ANGPTL3-Targeted Drug Development for Diabetes
Angiopoietin-like protein 3 (ANGPTL3) regulates lipid metabolism and insulin signaling pathways, leading to diabetic dyslipidemia and systemic insulin resistance. The dual regulatory role of ANGPTL3 makes it an effective therapeutic target to address the atherogenic dyslipidemia and metabolic dysfunction in type 2 diabetes mellitus (T2DM). Ace Therapeutics is committed to providing comprehensive ANGPTL3 inhibitor development services to help clients achieve breakthroughs in drug discovery and development for diabetes and related metabolic disorders. Our services cover multiple stages from early screening and optimization to preclinical studies, helping our clients to efficiently develop ANGPTL3 inhibitors with application value.
Introduction to ANGPTL3
ANGPTL3is a liver-derived protein that plays a crucial role in regulating plasma lipoprotein metabolism by inhibiting lipoprotein lipase and influencing lipid levels. Potential role of ANGPTL3 in diabetic dyslipidemia, including:
- Enhanced insulin sensitivity: Deficiency of ANGPTL3 is associated with enhanced insulin sensitivity, suggesting that ANGPTL3 may be a potential target for the therapy of insulin resistance and related metabolic disorders.
- Regulation of lipid levels: ANGPTL3 inhibitors can decrease LPL and very low-density lipoprotein (VLDL) levels, thus effectively treating lipid metabolism disorders associated with type 2 diabetes.
- Impact on HDL function: Inhibition of ANGPTL3 may also affect high-density lipoprotein (HDL) function in type 2 diabetes individuals, further improving their lipid metabolism profile.
Fig. 1 Mechanisms leading to diabetic dyslipidemia. (Chen, J.; et al., 2024)
ANGPTL3 Inhibitor Development Services at Ace Therapeutics
Ace Therapeutics helps clients accelerate the development process of ANGPTL3 inhibitors through multi-dimensional and full-process R&D support.
- Early screening and optimization: We provide high-throughput screening services to identify compounds with potential inhibitory activity against ANGPTL3 from a large library of compounds, and further improve their inhibitory effect and selectivity through structural optimization.
- In vitro studies: We validated the inhibitory effect of the candidate compounds on ANGPTL3 and assessed their effects on LPL and VLDL levels by cellular assays and enzyme activity measurements.
- In vivo studies: We perform in vivo experiments using diabetic animal models to assess the effects of antidiabetic drug candidates on lipid metabolism, insulin sensitivity, and HDL function, alongside conducting pharmacokinetic and pharmacodynamic studies.
- Preclinical studies: We provide complete preclinical research services, including safety evaluations, pharmacodynamic studies and pharmacokinetic studies, to support the subsequent development of inhibitors for ANGPTL3.
Advantages of Our ANGPTL3 Inhibitor Development Services
- Personalized service: We provide personalized diabetes modeling and preclinical testing services according to the specific needs of our clients.
- Advanced equipment: We are equipped with advanced laboratory equipment and analytical instruments, which enable us to perform in vivo and in vitro analyses efficiently and accurately.
- Professional team: We have a team of experienced scientists and researchers with profound background in ANGPTL3 research and rich experience in drug development.
Ace Therapeutics is committed to utilizing our expertise and experience in the field of diabetes to help our clients develop innovative medicines. If you are interested in our ANGPTL3 inhibitor development service, please feel free to contact us. We will be happy to provide you with professional services and solutions to help you succeed in drug discovery.
References
- Chen, J.; et al. ANGPTL3 as a target for treating lipid disorders in type 2 diabetes patients. Lipids in Health and Disease. 23.1 (2024): 356.
- Dhankhar, S.; et al. Novel targets for potential therapeutic use in Diabetes mellitus. Diabetology & Metabolic Syndrome. 15.1 (2023): 17.
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