WF-10, The Drug That Saved My Life

Note on the video.

The more I do this work, the more convinced I become in the necessity of having a survivor’s mindset — an unwillingness to give up — a resourceful mindset in combination with in-depth research into possible cures after one has received a terminal diagnosis.

In this video, I combined a video I created on that combination with a video NotebookLM created based on the article below. NotebookLM creates videos that are just okay, but over time I hope to develop other, better, techniques. In the meantime it is an adequate summary of this Substack.

. . .

In 1990, a couple of grape-sized lumps appeared on the side of my neck. They wouldn’t go away so I went to my local doctor. He told me that I had a reaction to insect bites and it was nothing to worry about. They would go away on their own. In those days I ran a lot in the woods and frequently got deerfly bites on my neck and shoulders.

Months went by. No change, so I phoned a radiation oncologist at a nearby hospital and made an appointment. He took a blood test, looked at my neck and said, “I think you’ve got cancer. But, then again, I think everyone has cancer, because that’s all I see all day long. So we need to do some tests – a bone marrow aspirate, a lymph node biopsy.” He phoned me a few days after the tests and told me that I had stage 4a non-Hodgkin’s lymphoma. Stage 4a means it had infiltrated my bone marrow. There was no known cure. I had two young sons, four and one years old. My world felt like it was closing in on me.

It took me over ten years to find a cure. First, there was a couple of years of “wait and see” – there is no statistical advantage to early treatment for indolent lymphomas. The disease attacks your bone marrow as does chemotherapy so sooner or later lymphoma patients did, in those days, go into a downward spiral. Chemo attacks fast-growing cells – that’s why people experience nausea (stomach lining destruction) and hair loss, among other side effects. Indolent lymphoma is relatively slow growing. The chemo first kills off the fastest-growing cancer cells. The slow-going lymphoma cells replicate and gradually wear down a patient’s bone marrow, a major engine in immune systems. Eventually, with depleted bone marrow, the cancer takes over. As I understand it, fungal infections are also often a problem.

I went through eleven oncologists, one naturopath and one osteopath over the next twelve years. Most were experts in the problem. Given that there was no proven cure, I needed a doctor with imagination, someone experimental by nature, but also someone with state-of the art expertise. I travelled a lot of dead ends including a clinical trial at the NIH in Bethesda, Maryland and one at the Dana Farber in Boston. I tried 714-x – a drug I had to inject daily into the area just above my groin. I bought it from someone operating out of a garage outside of Sherbrooke, Quebec. A friend gave me Andrew Weil’s home phone number. Dr. Weil has written many books on natural healing, including the bestseller Spontaneous Healing. He answered the phone and in a grouchy almost angry voice told me to eat maitake mushrooms and hung up. I did, and not only that began a study of all wild mushrooms. Eventually I met with Paul Stamets, widely regarded as one of the world's leading mycologists and a preeminent expert on North American fungi. I ate lots of wild mushrooms. My cancer kept growing.

I read books, including one on macrobiotics. Then I went to several health food stores in the area where I was living and asked if anyone knew of a macrobiotic chef in the area. Everyone mentioned the same guy who had not only studied with Michio Kushi, the primary advocate for macrobiotics in North America, but also had a phenomenal organic garden. I paid him for cooking lessons. When his marriage broke up, he and I rented a house together. Years later Michio, his wife and daughter all died of cancer. It didn’t work for me either. But I kept looking, kept experimenting. When it came time to get chemotherapy – I had 52 tumors throughout my body, including one in my mesentery that was 22 x 17 cm -- I convinced an oncologist in Canada, to give me Fludaribine, an experimental chemotherapy. I had to check into the hospital and get a 24 hour a day infusion. I had always been interested in painting, so while there I took books of art that resonated with me out of the hospital library, all the while tethered to an IV pole. I took them back to my room and painted the same images over and over until I learned the art of watercolor. The cancer kept growing.

I began a regimen of CHOP, the standard chemotherapy for non-Hodgkin’s lymphoma. The cancer kept growing. I enrolled in an experimental clinical trial at the Dana Farber for an autologous bone marrow transplant. In preparation, to reduce my tumor burden as much as possible, I got more chemo. My blood counts plummeted, I was anemic, a borderline hemophiliac and had shingles. My blood counts were too low to proceed, so was removed from the clinical trial. My oncologist told me that there was nothing more she could do for me. I was on my own.

Actually, in retrospect, it may have been a good thing that I was removed from that experimental bone marrow program. Everyone I read about who underwent the treatment died of complications even if cured of cancer. A prominent example was Paul Tsongas, the Democratic candidate for president in 1992. He went into remission from lymphoma but died of liver failure thirteen years later. The liver failure was linked directly to the treatment.

During this entire period, I was continuing to read about experimental therapies, phoning physicians, clinicians and medical researchers. I attended conferences and during breaks would track down the physicians who spoke and ask them, “What’s the most exciting research or clinical trial right now in indolent, B-cell, non-Hodgkin’s lymphoma?” I’d call authors of research papers. Most of them wouldn’t come to the phone, but those that did pointed me in interesting directions.

Somewhere during this time, I heard an interview on NPR that was important for me. A young man who had rowed alone across the Atlantic, and gotten blown off course, ran out of food and almost out of fresh water, said that he chanted to himself, over and over, “I am a survivor. I am a survivor. . .” After listening to the interview, that became my mantra too. Before I fell asleep at night, and as soon as I woke up in the morning, I chanted to myself, “I am a survivor.” I can’t prove it of course, but I think it was important to my recovery. It guided me in the right direction, even if on a subconscious level.

I came across an article about German physicians who returned from volunteering at Chernobyl exposed to sublethal radiation. They had skin lesions and internal bleeding. A chemist there, Friedrich-Wilhelm Kuehne, had developed a successful skin cream to treat severe burns. He modified it for these radiation skin lesions and it worked. He then created an infusion version for internal bleeding. Not only did it work, but none of the physicians got leukemia, a very common side effect of radiation exposure. That compound was WF-10.

Next, a urologist who had prostate cancer that had metastasized, and who happened to be a relative of Dr. Kuehne, decided to experiment on himself. He underwent a lethal dose of radiation to cure the prostate cancer, then took WF-10 to combat the effects of the radiation. Though the therapy was extremely painful, he survived. Cancer cured.

During a visit to Halifax, Nova Scotia to interview an artist, Gabriel Gély, for Heron Dance, my art journal, I had a chance encounter with a former client from the days I worked on Wall Street. My head was bald from chemo. He asked me what was going on. I told him about my cancer journey. He mentioned that he had an investment in a company in Germany that made a drug that may have some cancer treatment value, WF-10. With his introduction, I contacted the company, obtained the drug, and found, after calling many, many physicians one willing to administer it in the US. Within a month my blood counts had improved and my cancer had stopped growing. I wasn’t cured, but I was, for the first time in years, doing well. I felt healthy.

WF-10 kept me going long enough for the release of Rituxan, a monoclonal antibody used to treat B-cell lymphoma. Rituxan, the first monoclonal antibody, was made in part by inserting mouse antibody genes into cultivated mammalian cell lines (typically Chinese Hamster Ovary cells) that then mass-produce the antibody. Production now occurs in engineered cultured cells. I assume it works because of human’s long association with rodents, and the resulting defense systems we’ve built up over the millennium to protect ourselves. Our immune systems encounter the rodent cells and mass produce a defense that then defends against the invader. The antibody created also works against lymphoma. Regardless of whether or not I’m right about that, it worked. My lymph nodes disappeared. My blood counts recovered with the exception of platelets. Those, now normal, have taken all these years to fully recover.

The story of WF-10 is one of both triumph and tragedy. Triumph because it has proven effective against a number of debilitating diseases: HIV and diabetes, for instance. It seems to have some efficacy against cancer but its real value may be in restoring the depleted immune systems of those who have undergone chemotherapy or radiation. The tragedy is that the company that produces it ran out of money in the FDA approval process – during the clinical trials. Companies frequently spend over a billion dollars getting a new drug approved, and that doesn’t count the many that fail to show efficacy during the process. WF-10 is currently available only in Thailand.

Here’s a history of WF-10 clinical trials:

WF-10 (TCDO) Clinical Trial Timeline

1. Oncology (Pancreatic Cancer)

• Trial: Phase II, adjunctive WF‑10 + capecitabine for unresectable pancreatic cancer

• Registration: EU Clinical Trials Register (EudraCT ID: 2004‑001621‑14)

• Sponsor/Site: Dimethaid AG; European Pancreas Center, University of Heidelberg

• Status: Ended December 15, 2008; published results:

WF10 Stimulates NK Cell Cytotoxicity by Increasing LFA-1-Mediated Adhesion to Tumor Cells

Here’s a paragraph from the research study published after the trial ended:

WF10, or Immunokine, is based on the chlorite ion matrix tetrachlorodecaoxygen and is currently being evaluated in various clinical indications including the adjuvant therapy of inoperable pancreatic cancer and various inflammatory conditions. WF10 is known to have various immunological effects by stimulating innate immune functions, while inhibiting adaptive immune functions [10]. In contrast to control animals, sublethally irradiated rats treated with WF10 developed significantly less hematological or solid tumors than controls [11, 12]. This antitumor effect of WF10 could be explained by stimulating the innate natural cytotoxicity against tumors. We, therefore, investigate the effect of WF10 on NK cell cytotoxicity.

2. Wound Healing & Radiation Injury

• Radiation Dermatitis / Mucositis (France, 1991)

  • Randomized crossover trial (103 patients) showing lesion improvement with WF‑10

  • No formal NCT/EudraCT ID found

  • Cited in Drugs R D (2004) review (PubMed, PubMed)

• Radiation Cystitis (Thailand, post-1998)

  • WF‑10 approved for postradiation cystitis following a trial in 20 patients

  • Used under physician request protocols in Germany (PubMed)

• Chronic/Difficult Wounds (TCDO vs. PVP‑iodine, Germany, 1986)

  • Controlled study: 29 patients treated with TCDO (Oxoferin), compared vs beta‑iodine; showed superior wound healing and granulation tissue quality (PubMed)

3. Hematology / Immune Dysfunction (Infectious & Diabetic Ulcers)

• Diabetic Foot Ulcers (Double-blind RCT)

  • Journal of Foot & Ankle Surgery, 2011 (published Mar 2013).

  • 40 participants: standard therapy + WF‑10 vs placebo.

  • WF‑10 group showed significant improvement in wound severity, reduced infection/inflammation, and better granulation formation.

4. Other Mentions

• Drugs R D Review (2004)

  • Phase III trial in AIDS patients. This was a 1995 randomized trial of late stage HIV patients. It was a multi centric clinical trial involving San Francisco General, Miami and 20 more centers. The study was in the follow up period of 2 years but closing could not be acheived for financial reasons. Interim data showed that WF10-treated subjects out-survived those that received the placebo. More on that trial and its results here.

  • Cervical cancer (1989), radiation-related issues, etc.

  • Reports WF‑10 is approved in Thailand for postradiation inflammatory conditions and available under Canada’s Special Access Program (PubMed)

Summary Table

Summary:

• WF-10 saw some success in wound healing, radiation injuries, and ulcers, though these were small-scale (Phase II or lower).

• Clinical development stalled post-2008, and no large trials or publications emerged after that.

• Today, WF-10 exists primarily through topical derivatives like Oxoferin/Oxovasin, used for wound healing.

A primary benefit of WF-10 is its ability to boost macrophages, a critical blood element in the immune system. Macrophages are phagocytes: they “swallow” and digest bacteria, viruses, dead cells, and debris. This helps clear infections and clean up tissue damage. After digesting microbes, macrophages display antigens (pieces of what they ate) on their surface. This alerts and activates T cells, which are key to adaptive (long-term, targeted) immunity. T cells play a role in emerging cancer treatments as described in the chapter of this book on CAR-T and CAR-NK therapies. Macrophages also release cytokines (chemical signals) that call in and direct other immune cells.

If you are interested in WF-10, please be in touch. I might not be able to figure out a way to have it administered in the US, but I’ll contact OXO Translational Science GmbH in Germany and get back to you with options.

Macrophages

In addition to WF-10, a number of other compounds are also effective at boosting macrophages. These are easy to get in the US, either through an oncologist or, in many cases, over-the-counter:

1. Pathogen-Derived Molecules

These are often recognized by pattern recognition receptors (PRRs) on macrophages:

• Lipopolysaccharide (LPS) – from Gram-negative bacteria, a strong activator via TLR4 (used experimentally, not safe as therapy).

• CpG oligodeoxynucleotides – bacterial DNA motifs, recognized by TLR9, drive macrophage activation.

• Flagellin – bacterial protein recognized by TLR5.

2. Cytokines (Immune Signaling Proteins)

• Interferon-γ (IFN-γ) – classically activates macrophages into an M1 phenotype (tumoricidal, antimicrobial).

• Granulocyte-macrophage colony-stimulating factor (GM-CSF) – promotes macrophage proliferation and functional activation.

• Tumor necrosis factor (TNF) – enhances phagocytic and pro-inflammatory capacity.

3. Small Molecules & Drugs

• Imiquimod (Aldara® cream) – TLR7 agonist, used topically for skin cancers and warts; boosts macrophage and dendritic cell activity.

• Lentinan – mushroom-derived β-glucan analogue, enhances macrophage and NK function.

• Muramyl dipeptide (MDP) – bacterial cell wall component, tested as an immune stimulant.

• Checkpoint inhibitors (e.g., anti-PD-1, anti-CD47 antibodies) indirectly enhance macrophage phagocytosis of tumor cells by lifting inhibitory signals.

4. Natural Compounds & Nutraceuticals

• Vitamin D – enhances macrophage antimicrobial responses, especially against tuberculosis.

• Curcumin (from turmeric) – modulates macrophage polarization (often shifting toward M2, anti-inflammatory).

• Resveratrol, quercetin – polyphenols that influence macrophage cytokine output.

• Probiotics – some Lactobacillus strains increase macrophage phagocytosis via gut-immune signaling.

5. Clinical/Experimental Therapies

• BCG vaccine (for TB and bladder cancer) – a classic macrophage stimulator; induces “trained immunity” and is used intravesically to activate macrophages against bladder cancer.

• Monoclonal antibodies (rituximab, trastuzumab) – don’t directly activate macrophages, but engage them via Fcγ receptors to mediate antibody-dependent cellular phagocytosis (ADCP).

• Cytokine therapies (IL-2, IL-12, IFN-α) – tested in cancer immunotherapy to augment macrophage and NK functions.

Of these, the following are non-prescription:

• β-Glucans (yeast, oats, mushrooms)

  • Found in dietary supplements and functional foods.

  • Activate macrophages via Dectin-1 and CR3 receptors.

  • Available as capsules, powders, or extracts (e.g., baker’s yeast β-glucan, reishi or shiitake mushroom products).

  • There are a number of versions of Beta Glucan on the market. I’ve used several. Notes on a particularly interesting one, Wellmune WGP, follow.

• Vitamin D

  • Essential for proper macrophage antimicrobial activity.

  • OTC in tablets, capsules, drops.

  • Deficiency is linked to impaired innate immunity.

• Vitamin C

  • Antioxidant, enhances macrophage phagocytosis and ROS production.

  • Widely available as OTC supplements.

• Zinc

  • Important for macrophage differentiation and function.

  • OTC as lozenges, tablets, multivitamins.

• Probiotics (e.g., Lactobacillus, Bifidobacterium strains)

  • Some strains stimulate macrophage phagocytosis and cytokine production.

  • Available in capsules, yogurts, fermented foods.

• Medicinal mushroom extracts (e.g., Reishi/ Ganoderma lucidum, Shiitake/ Lentinula edodes, Maitake/ Grifola frondosa)

  • Contain β-glucans and polysaccharides with macrophage-activating effects.

  • OTC as powders, teas, tinctures.

• Curcumin (turmeric extract)

  • Modulates macrophage activity; effects can be pro- or anti-inflammatory depending on dose and context.

  • Available as OTC supplements.

• Resveratrol / Quercetin (plant polyphenols)

  • Influence macrophage cytokine secretion and oxidative burst.

  • OTC in capsules or dietary sources (berries, red grapes, onions).

Beta Glucan is widely used in Europe as an immune system booster. It isn’t prescribed by physicians in America because it can’t be patented and therefore won’t have drug company sponsorship or marketing. It has, nevertheless, been the subject of at least 200 research studies, as indicated in this NIH article:

β-Glucan Metabolic and Immunomodulatory Properties and Potential for Clinical Application

Conclusions

β-glucans are natural molecules that have significant therapeutic promise, particularly as metabolic and immune-modulatory agents [189]. Enthusiasm for their therapeutic potential is reflected in the high number of clinical trials of β-glucans that have been completed or are in progress.

Cancer Therapy

One of the most interesting applications of β-glucans is for cancer treatment, specifically as an adjuvant to enhance “conventional” cancer chemotherapeutics. β-glucans regulate complement-dependent cytotoxicity (CDC). β-glucans are recognized as PAMPs, triggering the response of immune effector cells. This will then elicit an anticancer immune response through the formation of a complex. When they enter the bloodstream, they are bound by endogenous plasma anti-β glucan antibodies (ABA). This binding activates complement and complement protein iC3b binds to the ABA, resulting in β-glucans—ABA—iC3b complex [146,147]. This complex binds to immune effector cells and activates specific aspects of innate immune function including CR3 phagocytosis. The activation and formation of this complex facilitate the direct killing of antibody-targeted tumour cells [146,147].

This mechanism was observed in both a pre-clinical model [148] and demonstrated with whole blood from healthy volunteers. The authors found that anti-cancer properties are dependent on the formation of the complex with naturally occurring ABAs [146]. In the preclinical model, mice were administered anti-tumour monoclonal antibodies (mABs) in combination with β-glucans. Results showed that the dual treatment produced significantly greater tumour regression in both mammary and hepatic tumours. The combinational treatment had a greater effect on each treatment individually. Interestingly, mice that were deficient in CR3 or serum CR3 or granulocytes did respond to treatment [148].

. . .

Years ago, in my research into Beta Glucan, I contacted a scientist at Biothera Pharmaceuticals, a manufacturer in the US of Beta Glucan, who told me not only that his company was doing research for the US Government into the use of Beta Glucan to treat military personnel, should they become exposed to radiation, but that he was giving it to his mother who had lymphoma. He thought that the drug was having a positive impact but had no specifics to share. Of particular importance, and something I’ve not seen or heard anywhere else, he told me that Beta Glucan was much more effective taken on an empty stomach. I get up a three times a night to use the bathroom, and for years, when it became impossible to get WF-10, I took 2100mg of Beta Glucan with each urination. I followed this practice during the night to take advantage of my empty stomach.

The indication of a benefit to those exposed to radiation was particularly interesting given that WF-10 has similar properties. This is what I found after further research:

Earlier preclinical research has demonstrated that yeast beta glucan enhanced the production of white blood cells – a process known as hematopoiesis – following radiation exposure and reduced infectious complications of myelosuppression. The findings support the potential for developing therapies for cancer patients undergoing radiation or chemotherapy, as well as protecting military personnel and civilians from "dirty bombs" or nuclear accidents.

Funding for the study came from the National Institute of Health, the U.S. Army Breast Cancer Research Program, the Kentucky Lung Cancer Research Board and Biothera and this:

What the Evidence Shows

1. Early Research at the U.S. Armed Forces Radiobiology Research Institute (AFRRI)

• Patchen et al. conducted important studies in the early 1980s demonstrating that administration of β‑1,3-glucan significantly helped mice recover from radiation-induced bone marrow injury and improved survival rates after lethal radiation exposure. These studies were experimental and preclinical, using purified forms of β‑glucan.
  “Currently, we [U.S. Armed Services] are using glucan to enhance hemopoietic proliferation in conjunction with hemopoietic injury induced by radiation.” betaglucandata.com+2doveclinic.com+2pmc.ncbi.nlm.nih.gov+3betaglucan.org+3betaglucan.org+3

• Additional reports noted that oral β‑glucan protected about 70% of mice from lethal radiation when given after exposure, and stimulated white blood cell recovery via CR3-mediated mechanisms.

The Biothera Beta Glucan is more expensive than others I’ve bought, but the purification process used probably makes it worth it. It is available on Amazon as Wellmune.

Biothera’s Contributions to β-Glucan Research & Standards

1. Development of Wellmune® (WGP®) – a Proprietary β-Glucan Ingredient

• Biothera developed and markets Wellmune WGP®, a highly purified yeast-derived β‑1,3/1,6‑glucan, removing mannans, proteins, and lipids to enhance bioactivity and purity.

• They emphasize that not all β‑glucans are alike, and biological activity varies by molecular structure and yeast strain. PMC+11NutraIngredients-USA.com+11SupplySide SJ+11

2. GRAS Status for Food Use

• In December 2006, Biothera’s WGP 3-6 and BetaRight® 3-6 became the first yeast β‑glucans to achieve Generally Recognized As Safe (GRAS) status under FDA guidelines—supported by extensive safety and manufacturing data. New Hope

3. Establishing Analytical Standards (GEM Assay)

• Biothera chemists introduced the Glucan Enzymatic Method (GEM)—a more accurate and precise assay for measuring β‑glucan content in raw ingredients and finished products. Published in the Journal of Agricultural and Food Chemistry, this method avoids polysaccharide misestimation inherent in older assays. Annals of Oncology+6SupplySide SJ+6NutraIngredients-USA.com+6

More on Beta Glucan can be found here. (I receive no compensation, direct or indirect, from any company or product mentioned).