Ace Therapeutics is a contract research organization engaged in cardiovascular disease research. We aim to provide comprehensive solutions and R&D outsourcing services for our clients worldwide to accelerate cardiovascular drug discovery and development.
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The development of novel therapeutics for cardiovascular disease confronts multiple translational challenges.
We understand the difficulties of the current research into cardiovascular disease, and are committed to providing animal model construction services, conventional genetically engineered animal models, and customized functional animal diets for the basic research and drug development of cardiovascular diseases.
Animal Fetching
Model Construction
Model Evaluation
Given the complex pathophysiology and chronic progression of atherosclerosis, well-characterized animal models that faithfully recapitulate key aspects of human disease pathogenesis have become indispensable tools for investigating disease mechanisms and evaluating novel therapeutic interventions. Recent advances in preclinical model development have yielded increasingly sophisticated systems that more accurately mimic human atherosclerotic progression, enabling rigorous investigation of disease pathogenesis and accelerating the discovery of innovative treatment strategies.
Well-established animal models of hypertension serve as essential tools for investigating hypertensive disorders and their associated complications, with two primary classifications. Genetic hypertension models, which develop elevated blood pressure without external manipulation, provide valuable systems for studying the fundamental mechanisms of essential hypertension and evaluating novel antihypertensive therapies. Experimentally induced hypertension models, created through pharmacological, dietary, or surgical interventions, offer rapid induction timelines and are particularly suited for investigating secondary hypertension mechanisms triggered by specific environmental or pharmacological factors.
Thrombosis, characterized by pathological intravascular clot formation, represents a critical mechanism underlying major cardiovascular and cerebrovascular events, including acute myocardial infarction and ischemic stroke, through its dual manifestations as arterial and venous thromboembolism. Given the central role of thrombotic processes in numerous life-threatening conditions, well-validated animal models of thrombosis have become indispensable for elucidating disease mechanisms and advancing the development of novel antithrombotic therapies with improved efficacy and safety profiles.
The myocardial ischemia-reperfusion arrhythmia model serves as a well-established preclinical system for investigating ischemic cardiomyopathy pathophysiology, wherein transient coronary occlusion followed by controlled reperfusion induces characteristic electrophysiological disturbances that mimic clinical manifestations of ischemic heart disease. This model specifically recapitulates the pathophysiological cascade of myocardial injury resulting from temporary blood flow interruption and subsequent restoration, providing critical insights into ischemia-reperfusion injury mechanisms and potential therapeutic interventions.
Many existing antiarrhythmic agents paradoxically exhibit proarrhythmic potential or induce other cardiovascular complications, highlighting the critical need for developing safer and more effective therapeutic alternatives. The establishment of physiologically relevant arrhythmia models is fundamental to this endeavor, with murine models (mice and rats) serving as the predominant preclinical systems due to their conserved cardiac anatomy and electrophysiological properties that closely mirror human pathophysiology, making them indispensable for investigating arrhythmia mechanisms and evaluating novel pharmacological interventions.
Heart failure arises from diverse etiologies that ultimately impair myocardial contractility, leading to insufficient cardiac output to meet systemic metabolic demands and subsequent development of characteristic clinical manifestations. To recapitulate this complex pathophysiology, researchers have established multiple preclinical models through distinct induction methods, including pharmacological cardiotoxicity, chronic metabolic stress from high-fat diets, and surgical hemodynamic overload via vascular constriction, each exhibiting unique patterns of cardiac functional deterioration and remodeling that mirror specific clinical heart failure phenotypes.
Hypertrophic cardiomyopathy represents a maladaptive myocardial response to sustained pathological stimuli, characterized by cardiomyocyte hypertrophy and architectural remodeling. To investigate this complex pathophysiology, researchers have established multiple validated preclinical models that accurately recapitulate disease features, including pressure-overload models induced by surgical aortic constriction, pharmacological models utilizing cardiotropic agents, and genetically engineered models with targeted mutations.
Heart valve disease pathogenesis involves intricate inflammatory and apoptotic pathways, though the precise molecular mechanisms remain incompletely characterized, necessitating the development of physiologically relevant animal models to elucidate disease progression. An optimal preclinical model of valvular pathology should combine rapid induction kinetics with hallmark features of valve inflammation and fibrosis, while demonstrating quantifiable structural abnormalities through advanced imaging modalities to facilitate comprehensive mechanistic and therapeutic investigations.
Cardiovascular infections caused by diverse pathogens including bacteria, viruses, mycoplasma, chlamydia, and rickettsia can manifest as distinct clinical entities such as infective endocarditis, myocarditis, pericarditis, valvulopathies, and systemic vasculitis. Contemporary research utilizes pathogen-specific animal models, with enterovirus-infected models (particularly coxsackievirus B3 and EV71 strains) effectively mimicking the clinical progression of viral myocarditis, enabling mechanistic studies of host-pathogen interactions and therapeutic development.
Ace Therapeutics specializes in the preclinical development of novel cardiovascular therapeutics tailored to disease mechanisms, drug modalities, and specific therapeutic targets. Our end-to-end solutions ensure optimized efficacy, safety, and translational potential for your candidate.
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At Ace Therapeutics, we deliver end-to-end preclinical research services for cardiovascular drug development, encompassing rigorous in vitro and in vivo evaluations across pharmacodynamics, safety pharmacology, toxicology, and pharmacokinetics to generate robust datasets that inform clinical trial design and risk assessment.
In Vitro Pharmacodynamic Evaluation of Cardiovascular Drugs
Our comprehensive in vitro pharmacodynamic evaluation platform enables systematic characterization of drug mechanisms and pharmacological effects during early discovery phases, providing critical data to de-risk cardiovascular drug development through predictive assessment of therapeutic potential and target engagement.
In Vivo Pharmacodynamic Evaluation of Cardiovascular Drugs
Our specialized in vivo pharmacodynamic evaluation platform enables direct measurement of critical drug activity parameters in physiologically relevant systems, providing essential preclinical data to characterize therapeutic efficacy, dose-response relationships, and mechanism of action for cardiovascular drug candidates.
In Vitro Pharmacokinetics Evaluation of Cardiovascular Drugs
Achieving an ideal pharmacokinetic profile represents a critical determinant of clinical success for drug candidates. Our advanced in vitro pharmacokinetic technology platform delivers scientifically validated solutions for characterizing key ADME parameters of cardiovascular therapeutics, enabling data-driven optimization of drug candidates' pharmacokinetic properties to enhance therapeutic potential and clinical translatability.
In Vitro Pharmacodynamic Evaluation of Cardiovascular Drugs
Prior to initial human administration, comprehensive assessment of a drug candidate's pharmacokinetic profile through validated animal studies is essential to ensure safe and effective clinical translation. Our established preclinical platform provides robust in vivo pharmacokinetic evaluation services specifically optimized for cardiovascular therapeutics, delivering critical data on absorption, distribution, metabolism and excretion (ADME) parameters to support regulatory submissions and clinical trial design.
General Toxicity Evaluation of Cardiovascular Drugs
Systematic general toxicity evaluation constitutes a critical component of the preclinical safety assessment for cardiovascular therapeutics, encompassing comprehensive characterization of acute, subchronic, and chronic toxicity profiles. Our preclinical platform delivers end-to-end general toxicity evaluation services specifically designed for cardiovascular drugs.
Genetic Toxicity Evaluation of Cardiovascular Drugs
Genotoxicity represents the deleterious effects on genetic material including DNA damage and chromosomal aberrations, a particular concern for cardiovascular therapeutics due to their typically chronic administration regimens. Our preclinical genotoxicity evaluation platform provides comprehensive assessment of potential mutagenic risks for cardiovascular drug candidates through validated in vitro and in vivo studies, enabling early identification of genetic safety concerns during lead optimization and preclinical development phases.
Reproductive Toxicity Evaluation of Cardiovascular Drugs
Reproductive toxicity evaluation provides essential safety data required for clinical trial authorization and regulatory approval, establishing critical risk-benefit profiles for drugs with potential effects on fertility, embryonic development, and postnatal growth. Our reproductive toxicity testing platform delivers complete evaluation services for cardiovascular therapeutics.
Safety Pharmacology Evaluation of Cardiovascular Drugs
Safety pharmacology evaluation provides critical insights into potential adverse physiological effects of novel cardiovascular drugs at therapeutic and supratherapeutic doses, enabling early identification of functional risks to vital organ systems. Our safety pharmacology platform delivers comprehensive cardiovascular assessments, including:
Ace Therapeutics provides scientifically validated, regulatory-ready solutions that bridge discovery research and clinical development, delivering robust preclinical data packages to accelerate your cardiovascular therapeutics while maintaining the highest standards of scientific rigor and regulatory compliance.
Q: What’s your approach to repurposing drugs for CVD?
A: We leverage computational biology and network pharmacology to identify repurposing candidates, followed by rapid in vitro / in vivo validation in relevant CVD models.
Q: Do you support gene therapy or RNA-based CVD therapeutics?
A: Yes, from AAV vector design (e.g., for familial hypercholesterolemia) to LNP-formulated siRNA/mRNA delivery (e.g., targeting PCSK9).
Q: How do you address the translatability gap between preclinical models and human CVD?
A: We employ a tiered model strategy, combining genetically engineered rodents, large-animal models (e.g., porcine MI models), and human iPSC-derived cardiomyocytes/3D tissue constructs to improve clinical relevance.
Q: How can small molecules overcome safety challenges in CVD (e.g., QT prolongation)?
A: Our early-stage screening includes multi-ion channel profiling (hERG, Nav/Cav) and structural optimization to mitigate proarrhythmic risks while maintaining efficacy.
Ace Therapeutics offers comprehensive solutions and R&D services to researchers worldwide to advance the field of cardiovascular diseases.
We do not provide medical care for patients.
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