Transposition of the Great Arteries (TGA)
Transposition of the great arteries (TGA) is a critical congenital heart disease (CHD) due to embryologic error in which great arteries are not connected to the correct ventricles. Protheragen is a premier research service provider with an established reputation for rare cardiovascular disease research, such as TGA. Leveraging years of rare disease research and development experience, we offer a one-stop solution for drug discovery and development that bridges cutting-edge science with potential therapies.
Introduction to Transposition of the Great Arteries (TGA)
Transposition of the great arteries (TGA) is one of the most frequent cyanotic congenital malformations of the heart in the neonate and constitutes approximately 3% of CHDs. In such individuals with TGA, the aorta is attached to a morphologic right ventricle and the pulmonary artery to a morphologic left ventricle. TGA sets in motion a cascade of maladaptive responses in a cardiac function where poorly oxygenated blood flows into the systemic circulation and the better-oxygenated blood continually arrives at the lung.
Fig.1 The TGA mouse model of retinoic acid-treated. (Nakajima Y., 2016)Pathogenesis of Transposition of the Great Arteries (TGA)
Transposition of the great arteries (TGA) is a group of complex congenital heart malformations, whose etiology is not clear. The morphological pattern causing TGA is essentially, the inverted rotation of conotruncus secondary to hypoplasia of subpulmonic conus in the presence of persistent subaortic conus. Genetic, epigenetic, and environmental factors contribute to the development of the anomaly. It may manifest as a solitary abnormality or combined with other cardiac malformations.
Therapeutics Development for Transposition of the Great Arteries (TGA)
Surgical therapy is the main therapy of TGA, and drugs are primarily adopted for preoperative and postoperative therapeutic, that is, opening the ductus arteriosus or dealing with complications.
| Drug Names | Mechanism of Action | Targets | NCT Number | Research Phase |
|---|---|---|---|---|
| Milrinone | Phosphodiesterase-3 (PDE3) inhibitor potentiates cardiac output. | PDE3 | / | Approved |
| Levosimendan | Improves cardiac output in TGA by increasing myocardial contractility and causing vasodilation via troponin C sensitization and activation of the ATP-sensitive potassium channel. | PDE3 | NCT01120106 | Phase II |
| Eplerenone | Aldosterone receptor antagonist which alleviates TGA-related symptoms by increasing diuresis to reduce fluid overloading and cardiac workload. | MR | NCT01971593 | Phase IV |
Disclaimer: Protheragen focuses on providing preclinical research services. This table is for information exchange purposes only. This table is not a treatment plan recommendation. For guidance on treatment options, please visit a regular hospital.
Our Services
Protheragen provides an integrated services platform that includes diagnostics, therapeutics, and disease model development for rare cardiovascular diseases. Our cutting-edge technologies and customized approaches result in accuracy and efficiency, and our strong disease models supply invaluable information on the progression of the disease and the response to compounds. Our preclinical services also include extensive pharmacokinetic studies and comprehensive drug safety testing.
Therapeutic Development Services
Diverse Platforms
Animal Model Development for TGA
Models of TGA in animals permit investigators to study the pathogenesis of disease, monitor the course of disease, and develop novel diagnostic and therapeutic strategies with consideration for safety and efficacy. Our company is invested in advancing pioneering research in this space by providing personalized animal model development services for rare cardiovascular diseases such as TGA.
TGA animal models are obtained via retinoic acid or retinoic acid competitive antagonist administration in pregnant mice.
- Retinoic acid-induced model
- Other models
- BMS-493-induced model
Through the application of cutting-edge innovations combined with unrivaled experience, Protheragen enables our partners to conquer the obstacles of rare cardiovascular disease drug development. Our seamless approach expedites the discovery and development process while reducing risk and maximizing therapeutic potential. If you would like to learn more about our content moderation services get in touch with us.
Reference
- Nakajima, Yuji. "Mechanism responsible for D-transposition of the great arteries: Is this part of the spectrum of right isomerism?" Congenital anomalies 56.5 (2016): 196-202.
For research use only, not for clinical use.