3 Bromopyruvate

Other names: 3BP, 3-Bromopyruvic Acid
CAS number:1113-59-3


The info shared here came from multiple directions. That includes literature research, personal experience, a lot of ideas discussed and shared on Cancer Compass, discussion with a good number of professors and doctors, discussion with German clinics, discussions with patients.

My opinion:

For an update on my opinion related to 3BP please check the following post too: https://www.cancertreatmentsresearch.com/?p=725

I went through ups and downs with my opinion regarding 3BP anti-cancer effectiveness. But today, based on what I saw, based on the science behind, based on input from various doctors and clinics around the world using 3BP, and input from many patients, I believe 3BP has serious anti cancer potential. BUT, what I also learn more and more is that it has its challenges too. It is challenging to administer 3BP so that we get the best outcome. However, based on all the input I mention above, I think we are on the right track to identifying the right administration protocol.

The administration protocol can make the difference between failure and success. As a result, some doctors/clinics will stopped using 3BP because of very limited or even negative results and others are getting great results.

If 3BP is not used as a part of correct treatment protocol (e.g. including other glycolisis inhibitors and/or angiogenesis inhibitors), in some cases, according to a few US doctors, the 3BP treatment may lead first to a decline of tumor size and after that to a faster growth in the same way as chemo does in some cases. I believe this is because 3BP may kill the outside layer of tumor related to cells sensitive to 3BP (via MCT1 transporters), exposing the patient to highly glycolitic cells not sensitive to 3BP. If this view is true, in the next treatment step the highly glycolitic cells may potentially be killed by e.g. 2DG or high dose Vitamin C or their growth may be inhibited by angiogenesis inhibitors.

Here is the treatment protocol I currently believe can address some of the potential issues suggested above: https://www.cancertreatmentsresearch.com/?p=184

Warning: During the summer of 2016, a clinic in Germany using 3BP IV had an unfortunate experience, seeing three of its patients death in a short time frame of a few to several days. One of the treatments used for their patients was 3BP, next to others such as Vitamin C, etc. 3BP was suspected to cause the death of the patients (Ref.). However, it is difficult to understand how 3BP would have triggered such a result given that the clinic was using 3BP for more than a year to treat its patients. The case is currently under investigations. Association of this unfortunate event with 3BP is also difficult to understand since multiple clinics and patients around the world used 3BP for long time frames, even longer than one year, without reporting any side effects. Nevertheless, this event should make us realize that stage IV cancer treatments, whether conventional or not, represent a step in uncharted territory where the risks are little known or totally unknown.

Update on the above Warning @ April 2018: According to a recent communication (Ref.) it seems that the German clinic used 3x to 6x higher dose compared to the dose considered to be safe. In the same statement, the investigation team does not rule out the potential anticancer effects of 3BP. (I find this last addition in their statement fair and interesting)

My opinion on the above: Based on various pieces of information from various sources, I believe that the issues at the German clinic were due to high dose of 3BP used in patients that were not previously exposed to 3BP. Based on my understanding and observation, 3BP is most effective during the first exposures since it mostly acts on cells that have MCT1 expression. More specifically, MCT1 (the dors through which 3BP enters the cancer cells) are also the transporters used by cancer cells to absorb lactic acid in order to be converted into energy through respiration. As a result, these cells are those forming the outside layers of tumors, and are located there due to the required access to oxygen. When the tumors are larger, there is an abundance of such cancer cells. When those are exposed to high dose of 3BP, there will be a sudden cancer cell death leading to tumor lysis syndrome. This is known to lead to generation of ammonia. When ammonia is too high it induces hepatic failure. Next, ammonia builds up into the bloodstream and affect the function of the nervous system. If not treated in time, this in turn can lead to the death of the patient (Ref.). Tumor lysis and build up of ammonia was also what happened in case of Yvar, the Dutch boy treated first time with 3BP at the Frankfurt Hospital in Germany (Ref.). Fortunately, his father identified that in time and the ammonia was successfully removed from the blood with hydration and intravenous Hepa Mertz. This experience is discussed in more details in the book “Tripping over the Truth” at page 95 (Ref.). In conclusion, in my opinion, using high dose 3BP in patients that were never exposed to 3BP and with high tumor load is dangerous. This is why I would always start with a lower dose (e.g. 0.25 of the normal dose) and move up step by step towards the target dose during the course of several weeks.


The anti-cancer potential of 3BP has been demonstrated by Dr. Ko while working in the lab of Prof. Pedersen at Johns Hopkins University sometime around 2002. Here is a link to Prof. Pedersen’s lab. Dr. Geschwind who at that time was working at Johns Hopkins University as well, publish his own patents in addition to those of Dr. Ko. As a result, there were two groups of researchers claiming the rights and both created their own company.

As a side note, I did have a few e-mail conversations with Prof. Pedersen and I appreciate his great honesty. I am also very  impressed to see how he is always giving the whole credit to Dr. Ko for the discovery (while to my knowledge, most in the academic world would not do the same). Here is a comprehensive presentation of prof. Pedersen at the NCI and NIH in Unated States. Interestingly, Prof. Pedersen sent a personal letter to President Obama about this matter on January 22, 2013. The president’s mother died of ovarian cancer at the early age of 53. Months later, Prof. Pedersen had still received no response from the president. (Ref.)

Regarding the two main companies associated with the patents on 3BP, that of Dr. Ko is not very visible. However, while not visible, I think Dr. Ko is conducting clinical trials by supporting some doctors, mostly outside of the US, with both the administration protocol and the formulated 3BP. Dr. Ko’s company is called KoDiscovery and is located in Baltimore,  Maryland, United States. What is also clear is that she was the one who supported the first known application of 3BP in humans which also had great success (see case report below). Dr. Geschwind, on the other hand, has gained FDA approval with his company Presciencelabs intending to soon start clinical trials (this was stated in 2013 and three years latter there is still no trial). The patent battle seems to be the reason why things are moving so slowly.

Here are recent news (Nov 2015) related to the legal discussions between the inventors: http://holmansbiotechipblog.blogspot.ca/2015/11/court-dismisses-disaffected-professors.html

There are so many points to discuss about this substance but here are the most relevant points in my view:
– this is a substance with good potential against cancer
– it has clear science behind it and there is a lot of academic research supporting its potential
– it has been used on animals with great success
– it has been used on humans with success (both published and unpublished reports used with effectiveness on: liver cancer, melanoma, lung cancer, adrenal cancer, breast cancer, pancreatic cancer, prostate cancer, etc.)
– it is a very low cost substance
– it can be easily accessed
– it is water soluble so that it can be administered via IV, orally, topically, via nebulizer, or enema
– it is relevant for most types of cancers: it is a metabolic treatment (inhibiting energy production in cancer) and not genetic – this means that the response is not dependent on the very complex genetic profile
– a requirement is that the cancer is visible on PET – however there is no certainty that all cancers visible on PET will respond. In addition to the PET visibility, it needs to have an expression of the MCT1 transporters (see below under Mechanism)
– it is toxic to cancer cells and non-toxic to normal cells through MCT1 selectivity (it is non toxic at the right dose which is discussed below)

Some of the main challenges related to this substance are that its stability is very limited, and it is an acidic substance. The stability declines when temperature increases and when the pH of the solution in which 3BP is mixed increases. Light will also negatively affect its stability.

When delivering to humans, the acidity has to be reduced, i.e pH of the solution has to be increased, which in turn will reduce its stability. However, there are ways to balance those aspects so that the substance can be administered to humans at an acceptable pH while still being effective. There are several patents addressing that, and Ko’s patent is one of those.

Case reports

1. Dr. Ko provide the 3BP  used for the first time officially on humans, by Prof. Vogl. Specifically, it has been administered to a Dutch boy in 2012 at Frankfurt University in Germany, via a technique called TACE, administrating 3BP locally to the liver. The boy was in a terminal phase (liver cancer) and a few applications of the 3BP via TACE succeeded to kill his cancer. As a result the boy had his life extended. The boy passed away a few years later due to a reason other than cancer. What is extremely important is that the cancer had been eliminated and this was a huge result.  Here is the published case. The intervention was performed by Prof. Vogl.
It is amazing that the treatment had such great success in the context that conventional medicine had nothing to offer and that society did not react to this and push 3BP fast to application on humans. However, there is an entire world that has been developed “underwater” and in this world 3BP is today applied on humans even via TACE.

2. 3BP has been applied on a late-phase melanoma cancer patient, via IV administration, at a hospital in Egypt (read the publication here). The patient did not survive due to extensive lung damage caused by cancer, but importantly, the 3BP succeeded to completely deactivate the cancer. Next to showing the high relevance of 3BP in eradicating cancers relying on glycolysis, this report also shows that the effectiveness of such pro-oxidant strategies can be strongly supported by concomitant depletion of glutathione with common drugs such as paracetamol (acetaminophen in US and Canada). (Note: it is well known that glutathione is one of the main factors leading to resistance of cancer to pro-oxidant therapies, and I am wondering why cancer patients do not typically receive paracetamol specifically administered before the administration of various chemotherapies).

Anecdotal reports/stories

Besides the liver cancer and melanoma cases reported in the literature, here are a few examples of stage IV cases that I am aware of:

prostate cancer: a cancer scientist for 30 years treating his prostate cancer during chemo treatment. Chemo alone had no anti-cancer effect. Adding 3BP + paracetamol (used to reduce glutathione) lead to decline in PSA level. He used oral administration only at 2mg/kg/day (solution at pH 4 to 5). Treatment at home.
breast cancer: a 40 to 50 years old lady with various metastases using a few IVs and intensive oral and topical administration (unknown dosage). She was given a few months to go and after about one to two months treatment many of her tumors were gone. 
– adrenal cancer: one month treatment IV (2x/week) led to a reduction of tumor markers of about 10% and a reduction of tumor of 16% in a month as shown on CT scan.
lung cancer: about one month oral and topical administration leading to eradication of a one cm tumor in the lung and 50% decrease of a lymph note. Treatment at home.
pancreatic cancer: Patient utilized 3BP, IV€™s, an oral protocol, hyperthermia, EWOT, fresh green juices, colonics, etc. This led to serious reduction of the tumor markers. Case reported at Dayspring Clinic
breast cancer: another patient treated and reported at Dayspring Clinic
– lung cancer – extensive stage small cell lung cancer (ES-SCLC): 3BP + Salinomycin treatment during about one month leading to complete disappearance of SCLC as shown on CT. Treating doctors were Dr. Jason Williams in Bogota, Dr. Mark Rosenberg in the U.S. and Dr. Leonardo Gonzalez at a clinic in Columbia. Reference.

In many cases, after the first 3BP IV administration, a reduction in pain has been observed.

Note: also to my knowledge there were patients treated with 3BP and not responding. As we will see below, besides administrating 3BP in the right way, the key for 3BP action is the expression of MCT1 which if not present may also be forced with various supporting treatments.


3BP is generally presented as an inhibitor of glycolysis (one of the major mechanisms for energy production in cancer) and has shown remarkable efficacy in not only preventing tumor growth, but even eradicating existent tumors in animal studies and in humans. Its mechanism of action is still a matter of debate but in general it is believed to be an alkylating agent, inhibitor of HK2 enzyme, which is essential in cancer cells for both glycolysis and respiration.

In order to get into the cancer cell and inhibit the HK2 enzyme, 3BP seems to use the MCT1 transporter (Ref) which is over expressed in many cancers visible on PET scan. Highly glycolytic cancers are producing a lot of lactate as a result of the high glycolysis. Lactate together with a proton is pushed out of the cancer cell through MCT4 transporters. As a result cancer cells are also pushing out protons in order to maintain their high intracellular pH. In turn this increases the amount of lactic acid (and thus the acidity) around the tumors. In time, if the outside layer of cancer cells have also access to oxygen, they may develop the capability of using lactic acid as a source of energy for the respiration process. This means that they will start directly importing lactate, through a transporter located on their membrane (i.e. MCT1), convert that into pyruvate and use that further to produce ATP. These are the cancer cells that are believed to be sensitive to 3BP. Why? Because 3BP has a chemical structure such that it can be transported through the same transporter (MCT1) through which lactic acid is imported. Since MCT1 is over expressed in cancers, 3BP will selectively be absorbed by the cancer cells (like we discussed not all but those who have MCT1) and will not affect the normal cells. Understanding this mechanism has great implications on how 3BP administration will be supported.

What we can understand from the above is that the acidic environment around the tumors is supporting 3BP effectiveness and treatments of patients with alkaline substances such as NaBic (e.g. Simocini protocol) should be avoided during the 3BP administration. Next to that, oxygen is required for the cell respiration and thus for the existence of tumor cells that are sensitive to 3BP. Of course, we should avoid any inhibitor of the MCT1 transporter. I will discuss them more in the “Antagonists” section below, but some of them are Ibuprofen, Quercetin, Statins, etc.

In some special cases, 3BP may cross BBB (blood brain barrier):
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1220552/pdf/10510291.pdf   (see page #14)
Starvation should help on this line.

3-BP has non-glycolytic targets as well, such as V-ATPases 20, SERCAs 24, Carbonic Anhydrases 51 and HDACs 52 (Ref.)

Here is a nice overview on the relative expression of MCT1 in cancer cell lines (in red box) and their normal tissue of origins (in white box):

MCT1 expression


In glioblastoma cells, it takes about 3-4 hours to reach a high level of ATP depletion, after the cells were exposed to 3BP: Refrence

Here is a good discussion on “Enhancing 3-Bromopyruvate Toxicity in Tumor Cells By Inducing Hyperglycemia” http://pharmacologia.com/abstract.php?doi=pharmacologia.2013.571.575


3BP in its raw state is highly acidic.

If the solution to be administered is prepared well, there should be no concerns. People have been treated for months with no issues. No specific side effects are observed. However, note that long term side effects are not expected but also not known.

If the solution is not prepared or administered in the right way, various issues may emerge from inflammation of the veins to anything that an acidic substance may do in the body. This is why both the pH combined with the administration time have to be balanced.

If a cancer treatment is very effective in killing cancer cells, it may trigger an effect called Tumor Lysis Syndrome (TLS) which may include one or more of the following:  a high blood potassium, high blood phosphorus, high blood uric acid and high urine uric acid, low blood calcium, and consequent acute uric acid nephropathy and acute kidney failure. In case this happens, here is what can be done. This applies for any effective treatment including chemotherapy (when that is effective).

Preparation & Administration

Substance used: 3-Bromopyruvic Acid at purity >95%, preferably >98%. CAS Number 1113-59-3.
Depending on purity, at 95% 3BP is orange crystals, and at 100% white crystals. It can be administered topically, nebulized, taken orally, or by IV. Below are the formulations I am aware of and like all the content I share here it comes with my disclaimer:


– 100mg 3BP mixed with 2ml water (preferably distilled but not necessarily) in a glass vial
– to the above solution add 50mg sodium bicarbonate (NaBic) powder and mix
– to the above solution add 4ml DMSO
– the resulting solution is applied one or several times/day in the tumor area; if the tumor is at the surface, it can be started with one tumor only and observe the reaction – adapt applied dose accordingly

Tools and materials needed for the above:
digital scale that measures 1mg
DMSO – can be found at various sources on the web. Some of the best is claimed to be this one but this should also be fine.
NaBic – can be found at various sources on the web, for example here


– 2mg/kg to 4mg/kg 3BP (for example, a person of 60kg would need 12omg if he/she intends to use 2mg/kg)
– 3BP is mixed with drinking water until pH of the solution is about 4 (bets is to use water with as little chlorine (Cl) as possible, since Cl is displacing the bromine in the 3BP) – some are using pH as low as 3 and state not to have side effects but I would stay with 4
– drink every morning one hour before eating (some split the dose in two or even in three and take one part in the morning and one in the evening before dinner)
– a few times/week use pre and probiotics as 3BP may also kill teh good gut bacteria
– as with anything I would always start at lower dose, i.e. 0.5mg/kg and build up to the target dose

My understanding is that most of the people have no issues with this – some people may vomit after the first times but that seems to go away after several days (we had no issue with it)

Update 20160104I am aware of 3 major options for the mixture of oral 3BP:

1. distilled water – this will require probably about one liter of water to get about 2mg/kg 3BP to a pH of about 4 to 5 – the drawback of this options is that it has too much water
2. ~100-200 ml distilled water + 2mg/kg 3BP + NaBic enough to get to a pH of about 4
3. ~100 ml commercial water (such as Evian) +2 mg/kg – add water until pH of the resulting solution is 4 to 5 – the drawback of this option (I only now realize) is that it has Cl inside that will displace bromine from 3BP

Tools and materials needed for the above:
digital scale that measures 1mg
pH measurement tool (preferably an electronic version) available on e.g. eBay or Amazon
– optional a system for controlling water composition: http://www.waterstreetstations.com/


– 44mg 3BP add 5 ml water (distilled if possible or low Cl amount) and mix
– add 30mg sodium bicarbonate powder (to increase the pH) and mix
– add the above solution (5ml water+3BP+NaBic) to 15ml water
– this should lead to a solution with a pH between 6 and 7
– check pH and make sure is not below 6 so that is friendly to the lungs
– we use 5ml of the solution above which is the max that can go into our nebulizer at one time, and add to this 10 drops of DMSO
– the solution above should be OK and represent no danger if the pH is as indicated
– if everything is good the 3BP concentration can be increased as long as the pH is maintained between 6 and 7

Any modification of the dose should be done step by step and the reaction to that observed.

Tools and materials needed for the above:
digital scale that measures 1mg
pH measurement tool (preferably an electronic version) available on e.g. eBay or Amazon
DMSO – can be found at various sources on the web. Some of the best is claimed to be this one but this should also be fine.
NaBic – can be found at various sources on the web, for example here
Nebulizer here is one that we use but any should be good


Note: My ideas on 3BP treatment strategy is discussed on a different page – click here to get there 🙂

This administration method requires more discussion:

Unbuffered: One way to administrate 3BP is unbuffered, which is the method used in Egypt for the treatment of the melanoma patient (Ref). They saw impressive results and that is a good reference point for the effectiveness of this method. However, because the solution is unbuffered, the administration time has to be longer otherwise the patient will be put in danger. (This is why probably most of the clinics will not use this method since each patient would require to stay longer in the clinic while the clinics prefer shorter times.) I will refer to the target dose where effectiveness is expected but it should always be started at lower doses and increased if no adverse reactions are observed. This is how this can be prepared:

– target dose is 2mg/kg to 2.5mg/kg
– take the 3BP powder as measured with a digital scale and add in a sterile cup/vial. If the choice is 2mg/kg and the patient weighs 60kg, there will be a total of 120mg to be used for an IV
– mix the powder with 20ml sterile water for injection (not saline!)
– when the solution is well mixed (i.e. no 3BP powder visible) take all the solution into a syringe (if we do not have a 20ml syringe we may need to perform this action multiple times but if we have 20ml syringe, we will need to perform it only once).
– take out the used needle and instead put a o.2um sterile filter on the syringe – at the other side of the filter mount a new sterile needle.
– inject this 3BP solution into the 500ml NaCl (saline) bottle/bag (do not reduce to 250ml because it will be even more acidic).
– put aluminum foil around the NaCl bottle/bag so that the exposure to light is limited.
– administer this solution in about 2.5 hours via a port-a-catch/port/PICC (if this solution is administrated via the arm directly into the vein, there may be inflammation developing in time and the veins will not be accessible for IV for long time before they recover) – this time frame should be respected and not shortened.

Buffered (i prefer the un buffered approach):

– target dose is 2 mg/kg – a little higher can be used in the buffered version
– take the 3BP powder as measured with a digital scale and add in a sterile (or very clean) cup/vial. If the choice is 2mg/kg and the patient weighs 60kg, there will be a total of 120mg to be used for an IV
– mix the powder with 20ml sterile water for injection (not saline!)
– when the solution is well mixed (i.e. no 3BP powder visible) take all the solution into a syringe (if we do not have a 20ml syringe you may need to perform this action multiple times but if we have 20ml syringe, you will need to perform it only once).
– take out the used needle and instead put a o.2um sterile filter on the syringe – at the other side of the filter mount a new sterile needle.
– inject this 3BP solution into the 500ml NaCl (saline) bottle (not 250ml because it will be even more acidic) and shake the saline bag gently.
– next, inject NaBic 8.4% solution: for every ~60mg 3BP I use 1ml  NaBic 8.4% solution. Therefore, if 120mg 3BP is used, 2ml NaBic 8.4% solution will have to be added. After that we need to shake the bottle/bag gently. Note that to my knowledge, Dr. Ko doesn’t like to use NaBic. She is using other buffers. However, note that 3BP solutions should never be neutralized with concentrated solutions of strong bases such as NaOH because the high concentration of hydroxide ion directly displaces the bromide, rapidly producing 3HP (Ref.)
– put aluminum foil around the NaCl bottle/bag so that the exposure to light is limited.
– administer this solution in about 2.5 hours via a port-a-catch/port/PICC (if this solution is administered via the arm directly into the vein, there may be inflammation developing in time and the veins will not be accessible for IV for a month or so before they recover) – this time frame should be respected and not shortened.

– best to prepare the 3BP solution before the IV, and administer asap.
– best to limit the exposure of the solution to light – if possible administer in a room with low intensity of light – we can wrap the saline bag in aluminium foil as well.
– NaBic addition will decrease the stability of 3BP in solution. As a result it is better if we split the dose in two bottles and prepare the second once the first is finished, e.g. if a total of 120mg 3BP is intended to be administrated, first add 60mg 3BP to a saline bag of 250ml and 1ml NaBic 8.4% and administrate in one to one and a half hour and than prepare and administrated the other 60mg 3BP in the same way. In this way we will get the most out of the IV.

Tools and Materials needed for the above:
– digital scale that measures 1mg
– a Port-A-Catch, port or a PICC line installed (administration in the arm is possible according to the Egypt-case but will lead to inflammation soon – not recommended)
– 0.2um sterile filters for syringe
– glass vials to mix 3BP with water for injection, like this or similar
– Of course there is a need for all the typical stuff required for IV like saline (250ml and 500ml bottles), delivery kit, syringes, needles, water for injection. In Germany everything can be ordered online from here 
– Some bottles of NaBic solution 8.4% will also be required – here is an example

Administration Protocol and Treatment Strategy has been discussed on the following page: https://www.cancertreatmentsresearch.com/?p=184

Source & Cost

There are many suppliers selling 3BP on the web, and most is manufactured in China. It is easy to order 3BP on Alibaba but is a bit more difficult to know which source to trust.

I personally believe that the difference between various sources is related to the following:

– manufacturing conditions – that included the environment in which 3BP was produced and the elements that have been used in production. This may be reflected in the purity level and the rest of components that are in the product we ordered, i.e. rest of 3% if the product has 97% purity
– storage conditions – 3BP has to be stored around 4C. I can imagine that not many of them will have the right storage capabilities next to the fact that many from China are not the manufacturers but trading agencies.

I do know some people using Chinese version even for IV, but I would not do that. Myself, I have some Chinese version for backup but always use the western version. It would be best if for IV the source would be at the level of Sigma Aldrich or similar. The difficulty with Sigma is that they only sell it to businesses or academic institutions. So anyone who would like to have Sigma products, has to have a company and a business address (they always first check the address on Google map – that is their first filter) or represent a university. If that is not the case, we may find a friend with a company or somebody working or studying at a university.

In conclusion,
– if we order from China we need to make sure we have a recommended supplier from whom someone else already ordered.
– for IV, western sources is the way (if possible, not only for IV).
– since recently there is also a source (pharmacy) in Europe/Germany who would sell IV ready solution – vial of 200mg at 30 euro – Update September 2016: This option is not available anymore

Regardless of the source, price is so little that it doesn’t need to be discussed here.

Relevant Literature

– Check the reference list on the following section of this site: https://www.cancertreatmentsresearch.com/?p=184
– Thesis from Heidelberg on 3BP killing pancreatic CSC. Reference
– In renal cell carcinoma, ccRCC, the activity of most other pathways than that of glycolysis has been shown to be reduced and is expected to be highly sensitive to 3BP (Ref.)
– A good list from Cancer Cure
– the inhibition of CA-IX (which is easy to be done), in combination with a hexokinase II inhibitor, may be therapeutically useful in patients with HCCs that are aggressively growing in a hypoxic environment (Ref)

Synergists & Antagonists

A good part of my ideas have been discussed in this post and others here.

Synergistic, Complementary or Supporting:  Curcumin, Curcumin22DG, Glutamine Deprivation e.g. Phenyl Butyrate, Chloroquine, Paracetamol/acetaminophen, Methyl Jasmonate, Fasting, Hypoglycemiareduction in extracellular pH enhanced 3-BrPA uptakeButyrate,  Lactate, Ketosis, Exercise, TestosteroneAcetazolamide, Citrate, Citrate2, Rapamycin

Will make tumors more sensitive to chemo due to ATP depletion http://cancerres.aacrjournals.org/content/early/2011/12/20/0008-5472.CAN-11-1674.full.pdf
Inhibition of glucose turnover by 3-bromopyruvate counteracts pancreatic cancer stem cell features and sensitizes cells to gemcitabine http://www.ncbi.nlm.nih.gov/pubmed/25015789
Stalling the engine of resistance: targeting cancer metabolism to overcome therapeutic resistance http://www.ncbi.nlm.nih.gov/pubmed/23610447

Antagonists: All the MCT1 inhibitors such as Quercetin, Luteolin, Atorvastatin (and other statins), Diclofenac, Phloretin, Naringenin, Apigenin, Genistein, Ibuprofen, Silybin, Disulfiram?

What is not clear to me yet is whether those drugs/supplements that will reduce mito ATP production should be used or not. Example of such elements: Metformin, Paw Paw/Graviola, Doxycycline. Some say yes and some not, due to various reasons. To be clarified.

Clinics Treating Patients with 3BP

US: Dayspring Cancer Clinic
My review: Comprehensive treatment around 3BP. Adding various other treatments to increase effectiveness in case sensitivity of specific cancer is not there or is limited. I recommend this clinic.

US: Advanced Rejuvenation Institute
My review: Unknown

Canada: Cancerimmunotherapycentres
My review: Unknown

Forums on 3BP:

Cancer Compass  – Inspire – Longecity

Other relevant links:

Cancer Cure Medicine – Is a Cancer Cure Being SuppressedWehaveacure – TheCancerCure – Cancer Cured, Again – War on Cancer

Reference on formulation and stability (fore more references see https://www.cancertreatmentsresearch.com/?p=184)

The antitumor agent 3-bromopyruvate has a short half-life at physiological conditions

Composition and method for the efficacious and safe administration of halopyruvate for the treatment of cancer This invention provides compositions and methods for the treatment of cancer. An inhibitor cocktail buffer includes at least one sugar, a non-potassium containing buffer, and an inhibitor:

1 Water only 0.33
2 Glycerol, 1% 0.34
3 Inositol, 4% 0.44
4 Sorbitol, 55% 0.47
5 Sodium Phosphate, pH 7.4, 0.5 M 0.17
6 All four agents above 1.00

Therapeutics for cancer using 3-bromopyruvate and other selective inhibitors of ATP production The present invention relates to methods of treating a cancerous tumor using selective inhibitors of ATP production. The present invention also relates to pharmaceutical preparations comprising such inhibitors and methods for administering them intraarterially directly to a tumor, as well as methods for identifying compositions that selectively inhibitor ATP production for use in the invention.

Anti-cancer composition and method utilizing 3-bp and liposomal reduced glutathione The invention proposes a method of treatment of cancers exhibiting a CD163 characteristic by a liposomally formulated reduced glutathione. The invention proposes a method of treatment of cancer of a combination of liposomally formulated reduced glutathione to cooperate with an anti-cancer agent 3-bromopyruvate and its analogs Bromopynivic acid and 3-BrOP (3-bromo-2-oxopropionate-l -propyl ester) (collectively “3BP” or “3-BP”) to ameliorate the 3BP side effects and enhance its cancer-killing capacity and enhance the detoxification of the body of dead cancer cell debris.

Compositions and methods for the treatment of cancer The present invention discloses anti-cancer compositions, and associated methods, including an anti-cancer composition comprising: a cellular energy inhibitor having the structure according to formula I wherein X is selected from the group consisting of: a nitro, an imidazole, a halide, sulfonate, a carboxylate, an alkoxide, and amine oxide; and R is selected from the group consisting of: OR′, N(R″)2, C(O)R′″, C1-C6 alkyl, C6-C12 aryl, C1-C6 heteroalkyl, a C6-C12 heteroaryl, H, and an alkali metal; where R′ represents H, alkali metal, C1-C6 alkyl, C6-C12 aryl or C(O)R′″, R″ represents H, C1-C6 alkyl, or C6-C12 aryl, and R′″ represents H, C1-C20 alkyl or C6-C12 aryl. The anti-cancer composition can additionally comprise at least one sugar, which stabilizes the cellular energy inhibitor by substantially preventing the inhibitor from hydrolyzing. Also, the anti-cancer composition can comprise a hexokinase inhibitor. Further, the anti-cancer composition can comprise a biological buffer that is present in an amount sufficient to at least partially deacidify the cellular energy inhibitor and neutralize metabolic by-products of the cellular energy inhibitor.

A composition and method for the efficacious and safe administration of halopyruvate for the treatment of cancer

Methods and compositions for administration of 3-halopyruvate and related compounds for the treatment of cancer The present disclosure relates to the discovery that compounds of the invention, particularly 3-bromopyruvate and related compounds, can be safely administered at concentrations effective for the treatment of cancer when formulated with an acidity of greater than or equal to pH of 2 and less than or equal to a pH of 6. Disclosed herein are novel and improved methods and compositions for the treatment ofcancer using 3-halopyruvate and related compounds.

Methods of treatment using 3-bromopyruvate and other selective inhibitors of atp production

Methods of treating tumors having elevated mct1 expression In some aspects, compositions and methods useful for classifying tumor cells, tumor cell lines, or tumors according to predicted sensitivity to 3-bromopyruvate (3-BrPA) are provided. In some aspects, methods of identifying subjects with cancer who are candidates for treatment with 3-BrPA are provided. In some aspects, compositions useful for subjects with cancers that express increased levels of MCT1 are provided. In some aspects, methods of treating subjects with cancers that express increased levels of MCT1 are provided. In some aspects, methods of identifying anti-tumor agents the efficacy of which is at least in part dependent on transporter-mediated uptake are provided.

Method of treating cancer with combinations of histone deacetylase inhibitors (hdac1) substances A method for treating cancer is described using combination therapies comprising the use of hyperbaric oxygen with histone deacetylase inhibitors, with and without glycolytic therapies. The patient is subjected to a hyperbaric environment of substantially pure oxygen. A predetermined dose of one or more HDACI substances is administered to the patient. In addition, glycolitic inhibitors may also be administered. Dosages, pressures, and durations are selected as described herein to have a therapeutic effect on the patient.

Propyl 3-bromo-2-oxopropionate and derivatives as novel anticancer agents The present invention is directed to compositions that inhibit glycolysis, perferentially in cancer. Specifically, the anticancer compositions comprise 3-halo-2-oxopropionate and its derivatives, such as ester derivatives. However, in specific embodiments, the anticancer composition is sodium 3-halo-2-oxopropionate, such as sodium 3-bromo-2-oxopropionate and a stabilizing agent, such as carbonic acid. In particular embodiments, the compositions of the present invention further comprise a metabolic intermediate for normal cells to utilize in a pathway for an alternate energy source, thereby providing protection to normal cells. In other embodiments, the 3-halo-2-oxopropionate or its ester derivative is used in combination with an additional cancer therapy, such as radiation and/or a drug.

Methods of treating tumors having elevated mct1 expression  In some aspects, compositions and methods useful for classifying tumor cells, tumor cell lines, or tumors according to predicted sensitivity to 3-bromopyruvate (3-BrPA) are provided. In some aspects, methods of identifying subjects with cancer who are candidates for treatment with 3-BrPA are provided. In some aspects, compositions useful for subjects with cancers that express increased levels of MCT1 are provided. In some aspects, methods of treating subjects with cancers that express increased levels of MCT1 are provided. In some aspects, methods of identifying anti-tumor agents the efficacy of which is at least in part dependent on transporter-mediated uptake are provided.

Characterization of acetate transport in colorectal cancer cells and potential therapeutic implications. https://www.ncbi.nlm.nih.gov/pubmed/27661124

Acetate, together with other short chain fatty acids has been implicated in colorectal cancer (CRC) prevention/therapy. Acetate was shown to induce apoptosis in CRC cells. The precise mechanism underlying acetate transport across CRC cells membrane, that may be implicated in its selectivity towards CRC cells, is not fully understood and was addressed here. We also assessed the effect of acetate in CRC glycolytic metabolism and explored its use in combination with the glycolytic inhibitor 3-bromopyruvate (3BP). We provide evidence that acetate enters CRC cells by the secondary active transporters MCT1 and/or MCT2 and SMCT1 as well as by facilitated diffusion via aquaporins. CRC cell exposure to acetate upregulates the expression of MCT1, MCT4 and CD147, while promoting MCT1 plasma membrane localization. We also observed that acetate increases CRC cell glycolytic phenotype and that acetate-induced apoptosis and anti-proliferative effect was potentiated by 3BP. Our data suggest that acetate selectivity towards CRC cells might be explained by the fact that aquaporins and MCTs are found overexpressed in CRC clinical cases. Our work highlights the importance that acetate transport regulation has in the use of drugs such as 3BP as a new therapeutic strategy for CRC.

Recent (2016) update on 3BP patent: Methods and compositions for administration of 3-halopyruvate and related compounds for the treatment of cancer https://www.google.com/patents/US9492417 indicating combination with Sodium Bicarbonate as a buffer as suitable to balance 3BP acidity and increase the daily dose.


This site is not designed to and does not provide medical advice, professional diagnosis, opinion, treatment or services to you or to any other individual. Through this site and linkages to other sites, I provide general information for educational purposes only. The information provided in this site, or through linkages to other sites, is not a substitute for medical or professional care, and you should not use the information in place of a visit, call consultation or the advice of your physician or other healthcare provider. I am not liable or responsible for any advice, course of treatment, diagnosis or any other information, services or product you obtain through this site. This is just my own personal opinion regarding what we have learned on this road.

Please read an extended version of the Disclaimer here: https://www.cancertreatmentsresearch.com/?page_id=1794

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Thanks Daniel, Life is OK.

So, systemic 3BP is effective up to and intraarterial 3BP is viable above certain size thresholds. Praying Dr. Ko will push thru all the obstacles. Here’s an article:



PMID: 28450161

How is the 3-BP getting into the cell?
3-BP through the MCT-1 makes sense, but POH-3-BP?


I am pretty much locked into the homeeville Anglo webspace.
Might others from different regions of global cyberspace chime in on what they are seeing when they search for 3-BP info that is local to where they are from?

I have been trying to break into different regional webspaces to see their point of view on 3-BP, though often I seem to get bounced back to here or the Compass etc. .

Would love to know what the local opinion might be of 3-BP globally. Might also be able to pick up on reports for other clinics that have been outside of our search engine range.


Yes, I am also very unsure about them. I can fully understand how many would want to be part of the 3-BP story, though
the question of whether they have authorization to provide such treatment is very unclear. It is possible that we are now
moving towards the start of a clinical trial with 3-BP and more clinics could enter the fray.

Yet, it is not certain that bringing on board a great number more clinics that do not have a long standing background in 3-BP will
be of long term benefit. Clinics without the required technical skills might simply create more Brachts.


Dear D, the research up till this point has talked of a possible ROS generation angle to 3-BP as you have noted.

“Furthermore, our results offer alternative interpretations of 56 previously published models on the role of supplemental antioxidants: Rather than 57 quenching reactive oxygen species (ROS), supplemental NAC or GSH directly interact 58 with 3-BP, thereby neutralizing the drug’s cytotoxic potential before it can trigger ROS 59 production. ”

“Surprisingly 442 however, in the presence of antioxidants (NAC or GSH) this inhibitory effect was 443 completely prevented, even though these were cell-free reaction conditions without the 444 possibility of free radical production by intact mitochondria or other cellular processes. 445 This outcome suggested that the protective effects of NAC or GSH might not be via their 446 conventional quenching of free radical species. (See Discussion regarding an alternative 447 model explaining cytoprotection by NAC and GSH.)”

These quotes are form the recent POH article PMID: 28450161.

It is possible that ROS is not involved with 3-BP efficacy.


D, I have been posting to the Compass thread about ethyl pyruvate.
This sounds like it has potential.

It has been given in a high dose IV phase II trial for high risk cardiac patients where it was not successful, though
there would seem to be an ATP depletion side of it. It is considered GRAS, yet the one problem noted was that
it might be very unstable when injected (another reference talked of a Ringer’s solution with EP that was stable).

I am somewhat surprised how many of these 3-BP like drugs are out there and could have significant anti-cancer effect.
If they could stabilize EP for human IV dosing at 10 mM then this would be the concentration that resulted in irreversible
ATP depletion.


Hi Folks,

I looked at the suggested websites and it seems there is a clinic in Bangkok, the medical director is called – no kidding – Dr. Porntip 😀 Full name is actually Dr. Porntip Chooparnich Here is the link: http://www.mithrabiomaxx.com/PDF/Brio-Clinic-Bangkok.pdf There is at least one other doctor, with a German sounding name and look.

I did see the “under the radar” statement, which is very strange. In the roll-down menus of http://www.mithrabiomaxx.com/index.php under “Therapy Programs” at e.g. http://www.mithrabiomaxx.com/basic-programB.php there is something called Chlorin e6 as a photosensitizer. Does anyone know what that could be? Also, do they have a price list?



Hello, greetings to everyone! I am thinking about oral use of 3-BP. And I am worried about bromine displacement by chlorine in the stomach acid. Would capsulation be a good approach to avoid 3-BP degradation? Also, I found info about buffer that stabilizes 3-BP. Is that another reasonable precaution with oral use, or buffering the solution is needed only with i.v. administration? Share your thoughts, thank you!


Daniel I have 2 questions :-

1 – why we should mix 3-BP with water instead of NaCl ? I’m used to mix DCA with NaCl before , also today I tried to mix 3-BP with NaCl and it dissolved completely , but I’m not sure what is the issue in the first place , is it about the solubility is poor in NaCl or its not good for its stability ?

2 – did you see effectiveness when you administrate 3-BP at night ? or you noticed only good respond when you give it in the morning when the patient is still fasting ?

wish you good weekend for you and all other friends here


Dear Emad,
I dont know why but i cannot use my mail.For your question:Yes please,If you could help me with a video,i will be very happy.
I will create another mail if it will not work next days.
Bye the way sal and 3-bp is a perfect combination,i like both.Are you using again salt version of sal?My mother had an antibiotic allergy when she was young and we dont know now.I am afraiding to use sal because of it.

You should look at blood counts as i read after 3-BP.It may be very effective with salinomycin.

Kind Regards


I will show you how to prepare DCA , the same will go for the others

but I can’t advise you to go ahead with it , its for only general information not for you to start with it right away

if you watch this video you will probably not need any other video from me


also you can search for a lot of videos on youtube

search for “0.2 um filter” and you will get it all

yes I’m using salt version of Sal , i don’t know if its like the base version but the side effects are the same

you need to be careful from allergy , for any reason you should always start on very low doses

for Sal , its hard , its already small dose its barely visible , you should have some help from experts if you can , its better than having risk doing things by yourself

I can remember one time i pushed the dose slight more than 0.2mg/kg of Sal and the side effects were strong and it was a scary night to me , but when it comes to cancer , its the only scary thing compared to any other thing in this world

regarding blood counts , we will not do it right now , we have to see what is happening with scans

speaking about scan , I’m wish to hear better results about your dear mother soon , i will pray for that


Thank you very much Emad.I watch all and helpful.


You always welcome brother

I understand from your comment that you did know how to make any solution sterile and ready for IV

if you still need a video please ask me


Thanks Emad,everything is clear.I want to use 3BP before phlorizin+hyperthermia.
I am searching for 3bp cases now,there is not too much on internet.
Your experience is great for all of us.I hope it works Emad.And T4 depleteion will also work.
Than we can make combinations.Did you find any other cases with 3bp?
There is one:they use 3bp with paracetamol(glutathione depletion).
In some forums they say metformin+3bp causes lactic acidosis.
I am sure Daniel knows more.


And Emad i wonder if salinomycin worked or not for your mother.
I think it didnt work,what do you think?May be because of salt version.
Because while searching,salinomycin is a perfect drug for cancer stem cells especially,
and Daniel saw very good responce.Did you search for other antibiotics?
Targeting mitochondria with antibiotics and you can add an anti worm-parasite drug.
Now you are on a very good and brave protocol.I think the best protocol and i hope very much for it to work.
Always wishing best for you.


Yes I still didn’t get the desired results from using Sal but also I’m still not aggressive on using it

in trials they are giving it every second day , I’m still giving it once or twice weekly not more

I may try other things like anti worm-parasite drugs but just when I can’t see any positive effect from Sal

its maybe due to salt version not effective but I can’t understand this , they look very similar

the same shape , the same side effects , the same look and feel and the both cause tremor if this is a sign of a response

also in the research field they are talking about both of them like they are the very same and no difference between them , I still believe on it whenever I see the good results in articles talking about it

hope combining it with 3bp will make it strong

wish the best for you too brother 🙂


Hi Daniel!

Just checking in and it’s great to see you working this site!

3BP was mentioned in passing in an article from Yale: “… our team has demonstrated the efficacy of the first anti-glycolytic agent 3-Bromopyruvate (3-BrPA) in several animal models.” http://medicine.yale.edu/lab/radresearch/research.aspx And “… Cancer cells have long been known to exhibit altered energy metabolism. This metabolic phenotype includes a dependence on glycolysis (cytoplasmic) rather than oxidative phosphorylation (mitochondrial respiration) for the production of intracellular energy (e.g. ATP). The biological significance of this altered metabolic phenotype is underscored by its recent classification as one of the hallmarks of cancer.”

I see Single Cause Single Cure has changed the name to Foundation for Metabolic Cancer Therapies and has recently funded Drs. Pete Pedersen and Thomas Seyfried and others. Looks like metabolic research might be progressing but in the normal slow fashion. It’s nice to see more dollars thrown that way.

I will never forget you and Miha.

Take care


Is there a little chance that IV can take the 3-bp / salinomycin IV infusions for 3 weeks, as is the protocol, without an implanted port?
It just started for 2 days, today is about to reach the maximum of 3-bp and the hand is already swollen. Do you think that the treatment cycle may end in these conditions?


D, could you help out?

I have been wondering about the vitamin C 3-bp combo. You noted the possible synergy in your post. What I am interested in is the gsh depletion potential of vitamin C. I thought that one could lead in with a week or two of vitamin C and then start up with the 3-bp. What I am not sure about is whether normal cells would also become gsh depleted. Safety would be a concern if normal cells were depleted. Do you have any references that show that normal cells don’t deplete? I have been looking around, though I have not found anything.

Noticed that over the last few days there have been some media mentions of Bracht.


D, Hope you’re having a wonderful summer!

I am only beginning to appreciate how much larger MCT-1 levels are in ALL progressing cancer patients.
(0.31–1.09) versus (0.01–0.05)
For example, Table 4.

Also ” it can be said that those women with MCT1, MCT4 and CD147 expressions respectively ranging between 0.01–0.05, 0.0005–0.002 and 0.063–0.072 are considered healthy; those whose MCT1, MCT4 and CD147 expression levels respectively ranged between 0.08–0.28, 0.001–0.006 and 0.32–0.37 are cancer patients with low odds of progression; finally, samples with results showing relative expression in MCF7 between 0.31–1.09, 0.03–0.08 and 0.53–0.80 respectively for MCT1,
MCT4 and CD147 indicate disease with chances of disease progression”


I had thought that perhaps some patients could have MCT-1 levels as low as those without illness.

For me, this suggests that 3-BP might help a broad range of patients to deplete their GSH selectively in the cancer cells. It would not even require 3-BP to appear to cause direct cancer cell lysis: 3-BP could simply wear down the GSH in the cancer cells. Afterwards, one could switch to vitamin C possibly with vitamin K3 for the knock out punch.

Too bad the FDA requires that all treatments need to be shown to be safe and effective!
Showing only that 3-BP were safe would allow the combo to go forward.
With the above plan, 3-BP monotherapy would seem totally ineffective, however, when the vitamin C/K3 was added in it could be
seen to be much more effective.



does anyone knows how to prepare 3bp for enema?

any direction would be apreciated



Hello there

it seems noone have information on enemas administration

anyone have information on intratumoral injection of 3bp?

thanks in advance


This was a surprise to me. The study looked at lymphoma cells and some of the cells had very low MCT-1 levels. Not surprisingly this meant that 3-BP was not very effective. What was surprising was that even while 3-BP was not effective 3-BrOP was.

“Thus, because of its better cell permeability and chemical stability, the ester pro-drug of 3-BrPA, 3-bromo-pyruvate propyl ester (3-BrOP) was used instead. 3-BrOP showed very high citotoxicity at low dosage (Figure ​(Figure2C),2C), suggesting that the ability of 3-BrOP to enter the cells and release 3-BrPA via hydrolysation by cellular esterases accounts for the > 10 fold difference in the potency of the two compounds.”

Wow! How does 3-BRoP enter a cell that blocks 3-BP entry?

We need to keep an eye out for these articles because it was not listed using a 3-BP search.
A considerable amount of 3-BP research flies under the radar.

Reversal of the glycolytic phenotype of primary effusion lymphoma cells by combined targeting of cellular metabolism and PI3K/Akt/ mTOR signaling


This Article says DCA (Similar agent to 3bp) shouldn’t be used in acidic form and 3bp is available in this form only on internet I think


Hi Daniel,
n the preparation IV 3BP does not put you may need a PH METER ,this is because the mixture with the correct quantities has a ph suitable for intravenous infusion?, even when NaBic is not added in the version without buffer)?thank you


Hello, is disulfiram contraindicated with 3-BP? Also, as Salinomycin is very difficult to obtain, is there an adequate substitute that effectively kills CSC?


vis, if you could access a chem lab and make up some 3-BP nanoparticles that would probably be very helpful.
There are a wide range of published formulations for chemicals that should magnify the effects while enhancing the safety. The lab work does not seem very complex. We have talked about this off thread for a few years, though we have not made progress with this idea. However, it would likely be well worthwhile if you could manage it.