Hemostemix Announces Its 10Th Publication: A Molecular Strategy For The Treatment Of Heart Failure: Response To Biocardia's Cardiamp Heart Failure Trial

(MENAFN- Newsfile Corp) Calgary, Alberta--(Newsfile Corp. - July 3, 2025) - Hemostemix Inc. (TSXV: HEM) (OTCQB: HMTXF) (FSE: 2VF0) is proud to share the Journal of Biomedical Research and Environmental Science published Autologous Angiogenic Cell Precursors-A Molecular Strategy for The Treatment of Heart Failure: Response to BioCardia's Cardiamp HF Trial.

Recent research has revealed the importance of choosing the right patients and the right type of stem cell to effectively treat inflammatory heart disease. Many traditional approaches using bone marrow-derived cells have failed in large trials, especially when applied broadly to patients with different forms of heart failure. However, Hemostemix's ACP-01 stands apart, due to its specific molecular characteristics and its ability to precisely target the root causes of non ischemic dilated cardiomyopathy (DCM): inflammation, fibrosis, and poor blood flow.

In Hemostemix' two earlier studies of DCM patients, cardiac function as measured by left ventricle ejection fraction percent (LVEF%) increased by up to 47.1% following one treatment (Stem Cell Research & Therapy, November 2023), with the most marked improvements observed in patients with severe dilated cardiomyopathy (LVEF% < 20%).

Study/Case Series

Patient Type

Baseline LVEF

Post-ACP-01 LVEF

Time Frame

Key Outcomes

Previous Dilated Cardiomyopathy Study Results for ACP-01

Hemostemix Phase 1 Data

Ischemic/Non-ischemic

18-25%

35-45%

3-12 months

Improved NYHA class, 6MWT

Compassionate Use Cases

End-stage DCM

≤20%

↑ by 10-25% points

6-12 months

Reduction in CHF symptom

A Molecular Strategy for the Treatment of Heart Failure

The Science of ACP-01: Targeted Repair at the Cellular Level

ACP-01 is made from autologous cells, taken from the patient's blood, reducing the risk of rejection or immune attack-response. ACP-01 consists of angiogenic cell precursors , which are biologically programmed to migrate to the site of injury, attract NK cells to reduce inflammation and fibrosis, and drive angiogenesis to improve microcirculation,

Migrate Precisely to Areas of Injury

Unlike other cell therapies, ACP-01 maintains high expression of CXCR4 , a receptor that guides cells to injured tissue by following CXCL12 chemokine signals. This homing mechanism ensures ACP-01 migrates exactly to where the damage is occurring; and, it supports tissue repair through paracrine signaling, which is the communication between cells that stimulates healing in neighbouring cells.

Attract Natural Killer (NK) Cells to Reduce Inflammation and Fibrosis

Dilated cardiomyopathy is associated with excessive inflammation and scarring (fibrosis) of the heart muscle. ACP-01 produces high levels of CXCL8 , a chemokine that attracts NK cells , a type of immune cell. NK cells help by:

• Suppressing fibrotic activity in cardiac fibroblasts (the cells that produce scar tissue).

• Blocking the buildup of inflammatory cells in the heart.

• Protecting the heart from viral damage , a known trigger for DCM.

Scientific studies have shown that when NK cells are active in the heart, they reduce collagen buildup (a key component of scar tissue), and support anti-inflammatory signalling.

Drive Angiogenesis to Improve Microcirculation

ACP-01 helps repair the heart by improving blood supply. These cells:

• Are programmed to form blood vessels

• Express high levels of VEGF and angiogenin , two key molecules in the formation of new blood vessels.

• Contain CD34+ cells , which are essential for organizing and guiding new vessel growth.

• Mobilize more CD34+ cells through CXCL8 signaling to amplify vascular repair .

Restoring microcirculation is critical for reducing the size of the damaged heart area, and for preventing further loss of function in the surrounding healthy heart tissues.

Why ACP-01 Succeeds Where Others Fail

Unlike bone marrow-derived therapies, ACP-01 is designed specifically to address the molecular drivers of DCM- chronic inflammation , fibrosis , and poor perfusion . Its mechanism of action and precision is driven by its composition and each patient's innate cellular communication pathways. Additionally, being autologous, ACP-01 avoids the complications of immune rejection, and it improves the consistency of cell survival and function.

Next Step: Treatment of nao-option patients in Florida

Building on Florida's new law that permits the use of non FDA approved stem cell treatments and Hemostemix's scientific findings, the Company is offering its therapy to patients with non-ischemic dilated cardiomyopathy, offering a life-changing, less invasive solution.

"ACP-01 is a personalized, biologically intelligent solution for the problem of dilated cardiomyopathy," said Dr. Fraser Henderson , CMO, Hemostemix. " Robust expression of specific cytokines by ACP create a cellular mileau that increases blood vessel formation and blood flow, while modulating inflammatory response to injured heart, countering scar and fibrosis. Moreover, receptor driven migration of ACP-01 cells to injured heart muscle promote local growth factor influences, preventing cardiac cell death. DCM patients who have run out of options now have a new path forward to regenerate heart function."

"With ACP-01, we're not just treating symptoms- it rebuilds the heart itself," said Thomas Smeenk, CEO of Hemostemix. "This is personalized medicine in action that is safe, targeted, and rooted in real science."

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