3BP IV Administration Protocol and Treatment Strategy - Mihaela Catalina Stanciu Foundation For Life

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3BP IV Administration Search …
Protocol and Treatment

Strategy If you like,
please share
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. Login
Username
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 Password
elements may be combined.
Application Remember Me
– 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 Register
cycle. Preferably, perform 3 cycles. Lost Password
– 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 Help this
– Glutamine deprivation increases 3BP absorption (Ref. page 105-107, Ref2) –>
work to
1 of 20 3/12/2019, 11:46 PM
avoid red meet and use glutamine inhibitors (e.g. Phenylbutyrate); see also the
continue,
following: Ref.
– Glucose deprivation increases 3BP absorption (diet and e.g. Metformin) (Ref.) please Donate
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)
Recent
– Avoid antioxidants as much as possible, supplements and IVs (keep those that are Comments
essentials to protect organs, etc.) – alternatively, use strong anti oxidants
Manuone on
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, Jcancom on
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 Jcancom on
e.g. Myo-inositol TrisPyroPhosphate, Hydrogen Peroxide, EWOT, etc. If possible
go to hyperbaric chamber.
IV administration (this is just my idea) Jcancom on
Day 1: Daniel on
Optionally Ozone therapy or IV Hydrogen Peroxide (H2O2)

Administer 3BP IV as indicated here
johan on
Wait one hour for 3BP effectiveness
Administer high dose IV Vitamin C
Day 2: Jcancom on
Administer 3BP IV as indicated here or replace this with Salinomycin IV (see

Jcancom on
post on Salinomycin)
Day 3:
Optionally Ozone therapy or IV Hydrogen Peroxide (H2O2) Jcancom on

Day 4: Daniel on
Administer 3BP IV as indicated here or replace this with Salinomycin IV (see Atom on
post on Salinomycin)
Day 5: Caio Barcelona on
2 of 20 3/12/2019, 11:46 PM
Optionally Ozone therapy or IV Hydrogen Peroxide (H2O2) Daniel on

Wait one hour for 3BP effectiveness
Administer high dose IV Vitamin C
Daniel on
Note:
– administering oxygen during 3BP administration will help ZdenekSipek on
– 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 michellewood1 on
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. Daniel on Contact
– 3BP is not good substrates for efflux pumps involved in the drug resistance, less johan on
chance to develop resistence to 3BP due to MDRs (Ref.)
Supplements and Drug administration Manuone on
– administrate paracetamol (acetaminophen) 3x-4x/week, 1.5g to 3g/day

(Paracetamol can induce liver toxicity. It helps to reduce glutathione level and
johan on
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
Forum:
buy here
– If possible use 200mg/day Myo-inositol TrisPyroPhosphate under the tongue – a Recent Posts
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 manuone, I am so glad
– 150mg to 250mg Chloroquine daily – to inhibit autophagy that you are never fully
satisfie...
– Celecoxib 600mg/day – to inhibit angiogenesis By Jcancom, 2 days ago
– 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 Thanks for sharing the
info Daniel! I keep
well. thinking all...
By Manuone, 2 days ago
Others
Next to the above,

– use strategies to enhance the immune system
Researchers in Memorial
– use other anti-angiogenesis inhibitors such as Thalidomide, Tetrathiomolybdate, Sloan Kettering’s Brain
3 of 20 3/12/2019, 11:46 PM
Albendazole, Plerixafor in case we see strong anti-cancer response from 3BP or any Tumor C...
By Daniel, 3 days ago
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,

Curcumin2, 2DG, Glutamine Deprivation e.g. Phenyl Butyrate, Chloroquine, Pancreatic cancer (PC)
and glioblastoma
Paracetamol, Methyl Jasmonate, Fasting, Hypoglycemia, reduction in extracellular multiforme (GBM...
pH enhanced 3-BrPA uptake, Butyrate, Lactate, Ketosis, Exercise, By Daniel, 3 days ago
Testosterone, Acetazolamide, 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, Thank you for your
Disulfiram? answer Daniel! It might
be Digitalis...
– Strong anti oxidant supplements such as NAC (N-Acetyl Cysteine) By ZdenekSipek, 5 days
ago
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 Researchers at the
Columbia University
used with 3BP. College of Denta...
By johan, 6 days ago
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.
"What we found is if you
cripple perhaps the most
Relevant Literature signi...
By johan, 1 week ago
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
Background/Aim:
signaling promotes glutamine uptake and metabolism in oxidative cancer cells. It
Metronidazole (MNZ) is
depends on the uptake of extracellular lactate by monocarboxylate transporter 1 a common antibio...
By Daniel, 2 weeks ago
(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 Thanks a lot both!
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cells Oxygenated cancer cells have a high metabolic plasticity as they can use By Daniel, 2 weeks ago
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 Sunt convins ca te vei
known concerning the relationship between oxidative lactate metabolism and recupera.Stiu cat esti de
respon...
glutamine metabolism. Using SiHa and HeLa human cancer cells, this study reports By
that intracellular lactate signaling promotes glutamine uptake and metabolism in stefanjoita@yahoo.com, 2
weeks ago
oxidative cancer cells. It depends on the uptake of extracellular lactate by
monocarboxylate transporter 1 (MCT1). Lactate first stabilizes hypoxia-inducible
factor-2Î± (HIF-2Î±), and HIF-2Î± 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 Statistics
(GLS1), resulting in improved glutamine uptake and catabolism. Elucidation of this since August
metabolic dependence could be of therapeutic interest. First, inhibitors of lactate
uptake targeting MCT1 are currently entering clinical trials. They have the potential
2015
to indirectly repress glutaminolysis. Second, in oxidative cancer cells, resistance to Today's Visits:
glutaminolysis inhibition could arise from compensation by oxidative lactate
9
metabolism and increased lactate signaling. –> my conclusion: use glutamine
Today's Visitors:
inhibitors at the same time with 3BP, but start first with the administration of
5
glutamine inhibitors in order to potentially increase the balance towards oxidative
Total Visits:
lactate metabolism and as a result induce/increase sensitiveness to 3BP.
1,954,616
Total Visitors:
3-BrPA eliminates human bladder cancer cells with highly oncogenic signatures via
engagement of specific death programs and perturbation of multiple signaling and 671,218
metabolic determinants. Interestingly, MCT1- and macropinocytosis-mediated Total Comments:

influx of 3-BrPA in T24 represents the principal mechanism that regulates cellular 7,124
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 On Facebook
trafficking. Altogether, it seems that 3-BrPA represents a promising agent for
since 2019
bladder cancer targeted therapy.
The cytotoxicity of 3-bromopyruvate in breast cancer cells depends on extracellular MCS Foundation For
pH: At pH 6.0, the affinity of cancer cells for 3BP transport correlates with their 131 likes
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- Like Page
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].
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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.
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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.
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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 Î¼M 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
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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
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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-Î± and pH
regulators: VATPase and MCT1 and production of cytokines: IL-10, IL-6 and IFN-
Î³
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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10 of 20 3/12/2019, 11:46 PM
PROTOCOLS & STRATEGIES, TOP TREATMENTS 29 COMMENTS
← If TLS (Tumor lysis syndrome) Tetrathiomolybdate (TM) →

occurs
29 thoughts on “3BP IV Administration

Protocol and Treatment Strategy”
LetterRip
AUGUST 25, 2015 AT 4:32 AM
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) .
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Daniel
AUGUST 25, 2015 AT 7:48 PM
please have a look if it is still a contradiction – I meant each day Monday to

Friday and the weekends off.
I will add references in time but I had to make a choice, i.e. focus on putting
things together to have a complete protocol shared vs making a scientific story
(which I initially wanted to do). I decided to focus on the first since that is of
11 of 20 3/12/2019, 11:46 PM
value and not accessible today for most of us. The theory can be find in
multiple places but the application not. In time I will add references. But please
note that this is a result of both science and clinical experience of others which
is of higher value compared with the theory.
Blood tests: again no reasons was due to time limitation but here is a short
answer: main goal is to follow tumor evolution and TLS
LDH-reflection of glycolisis and tumor evolution but also reflection of TLS;
markers same as LDH;
all the others are meant to monitor TLS in case that happens
Vit C is acting as a pro oxidant at cellular level
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LetterRip
AUGUST 25, 2015 AT 6:34 AM
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
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Daniel
AUGUST 25, 2015 AT 7:50 PM
Thanks – very good point – agree that may happen if not done well – I know I
was speaking with some alternative doctors who had own techniques not to get
the damage – when I have time will search for the difference in administration
techniques
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LetterRip
AUGUST 25, 2015 AT 11:43 PM
Thanks, would be interested to see the research and reasoning.
12 of 20 3/12/2019, 11:46 PM
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LetterRip
AUGUST 25, 2015 AT 6:41 AM
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
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Daniel
AUGUST 25, 2015 AT 7:55 PM
this one is added based on clinical evidence on synergy

side effects associate with B17 are for oral administration, not IV
its anti cancer effects are debated but what is not debated today?
note that major alternative cancer clinics in Germany lead by major Univ Prof
are using B17 IVs
genetic labs such as RGCC show strong effectiveness of B17 against CTCs
from most patients (I have statistics demonstrating that)
yes, it seems that the source matters and in Germany there are some very good
sources but a bit expensive – 60 euro/6grams
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ALBERTO
APRIL 30, 2017 AT 11:55 AM
Dear Daniel, could you post or send me the information about B17 against
CTCs? Would be very helpful
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13 of 20 3/12/2019, 11:46 PM
Daniel
APRIL 30, 2017 AT 3:59 PM
Hi Alberto. I am not so convinced of B17 anymore as I know many

(including us) who use it without clear benefits regardless if from
Mexico or Germany. If I would still want to use it, I would do that
without heaving too much expectations. This is my current view, and it
may change if I will hear of positive results.
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LetterRip
AUGUST 25, 2015 AT 6:48 AM
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
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Daniel
AUGUST 25, 2015 AT 7:56 PM
not only anti VEGF but also pro oxidant due to the interaction with Fe which
can be found in large amounts in the cancer cells
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LetterRip
AUGUST 25, 2015 AT 6:51 AM
Curcumin also acts to inhibit VEGF, so agreed to have it as an alternative to

artensuate makes sense.
If the goal is VEGF blockage/inihibition you might also consider drugs that doctors
will be more familiar with such as Lenvatinib
14 of 20 3/12/2019, 11:46 PM
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LetterRip
AUGUST 25, 2015 AT 6:53 AM
For ozone therapy – see the comment and concern above regarding hydrogen
peroxide and ozone therapy causing RBC damage.
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Daniel
AUGUST 25, 2015 AT 7:57 PM
answered that
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ALBERTO
APRIL 30, 2017 AT 9:47 PM
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
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LetterRip
AUGUST 25, 2015 AT 6:59 AM
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
15 of 20 3/12/2019, 11:46 PM
effect?
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Daniel
AUGUST 25, 2015 AT 8:11 PM
increases O2 production by redirecting pyruvate inTO mito same as DCA:

alpha-Lipoic acid induces apoptosis in human colon cancer cells by increasing
mitochondrial respiration with a concomitant O2-*-generation.
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Geoff Taylor
APRIL 12, 2016 AT 5:45 PM
Question is Ethyl 3-Bromopyruvate acceptable?
Thanks
Geoff
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Daniel
APRIL 12, 2016 AT 8:40 PM
Ethyl 3-Bromopyruvate is NOT the same with what was used to treat people and in
most of the published studies.
3-Bromopyruvic acid is what was used. This chemical has its identity number CAS
1113-59-3.
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Wray Whyte
MAY 2, 2016 AT 4:20 PM
16 of 20 3/12/2019, 11:46 PM
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
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Daniel
MAY 2, 2016 AT 6:03 PM
Dear Wray, thank you for the kind words. I will let you know by email what is
my source but any major Western Supplier will be just as good. Regarding the
donation, you are one of the very few thinking about supporting this website
and I would like to thank you for that too. If you push the donate button there is
also an option in the lower-left corner stating “Don’t have a PayPal account”.
This should be an option to donate without having a PayPal account and they
seem to accept Visa too. If that is still not working, please let me know and I
will check what are the other options.
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Sylvia Smith
JUNE 11, 2016 AT 5:54 AM
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.
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17 of 20 3/12/2019, 11:46 PM
Daniel
JUNE 11, 2016 AT 11:59 AM
Dear Sylvia. The best is too check with dr. Jason Williams, after sending him the
history etc. If based on the documents, he says 3BP is the most suitable option, I
would indeed go for Dayspring as they are the best world wide on 3BP. I hope this
helps.
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Saška Tomič
AUGUST 2, 2016 AT 1:26 PM
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.
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Daniel
AUGUST 2, 2016 AT 1:52 PM
Dear Saska, I am sorry to hear about your challenges. I cannot suggest anything
else other than to follow your doctor. Next to that, a relevant idea could also be
to check with Prof. Vogl at Frankfurt University and see if he can help your
father. He is using TACE and with that he can administer chemo so that it only
targets the liver. The technique can be very effective and has helped many
people. Just check on Google and you will find his contact details. I hope this
helps.
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18 of 20 3/12/2019, 11:46 PM
Macarena Oliverio
JUNE 22, 2017 AT 4:45 AM
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!!
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alternmed
JUNE 24, 2017 AT 2:19 AM
hi guys
just found this testimony on 3bp enemas
http://www.dayspringcancerclinic.com/3bp-cases/
anyone knows how to do it in enemas?
thanks
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Daniel
JULY 1, 2017 AT 12:53 AM
Thank you for pointing this out Alternmed!
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HOME TREATMENTS BY MECHANISM VISITOR STORY

CANCER TREATMENT CLINICS NEWS & OTHERS FORUM

POSTED ON AUGUST 23, 2015 BY DANIEL

Protocol and Treatment

IV administration (this is just my idea) Jcancom on

Optionally Ozone therapy or IV Hydrogen Peroxide (H2O2)

Administer 3BP IV as indicated here or replace this with Salinomycin IV (see

Optionally Ozone therapy or IV Hydrogen Peroxide (H2O2) Jcancom on

Day 5: Caio Barcelona on

Optionally Ozone therapy or IV Hydrogen Peroxide (H2O2) Daniel on

Supplements and Drug administration Manuone on

– administrate paracetamol (acetaminophen) 3x-4x/week, 1.5g to 3g/day

Next to the above,

A short list of Synergy, Complementary or Supporting elements: Curcumin,

Testosterone, Acetazolamide, Citrate, Citrate2, Rapamycin

Do not use the following antagonists:

Great presentation on Monocarboxylate Transporters: http://www.njacs.org/wp-

The effect of 3-bromopyruvate on human colorectal cancer cells is dependent on

metabolic determinants. Interestingly, MCT1- and macropinocytosis-mediated Total Comments:

responsiveness to the drug. Besides its capacity to affect transcription in gene-

3-bromopyruvate inhibits glycolysis, depletes cellular glutathione, and

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

Hexokinase II inhibitor, 3-BrPA induced autophagy by stimulating ROS formation

Local delivery of cancer-cell glycolytic inhibitors in high-grade glioma: The

Inhibition of glucose turnover by 3-bromopyruvate counteracts pancreatic cancer

Monocarboxylate transporters as targets and mediators in cancer therapy

Glycolysis inhibition and its effect in doxorubicin resistance in

Mitochondria: 3-bromopyruvate vs. mitochondria? A small molecule that attacks

Transport of 3-bromopyruvate across the human erythrocyte membrane: 3-BP

Safety and outcome of treatment of metastatic melanoma using 3-bromopyruvate: a

Killing multiple myeloma cells with the small molecule 3-bromopyruvate:

Effect of 3-bromopyruvic acid on human erythrocyte antioxidant defense

Regulation of the proliferation of colon cancer cells by compounds that affect

Anticancer efficacy of the metabolic blocker 3-bromopyruvate: specific molecular

Glycolysis inhibitors as a potential therapeutic option to treat aggressive

D-Amino acid oxidase-induced oxidative stress, 3-bromopyruvate and citrate

Glutamine deprivation enhances antitumor activity of 3-bromopyruvate through the

EPR oxygen imaging and hyperpolarized 13C MRI of pyruvate metabolism as

Aerosolized 3-bromopyruvate inhibits lung tumorigenesis without causing liver

3-Bromopyruvate inhibits calcium uptake by sarcoplasmic reticulum vesicles but

A translational study “case report” on the small molecule “energy blocker”

Flow cytometric evaluation of the effects of 3-bromopyruvate (3BP) and

3-Bromopyruvate antagonizes effects of lactate and pyruvate, synergizes with

Transport by SLC5A8 with subsequent inhibition of histone deacetylase 1

MCT1-mediated transport of a toxic molecule is an effective strategy for targeting

Systemic administration of 3-bromopyruvate in treating disseminated aggressive

The Monocarboxylate Transporter Family€”Role and Regulation

Novel molecular mechanisms of antitumor action of dichloroacetate against T cell

Targeting cancer metabolism: a therapeutic window opens

Glucose deprivation increases monocarboxylate transporter 1 (MCT1) expression

GLUTAMINE DEPRIVATION ENHANCES ANTITUMOR ACTIVITY OF

PROTOCOLS & STRATEGIES, TOP TREATMENTS 29 COMMENTS

← If TLS (Tumor lysis syndrome) Tetrathiomolybdate (TM) →

29 thoughts on “3BP IV Administration

Could the recommendation in the protocol be referenced to the literature supporting

please have a look if it is still a contradiction – I meant each day Monday to

Thanks, would be interested to see the research and reasoning.

Mention of B17 makes me rather questioning- laetrile/amygdilin/B17 is generally

this one is added based on clinical evidence on synergy

Hi Alberto. I am not so convinced of B17 anymore as I know many

Curcumin also acts to inhibit VEGF, so agreed to have it as an alternative to