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The COC Protocol in Breast Cancer

This document is a summary of the rationale and some of the current scientific evidence which supports the use of the COC Protocol medications alongside standard-of-care treatments for breast cancer. We understand that cancer is a very personal condition, and every patient has a unique set of challenges. For more information regarding your own personal situation please get in touch with the Care Oncology Clinic at 800-392-1353 in the United States, or visit the website at https://careoncology.com.  

If you are new to Care Oncology please note the following:

  1. You do not need to travel. You can meet with our team of oncologists and oncology nurses through secure video for ongoing support.
  2. The Care Oncology adjunct protocol medications are shipped directly to your home from our US Partner Pharmacies and can be used alongside your standard of care treatment.
  3. We are incredibly proud to announce that we have passed the Validation Institute’s extremely rigorous validation process of data analysis, outcome claims, and value calculation. We have worked hard to get to this point. Early on, we recognized the tremendous value a responsibly delivered program of repurposed drugs offered to cancer patients, yet, it was not being offered at scale. Four years ago, we set out to change this knowing it was a marathon, not a sprint.

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The COC Protocol and breast cancer: Key points

  • The COC Protocol is a combination of four commonly prescribed medications (atorvastatin, metformin, mebendazole, and doxycycline) with the potential to target breast cancer and help improve the effectiveness of standard anticancer therapies.
  • A number of observational studies have linked metformin or statin use to improved outcomes in patients with breast cancer.
  • Laboratory studies on breast cancer cells grown in dishes show that metformin and statins can directly target and damage breast cancer cells – weakening them and making them more vulnerable to standard treatments.
  • Results from small ‘window of opportunity’ clinical trials in patients with operable breast cancer generally show that taking metformin or statin pre-surgery can lead to potentially positive changes to molecular markers of cancer, including those which regulate breast cancer cell growth and division. More trials investigating if metformin or statins can affect disease response are underway.
  • Doxycycline can block growth of both HER2 positive and triple-negative breast cancer stem cells incubated in dishes in the lab, and helped to improve resistance-related changes induced by the standard chemotherapy paclitaxel.
  • Doxycycline has just reached early clinical trials in breast cancer patients. Results from the first small study show that patients with early-stage breast cancer who took doxycycline for just 14 days before surgery reduced levels of molecular markers for presence of cancer stem cells by an average of around 40%. Beneficial effects were noted for all but one of the patients treated (8/9).
  • Mebendazole can slow the growth and division of breast cancer cells grown in the lab, including breast cancer cells which are more resistant to chemotherapy. More human studies are needed.

The COC Protocol and breast cancer: Published evidence

The COC Protocol is a combination regime of four commonly prescribed medications, each with evidence of metabolically-based anticancer activity, and well understood safety profiles. These medications are: metformin, atorvastatin, doxycycline, and mebendazole. Some of the studies which support the use of the COC Protocol as an adjunctive therapy alongside current standard treatments for breast cancer are presented below. This evidence mainly comes from laboratory studies, large epidemiological studies (which investigate links between taking medications and breast cancer outcomes in groups of individuals), and early stage clinical trials.

You may notice that many of the studies below only focus on individual COC Protocol medications. We are the first to design an adjunct therapy which combines all four. We do believe that combining these medications will achieve the greatest results, and our own research program, called METRICS, is already producing more of the evidence needed to show this. You can read more about why we believe these medications work together so well to help target cancer, and about the METRICS program itself, in further sections below.

Metformin and breast cancer

Metformin use linked to potential breast cancer benefits

Many observational studies now provide evidence supporting the use of metformin in breast cancer. Metformin is licensed to treat type 2 diabetes, and observational studies in groups of patients with diabetes tend to show that those who take metformin have better chances of an improved outcome if they develop breast cancer (Aksoy et al., 2013; El-Benhawy and El-Sheredy, 2014; Sonnenblick et al., 2017). Metformin use has been linked to improved survival in patients with breast cancer (Kim et al., 2015; Xu et al., 2015), improved response to breast cancer treatment (Jiralerspong et al., 2009), and less chance of breast cancer spreading and relapse (Chen et al., 2017; Jacob et al., 2016).

It’s likely that some of the beneficial effect of metformin found in these studies is due to metformin’s ability to improve a patient’s diabetes and/or weight by reducing glucose levels, which can help reduce the risk of developing breast cancer, and improve a patient’s health and ability to tackle breast cancer if they do have it (Hatoum and McGowan, 2015). But laboratory studies also show that metformin is doing more than this. In fact metformin can actively work directly against breast cancer cells, reducing their ability to take up and use energy, and blocking their ability to grow, spread, survive, and relapse (Alimova et al., 2009; Hadad et al., 2014; Orecchioni et al., 2015).

Different types of breast cancer require different treatments. Trastuzumab, for example, is specifically used to treat human epidermal growth factor receptor 2 (HER2) positive breast cancer. Tamoxifen is effective against estrogen receptor (ER) positive breast cancer. Importantly, cancer cell studies in the lab demonstrate that metformin has anticancer activity against many different breast cancer cell types, including ER positive (Giles et al., 2018), HER2 positive (Chen et al., 2013), and potentially harder-to-treat subtypes such as triple-negative cancer cells (Deng et al., 2012; Vazquez-Martin et al., 2011; Wahdan-Alaswad et al., 2014). This means metformin has the potential to work effectively alongside standard treatments for breast cancer, regardless of the cancer subtype. 

Metformin targets breast cancer stem cells

Metformin has also been shown to target breast cancer stem cells (Bao et al., 2014; Cufi et al., 2012; Hirsch et al., 2009). This activity against breast cancer stem cells, along with its ability to target different subtypes of breast cancer, help to explain why lab studies show it can work in combination with a number of standard treatments, including trastuzumab (Cufi et al., 2012), tamoxifen (Ma et al., 2014), and standard chemotherapy agents (Iliopoulos et al., 2011). Animal and cell studies show that metformin both helps to improve the effectiveness of standard treatments (Bradford and Khan, 2013; Liu et al., 2012; Zhang et al., 2014) and also delays relapse of cancers which have been treated with these therapies (Iliopoulos et al., 2011).

In addition, lab studies also show that metformin can also help to prevent breast cancer cells from becoming resistant to chemotherapy, and improve the sensitivity of already resistant cancer cells to treatment (Davies et al., 2017).

Metformin improves markers of breast cancer in early clinical studies

As a result of the large amount of supportive data for metformin in breast cancer generated by observational and laboratory studies, various clinical trials investigating metformin in breast cancer are now underway (Camacho et al., 2015). Overall, collective analyses of the results of these early-stage trials (meta-analysis) are beginning to suggest a generally positive effect when metformin is added to standard cancer therapies (Rahmani et al., 2019; Zhang et al., 2019b). 

A number of ‘window of opportunity’ trials are investigating if taking metformin for around two weeks prior to surgery can help to improve molecular markers of the disease in patients with operable early-stage breast cancer. Results from these studies generally suggest that taking metformin can lead to potentially positive changes to molecular markers of cancer, including those which regulate breast cancer cell growth and division (Bonanni et al., 2012; Cazzaniga et al., 2013; Hadad et al., 2011; Kalinsky et al., 2014; Niraula et al., 2012), as well as potentially improving the regulation of hormones and other factors for some patients (Kalinsky et al., 2014; Niraula et al., 2012). These studies are now helping scientists understand exactly how and when metformin could help patients with breast cancer (Bonanni et al., 2012; DeCensi et al., 2014, 2015; Rahmani et al., 2019).

Phase 2 ‘neoadjuvant’ trials are generally longer and more complex trials which investigate metformin alongside courses of standard treatments to treat different types of breast cancer. The aim of these trials is to establish if metformin really does help improve the effectiveness of standard treatments, as lab studies suggest (Kim et al., 2014). In one recent study (the METTEN study) (Martin-Castillo et al., 2018), in women with HER2 positive early-stage breast cancer, more patients taking metformin responded well to chemotherapy/targeted treatment (65.5%) compared to patients not taking metformin (58.6%). This difference was not statistically significant; which means this result could have been reached by chance. However, Phase 2 trials are generally underpowered for reaching statistical significance in this way, and the researchers called for progression to larger Phase 3 trials which can be properly designed to determine just how real this effect is (Martin-Castillo et al., 2018). Potentially encouraging results from other Phase 2 trials, such as one in overweight individuals with metastatic breast cancer have also been reported (Yam et al., 2019). It’s also worth noting that as expected, not all metformin cancer trials have reported positive results. For example, other Phase 2 trials have found metformin with standard therapy had no real difference compared to standard therapy alone in certain circumstances (Mark et al., 2019; Nanni et al., 2019). We do believe that metformin will be most effective in any setting when given in combination with other anti-metabolic medications.

Larger studies are needed to help resolve these issues, and a Phase 3 trial is now underway to investigate metformin in breast cancer. Although the trial is not due to be completed until 2020, initial results from the first 6 months of the trial showed that patients who started taking metformin immediately following completion of surgery and standard chemotherapy cycles had favorable changes in a molecular marker of breast cancer (Dowling et al., 2018), and improved metabolic factors (Goodwin et al., 2015).

Statins and breast cancer

Observational studies link statins to better breast cancer outcomes

Statins are usually given to help manage cardiovascular disease. However observational studies on large groups of people taking statins have also found that individuals with breast cancer who are taking statins may also have reduced risk of their cancer recurring following treatment, compared to patients who are not taking statins (Ahern et al., 2014; Manthravadi et al., 2016). For example, in one study in almost 2000 survivors of breast cancer, those who started taking stains within three-years after diagnosis had a reduced chance of their cancer coming back (Kwan et al., 2008). In another study, just 6 months of statin use post-diagnosis was linked to improved rates of relapse (Chae et al., 2011).

Importantly, the beneficial effect of statins in these and other studies was more strongly linked to more fat-soluble ‘lipophilic’ statins (like atorvastatin). In some laboratory studies, lipophilic statins have also been shown to have superior anticancer effects at the cellular level compared to less fat‑soluble statins (Liu et al., 2017).

Observational studies also link statin use to improved disease response to treatment and survival in patients with breast cancer, even for patients with breast cancer types which can be more aggressive (Manthravadi et al., 2016; Murtola et al., 2014; Zhong et al., 2015). For example, in one study in patients with inflammatory breast cancer, patients taking atorvastatin while being treated for cancer had a longer period of time before their disease progressed, compared to those not taking a statin (Brewer et al., 2013).

Statins target breast cancer cells

Statins, particularly fat-soluble lipophilic statins like atorvastatin, reduce growth and division of breast cancer cells and increase breast cancer cell death in laboratory studies


German Diabetes Association”,”page”:”47-48″,”volume”:”111″,”issue”:”1″,”source”:”PubMed”,”abstract”:”The effect of five statins, i.e. atorvastatin, fluvastatin, lovastatin, pravastatin and simvastatin was investigated on the proliferation of the human breast cancer cell line MCF-7. All statins except of pravastatin were able to inhibit cell proliferation up to 90 % at a concentration of 50 micro M. Between the effective statins no significant difference was observed indicating a class-specific effect. These data suggest that statins may have clinical significance in the primary prevention of human breast cancer beyond their cholesterol-lowering effect. However, clinical proof must be awaited before drawing any further conclusions.”,”DOI”:”10.1055/s-2003-37501″,”ISSN”:”0947-7349″,”note”:”PMID: 12605351″,”journalAbbreviation”:”Exp. Clin. Endocrinol. Diabetes”,”language”:”eng”,”author”:[{“family”:”Seeger”,”given”:”H.”},{“family”:”Wallwiener”,”given”:”D.”},{“family”:”Mueck”,”given”:”A. O.”}],”issued”:{“date-parts”:[[“2003″,2]]}}}],”schema”:”https://github.com/citation-style-language/schema/raw/master/csl-citation.json”} (Alarcon Martinez et al., 2018; Mück et al., 2004; Seeger et al., 2003). Studies also show that statins can potentially block the invasiveness of breast cancer cells in the lab, suggesting they can also help slow cancer spread to other parts of the body (Kanugula et al., 2014; Wolfe et al., 2015). In a mouse model of metastatic breast cancer, statin treatment delayed the growth of cancer which had already spread by up to 80%, with beneficial activity noted within a week of starting treatment (Vintonenko et al., 2012).

Other studies also show that statins can help sensitize breast cancer cells to standard radiotherapy and chemotherapy treatments (Kozar et al., 2004; Van Wyhe et al., 2017). One study found simvastatin could sensitize triple-negative or inflammatory breast cancer cells to radiotherapy in the lab. The same study went on to observe in a patient population that women with inflammatory breast cancer who took statins during their treatment had less chance of their cancer coming back within 3 years (Lacerda et al., 2014).

Similar to metformin, statins can produce these anticancer effects across different breast cancer types, including ER positive, HER2 positive, and triple-negative breast cancer. In fact some lab studies show statins are particularly effective against triple-negative breast cancer cells (Campbell et al., 2006; Yao et al., 2017).

Clinical trials investigating statins in breast cancer are now underway

A few early-stage clinical trials now show robustly positive results in terms of statins in breast cancer. Early phase ‘window of opportunity’ trials have investigated if early, pre-surgical statins can help to improve molecular markers of the disease in patients with operable disease. So far these studies show improved cancer molecular profiles in patients with statin treatment, suggesting atorvastatin and other statins in this context may have beneficial effects on cancer cell growth and division and cell death, even in women with high-grade more aggressive tumors (Bjarnadottir et al., 2013, 2015; Feldt et al., 2015; Garwood et al., 2010).

Based on these promising results, a number of Phase 2 studies investigating adjunctive statins for a variety of different types of breast cancer, including triple-negative breast cancer, are now underway. These studies should help establish just how statins can help patients with breast cancer.

Mebendazole and breast cancer

Interest in mebendazole as a potential anticancer treatment is mostly based on promising mechanistic studies and compelling reports from case studies in cancer patients (Nygren and Larsson, 2014; Pantziarka et al., 2014).

Mebendazole is thought to kill cancer cells partly by disrupting special structures inside the cell, called microtubules (Pantziarka et al., 2014). It works in a similar way to vincristine, a chemotherapy drug currently used for treatment of some types of cancer, including advanced-stage breast cancer (De Witt et al., 2017).

Studies on breast cancer cells grown in the lab show that mebendazole and related drugs from the same class (called benzimidazoles) can slow the growth and division of several different types of breast cancer cells, including cells resistant to chemotherapy (Coyne et al., 2013; Hou et al., 2015; Mukhopadhyay et al., 2002). In one study, mebendazole potently reduced survival of chemotherapy-resistant breast cancer cells by as much as 63.1% (Coyne et al., 2013). Studies have also demonstrated robust anticancer activity of benzimidazoles against triple‑negative breast cancer (Hou et al., 2015; Zhang et al., 2015). Importantly, in one study a benzimidazole was also shown to directly target breast cancer stem cells (Hou et al., 2015).

Emerging laboratory-based evidence also suggests that benzimidazoles can enhance the activity of standard breast cancer treatments such as doxorubicin and fluorouracil (Hou et al., 2015). In one lab study, mebendazole increased the effectiveness of radiation therapy on triple-negative breast cancer cells, and prevented resistance to treatment developing (Zhang et al., 2019a). In addition, a series of studies using chemotherapy-resistant ER/HER2 positive breast cancer cells grown in the lab, consistently showed that mebendazole not only reduced survival of cancer cells, it also helped to complement and enhance the activity of specially-developed targeted forms of breast cancer chemotherapy drugs epirubicin and gemcitabine (Coyne et al., 2014, 2012, 2013).

Doxycycline and breast cancer

Aside from being an effective antibiotic, doxycycline also possesses other extremely valuable properties, including anti-inflammatory and anticancer activity. This gives doxycycline real therapeutic potential in treating a range of other diseases, including cancer (Bahrami et al., 2012).

Lab studies and animal studies have long shown that doxycycline can block breast cancer cell growth, division, and movement (Duivenvoorden et al., 2002; Fife and Sledge, 1995, 1998). More recent studies also show that doxycycline can stop cancer cells from repairing their DNA when it becomes damaged, for example, by chemotherapy (Peiris-Pagès et al., 2015). Indeed, lab studies show that doxycycline can help improve the effectiveness of chemotherapy activity against breast cancer cells (Foroodi et al., 2009; Lamb et al., 2015a).

Most recently, focus has fallen on understanding how doxycycline can block breast cancer stem cell growth (Ozsvari et al., 2017; Zhang et al., 2017). A very recent study on cells grown in the lab has shown that doxycycline can block growth of both HER2 positive and triple-negative breast cancer stem cells, and helped to improve resistance-related changes induced by the standard chemotherapy paclitaxel (Lin et al., 2018). In a different lab study, a combinatorial approach including doxycycline very effectively eradicated breast cancer stem cells (Fiorillo et al., 2019).

Doxycycline has just reached early clinical trials in breast cancer patients. Results from the first small study, published in October 2018, show that patients with early-stage breast cancer who took doxycycline for just 14 days before surgery reduced levels of molecular markers for presence of cancer stem cells by an average of around 40%. Beneficial effects were noted for all but one of the patients treated (8/9) (Scatena et al., 2018). Larger clinical trials are now underway.

Our own evidence: The METRICS Study

What is METRICS?

METRICS is our own in-house research program. A great deal is already known about the safety and effectiveness of the COC Protocol medications in cancer. But it is also our responsibility to acknowledge that we don’t have all the answers, and that we still need to generate good quality clinical research investigating the COC Protocol in patients with cancer, to ensure the COC Protocol is as effective and safe as it can be.

To enable us to fund this research, we have developed a novel, affordable system where our clinical study, METRICS, is essentially ‘patient-funded’. Every consenting patient who enters the clinic is enrolled into METRICS, and these fees are helping to fund the study. This is a new model of clinical research, aimed at bridging the funding and data gaps which are currently hindering the repurposing and further clinical development of already licensed medications.

METRICS first results

In a first success for METRICS, results from our initial pilot study were recently published in the peer-reviewed scientific journal Frontiers in Pharmacology. The paper can be accessed freely online here.

The METRICS pilot study was an observational retrospective study, which means that our researchers looked back and analyzed patient clinical records to find out what happened. They collected data and recorded the outcomes from 95 patients with an advanced type of brain cancer called glioblastoma who attended the Care Oncology Clinic and who took the full COC Protocol alongside their usual standard treatments. This study did not have a control group, so our researchers compared the results from METRICS with previously published results from earlier studies in patients with the same type of cancer, and who also took standard-of-care treatments.

Initial results suggest that patients who attended our clinic and took the COC Protocol as part of their usual care were much more likely to survive at least 2 years (64.0% of patients in our study survived at least 2 years, compared to 27-29% for patients included in previously published studies), and tended to have longer survival times overall than would usually be expected for patients with this type of cancer (patients survived an average of 27 months in our study, compared to 15-16 months in earlier studies)(Agrawal et al., 2019).

These results are extremely promising, but they are also still preliminary. We don’t yet know exactly how the COC Protocol may have impacted survival times for example, or how other factors such as certain patient characteristics may have also influenced these results. But this first, initial evidence is certainly encouraging, and it suggests to us that we are heading in the right direction. Our next planned stage is to conduct a larger, well-designed study. You can find out more about future METRICS plans by looking online or contacting the clinic.

More about the COC Protocol

What is the COC Protocol?

The COC Protocol is a combination treatment regimen comprised of licensed medications, specifically designed by Care Oncology for adjunctive use alongside a patient’s usual treatments (i.e. standard-of-care).

The four medications included in the COC Protocol regimen are: metformin, a very common anti-diabetes drug; atorvastatin, a type of statin used to manage cardiovascular conditions; doxycycline, a type of antibiotic often used to treat chronic infections like acne; and mebendazole, a medicine commonly used to treat parasite infections in children and adults.

We chose these four medications from thousands of potential candidates specifically because they fit our predetermined selection criteria. These criteria include solid evidence of effectiveness against cancer, a coherent mechanism of action, and importantly, a good safety profile. These three central tenets have shaped our approach from the very beginning.

Safety is paramount

Cancer is a complex disease with complex treatments, and we believe that the addition of further therapies alongside standard treatments should be very carefully evaluated. Not just from the perspective of effectiveness, but also, importantly, in terms of safety. This is why our whole approach is based on evidence – mostly published scientific studies, and also, increasingly, our own data.

Many different medications on the market have at least some published evidence supporting their relatively effective use in cancer, but few of these medications have the level of evidence of both safety and effectiveness that we require for the COC Protocol. Large amounts of detailed data already exist for each of the protocol medications, garnered from years of use in the general population – and this helped to give us a crucial head-start during development.

We have painstakingly searched through decades of published data on each of the COC Protocol medications, exploring how they work in different patient populations (including patients with cancer), and on cell and animal models in the lab. These data, alongside our own clinical experience, help to ensure that we have a good understanding of how these medications will behave in patients with differing stages and types of cancer, both in combination with each other and also in combination with numerous other cancer therapies. This knowledge is paramount, and from our studies, this type of evidence is just not there yet for many other off‑label anticancer drug candidates – especially when given in combination.

An anti-metabolic therapy which can potentially target any cancer

The COC Protocol is designed to work by restricting the overall ability of cancer cells to take up and use (i.e. ‘metabolize’) energy.

Cancer cells need huge amounts of energy to survive, and the vast majority of cancers use an adaptive process called aerobic glycolysis to generate the excessive energy they need (Kroemer and Pouyssegur, 2008). Each of the medications in the protocol can target the various molecular metabolic processes involved in and surrounding aerobic glycolysis, and this can help lower the overall metabolic rate of the cancer cell (Jang et al., 2013).

We believe the COC Protocol medications can work in combination to consistently restrict energy supply and use, while simultaneously preventing cancer cells from adapting and using other pathways to take up energy (Jagust et al., 2019). As a result, cancer cells become increasingly weaker and less able to take in and use the nutrients (e.g. such as glucose and essential amino acids glutamine and arginine) they need from their surroundings (Andrzejewski et al., 2018; Liu et al., 2016). This makes it more difficult overall for cancer cells to survive, grow, and spread in the body. Gradually, the weakened cells (including more resilient and previously treatment- resistant cells) become more vulnerable to attack from other cell‑killing cancer therapies such as radiotherapy, chemotherapy, hormonal therapy, and targeted therapies (Bradford and Khan, 2013; Chen et al., 2012; Lacerda et al., 2014; Lamb et al., 2015a; Pantziarka et al., 2014).

By targeting the adapted metabolic mechanisms which are common to most cancers (but not usually healthy cells), we believe that the COC Protocol can be effective and selective for virtually any cancer regardless of specific type, stage, or location of cancer. Published epidemiological and lab studies increasingly support the potentially broad range of this therapy (Chae et al., 2015, 2016; Iliopoulos et al., 2011; Lamb et al., 2015b; Pantziarka et al., 2014).

Mechanistic coherence in action – the power of combination

The true power of the COC Protocol lies in the specific combination of medications we use. We developed the protocol not just as a regimen of four individual treatments each with anticancer activity, but also to work as a single combined treatment- with the potential to produce powerful synergistic effects (Mokhtari et al., 2017).

Each medication in the COC Protocol targets cancer cell metabolism in a distinct and complementary way, and we have termed this action ‘mechanistic coherence’. Put simply, mechanistic coherence describes how each medication can attack the cancer cell from a different angle. For example, cancer stem cells are a particularly resilient type of cancer cell, and each medication targets these cells in a different way: metformin targets the cell’s ‘batteries’ (called mitochondria) by making it very difficult for mitochondria to run the molecular reactions they need to produce energy, doxycycline blocks the cell-DNA machinery that mitochondria need to replicate and repair (Skoda et al., 2019), statins can alter cancer stem cell gene expression, making the cells more sensitive to other cancer therapies (Kodach et al., 2011), and mebendazole can interrupt numerous molecular processes involved in cell division to help block cancer stem cell growth (Hothi et al., 2012; Hou et al., 2015).

By combining all four agents together, the COC Protocol can hit cancer stem cells (and other cancer cells) across multiple ‘weak spots’, and like a one-two punch, this leaves the cells less able to dodge and recover.

Lab studies are beginning to highlight the effectiveness of this approach using COC protocol medication combinations. In one mechanistic study, combining statin and metformin greatly decreased the growth of prostate cancer cells more than either agent alone (Wang et al., 2017). Observational studies have also reported potentially ‘synergistic’ effects of these medications against various cancers (Babcook et al., 2014; Danzig et al., 2015; Lehman et al., 2012; Nimako et al., 2017). A clinical trial investigating metformin and doxycycline in breast cancer is now underway (NCT02874430), and our own research program, METRICS, is now also beginning to produce promising data.    

A long-term adjunctive therapy

The COC Protocol is primarily designed to be a long-term ‘adjunctive’ therapy, to help optimize standard treatments. However, as metabolic treatment with the COC Protocol is intended to run long-term, patients may also take the protocol as a maintenance regime after standard treatment has been completed or during breaks from standard treatment and as part of a long-term strategy to mitigate the risk of recurrence or metastases. For this reason, it is also worth noting that each of the COC Protocol medications also has reported beneficial mechanisms of action in cancer which are not dependent on the co-administration of standard therapies, and which may independently help to reduce the risk of relapse and metastatic spread.

The Care Oncology model

Active medical supervision of each patient

Although the COC Protocol medications have been used safely in the general population for many years, every patient who comes to us is unique. This is why every patient who attends the Care Oncology Clinic is placed under the direct care of clinicians with specialist knowledge of prescribing the COC Protocol medications in the context of cancer. Our clinicians individually assess the potential benefits and risks involved in taking the COC Protocol with each patient. They will only recommend the COC Protocol to patients when they believe it will be safe and beneficial to do so. Each COC Protocol prescription is tailored to the needs of the patient, and doses and regimens are carefully reviewed and adjusted based on how the patient progresses.

It is therefore essential that patients only take the COC Protocol while being carefully monitored at our clinic for the duration of their treatment.


Important Notice

Purpose of this article

This article is an overview of some of the scientific and medical published literature concerning the medications which comprise the patented Care Oncology protocol. Care has been taken to select relevant articles supporting the off-label use of these medicines in a clinical setting for the adjunct treatment of cancer. This article does not purport to be a comprehensive review of all the evidence, nor does it capture all of the potential side-effects of such treatment.

This article is for information purposes only and it does NOT constitute medical advice. The medicines discussed herein are available on prescription-only and should not be taken without consultation with your doctor or other professional healthcare provider. Care Oncology doctors will discuss the suitability of these medicines with you and will liaise with your doctor or oncologist to discuss their suitability for you.

You must NOT rely on the information in this article as an alternative to medical advice from your doctor or other professional healthcare provider. If you have any specific questions about any medical matter you should consult your doctor or other professional healthcare provider. If you think you may be suffering from any medical condition you should seek immediate medical attention. You should never delay seeking medical advice, disregard medical advice, or discontinue medical treatment because of information contained in this article.


The copyright in this article is owned by Health Clinics LLC and its licensors.


The Care Oncology (“COC”) Protocol is protected by United States patent US9622982B2 and by various additional international patents.



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