Alchemab Therapeutics unveils Alzheimer's candidate ATLX-1088 targeting CD33 at the Antibody Industrial Symposium
CAMBRIDGE, England, June 22, 2023 /PRNewswire/ -- Alchemab Therapeutics, an antibody discovery company identifying naturally occurring antibodies from individuals resilient to disease, today announced that it unveiled data on ATLX-1088, its newly-discovered preclinical Alzheimer's candidate, at the Antibody Industrial Symposium in Tours, France, 22-23 June 2023.
ATLX-1088 is a potential first-in-class human antibody targeting CD33, a cell surface protein which is thought to have a key role in Alzheimer's disease. Studies have found that higher expression of CD33 is associated with more advanced cognitive decline and worsening disease status – as high levels of CD33 inhibit normal function of brain-resident immune cells called microglia, which maintain neural networks and repair damage.
After identifying common antibodies unique to individuals resilient to Alzheimer's disease, Alchemab identified the target as CD33. By starting with the body's response to disease, as opposed to the target itself, Alchemab's platform inverts the traditional 'target-led' drug discovery process. In effect, the immune system is used as a search function to identify the most important disease modifying targets.
An additional benefit of this approach is that the disease modifying antibody has been naturally optimized by the immune system which can lead to potential beneficial properties from a therapeutic perspective.
Young Kwon, Chief Executive Officer of Alchemab, said: "Alchemab's unique approach to antibody research has led to the discovery of ATLX-1088, which we hope could be a new therapy for Alzheimer's. While there's been progress in the Alzheimer's field in the last few years, there's still a tremendous need for more and better therapies, and we hope ATLX-1088 could be an important treatment option given its broad effect on microglial cell function."
Alchemab's CD33 binding antibody has a novel mechanism of action, which, together with the data presented today, suggests a favorable pharmacokinetic and pharmacodynamic profile. This could lead to a potent drug with fewer side effects.
Data presented at the symposium shows ATLX-1088 results in a significant increase in the phagocytosis or removal of the toxic protein amyloid beta by microglia which may help to restore healthy brain cell function.
Jane Osbourn, Chief Scientific Officer of Alchemab, said: "This is the first time we have revealed data from this exciting drug candidate targeting CD33. There's strong evidence to show that knocking out CD33 results in lower amyloid-beta levels and reduction in amyloid plaque burden in the brain. We believe that ATLX-1088 could be an important step forward in treatment, potentially bringing a much needed new therapy to patients with this debilitating disease."
Presentation Title: Antibodies from Resilient Individuals: A novel approach for Antibody Drug Discovery
Presenter: Sandrine Legg, Director of Phenotypic Screening, Alchemab Therapeutics
Date and Time: Thursday 22 June 2023, 14:00 CEST
About Alchemab
Alchemab studies the unique antibody response of resilient individuals to develop drugs based on naturally derived antibodies to prevalent, hard-to-treat diseases which do not have disease modifying therapies. Alchemab's platform integrates data mining of patient-derived immune responses with the latest, multi-disciplinary drug discovery approaches to understand what keeps people well. The goal is to unlock nature's engineering and harness the incredible human immune system to find breakthrough drugs.
Alchemab's highly experienced team has broad expertise and capabilities across discovery and development. Through collaborations with world class institutions, Alchemab taps into large ecosystems and millions of patient samples which it analyzes using advanced computational approaches.
Alchemab is headquartered in London, UK with labs in Cambridge, UK and Boston, US.
For more information, visit www.alchemab.co.uk.
SOURCE Alchemab Therapeutics
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