NEWS

Dear Colleagues, Partners and Friends,

As this will be my final Message as Chairman, I would like to leave one principle that has guided our work for more than four decades:

Clinical observation must come first, scientific explanation must follow, and both must ultimately serve the patient.

Our scientific journey began with observations that were initially difficult to explain. In chronic non-healing wounds treated with Oxoferin and later OXOVASIN, clinicians around the world repeatedly observed a characteristic transition: wound odour and pain disappeared, healthy tissue colour returned, healthy granulation tissue developed and progressive healing followed — often accompanied by remarkable clinical control of local infection.

Importantly, these wounds did not necessarily become microbiologically sterile. The clinical condition changed and productive, non-fibrotic healing resumed.

At the same time, experimental and clinical studies demonstrated improved oxygenation of hypoxic tissue and accelerated wound repair. This led us early to consider oxygen not only in terms of supply, but in terms of its productive utilization by living tissue.

Earlier clinical and experimental studies had already demonstrated that WF10 can modify the pathological erythrocyte compartment, including the redox-active clearance of highly glycated, pre-haemolytic erythrocytes and the inactivation of extracellular heme-derived toxicity. The 2026 work now places these observations into a broader physiological framework of redox-governed reparative immunity and oxygen usability.

For many years, however, an important question remained unanswered: how could these apparently different observations — tissue oxygenation, erythrocyte restoration, control of destructive inflammation and productive tissue repair — be connected?

That has now changed.

In 2026, Bauerdick et al. in the Journal of Immunology demonstrated experimentally that WF10 shifts activated neutrophils away from destructive NETotic programmes towards apoptotic resolution pathways. For the first time, a central component of the transition repeatedly observed at the patient’s bedside could be demonstrated experimentally.

Our newly published work, “From Destructive Inflammation to Redox-Governed Reparative Immunity” (Wabnitz et al., Trends Open, 2026), integrates these findings with the earlier clinical and experimental observations into a broader physiological framework involving redox regulation, compartmentalization, erythrocyte and heme biology, functional hypoxia, immune resolution and tissue repair.

At the centre of this framework is oxygen usability.

Oxygen supply alone is not sufficient. Biological repair requires the restoration of physiological conditions that allow oxygen to be used productively for energy-dependent cellular programmes.

This perspective does not replace our earlier work.

It gives the earlier observations a common physiological context.

Healthy granulation, improved tissue oxygenation, restoration of erythrocyte homeostasis and the transition from a chronically inflamed wound towards productive, non-fibrotic healing were observed and investigated long before the term oxygen usability was introduced. The new framework helps us understand why these apparently different observations may belong to the same physiological process.

After more than four decades, I therefore see this not as the end of a scientific journey, but as the beginning of its clinical translation.

This scientific framework should guide the future clinical development and medical communication of OXO products. Scientific interpretation must remain grounded in evidence and in the work of our academic collaborators, while our clinical and commercial partners have the responsibility to translate this knowledge carefully and responsibly into medical practice.

I now leave this next phase to a new generation, our academic collaborators and our future clinical partners — with gratitude to all those who have contributed along this long journey, and with confidence that the principle with which we began will remain unchanged:

Clinical observation must come first, scientific explanation must follow, and both must ultimately serve the patient.

Science defines the foundation.
Clinical evidence validates it.
Responsible translation brings it to the patient.

Dr. Friedrich-Wilhelm Kühne
Chairman
OXO Translational Science

Kuala Lumpur, Heidelberg, Magdeburg/Wanzleben, Bangkok

OXO Translational Science GmbH (OXO TS) Germany, a pharmaceutical company engaged in drug development for treatment of inflammatory diseases and diabetic vascular complications, reports the publication of a new patent in the European Patent Bulletin entitled “Use of chlorite to treat red blood cell diseases and indications mediated thereby”. The patent application has been filed in on 22^nd August 2016 (EP16763581.2). An official communication under rule 71(3) EPC on the granting of the patent was sent on 27^th September 2022.

Red Blood Cell (RBC) dysfunctions are the reason for many currently uncurable or unstoppable diseases, e.g. Sickle Cell Anemia. Dysfunctional RBCs are also responsible for the damage of the endothelial cell wall of blood vessels (particularly in the microcapillaries) of individuals diagnosed with Diabetes Type 1 and Type 2. In these patients, RBC dysfunction is characterized by high levels of Hemoglobin A1c (HbA1c). The latter reflects glycation of hemoglobin with RBCs, which leads to metabolic, functional and structural disturbances of the cells. Highly glycated dysfunctional RBCs in Diabetic patients as well as hemolytic products from these cells lead to endothelial damage and vascular inflammation.

In October 2022 the Journal of Diabetes and Treatment published an article entitled “Redoxactive Clearance of Highly Glycated Red Blood Cells: A New Frontier in the treatment of Diabetic Vasculopathies”. This open-access article reports the results from a scientific clinical collaboration project between 1) the National University of Malaysia (Kuala Lumpur, Prof. Yazid Bajuri), 2) the University of Heidelberg, Department for Internal Medicine (Sonderforschungs-bereich SFB1118: ‘Reactive Metabolites as cause of diabetic complications’, Prof. Peter Nawroth), and 3) the OXO TS Research Group, (Wanzleben, Germany and Bangkok, Thailand)

In this controlled clinical trial, a number needed to treat (NNT) of only 20 patients (mean HbA1c > 10%) was sufficient to convincingly proof WF10, propriety drug of OXO TS, as a completely new therapeutic concept for reduction of ele-vated HbA1c levels and restoration of endothelial integrity. In the treatment group, receiving standard of care glucose lowering drugs AND the i.v. drug WF10, > 83% of patients achieved HbA1c values characteristic for NON-diabetic patient within 4 – 6 weeks, whereas in the control group, receiving ONLY standard of care medication, only 25% of
the patients achieved those values

Dr. Joerg Flemmig, Chief Scientific Officer at OXO TS and co-author of the paper, stated: “We are grateful to be able to provide a safe and meaningful drug for treatment of diabetic vascular complication. In our recent clinical studies, we were able to show that not high blood sugar levels per se but glycation-derived dysfunctional RBCs are responsible for diabetic vascular complications.”

WF10, the flagship drug of OXO TS, is approved in Thailand and the launch in ASEAN is lined up. Based on the European patent approval, the company is looking for partners to co-finance the pivotal Phase III study for EMA Approval.