Over the next six to eight weeks Dalton will be completing the quality control process which will culminate with the release of a first-ever, stand-alone cilastatin drug product to be used in a Phase II trial targeting drug toxin related AKI in hospitalized patients.
Arch has agreed to be an industry partner with a group of Canadian clinical researchers in a planned Phase II clinical trial targeting drug toxin-related AKI, which is expected to start in late 2024. The Company will be acting as a study partner for grant funding opportunities, providing cilastatin drug product and providing scientific and regulatory advice.
Arch has method of use patents in several jurisdictions including
About Cilastatin
Cilastatin is an enzymatic dipeptidase-1 (DPEP1) inhibitor originally developed in the early 1980´s by
Cilastatin has a slightly different mechanism of action compared with Arch’s novel drug candidate, LSALT peptide (Metablok) a non-enzymatic DPEP1 inhibitor. Whereas LSALT peptide specifically blocks DPEP1-mediated inflammation in the kidney, lungs and liver, cilastatin also has off target-effects that prevent toxin uptake in the kidneys. Thus, cilastatin is particularly effective for toxin-related AKI, but not suitable for other forms of non-toxin related AKI targeted by LSALT peptide.
Cilastatin as a potential treatment for AKI
AKI reflects a broad spectrum of clinical presentations ranging from mild injury to severe injury that may result in permanent and complete loss of renal function. Clinically, the causes of AKI include sepsis, ischemia-reperfusion injury, and various endogenous as well as exogenous (drug) toxins. There is no specific therapeutic treatment available in the market today that prevents AKI. In the worst cases, the kidneys fail, requiring kidney dialysis or kidney transplant for survival.
Exogenous toxins include a wide range of pharmaceutical drugs such as antibiotics (vancomycin, aminoglycosides), chemotherapeutic agents and radiographic contrast. Drug toxin-induced AKI represent approximately 30% of all AKI in hospitalized patients.
As stated above, cilastatin is particularly suited to preventing AKI caused by drug toxins due to a unique off-target effect that blocks their uptake into the kidney tissue. Several in vitro and in vivo studies indicate that cilastatin prevents AKI induced by multiple nephrotoxic drugs (exogenous toxins).
About
For more information on Arch Biopartners’ science and drug platform, please visit: www.archbiopartners.com/our-science
For investor information and other public documents the company has also filed on SEDAR+, please visit www.archbiopartners.com/investor-hub
The Company has 64,250,633 common shares outstanding.
Forward-Looking Statements
This press release contains forward-looking statements within the meaning of applicable Canadian securities laws regarding expectations of our future performance, liquidity and capital resources, as well as the ongoing clinical development of our drug candidates targeting the dipeptidase-1 (DPEP1) pathway, including the outcome of our clinical trials relating to LSALT peptide (Metablok) or cilastatin, the successful commercialization and marketing of our drug candidates, whether we will receive, and the timing and costs of obtaining, regulatory approvals in
The science and medical contents of this release have been approved by the Company’s Chief Science Officer
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For more information, please contact:Richard Muruve Chief Executive OfficerArch Biopartners, Inc. 647-428-7031 info@archbiopartners.com
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