Repurposed Drugs and Nutraceuticals: A New Frontier in Cancer Therapy"

"The Future of Cancer Treatment Is Already Here"

“ This post highlights the Power of Repurposed Drugs and Nutraceuticals while disrupting the traditional approach to cancer therapy. This post is central to understanding the new revolutionary approach to cancer management.” - Paul

What “repurposing” means in oncology

• Drug repurposing uses existing, usually non‑oncology, approved drugs (with known safety profiles) for new anticancer indications, often in combination with standard therapies.

• It is important to emphasize that all repurposed drugs are FDA approved often with a long safety record. Off-label drug use involves prescribing medications for indications, or using a dosage or dosage form, that have not been approved by the US Food and Drug administration. Off-label prescribing is legal in all states, is approved encouraged by the FDA and does not require patient consent.(1)

• ​Advantages of the use of off-label drugs include shorter development timelines, lower cost, and rapid movement into trials.

• For obvious reasons large randomized controlled trials testing these drugs are far and few between. Barriers include lack of commercial incentive, intellectual‑property issues, and complex trial design, making it hard to move from signal to standard of care. Essentially Big Pharma and the agencies they control do not want these studies to be performed. Chemotherapy in the USA is a $4Billon industry.

Major repurposed drug classes

• Metformin: Widely studied; preclinical data show inhibition of cancer cell metabolism via AMPK activation and mTOR suppression, and observational studies link use to lower incidence and improved outcomes in several cancers.

• Ivermectin and mebendazole: Both show anticancer effects in preclinical models, but evidence is largely limited to cell cultures, animal studies, and anecdotal clinical reports. Ivermectin inhibits cancer cell proliferation, metastasis, and angiogenesis in multiple tumor types and can induce apoptosis, autophagy, and other forms of programmed cell death. Mebendazole disrupts microtubule polymerization by binding the colchicine site on tubulin, leading to mitotic arrest, apoptosis, and inhibition of cancer cell proliferation. Additional reported actions include inhibition of angiogenesis (e.g., via VEGFR2), suppression of pro-survival and metastatic pathways, reduction of cancer stem cell populations, and radiosensitization or chemosensitization in various models.

• Melatonin: Melatonin shows broad anticancer (oncostatic) activity in preclinical models and modest, mainly adjunctive benefits in clinical studies, acting through antioxidant, pro‑apoptotic, immune‑modulating, and endocrine mechanisms. Evidence is strongest for use alongside chemotherapy or radiotherapy rather than as a stand‑alone anticancer drug in humans

• Statins (lipid lowering): Induce tumor‑specific apoptosis in some models and have been associated with improved survival in observational cohorts

• Beta‑blockers (e.g., propranolol): Preclinical and epidemiologic data suggest reduced metastasis and improved outcomes in some cancers, and early trials in angiosarcoma and perioperative settings are ongoing, but evidence is still preliminary.

• Doxycycline: Doxycycline shows several experimental anticancer actions, mainly by targeting mitochondrial function and cancer stem cell biology. Doxycycline binds mitochondrial ribosomes, impairing translation of mitochondrial DNA–encoded respiratory chain proteins, which reduces oxidative phosphorylation, ATP production, membrane potential and proliferation in multiple cancer cell lines while sparing normal fibroblasts.​ Cancer cells and cancer stem cells (CSCs) often rely heavily on mitochondrial metabolism, so this mitochondrial targeting preferentially stresses malignant cells and can lower the apoptotic threshold to chemotherapy.

Major nutraceuticals in cancer care.

• Nutraceuticals (e.g., curcumin, resveratrol, quercetin, sulforaphane, lycopene, omega‑3s, aged garlic extract, green tea extract, and vitamins D show antioxidant, anti‑inflammatory, pro‑apoptotic, anti‑angiogenic, and immune‑modulating effects in preclinical studies and limited clinical studies.

• Many demonstrate synergy with chemotherapy in models, enhancing cytotoxicity and sometimes reducing side effects such as oxidative damage, nausea, fatigue, and immunosuppression

Remarkably, unlike conventional chemotherapeutic drugs that mostly act via a single cellular biological pathway, almost all the repurposed drugs/nutraceuticals used as adjunctive treatments for cancer have multiple modes of action (see table 1). These mechanisms can generally be divided into two major groups, namely:

i. those that act directly on cancer cell pathways promoting cell death (apoptosis); and

ii. those that alter the tumor microenvironment (TME) restoring immune function and T cell cytotoxicity, limiting angiogenesis and metastatic spread, and inhibiting cancer stem cells.

Those nutraceuticals and repurposed drugs that have been demonstrated to reduce the risk of developing cancer are likely to be highly effective in treating cancer. Furthermore, it is likely that the metabolic pathways involved in cancer prevention play a major role in limiting cancer growth and spread. Consequently, an evaluation of a repurposed drug’s efficacy in preventing cancer is important in considering the role of that drug in the treatment of cancer.

Most published studies demonstrating the benefit of nutraceuticals and repurposed drugs are in vitro mechanistic experiments and studies performed in animal models. Prospective clinical studies are generally small, focusing on mechanisms of action or surrogate markers of efficacy. Indeed, most of the published clinical data consists of epidemiological studies, retrospective observational studies, small case series, and case reports with few prospective clinical studies. This is not unexpected due to the “war on repurposed drugs” that is being waged by Big Pharma and its supporters; there is little funding to support well-designed clinical studies using cheap, potentially effective, and lifesaving drugs. As multiple repurposed drugs are used together to treat patients it is almost impossible to design randomized prospective studies as this would require multiple treatment arms. It would also be unethical to have a placebo arm in which the patients receive no active treatment. The ideal would be a large prospective study comparing the outcome of a repurposed drug combination compared to the expected outcome for a specific cancer (e.g. The Metric’s study).(2) However, such studies are logistically difficult, resource intensive and expensive to perform, unlikely in a setting outside of Big Pharma.

Table 1. Summary of the anti-cancer pathways of the repurposed drugs and nutraceuticals.

Large, pharma-funded, randomized, double-blind controlled trials (RCTs) - considered by the medical establishment and those in the ivory towers to be the gold standard — have numerous limitations, however, and frequently don’t reflect real-world clinical practice. Furthermore, there is now strong scientific data and a growing consensus that well-conducted observational studies produce results statistically similar to those of traditional RCTs. (3) It is, therefore, possible, and indeed desirable to design prospective observational studies to study the clinical efficacy of the metabolic approach to cancer and specifically the combined use of multiple repurposed drugs. As the metabolic approach to cancer necessitates a combination of interventions, including caloric reduction and a ketogenic diet, and multiple off-label anticancer drugs, it would be nearly impossible to design a double-blind randomized study.

The METRICS study (NCT02201381) is an example of an off-label drug protocol for the treatment of patients with glioblastoma. (2) METRICS is a novel, participant-funded, open-label, non-randomized, single-arm real-world study designed to gather high-quality evidence on the safety, tolerability, and effectiveness of the combination of four off-label metabolically targeted medicines (metformin, atorvastatin, mebendazole, and doxycycline) as an adjunctive cancer treatment for glioblastoma and other tumors. (2) The retrospective arm of the METRICS study has produced very encouraging results, with a significant increase in disease-free survival of patients compared to a control group.

A 2014 ProPublica investigation found that “Big Pharma’s focus on blockbuster cancer drugs squeezes out research into potential treatments that are more affordable.” (4) A researcher at Harvard Medical School who has tried for many years to find funding for a study on the effects of aspirin on breast cancer told the reporter: “For some reason, a drug that could be patented would get a randomized trial, but aspirin, which has amazing properties, goes unexplored because it’s 99 cents at CVS.” (4)

The Repurposing Drugs in Oncology (ReDO) project has cataloged 268 approved drugs with anticancer effects. (5). In addition, over three thousand plant species have anti-cancer activity.(6) It would be impossible to review all the drugs in ReDo’s database in this monograph; rather, we have focused on and evaluated the drugs that appear to have the greatest clinical utility. These repurposed drugs are listed in priority according to the strength of the supporting clinical and mechanistic evidence.

Patients with cancer should consider taking at least 4-6 agents repurposed drugs and nutraceuticals. While remissions using a single agent (e.eg ivermectin, fenbendazole) have been reported, we believe that multiple agents acting on different metabolic pathways act additively/synergistically with each other and with conventional chemotherapy. The chapter entitled “approach to repurposed drugs outlines the preferred combination of agents for each particular cancer.” Table 3 outlines the most common cancers and their curability with standard chemotherapy. The curability with standard chemotherapy should be discussed with the patient to formulate a treatment plan that includes adjunctive therapy or adjunctive therapy alone. All patients who elect to receive chemotherapy should concomitantly receive adjunctive therapy; metronomic chemotherapy dosing may be preferred in these patients.

The patient’s response to treatment should be monitored with a PET scan (glucose uptake scan) every three months and then at least every 6 months once in remission/cancer stable. Patients should follow their tumor markers concomitantly. Circulating tumor DNA (in blood specimens) is an emerging technology that may prove useful for monitoring tumor progression. (7, 8) Patients and their healthcare providers should dynamically follow their tumor markers and adjust their treatment protocol accordingly. Patients who demonstrate a good clinical response should not stop their treatment protocol abruptly, as this may result in a relapse, (9) but rather reduce the number of interventions dynamically.

Table 2. Contrasting characteristics of standard chemotherapy and repurposed drugs and nutraceuticals

Antioxidant supplements (vitamins A, C, and E; coenzyme Q10, and N-acetyl cysteine) should be avoided in patients with cancer. In an experimental model, Wang et al demonstrated that vitamin C, vitamin E and n-acetylcysteine (NAC) increased tumor angiogenesis by BACH1 mechanism (redox-sensitive transcription factor BTB and CNC homology 1). (10) These antioxidants should specifically be avoided in patients undergoing chemotherapy and radiotherapy, as these interventions act largely by increasing oxidant injury, which is minimized by antioxidant supplements. (11, 12) Paradoxically, while oral vitamin C is a potent antioxidant, (13) high-dose intravenous vitamin C generates reactive oxygen species that potentiates the effects of chemotherapy and radiation therapy (see section on intravenous vitamin C). Moderate dose oral Vitamin C blocks glycolytic pathway and has been shown to be synergistic with doxycycline.(14, 15) High dose thiamine may in some contexts support tumor growth or survival, so “rational use” (avoiding unnecessary large chronic doses) is advised. Thiamine should only be given to correct thiamine deficiencies. Similarly, high B12 levels may promote cancer proliferation and high B12 levels should be avoided. Avoid chronic high‑dose B‑vitamin supplementation “just in case” in patients with active cancer.

Table 3: Tumor stratification according to response to chemotherapy

In order to support the Warburg metabolic reprogramming glycolytic enzymes are increased in cancer cells. Not surprisingly, the degree of upregulation of these enzymes is greatest in the deadliest cancers (see Tables 4 & 5)

Table 4. Alteration in glycolytic enzymes associated with the Warburg effect in cancer cells

Table 5. Alteration in the glycolytic enzymes in the 10 deadliest cancers

One of the major goals of repurposed drugs in patients with cancer to to target the glycolytic enzymes. Those agents with are most effective in targeting glycolytic enzymes in cancer are listed in Table 6.

Table 6. Ranking of agents targeting glycolytic enzymes (Warburg Effect)

Table 7. AI ranking of the top 5 anticancer drugs based on stem cell pathway effect on tumor microenvironment and safety

Ranking of the most important anticancer agents.

It is important to recognize that this ranking is dynamic and will evolve as new scientific evidence emerges and our understanding of these agents improves. Consequently, the position of individual compounds may change over time. Each of these agents will be reviewed in future posts.

For practical purposes, the agents are grouped into four broad tiers:

Tier 1: Agents with the strongest and most consistent anticancer signal, supported by substantial preclinical evidence and, in some cases, clinical data. These compounds demonstrate activity against one or more key hallmarks of cancer, including inhibition of proliferation, induction of apoptosis, targeting of cancer stem cells (CSCs), and modulation of the tumor microenvironment (TME).

Tier 2: Agents with promising but less extensive evidence, demonstrating meaningful activity in at least two of the three major domains: tumor cell control (proliferation/apoptosis), CSC targeting, and TME modulation.

Tier 3: Agents supported primarily by limited, indirect, or predominantly preclinical evidence, with insufficient clinical data to establish a significant anticancer role.

Tier 4: Agents with very weak, controversial, unsupported, or largely theoretical evidence for cancer control, and in some cases concerns regarding safety or potential harm.

Tier 1: Highest overall anticancer signal

These agents have reasonably strong data for inhibiting proliferation, inducing apoptosis, and modulating CSCs and/or TME across several models.

• Vitamin D3

  • In vitro/in vivo evidence of reduced proliferation, induced differentiation and apoptosis, inhibition of stem‑like phenotypes, and anti‑angiogenic and metabolic effects in many cancer types​

• Metformin

  • AMPK activation and mTOR inhibition decrease tumor cell proliferation and impact cancer metabolism and CSC populations in several models; observational and some interventional data show improved outcomes in some cancers​

• Melatonin

  • Pro‑apoptotic and anti‑proliferative in multiple tumor models; also, anti‑angiogenic and immunomodulatory (enhanced NK and T‑cell function). Meta-Analysis of 21 trials suggests improved response and survival when added to chemo/radiotherapy​

• Propranolol

  • Blocks stress‑mediated β‑adrenergic signaling, reducing angiogenesis and proliferation and modulating immune/TME; some perioperative/observational data​

• Ivermectin

  • Emerging data show mitochondrial dysfunction, induction of apoptosis, inhibition of proliferation and migration, and effects on CSC‑like populations; case‑based and small series use it in combination metabolic protocols​

• Mebendazole

  • Disrupts microtubules, causing mitotic arrest and apoptosis; preclinical data show potent inhibition of proliferation, including CSCs, and strong anti‑angiogenic effects; some in vivo work suggests survival benefits vs standard agents in glioma models​

• Green tea catechins (EGCG)

  • Decrease tumor cell viability and migration, induce apoptosis, inhibit angiogenesis, and modulate immune response and TME; spheroid models show selective toxicity for breast cancer vs normal breast cells​

• Curcumin (nanocurcumin)

  • Broad pro‑apoptotic, anti‑proliferative, anti‑inflammatory, and anti‑angiogenic effects, with evidence for targeting CSC pathways (e.g., Wnt/β‑catenin, NF‑κB) and TME modulation in preclinical studies

• Sulforaphane

  • Epigenetic regulator with strong preclinical evidence for inducing apoptosis, inhibiting proliferation, targeting CSC markers, and modulating detoxification and inflammatory pathways in the TME​

• Thymosin alpha-1

  • Thymosin Alpha-1 (Tα1) is a naturally occurring immune-regulating peptide that enhances dendritic cell function, restores CD8+ cytotoxic T-cell activity, and increases natural killer (NK) cell surveillance against cancer

• Atorvastatin / Simvastatin

  • HMG‑CoA reductase inhibition reduces proliferation, promotes apoptosis, and may affect CSCs and TME (cholesterol and prenylation pathways)​

• Omega‑3 fatty acids

  • May induce apoptosis, reduce proliferation, and exert anti‑inflammatory, pro‑resolving TME effects​

• Berberine

  • Anti‑proliferative, pro‑apoptotic, affects metabolic pathways and may influence CSCs, some synergy with metformin​

• Doxycycline

  • Targets mitochondrial biogenesis and may deplete CSC‑like populations; inhibits MMPs, impacting invasion and TME

• Mistletoe (Viscum album)

  • Lectins and other components induce apoptosis and inhibit proliferation; immunomodulatory with NK‑cell activation and some clinical data for disease control and improved quality of life. Administered by specialized integrative clinicians

• High‑dose intravenous Vitamin C

  • Acts as a pro‑oxidant at pharmacologic doses, generating hydrogen peroxide and inducing tumor‑selective cytotoxicity and apoptosis; also influences TME redox and may synergize with chemo/radiation in early trials​

• Resveratrol / Pterostilbene

  • Polyphenols with pro‑apoptotic, anti‑proliferative, anti‑angiogenic, and CSC‑targeting effects (e.g., Notch, Hedgehog, Wnt) in diverse tumor models​

Tier 2: Promising, multi‑domain activity

These agents show meaningful preclinical evidence or limited clinical support for at least two proliferation/apoptosis, CSCs, and TME.

• Modified citrus pectin - is a naturally derived polysaccharide that inhibits galectin-3, a key protein involved in cancer cell adhesion, aggregation, metastasis, fibrosis, and immune evasion.

• Luteolin - a potent plant flavonoid that inhibits PI3K–AKT–mTOR, STAT3, NF-κB, Wnt/β-catenin, and epithelial–mesenchymal transition (EMT), thereby suppressing cancer cell proliferation, cancer stem cells, angiogenesis, metastasis, and treatment resistance across multiple tumor types.

• Genistein - is a soy-derived isoflavone that exerts broad anticancer effects by inhibiting androgen receptor, IGF-1, PI3K–AKT–mTOR, NF-κB, and STAT3 signaling, thereby suppressing proliferation, angiogenesis, metastasis, and cancer stem cell activity.

• Aspirin / Diclofenac (COX inhibitors) – anti‑inflammatory, anti‑proliferative, anti‑angiogenic; aspirin has epidemiologic and some interventional data for colorectal and other cancers.​

• Cimetidine – immunomodulatory, anti‑adhesive, and anti‑proliferative; small clinical series in gastric cancer and melanoma show survival and response benefits.​

• Honokoil - is a naturally occurring polyphenol derived from Magnolia bark that exhibits broad anticancer activity by inhibiting tumor growth, inducing apoptosis, suppressing cancer stem cells, and reducing angiogenesis and metastasis.

• Itraconazole – inhibits Hedgehog signaling, angiogenesis, and tumor metabolism; some small trials show activity in lung and other cancers.​

• Niclosamide – targets multiple pathways (Wnt/β‑catenin, STAT3, NF‑κB) with apoptosis and CSC‑related effects in vitro.​

• Artemisinin – generates reactive oxygen species in iron‑rich cancer cells, leading to apoptosis and reduced proliferation, limited clinical translation so far.​

• Low-dose naltrexone - immunomodulating/endorphin hypotheses; limited cancer-specific controlled evidence.

Tier 3: Limited, mostly preclinical, indirect, or inconsistent translation

• Ganoderma lucidum and other medicinal mushrooms – β‑glucans and other components modulate immunity (TME) and may have direct anti‑proliferative/apoptotic effects

• Nigella sativa –(thymoquinone) – preclinical evidence of apoptosis induction

• Spironolactone – limited but emerging data for anti‑proliferative and DNA‑damage‑related effects

• Sildenafil/Tadalafil- immune/TME hypotheses; limited cancer-control clinical evidence

• Dipyridamole - some mechanistic synergy reports; little robust clinical translation

• Fenofibrate - notable preclinical anti-tumor/TME effects; clinical oncology use remains limited

• Lactoferrin - immune/mucosal/TME plausibility; limited direct cancer-control outcomes

• Ashwagandha (mostly supportive care/stress biology + preclinical anticancer

  signals)

• Aged garlic extract - reduces inflammation and oxidative stress, enhances immune surveillance and inhibits tumor proliferation and angiogenesis

• Lycopene - antioxidant, inhibition of cell proliferation, induction of apoptosis, and modulation of growth-factor signaling pathways

• Wheatgrass - antioxidant, anti-inflammatory, immune-modulating, and pro-apoptotic mechanisms, but evidence remains limited and largely preclinical

• Alpha lipoic acid - reduces oxidative stress and inflammation, activates AMPK, inhibits mTOR signaling, and promotes apoptosis in cancer cells, although most evidence remains preclinical

• Chlorine dioxide – in-vitro mechanistic data, limited clinical evidence

Tier 4: Very weak, controversial, harmful or largely theoretical for cancer control

These agents are reviewed in detail in a subsequent posting.

• Dichloroacetate – potential toxicity, limited benefit

• Bicarbonate alkali therapy – physiologically unsound, not scientifically supported.

• Cannabinoids (for cancer control) — strong role in symptom management in selected patients, but direct anticancer control in humans remains unproven; major oncology guidance focuses on communication/symptom domains rather than treating cancer itself.

• High dose ozone – not scientifically supported

• Systemic pancreatic enzyme therapy – not scientifically supported

• Insulin potentiation therapy – not scientifically supported

• Pao Pereira — limited high-quality translational evidence.

• Dandelion extracts - mainly anecdotal/preclinical; insufficient reliable translational evidence

• Dimethyl sulfoxide (DMSO) – not clinically useful and potentially harmful

• Shark cartilage — heavily marketed historically; clinical evidence has not supported meaningful cancer-control benefit

• Essiac – historically promoted; clinical evidence has not supported meaningful cancer-control benefit

• Gerson Therapy – contraindicated, fruit juice therapy will cause severe hyperglycemia and promote tumor growth

• Rife machine - no biological or clinical efficacy

• “Urine” therapy – not scientifically supported

• Homeopathic cancer remedies - no anticancer effect

• Colchicine - narrow therapeitc window, serious toxicity

• Laetrile (amygdalin) — long-standing controversy; lack of reliable efficacy evidence and meaningful safety concerns in real-world use

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Medical Disclaimer: The discussion of repurposed medications and nutraceuticals in this article is intended to review the scientific literature and does not constitute a recommendation for self-treatment. Decisions regarding the use of off-label therapies should be made in consultation with a qualified healthcare professional familiar with the patient’s medical history and current treatment plan. Please see the full Medical Disclaimer on the introductory page to Marik’s Cancer & Metabolic Healing Playbook.

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