Alchemab Therapeutics, an antibody discovery company identifying naturally occurring antibodies from individuals resilient to disease, has unveiled data on ATLX-1088, its newly-discovered preclinical Alzheimer’s candidate.
The data was announced at the Antibody Industrial Symposium in Tours, France, June 22-23, 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 optimised 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 favourable pharmacokinetic and pharmacodynamic profile. This could lead to a potent drug with fewer side effects.
Data presented at the symposium show 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.”