently mature and specific to the LV. By applying insights from cardiac development, researchers identified that precise mesoderm patterning and blocking of the retinoic acid pathway are critical steps for directing stem cells toward a near-homogenous population of LV-specific cardiomyocytes. Compared to those generated by standard protocols, these cells demonstrated superior metabolic activity, reduced proliferation, and greater structural and functional maturity. Engineered heart tissues built from these cells were better organized, generated higher contractile force, and could be paced to physiological rates. Critically, this level of maturity was achieved rapidly and without the maturation regimens typically required — representing a meaningful advance in the development of more accurate and practical human cardiac models.
PUBLICATION: Cell Reports Method (2023)
AUTHORS:Â Nicola Dark, Najah Abi-Gerges, Paul Miller, Marie-Victoire Cosson, Lorenza Bouissou, et al.
Bridging the gap between preclinical drug testing and clinical outcomes is essential for accurately evaluating the safety and efficacy of new cardiac therapies. A key aspect of this is understanding how drugs affect cardiomyocyte contractility and calcium handling — two processes central to heart function. This study directly compared primary human cardiomyocytes, isolated from donor hearts, with freshly isolated dog cardiomyocytes, assessing both their baseline function and their responses to five well-characterized inotropic agents. While dog cardiomyocytes showed greater amplitude in sarcomere shortening and calcium transients under baseline conditions, human cells exhibited longer durations of both measures. Notably, both cell types showed similar pharmacological responses across all five inotropes tested, spanning multiple mechanisms of action. These findings support the use of both human donor-derived and canine cardiomyocytes as complementary, reliable models for simultaneously evaluating drug-induced effects on cardiac contractility and calcium dynamics — and reinforce the value of primary human cardiomyocytes as a clinically relevant, non-animal alternative for cardiac safety profiling.
PUBLICATION: Journal of Pharmacological and Toxicological Methods (2023)Â
AUTHORS: BaoXi Gao, Najah Abi-Gerges, Ky Truong, Hugo Vargas, Alea Stafford, William Nguyen, et al.
For over a decade, cardiac safety testing has centered on evaluating a drug’s potential to cause dangerous heart rhythm abnormalities — specifically QT interval prolongation and Torsades de Pointes arrhythmia — following guidelines that rely heavily on hERG channel assays and in vivo measurements. While this approach has been effective, it carries significant drawbacks, including unnecessary compound attrition and the high cost of late-stage clinical QT studies. The Comprehensive In Vitro Proarrhythmia Assay (CiPA) initiative, a public-private collaboration, aims to modernize this paradigm by combining standardized multi-ion channel assays, computational modeling of human ventricular action potentials, and confirmation studies in stem cell-derived human cardiomyocytes — with the ultimate goal of more accurately predicting arrhythmia risk and eliminating the need for costly thorough QT studies. This perspective article examines the rationale behind CiPA, the progress made to date, and the challenges that remain if this new framework is to successfully replace existing guidelines and gain broad acceptance across the drug development community.
PUBLICATION: Journal of Biomolecular Screening (2016)
AUTHORS: Bernard Fermini, Najah Abi-Gerges, Jules Hancox, Khuram Chaudhary, Krystle Correll, Paul Levesque, et al.
A critical component of the CiPA initiative’s modernized cardiac safety framework is the use of computational models to predict arrhythmic risk — models that depend on accurate measurements of how drugs interact with the hERG ion channel. To address this, the Ion Channel Working Group developed and standardized a patch-clamp protocol capable of measuring both the potency and kinetics of hERG channel block, with an eye toward broad implementation on automated platforms across the industry. Testing a panel of twelve reference drugs, the group successfully characterized block potency, time course, and trapping behavior for the majority of compounds — though seven drugs exhibited binding kinetics too rapid to be reliably captured by a single protocol, highlighting an inherent challenge in developing a one-size-fits-all approach. The resulting dataset is now being used by CiPA’s In Silico Working Group to build drug-binding models for risk prediction and has been made freely available as a gold-standard reference for evaluating variability across high-throughput testing platforms.
PUBLICATION: Journal of Pharmacological and Toxicological Methods (2017)
AUTHORS: Monique Windley, Najah Abi-Gerges, Bernard Fermini, Jules Hancox, et al.
A promising strategy for counteracting dangerous drug-induced QTc prolongation — a marker of arrhythmia risk — involves co-administering agents that inhibit the late sodium current (INaL) or L-type calcium current (ICaL) alongside hERG-blocking drugs. While a clinical trial confirmed that INaL inhibitors lidocaine and mexiletine successfully shortened hERG-mediated QTc prolongation, the ICaL inhibitor diltiazem unexpectedly failed to do the same. This study set out to understand why, reexamining the ion channel pharmacology of all drugs involved using physiologically relevant patch-clamp protocols and ventricular tissue from adult human hearts. The findings revealed that diltiazem’s potency against ICaL had been significantly overestimated in prior studies, and that its concomitant hERG-blocking activity at clinical exposure levels likely negated any QTc-shortening benefit. In contrast, nifedipine — which selectively inhibits ICaL with minimal hERG activity — produced clean action potential shortening without the distortion seen with diltiazem, further supporting this interpretation. Together, these results clarify the mechanistic basis of the clinical trial outcomes and reinforce the importance of using physiologically relevant experimental protocols and human cardiac tissue when generating ion channel data intended to inform clinical cardiac safety decisions.
PUBLICATION: Frontiers in Pharmacology (2025)
AUTHORS:Â
A promising strategy for counteracting dangerous drug-induced QTc prolongation — a marker of arrhythmia risk — involves co-administering agents that inhibit the late sodium current (INaL) or L-type calcium current (ICaL) alongside hERG-blocking drugs. While a clinical trial confirmed that INaL inhibitors lidocaine and mexiletine successfully shortened hERG-mediated QTc prolongation, the ICaL inhibitor diltiazem unexpectedly failed to do the same. This study set out to understand why, reexamining the ion channel pharmacology of all drugs involved using physiologically relevant patch-clamp protocols and ventricular tissue from adult human hearts. The findings revealed that diltiazem’s potency against ICaL had been significantly overestimated in prior studies, and that its concomitant hERG-blocking activity at clinical exposure levels likely negated any QTc-shortening benefit. In contrast, nifedipine — which selectively inhibits ICaL with minimal hERG activity — produced clean action potential shortening without the distortion seen with diltiazem, further supporting this interpretation. Together, these results clarify the mechanistic basis of the clinical trial outcomes and reinforce the importance of using physiologically relevant experimental protocols and human cardiac tissue when generating ion channel data intended to inform clinical cardiac safety decisions.
PUBLICATION: Biochimica et Biophysica Acta (2016)
AUTHORS:
Ibogaine and its metabolite noribogaine have shown promise in treating substance use disorders and co-occurring mental health conditions, but their clinical potential has been limited by significant cardiac safety risks and complex mechanisms of action. Researchers have now developed a new class of iboga alkaloids — called oxa-iboga compounds — created by structurally modifying the iboga skeleton to incorporate a benzofuran group. Critically, these new compounds showed none of the proarrhythmic effects of ibogaine and noribogaine when tested in primary human cardiomyocytes. In animal models, oxa-iboga compounds demonstrated superior efficacy against opioid use disorder, acting as potent kappa opioid receptor agonists while displaying atypical behavioral profiles compared to standard agents in that class. Most notably, a single dose or short treatment course of oxa-noribogaine produced long-lasting reductions in morphine, heroin, and fentanyl consumption, reversed opioid-induced hypersensitivity to pain, and suppressed drug-seeking behavior in relapse models. These findings position oxa-iboga compounds as a mechanistically distinct and potentially safer class of therapeutics for addressing the opioid crisis.
PUBLICATION: Nature Communications (2024)
AUTHORS:Václav Havel, Najah Abi-Gerges, Andrew C. Kruegel, Benjamin Bechand, Scot McIntosh , Leia Stallings, et al.Â
Ibogaine and its metabolite noribogaine have shown promise in treating substance use disorders and co-occurring mental health conditions, but their clinical potential has been limited by significant cardiac safety risks and complex mechanisms of action. Researchers have now developed a new class of iboga alkaloids — called oxa-iboga compounds — created by structurally modifying the iboga skeleton to incorporate a benzofuran group. Critically, these new compounds showed none of the proarrhythmic effects of ibogaine and noribogaine when tested in primary human cardiomyocytes. In animal models, oxa-iboga compounds demonstrated superior efficacy against opioid use disorder, acting as potent kappa opioid receptor agonists while displaying atypical behavioral profiles compared to standard agents in that class. Most notably, a single dose or short treatment course of oxa-noribogaine produced long-lasting reductions in morphine, heroin, and fentanyl consumption, reversed opioid-induced hypersensitivity to pain, and suppressed drug-seeking behavior in relapse models. These findings position oxa-iboga compounds as a mechanistically distinct and potentially safer class of therapeutics for addressing the opioid crisis.
PUBLICATION: FEBS Open Bio (2024)
AUTHORS: Ibragim Gaidarov, Najah Abi-Gerges, Todd Anthony, H Kiyomi Komori, Catherine Crosby, et al.Â
Ibogaine and its metabolite noribogaine have shown promise in treating substance use disorders and co-occurring mental health conditions, but their clinical potential has been limited by significant cardiac safety risks and complex mechanisms of action. Researchers have now developed a new class of iboga alkaloids — called oxa-iboga compounds — created by structurally modifying the iboga skeleton to incorporate a benzofuran group. Critically, these new compounds showed none of the proarrhythmic effects of ibogaine and noribogaine when tested in primary human cardiomyocytes. In animal models, oxa-iboga compounds demonstrated superior efficacy against opioid use disorder, acting as potent kappa opioid receptor agonists while displaying atypical behavioral profiles compared to standard agents in that class. Most notably, a single dose or short treatment course of oxa-noribogaine produced long-lasting reductions in morphine, heroin, and fentanyl consumption, reversed opioid-induced hypersensitivity to pain, and suppressed drug-seeking behavior in relapse models. These findings position oxa-iboga compounds as a mechanistically distinct and potentially safer class of therapeutics for addressing the opioid crisis.
PUBLICATION: FEBS Open Bio (2024)
AUTHORS: Ibragim Gaidarov, Najah Abi-Gerges, Todd Anthony, H Kiyomi Komori, Catherine Crosby, et al.Â
Accurately predicting how drugs affect the human heart is a critical challenge in preclinical development — current models frequently miss cardiotoxic compounds or falsely flag safe therapies, slowing the path to new treatments. Adult primary human cardiomyocytes are emerging as a powerful solution, offering native physiological and pharmacological properties that artificial cell models and animal models simply cannot replicate. Advances in donor heart recovery and cardiomyocyte isolation methods have expanded access to these cells, which have already demonstrated value in assessing cardiotoxicity risk and identifying new treatments for conditions like heart failure and atrial fibrillation. By incorporating data from adult human primary cardiomyocytes into structured decision-making frameworks, researchers can gain the holistic insights needed to more reliably predict drug effects on the human heart.
PUBLICATION: Current Pharmaceutical Biotechnology  (2020)
AUTHORS: Najah Abi-Gerges, Andre Ghetti, Paul Miller
Isolated human Purkinje fibres (PFs) in combination with electrophysiology are a unique tool that can be used to understand subtle differences between drugs on cardiac conduction. Ozanimod is an oral once-daily immunomodulator that has shown therapeutic benefit in clinical trials of relapsing multiple sclerosis and ulcerative colitis. The goal was to determine whether the higher selectivity of Ozanimod explains its improved clinical profile. The data agreed that Ozanimod has no effect on the measured conduction parameters.
AUTHORS: Najah Abi-Gerges, Paul E. Miller, Andre Ghetti, Fiona L. Scott, Kristen R. Taylor Meadows, Bryan Clemons, Paul Frohna, Guy Page, Gregory J. Opiteck
Cardiac safety remains the leading cause of drug development discontinuation. AnaBios has developed a human cardiomyocyte-based model that has the potential to provide a predictive preclinical approach for simultaneously predicting drug-induced inotropic and pro-arrhythmia risk. The human ventricular trabeculae-based model can clearly differentiate between pro-arrhythmia and non-proarrhythmic drugs and has the potential to enable a generation of reliable and predictive human-based cardiotoxicity data at the pre-clinical stage.
AUTHORS: Najah Abi-Gerges, Ashley Alamillo, Phachareeya Ratchada, Guy Page, Yannick Miron, Nathalie Nguyen, Paul E Miller and Andre Ghetti
Heart failure remains a major unmet medical need. To facilitate the identification of molecules with the most desirable efficacy profile, AnaBios developed a human cardiomyocyte contractility assay for the identification of positive inotropes with the potential to correct contractility deficits in heart failure. This adult human primary cardiomyocyte-based platform will facilitate the identification of molecules with the most desirable pharmacological correction of specific forms of contractility deficit.
AUTHORS: Najah Abi-Gerges, Tim Indersmitten, Ky Truong, William Nguyen, Ismael Tapia, Nathalie Nguyen, Guy Page, Paul E Miller and Andre Ghetti
Drug-induced effects on cardiac contractility can lead to serious adverse events including heart failure and limit the utility of innovative treatments. AnaBios sought to develop a human cardiomyocyte contractility assay that has the potential to simultaneously predict drug-induced inotropic risk and generate multi-parameter data to profile different inotropic mechanisms of action. The created adult human primary cardiomyocyte-based platform is scalable, efficient, and predictive for preclinical risk management.
AUTHORS: Najah Abi-Gerges, Tim Indersmitten, Ky Truong, William Nguyen, Nathalie Nguyen, Guy Page, Paul E Miller and Andre Ghetti
