Walden Biosciences, Inc. announced that it has entered into a research collaboration with Primula Group to lever a large body of genetic data on patients living with chronic kidney disease, including insights from close to 500,000 individuals in the UK Biobank.
Study to further understand the established role that suPAR plays in causing kidney disease
CAMBRIDGE, Mass., May 13, 2024 (GLOBE NEWSWIRE) -- Walden Biosciences, Inc. (Walden), a private, venture-backed biotechnology company advancing disease-modifying therapies to transform the treatment of kidney disease, today announced that it has entered into a research collaboration with Primula Group to lever a large body of genetic data on patients living with chronic kidney disease (CKD), including insights from close to 500,000 individuals in the UK Biobank. The study will be led by Dipender Gill, M.D. Ph.D., who is based at Imperial College London and has over 200 research papers on Mendelian randomization methods and application.
“We are delighted to collaborate with one of the world’s leading experts in Mendelian randomization to advance suPAR science and better understand the causative role of elevated suPAR levels in kidney diseases,” said Alex Duncan, Ph.D., Chief Scientific Officer of Walden. “Elevated levels of suPAR are known to injure kidney tissues, leading to podocyte dysfunction, kidney disease, and the associated proteinuria. The compromised kidney structure and function often leads to end-stage kidney disease, which can result in the need for dialysis or kidney transplant. Data from this study is expected to further support the clinical advancement of Walden’s anti-suPAR antibody, WAL0921, which is currently in Phase 2 clinical studies in CKD and expand the mechanistic insight into how elevated suPAR causes CKD.”
The study will investigate established variants from genetic analysis of the human PLAUR gene that encodes uPAR and affects circulating levels of soluble uPAR (suPAR), thereby affecting kidney function (Hindy et al., JCI, 2022). This study will elucidate the common and distinct effects of PLAUR variants on the circulating proteome, metabolome, and their potential clinical implications. The genetic variants will also be used as proxies to study the effect of pharmacological modulation of suPAR.
“The collaboration with Walden will build on earlier data supporting a causal role of suPAR in kidney disease and gives us a unique opportunity to help guide and transform the treatment of these patients, as well as identify other outcomes where targeting suPAR may be beneficial,” noted Dr. Gill.
Earlier this year, Walden completed a Phase 1+ clinical study of WAL0921, a first-in-class, proprietary, humanized monoclonal antibody that binds suPAR and inhibits its pro-inflammatory action on podocytes causing kidney dysfunction and disease. The Phase 1+ clinical study was a single center, placebo-controlled, single ascending dose study of WAL0921 in five cohorts that evaluated its safety, pharmacokinetics, and pharmacodynamics in 40 healthy subjects. Data from the study showed that WAL0921 was safe, well-tolerated, and demonstrated proof-of-biology through a rapid, dose-dependent reduction in free suPAR levels.
“We are pleased to be working with Dr. Gill to support this important work, as data from this collaboration will add to our growing understanding of the role that elevated suPAR plays in kidney disease and will support our ongoing Phase 2 study of WAL0921 in kidney disease,” stated Blaine McKee, Ph.D., Chief Executive Officer of Walden.
About Walden Biosciences
Walden Biosciences is a private, venture-backed clinical development-stage company focused on developing breakthrough, disease-modifying medicines to treat kidney diseases. Walden is applying novel, multi-disciplinary approaches that directly target the kidney to prevent damage, slow disease progression, and restore kidney function. Walden’s programs address novel targets for therapeutic intervention, directly targeting two cell types critical for kidney function: podocytes and proximal tubular cells. Dysfunction of these cells are critical hallmarks of the majority of kidney diseases. Walden’s clinical-stage program is a humanized monoclonal antibody that inhibits suPAR, a pro-inflammatory mediator that causes podocyte dysfunction and kidney disease. Walden’s second most advanced program is a small molecule that is designed to restore the function of dynamin, an enzyme responsible for the maintenance of the cytoskeletal architecture and function of podocytes and proximal tubule cells. All of Walden’s programs offer the promise to deliver disease-modifying, breakthrough therapies that are readily combinable with the standard of care to transform the treatment of kidney disease. For more information, please visit www.waldenbiosciences.com.
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