3BP IV Administration Protocol and Treatment Strategy

Update 03.03.2016: based on clear evidence IV Alpha Lipoic Acid (300-600mg) can inhibit the effectiveness of 3BP –> we may want to avoid that during 3BP treatment and use only when 3BP action is intended to be stopped.

For readers, you may want to first read this page and consider being treated at a clinic such as those suggested at the bottom of this page or any other you may trust.

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

Below is info consolidated from various sources I found and is just an example how elements may be combined.

Application

– Administer 3BP every day, 5 days/week (5 days on and 2 days off), during 3 weeks. This is a cycle. Take a few weeks break after a cycle then perform another cycle. Preferably, perform 3 cycles.
– At the beginning of every week, before IV administration, withdraw blood for the blood tests: follow LDH, tumor markers, Na, Ca, K, liver and kidney functions, uric acid levels, ammonia levels
Glutamine deprivation increases 3BP absorption (Ref. page 105-107, Ref2) –> avoid red meet and use glutamine inhibitors (e.g. Phenylbutyrate); see also the following: Ref.
Glucose deprivation increases 3BP absorption (diet and e.g. Metformin) (Ref.) Note that other reference is stating that cells grown in glucose deprived environment are less sensitive to 3BP. To try and understand both, I can imagine that the second reference refers to growing phase, while the first reference refers to the treatment phase. In this case both could be true.
– Based on the above last two points, fasting should lead to increased MCT1 expression . As a result, preferably, administer 3BP early in the morning before food (MCTs are upregulated with starvation)
Avoid antioxidants as much as possible, supplements and IVs (keep those that are essentials to protect organs, etc.) – alternatively, use strong anti oxidants like Glutathione (Ref.), NAC or Alpha Lipoic Acid, if due to any reason the 3BP action in the human body needs to be stopped. This is a good option as sometimes mistake in administrated dose are made. If a too high dose of 3BP has been applied by mistake, the doctor should imidiatly administrate such strong antioxidants, preferably via IV route.
– Do not administer supplements before 3BP IV
This is key: Before and during the treatment increase oxygen in the body with e.g. Myo-inositol TrisPyroPhosphate, Hydrogen Peroxide, EWOT, etc. If possible go to hyperbaric chamber.

IV administration  (this is just my idea)

Day 1:

  • Optionally Ozone therapy or IV Hydrogen Peroxide (H2O2)
  • Administer 3BP IV as indicated here
  • Wait one hour for 3BP effectiveness
  • Administer high dose IV Vitamin C

Day 2:

  • Administer 3BP IV as indicated here or replace this with Salinomycin IV (see post on Salinomycin)

Day 3:

  • Optionally Ozone therapy or IV Hydrogen Peroxide (H2O2)
  • Administer 3BP IV as indicated here

Day 4:

  • Administer 3BP IV as indicated here or replace this with Salinomycin IV (see post on Salinomycin)

Day 5:

  • Optionally Ozone therapy or IV Hydrogen Peroxide (H2O2)
  • Administer 3BP IV as indicated here
  • Wait one hour for 3BP effectiveness
  • Administer high dose IV Vitamin C

Note:
– administering oxygen during 3BP administration will help
– above use the 3BP solution version of choice (buffered or unbuffered – or it can be alternated between the weeks in order to identify which one produces the highest response).
– in high doses IVC acts as a pro oxidant – in this protocol, Vitamin C has multiple anti cancer roles one of which is to kill what 3BP may not, i.e. kill glycolitic cancer cells without MCT1.
– 3BP is not good substrates for efflux pumps involved in the drug resistance, less chance to develop resistence to 3BP due to MDRs (Ref.)

Supplements and Drug administration

administrate paracetamol (acetaminophen) 3x-4x/week, 1.5g to 3g/day (Paracetamol can induce liver toxicity. It helps to reduce glutathione level and increase effectiveness of 3BP. Assuming 3BP administration  is Monday to Friday, start Paracetamol administration on Sunday) Note: if Paracetamol intoxication occurs, use NAC (N-Acetyl Cysteine) for a few days –> therefore, have some NAC as home just in case.
Sodium Butyrate 2 capsules 3x/day (note: this one smells very bad …) – we can buy here
– If possible use 200mg/day Myo-inositol TrisPyroPhosphate under the tongue – a bit expensive but can be bought in groups from e.g. here. Is not required 200mg/day, even one time/week is still good as it will increase the capacity of hemoglobin to carry oxygen for nearly one week. This component is currently considered as an anti-cancer component alone and is in clinical trials under the name OXY111A
– 150mg to 250mg  Chloroquine daily – to inhibit autophagy
Celecoxib 600mg/day – to inhibit angiogenesis
– Shark Cartilage or Squalamine to inhibit angiogenesis – source
– Cimetidine 800mg/day – to reduce Treg and support immune system – source
– Use an anti-worm or anti-fungal (e.g. Mebendazole) or anti-biotic one-two weeks before and during the 3BP treatment (another very good idea from a great scientist)
– Use probiotics, specifically if we are going to follow the oral administration as well.

Others

Next to the above,
– use strategies to enhance the immune system
– use other anti-angiogenesis inhibitors such as Thalidomide, Tetrathiomolybdate, Albendazole, Plerixafor in case we see strong anti-cancer response from 3BP or any other treatment
– use Salinomycin IV one-two times/week depending on the response
– red meat should be avoided as is a important source of glutamine
– add Phenyl Butyrate if available – taken on prescription otherwise too expensive
– before the administration we may want to use Nitroglycerine or B3 (Niacin) vitamin to open up the veins and improve oxygenation.

A short list of Synergy, Complementary or Supporting elements:  Curcumin, Curcumin22DG, Glutamine Deprivation e.g. Phenyl Butyrate, Chloroquine, Paracetamol, Methyl Jasmonate, Fasting, Hypoglycemiareduction in extracellular pH enhanced 3-BrPA uptakeButyrate,  Lactate, Ketosis, Exercise, TestosteroneAcetazolamide, Citrate, Citrate2, Rapamycin

Do not use the following antagonists:
– All the MCT1 inhibitors such as Quercetin, Luteolin, Atorvastatin (and other statins), Diclofenac, Phloretin, Naringenin, Apigenin, Genistein, Ibuprofen, Silybin, Disulfiram?
– Strong anti oxidant supplements such as NAC (N-Acetyl Cysteine)

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. Currently I am also questioning weather DCA should be used with 3BP.

Great presentation on Monocarboxylate Transporters: http://www.njacs.org/wp-content/docs/2010-Spring-DrugMet-Mar. Includes list of elements interacting with MCTs and some studies of MCTs in different tissues.

Relevant Literature

The effect of 3-bromopyruvate on human colorectal cancer cells is dependent on glucose concentration but not hexokinase II expression Cells grown under lower glucose concentrations showed greater resistance towards 3BP.

Lactate promotes glutamine uptake and metabolism in oxidative cancer cells Using SiHa and HeLa human cancer cells, this study reports that intracellular lactate signaling promotes glutamine uptake and metabolism in oxidative cancer cells. It depends on the uptake of extracellular lactate by monocarboxylate transporter 1 (MCT1).

The above article suggests that by reducing intracellular lactate by 3BP or MCT1 inhibition will reduce glutaminolysis.

Lactate promotes glutamine uptake and metabolism in oxidative cancer cells Oxygenated cancer cells have a high metabolic plasticity as they can use glucose, glutamine and lactate as main substrates to support their bioenergetic and biosynthetic activities. Metabolic optimization requires integration. While glycolysis and glutaminolysis can cooperate to support cellular proliferation, oxidative lactate metabolism opposes glycolysis in oxidative cancer cells engaged in a symbiotic relation with their hypoxic/glycolytic neighbors. However, little is known concerning the relationship between oxidative lactate metabolism and glutamine metabolism. Using SiHa and HeLa human cancer cells, this study reports that intracellular lactate signaling promotes glutamine uptake and metabolism in oxidative cancer cells. It depends on the uptake of extracellular lactate by monocarboxylate transporter 1 (MCT1). Lactate first stabilizes hypoxia-inducible factor-2α (HIF-2α), and HIF-2α then transactivates c-Myc in a pathway that mimics a response to hypoxia. Consequently, lactate-induced c-Myc activation triggers the expression of glutamine transporter ASCT2 and of glutaminase 1 (GLS1), resulting in improved glutamine uptake and catabolism. Elucidation of this metabolic dependence could be of therapeutic interest. First, inhibitors of lactate uptake targeting MCT1 are currently entering clinical trials. They have the potential to indirectly repress glutaminolysis. Second, in oxidative cancer cells, resistance to glutaminolysis inhibition could arise from compensation by oxidative lactate metabolism and increased lactate signaling. –> my conclusion: use glutamine inhibitors at the same time with 3BP, but start first with the administration of glutamine inhibitors in order to potentially increase the balance towards oxidative lactate metabolism and as a result induce/increase sensitiveness to 3BP.

3-BrPA eliminates human bladder cancer cells with highly oncogenic signatures via engagement of specific death programs and perturbation of multiple signaling and metabolic determinants. Interestingly, MCT1- and macropinocytosis-mediated influx of 3-BrPA in T24 represents the principal mechanism that regulates cellular responsiveness to the drug. Besides its capacity to affect transcription in gene-dependent manner, 3-BrPA can also induce GLUT4-specific splicing silencing in both sensitive and resistant cells, thus dictating alternative routes of drug trafficking. Altogether, it seems that 3-BrPA represents a promising agent for bladder cancer targeted therapy.

The cytotoxicity of 3-bromopyruvate in breast cancer cells depends on extracellular pH: At pH 6.0, the affinity of cancer cells for 3BP transport correlates with their sensitivity, a pattern that does not occur at pH 7.4. In the three cell lines, the uptake of 3BP is dependent on the protonmotive force and is decreased by MCTs (monocarboxylate transporters) inhibitors. In the SK-BR-3 cell line, a sodium-dependent transport also occurs. Butyrate promotes the localization of MCT-1 at the plasma membrane and increases the level of MCT-4 expression, leading to a higher sensitivity for 3BP … We find that the affinity for 3BP transport is higher when the extracellular milieu is acidic. This is a typical phenotype of tumour microenvironment and explains the lack of secondary effects of 3BP already described in in vivo studies [Ko et al. (2004) Biochem. Biophys. Res. Commun. 324, 269-275].

Primary clear cell renal carcinoma cells display minimal mitochondrial respiratory capacity resulting in pronounced sensitivity to glycolytic inhibition by 3-Bromopyruvate (and here is a PDF version)

3-bromopyruvate inhibits glycolysis, depletes cellular glutathione, and compromises the viability of cultured primary rat astrocytes The data suggest that inhibition of glycolysis by inactivation of GAPDH and GSH depletion contributes to the toxicity that was observed for 3-BP-treated cultured astrocytes

The antitumor agent 3-bromopyruvate has a short half-life at physiological conditions This study found the first-order decay rate of 3-BP at physiological temperature and pH has a half-life of only 77 min. Lower buffer pH decreases the decay rate, while choice of buffer and concentration do not affect it.

Hexokinase II inhibitor, 3-BrPA induced autophagy by stimulating ROS formation in human breast cancer cells:  our results show that 3-BrPA triggers autophagy, increasing breast cancer cell resistance to 3-BrPA treatment and that CQ enhanced 3-BrPA-induced cell death in breast cancer cells by stimulating ROS formation

Local delivery of cancer-cell glycolytic inhibitors in high-grade glioma: The combination of intracranial 3-BrPA and TMZ provided a synergistic effect

Inhibition of glucose turnover by 3-bromopyruvate counteracts pancreatic cancer stem cell features and sensitizes cells to gemcitabine

Monocarboxylate transporters as targets and mediators in cancer therapy response: MCTs are attractive targets in cancer therapy, especially in cancers with a hyper-glycolytic and acid-resistant phenotype

Glycolysis inhibition and its effect in doxorubicin resistance in neuroblastoma: Glycolysis inhibitors such as 3-bromopyruvate could prove to become an effective means by which chemotherapy resistance can be overcome in human neuroblastoma.

Mitochondria: 3-bromopyruvate vs. mitochondria? A small molecule that attacks tumors by targeting their bioenergetic diversity: Contrary to predictions, 3BP interferes with glycolysis and oxidative phosphorylation in cancer cells without side effects in normal tissues.

Transport of 3-bromopyruvate across the human erythrocyte membrane: 3-BP uptake by erythrocytes was linear within the first 3 min and pH-dependent. The transport rate decreased with increasing pH in the range of 6.0-8.0. The transport was inhibited competitively by pyruvate and significantly inhibited by DIDS, SITS, and 1-cyano-4-hydroxycinnamic acid. Flavonoids also inhibited 3-BP transport: the most potent inhibition was found for luteolin and quercetin.

Safety and outcome of treatment of metastatic melanoma using 3-bromopyruvate: a concise literature review and case study. If the anticancer effectiveness of 3BP is less than expected, the combination with paracetamol may be needed to sensitize cancer cells to 3BP-induced effects.

Killing multiple myeloma cells with the small molecule 3-bromopyruvate: implications for therapy: The cytotoxicity of 3-BP, is potentiated by the inhibitor of glutathione synthesis buthionine sulfoximine.

Effect of 3-bromopyruvic acid on human erythrocyte antioxidant defense system: Thus induction of oxidative stress in erythrocytes by 3-BP is due to depletion of glutathione and inhibition of antioxidant enzymes.

Regulation of the proliferation of colon cancer cells by compounds that affect glycolysis, including 3-bromopyruvate, 2-deoxyglucose and biguanides: an additive effect was more notable in combined treatment with 3-bromopyruvateand 2-deoxyglucose.

Anticancer efficacy of the metabolic blocker 3-bromopyruvate: specific molecular targeting: Taken together, the specificity of molecular (GAPDH) targeting and selective uptake by tumor cells, underscore the potential of 3-bromopyruvate as a potent and promising anticancer agent. In this review, we highlight the mechanistic characteristics of 3-bromopyruvate and discuss its potential for translation into the clinic.

Repeated cisplatin treatment can lead to a multiresistant tumor cell population with stem cell features and sensitivity to 3-bromopyruvate

Deprive to kill: glutamine closes the gate to anticancer monocarboxylic drugs: our results identified the metabolic condition able to increase the selectivity of 3-bromopyruvate targets in neoplastic tissues, thereby providing a stage for its use in clinical settings for targeting malignancies and represent a proof of principle that modulation of glutamine availability can influence the delivery of monocarboxylic drugs into tumors.

Glycolysis inhibitors as a potential therapeutic option to treat aggressive neuroblastoma expressing GLUT1: 3-Bromopyruvate acid significantly suppressed the proliferation of neuroblastoma cells with high GLUT1 gene expression compared with those with low expression

D-Amino acid oxidase-induced oxidative stress, 3-bromopyruvate and citrate inhibit angiogenesis, exhibiting potent anticancer effects: Citrate is a natural organic acid capable of inhibiting glycolysis by targeting phosphofructokinase. Here, we report that DAO, 3BP and citrate significantly inhibited angiogenesis, decreased the number of vascular branching points and shortened the length of vascular tubules.

Glutamine deprivation enhances antitumor activity of 3-bromopyruvate through the stabilization of monocarboxylate transporter-1: our findings offer a preclinical proof-of-concept for how to employ 3-bromopyruvate or other monocarboxylic-based drugs to sensitize tumors to chemotherapy

EPR oxygen imaging and hyperpolarized 13C MRI of pyruvate metabolism as noninvasive biomarkers of tumor treatment response to a glycolysis inhibitor 3-bromopyruvate: the efficacy of 3-bromopyruvatewas substantially attenuated in hypoxic tumor regions (pO2<10 mmHg) … The discrepant results between in vitro and in vivo data were attributed to biphasic oxygen dependent expression of monocarboxylate transporter-1 in vivo. Expression of monocarboxylate transporter-1 was enhanced in moderately hypoxic (8-15 mmHg) tumor regions but down regulated in severely hypoxic (<5 mmHg) tumor regions.

Aerosolized 3-bromopyruvate inhibits lung tumorigenesis without causing liver toxicity: The ability of 3-bromopyruvate to inhibit mouse lung tumorigenesis, in part through induction of apoptosis, merits further investigation of this compound as a chemopreventive agent for human lung cancer.

3-Bromopyruvate inhibits calcium uptake by sarcoplasmic reticulum vesicles but not SERCA ATP hydrolysis activity: In this study, we show that the sarco/endoplasmic reticulum calcium (Ca(2+)) ATPase (SERCA) type 1 is one of the target enzymes of 3BrPA activity. Sarco/endoplasmic reticulum vesicles (SRV) were incubated in the presence of 1mM 3BrPA, which was unable to inhibit the ATPase activity of SERCA. However, Ca(2+)-uptake activity was significantly inhibited by 80% with 150 μM 3BrPA. These results indicate that 3BrPA has the ability to uncouple the ATP hydrolysis from the calcium transport activities.
we observed that the inclusion of 2mM reduced glutathione (GSH) in the reaction medium with different 3BrPA concentrations promoted an increase in 40% in ATPase activity and protects the inhibition promoted by 3BrPA in calcium uptake activity

A translational study “case report” on the small molecule “energy blocker” 3-bromopyruvate (3BP) as a potent anticancer agent: from bench side to bedside: Thus, a bench side discovery in the Department of Biological Chemistry at Johns Hopkins University, School of Medicine was taken effectively to bedside treatment at Johann Wolfgang Goethe University Frankfurt/Main Hospital, Germany. The results obtained hold promise for 3BP as a future cancer therapeutic without apparent cyto-toxicity when formulated properly.

Note: I just realized this paper has only 10 citations ?????? It should be thousands by now based on the magnitude of the published subject!

Flow cytometric evaluation of the effects of 3-bromopyruvate (3BP) and dichloracetate (DCA) on THP-1 cells: a multiparameter analysis: 3BP and DCA show no synergism, but have complementary destructive effects

3-Bromopyruvate antagonizes effects of lactate and pyruvate, synergizes with citrate and exerts novel anti-glioma effects: Serial doses of 3BP were synergistic with citrate in decreasing viability of C6 glioma cells

D-amino acid oxidase gene therapy sensitizes glioma cells to the antiglycolytic effect of 3-bromopyruvate: OSED utilizes D-amino acid oxidase (DAO), which is a promising therapeutic protein that induces oxidative stress and apoptosis through generating hydrogen peroxide (H2O2).

A novel facet to consider for the effects of butyrate on its target cells. Focus on €œThe short-chain fatty acid butyrate is a substrate of breast cancer resistance protein€ Butyrate is transported across teh membrane through MCTs with the help of protons and Natrium, both also transported inside the cell.

Transport by SLC5A8 with subsequent inhibition of histone deacetylase 1 (HDAC1) and HDAC3 underlies the antitumor activity of 3-bromopyruvate: 3-Bromopyruvate was transported into cells actively through the tumor suppressor SLC5A8, and the process was energized by an electrochemical Na+ gradient

MCT1-mediated transport of a toxic molecule is an effective strategy for targeting glycolytic tumors We identified the SLC16A1 gene product, MCT1, as the main determinant of 3-BrPA sensitivity. MCT1 is necessary and sufficient for 3-BrPA uptake by cancer cells.

Systemic administration of 3-bromopyruvate in treating disseminated aggressive lymphoma This, to our knowledge, is the first report of the use of 3-BrPA in a systemic tumor model. Based on these data, 3-BrPA holds promise for treatment of systemic metastatic cancers.

How does the metabolism of tumour cells differ from that of normal cells Thus, we may assume an hypothesis: 3BP could kills the tumours cells by the following determinant factors: (1) increased amounts of MCT 1 may enhance the transport of the compound and produce lethal intracellular levels (Figure 2); (2) increased binding of mitochondrial HK binding to VDAC/ANT/FoF1ATP synthase would affect mitochondrial respiration and thus favour inhibition by 3BP; (3) by lowering the levels of GSH 3BP would not counteract the effects of ROS. Indeed it is known that 3BP is transported by MCT1 and that it acts simultaneously at distinct steps of ATP-producing enzymes, i.e. GA3PDH, 3PGK, PyK, MDH, PDH, GDH, SDH, but does not affect the enzymes that use ATP, i.e. mt-HK, PGI, PFK I and SERCA (sarcoplasmic/endoplasmic reticulum Ca2+-ATPase) [48]. Furthermore, small metabolite analogues of the energy metabolism of tumour such as 3BP are not good substrates for efflux pumps involved in the drug resistance of several tumour cell lines.

The Monocarboxylate Transporter Family€”Role and Regulation

Novel molecular mechanisms of antitumor action of dichloroacetate against T cell lymphoma: Implication of altered glucose metabolism, pH homeostasis and cell survival regulation DCA treatment also altered expression of HIF1-α and pH regulators: VATPase and MCT1 and production of cytokines: IL-10, IL-6 and IFN-γ

Targeting energy metabolism in colorectal cancer – a PhD thesis on DCA and 3BP influence on CRC

Targeting cancer metabolism: a therapeutic window opens

Glucose deprivation increases monocarboxylate transporter 1 (MCT1) expression and MCT1-dependent tumor cell migration

GLUTAMINE DEPRIVATION ENHANCES ANTITUMOR ACTIVITY OF 3-BROMOPYRUVATE THROUGH THE STABILIZATION OF MONOCARBOXYLATE TRANSPORTER-1

Deprive to kill Overall, our results identified the metabolic condition able to increase the selectivity of 3-bromopyruvate targets in neoplastic tissues, thereby providing a stage for its use in clinical settings for targeting malignancies and represent a proof of principle that modulation of glutamine availability can influence the delivery of monocarboxylic drugs into tumors.

Disclaimer:

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 learn on this road. https://www.cancertreatmentsresearch.com/?p=1735

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29 Comments on "3BP IV Administration Protocol and Treatment Strategy"

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LetterRip
Member

Could the recommendation in the protocol be referenced to the literature supporting the recommendation or other reasoning?

The first line of the recommendation contradicts its self (5 days a week vs every day). So is it every day or 5 on 2 off?
It would be nice to have a reasoning for particular blood tests – some are obvious, others are not.
The overview seems to contradict specific recommendations in the protocol itself (ie recommendation of not using antioxidants – then day 1 and day 5 having a vitamin C IV) .

LetterRip
Member

IV hydrogen peroxide – I’d be concerned with damage to red blood cells leading to hypoxia.

” Documents from the board indicate that the case involved a woman he treated who had nearly died from a precipitous drop in hemoglobin caused by intravenous infusions of ozone and hydrogen peroxide, which destroyed many of her red blood cells.”

http://www.quackwatch.com/11Ind/pittman.html

LetterRip
Member

Mention of B17 makes me rather questioning- laetrile/amygdilin/B17 is generally viewed to have no anticancer activity, what is the evidence suggesting it should be a part of the protocol?

“Laetrile has shown little anticancer activity in animal studies and no anticancer activity in human clinical trials.

The side effects associated with laetrile toxicity mirror the symptoms of cyanide poisoning, including liver damage, difficulty walking (caused by damaged nerves), fever, coma, and death.”

http://www.cancer.gov/about-cancer/treatment/cam/hp/laetrile-pdq

LetterRip
Member

Agreed that artensuate does seem reasonable to include in the protocol based on research into its action via anti VEGF

http://www.ncbi.nlm.nih.gov/pubmed/11251172

http://ar.iiarjournals.org/content/35/4/1929.short

LetterRip
Member

Curcumin also acts to inhibit VEGF, so agreed to have it as an alternative to artensuate makes sense.

http://www.ncbi.nlm.nih.gov/pubmed/18596194

If the goal is VEGF blockage/inihibition you might also consider drugs that doctors will be more familiar with such as Lenvatinib

http://www.ncbi.nlm.nih.gov/pubmed/25197551

LetterRip
Member

For ozone therapy – see the comment and concern above regarding hydrogen peroxide and ozone therapy causing RBC damage.

ALBERTO
Guest

Disagree, ozone is not causing any dammage in RBC. Indeed, major hameotherapy could be very benefit in cancer. You can increase the oxigenation and high concentration og H2O2 which cause kill cancer cells

LetterRip
Member

Alpha-lipoic acid is an antioxidant, again this seems to contradict the advice to avoid antioxidants.

https://umm.edu/health/medical/altmed/supplement/alphalipoic-acid

Also Sloan Kettering suggests there is no benefit to it in the treatment of cancer,

https://www.mskcc.org/cancer-care/integrative-medicine/herbs/alpha-lipoic-acid

It does damage/apoptosis of liver mitochondria at high doses – is that the intended effect?

http://www.ncbi.nlm.nih.gov/pubmed/24753992
http://www.ncbi.nlm.nih.gov/pubmed/15843897

Geoff Taylor
Guest

Question is Ethyl 3-Bromopyruvate acceptable?

Thanks
Geoff

Wray Whyte
Guest

Hi Daniel I’ve found your site remarkable in it’s thoroughness on 3BP. I’ve read every page, and written an email to Dr Ko to see if I can get some 3BP. Although I would appreciate knowing your source. My oncologist in Cape Town is supportive in helping me, although 3BP is not available in any clinic in South Africa. The main reason I’m writing this is regards to your donation page. I prefer to use my Visa card, but Paypal is not accepting the info I enter. I use the Visa card on a regular basis to buy goods, play the EU lottery, give a donation etc on the internet. I never have a problem unless Paypal is involved! Is there some other way I can pay you? Maybe an electronic transfer to your account from my RBS card in the UK? I would need your bank details to do this. Looking forward to hearing from you. Take care Wray

Sylvia Smith
Guest

Daniel,
I am considering this treatment for Stage IV ovarian that is currently stable. Any history this being used successfully? On a PET scan
I have 5 spots of increased SUV with Values of 3.5, 5.1, 5.3, 5.2 with the largest 8.2. I also have two areas of 1 X 2 cm and 2X 2 cm that are not reactive to PET scan but seem to stable since April. Do you think I am a reasonable candidate and is Dayspring Clinic in Scottsdale worth considering or any other options? I live in Florida. Thank you.

Saška Tomič
Guest

Dear Daniel, my father has cholangiocarcinoma with mets all over liver.
We managed to get 3BP, and the only way he can use it is orally. He weighs 95 kg, and we were told to give him 100 mg of 3 BP in 100 ml of water every 12h.
We were also told to put him on B17 (orally), pancreatic enzymes, iodine and vitamin D3. The doctor specifically told not to go for Vitamin C injections during 3BP. He also put him off of Artemisinin he was taking prior 3BP. He was also taking sylimarin, dandelion, curcumin and artichoke extracts for liver protection, and had to stop.
Everything I read here contradicts our doctor’s instructions.

Please suggest what shall we do. What oral supplements can he consume along with 3BP? Is there a chance of liver failure due to 3BP? Cancer covers 70% of his liver and hasn’t metastized to the other organs yet. Doctors gave him max 3 months of life. He is not ‘yellowing’ yet. He hasn’t been on any chemo or radiation.

Macarena Oliverio
Guest

Hello, thnaks for all the information.
Does anyone have succes by IV? My mom has metastasis and I wnats to know if this helps?

Thanks again!!

alternmed
Member

hi guys

just found this testimony on 3bp enemas

http://www.dayspringcancerclinic.com/3bp-cases/

anyone knows how to do it in enemas?

thanks