Anti-AT1R Antibody Introduction

Anti-AT1R autoantibodies play an important role in the onset and progression of many diseases. For example, it has been found that AT1R plays an important role in diseases such as pre-eclampsia, hypertension, and vascular rejection of kidney transplants. Several studies have found that treatment with AT1R antagonists, plasma exchange, and intravesical immunoglobulin can improve the condition of patients with AT1-AA-positive vascular rejection, refractory hypertension, and other diseases. Thus, agonistic autoantibodies are an important modality for the treatment of related diseases. Based on our rich field experience and advanced technology platform, Creative Biolabs provides comprehensive services for custom agonistic antibody and agonistic autoantibody discovery to support agonistic antibody therapy development.

Structure of AT1R (Creative Biolabs Authorized) Fig 1. Structure of AT1R

Anti-AT1R Antibody

Angiotensin II type 1 (AT1) receptor (AT1R) belongs to the G protein-coupled receptor family and is widely expressed in immune cells, vascular endothelial cells, smooth muscle cells, etc. AT1R is mainly found in the kidney, heart, vascular smooth muscle cells, adrenal cortex, brain, platelets, and placenta. AT1R is the main receptor for angiotensin II (Ang II) in the glomerulus and can regulate Ang II release and perform its main pathophysiological roles, including the regulation of arterial blood pressure, the control of water-salt homeostasis, and the maintenance of normal intracellular environmental homeostasis, etc. Excessive activation of AT1R can lead to hypertension, vasoconstriction, and vascular smooth muscle migration and proliferation.

The main physiological effects of AT1R include stimulation of cell growth and positive time-varying force effects in cardiac tissue, stimulation of smooth muscle cell division and proliferation, contraction of vascular smooth muscle, stimulation of sympathetic nerves to increase the release of catecholamines, stimulation of the release of antidiuretic hormone and aldosterone secretion, and control of water intake and urinary sodium excretion. These functions are closely related to elevated blood pressure. ATR1 autoantibodies mediate a number of biological effects, such as cell proliferation and hypertrophy, vasoconstriction, and remodeling of the vascular wall and target organs, by acting on the ATR1 extracellular second cyclic peptide, which results in a range of associated clinical pathologies. It has been observed by immunizing animals with AT1 antibodies that the antibodies stimulate smooth muscle cell proliferation and lead to vascular wall thickening and remodeling. It may cause collagen deposition by promoting aldosterone secretion, causing the receptor structure to deform or not to be desensitized over time, thus being in continuous activation. In addition, it has also been shown that AT1R autoantibodies, when applied to vascular smooth muscle cells, result in the up-regulation of transcriptional activators such as NF-κB and AP1, which further regulate the expression of c-Jun, c-Fos, and other genes in the nucleus. These studies suggest that AT1R autoantibodies have agonist-like effects similar to those of Ang II and may be involved in the development of hypertension and hyperemesis gravidarum and related AT1R antibody-positive diseases. Therefore, agonistic antibody therapy based on AT1R autoantibodies is a potential treatment for these diseases.

Creative Biolabs has a wealth of knowledge and experience in custom agonistic autoantibody. We would be happy to share with you our knowledge and experience in anti-AT1R antibodies by phage display.

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