Dr Stanislaw BURZYNSKI

8/6/2019 Dr Stanislaw BURZYNSKI

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rexresearch.comrexresearch.comRex Research, POB 19250, Jean,Rex Research, POB 19250, Jean,NV 89019 USANV 89019 USA


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Dr Stanislaw BURZYNSKIDr Stanislaw BURZYNSKI

Antineoplaston TherapyAntineoplaston Therapy


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Antineoplaston (ANPAntineoplaston (ANPAntineoplastonsAntineoplastons is a name coined byis a name coined by

Stanislaw Burzynski for a group ofStanislaw Burzynski for a group ofpeptides, derivatives, and mixtures forpeptides, derivatives, and mixtures forwhich he claims antiwhich he claims anti--cancer activity.cancer activity.

These compounds have beenThese compounds have been

administered by Burzynski to canceradministered by Burzynski to cancerpatients since 1976.patients since 1976.


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The clinical efficacy of antineoplastonsThe clinical efficacy of antineoplastonscombinations for various diseases are thecombinations for various diseases are the

current subject of numerous FDA Phase IIcurrent subject of numerous FDA Phase IItrials by Burzynski and his associates.trials by Burzynski and his associates.

Antineoplastons are manufactured at aAntineoplastons are manufactured at afacility in Stafford, Texas for investigationalfacility in Stafford, Texas for investigational

use by the Burzynski Clinic, a publicuse by the Burzynski Clinic, a publiccompany that trades as a penny stock oncompany that trades as a penny stock onthe OTC Bulletin Board (BZYR)the OTC Bulletin Board (BZYR)


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BackgroundBackground

In 1967 Stanislaw Burzynski beganIn 1967 Stanislaw Burzynski beganinvestigating the use of antineoplastons afterinvestigating the use of antineoplastons afternoting significant peptide deficiencies in thenoting significant peptide deficiencies in the

blood of cancer patients as compared with ablood of cancer patients as compared with acontrol group[1][1].control group[1][1].

Burzynski first identified antineoplastons fromBurzynski first identified antineoplastons fromhuman blood.human blood.

Since similar peptides had been isolated fromSince similar peptides had been isolated fromurine, in 1970 Burzynski initially purified urineurine, in 1970 Burzynski initially purified urineas a bulk source of antinoeplastons.as a bulk source of antinoeplastons.


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Since his initial discovery, BurzynskiSince his initial discovery, Burzynskihas isolated dozens of peptide andhas isolated dozens of peptide andderivatives, some of which have beenderivatives, some of which have beenreportedly found to be active againstreportedly found to be active againstcancer with low toxicity.cancer with low toxicity.

Since 1980 he has been reproducingSince 1980 he has been reproducinghis compounds synthetically.[2]his compounds synthetically.[2]


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The first active peptide fraction identifiedThe first active peptide fraction identifiedwas called antineoplaston Awas called antineoplaston A--10 (310 (3--

phenylacetylaminophenylacetylamino--2,62,6--piperidinedione).piperidinedione). From AFrom A--10, antineoplaston AS210, antineoplaston AS2--1, a 4:11, a 4:1

mixture of phenylacetic acid andmixture of phenylacetic acid andphenylacetylglutamine, was derived [3]. Thephenylacetylglutamine, was derived [3]. The

active ingredient of antineoplaston A10active ingredient of antineoplaston A10--I isI isphenylacetylglutamine [4].phenylacetylglutamine [4].


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Phenylacetic acid is a toxic compoundPhenylacetic acid is a toxic compoundthat the body produces during normalthat the body produces during normal

metabolism.metabolism.

It is detoxified in the liver toIt is detoxified in the liver tophenylacetyl glutamine.phenylacetyl glutamine.


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The "antineoplaston AThe "antineoplaston A--10" compound10" compoundis an isolation artifact resulting fromis an isolation artifact resulting from

heating the urine under acidicheating the urine under acidicconditions.conditions.

The "antineoplaston AS2The "antineoplaston AS2--1" mixture is1" mixture is

the result of an alkaline hydrolysis ofthe result of an alkaline hydrolysis of"antineoplaston A"antineoplaston A--10". All compounds10". All compoundsare widely available cheap chemicals.are widely available cheap chemicals.


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TreatmentTreatment

For legal reasons Burzynski currently sells hisFor legal reasons Burzynski currently sells histreatments only in the context of clinical trials.treatments only in the context of clinical trials.

Patients receiving cancer treatment withPatients receiving cancer treatment with

antineoplastons must first qualify for one of theantineoplastons must first qualify for one of thecurrently available clinical trials.currently available clinical trials.

In order to qualify for most of the trials, aIn order to qualify for most of the trials, apatient must have first failed standardpatient must have first failed standard

treatment for the condition being treated, or ittreatment for the condition being treated, or itmust be a condition that is unlikely to respondmust be a condition that is unlikely to respondto currently available therapy and for which noto currently available therapy and for which nocurative therapy exists.curative therapy exists.


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Antineoplastons may be administeredAntineoplastons may be administeredintravenously or orally.intravenously or orally.

Patients who respond positively to initialPatients who respond positively to initialtreatment with intravenous antineoplastonstreatment with intravenous antineoplastonssometimes transition to the oral form.sometimes transition to the oral form.

Intravenous antineoplastons areIntravenous antineoplastons areadministered continuously with a portableadministered continuously with a portableprogrammable pump that the patient carriesprogrammable pump that the patient carrieson a shoulder strap in a canvas bag.on a shoulder strap in a canvas bag.


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The "antineoplastons," naturalThe "antineoplastons," naturalpeptides and metabolites, are notpeptides and metabolites, are not

generally cytotoxic like many historicalgenerally cytotoxic like many historical(and current) antineoplastic agents;(and current) antineoplastic agents;rather the highest usage levels carry arather the highest usage levels carry a

very high sodium load that requirevery high sodium load that requirecareful attention to fluid andcareful attention to fluid andelectrolyte balance.electrolyte balance.


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Burzynski suggests that antineoplastons A10Burzynski suggests that antineoplastons A10and AS2and AS2--1 both work by inhibiting1 both work by inhibiting

oncogenes, promoting apoptosis, andoncogenes, promoting apoptosis, andactivating tumor suppressor genes [4].activating tumor suppressor genes [4].

Several other mechanism of action haveSeveral other mechanism of action havebeen proposed.been proposed.

One of the factors that allows some cancersOne of the factors that allows some cancersto grow out of control is the presence ofto grow out of control is the presence ofabnormal enzymes, a byproduct of DNAabnormal enzymes, a byproduct of DNAmethylation.methylation.


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In the presence of these enzymes, theIn the presence of these enzymes, thenormal life cycle of the cells is disrupted andnormal life cycle of the cells is disrupted andthey replicate continuously.they replicate continuously.

Antineoplastons have been shown in theAntineoplastons have been shown in thelaboratory to inhibit these enzymes [8].laboratory to inhibit these enzymes [8].

Recent studies have shown that inhibitingRecent studies have shown that inhibitinghistone deacetylase (HDAC) promotes thehistone deacetylase (HDAC) promotes the

activation of tumor suppressor genes p21activation of tumor suppressor genes p21and p53. Phenylacetic acid contained in theand p53. Phenylacetic acid contained in theAS2AS2--1 mixture has been shown to be a1 mixture has been shown to be aweak HDAC inhibitor[9].weak HDAC inhibitor[9].


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ReferencesReferences 1. ^ Burzynski SR (1986). "Antineoplastons: history of the research1. ^ Burzynski SR (1986). "Antineoplastons: history of the research(I)". Drugs under experimental and clinical research 12 Suppl 1: 1(I)". Drugs under experimental and clinical research 12 Suppl 1: 1

9. PMID 3527634.9. PMID 3527634.2. ^ Ralph Moss (1996), The Cancer Industry ISBN 18810250982. ^ Ralph Moss (1996), The Cancer Industry ISBN 18810250983. ^ NCI Drug Dictionary, Definitions of antineoplastons A10 and3. ^ NCI Drug Dictionary, Definitions of antineoplastons A10 and

AS2AS2--114. ^ a b S.R. Burzynski, The Proposed Mechanism of Antitumor4. ^ a b S.R. Burzynski, The Proposed Mechanism of Antitumor

Activity of Antineoplastons (ANPs) in High Grade Glioma PathologyActivity of Antineoplastons (ANPs) in High Grade Glioma Pathology(HBSG) Integrative Cancer Therapies 2006; 40(HBSG) Integrative Cancer Therapies 2006; 40--47475. ^ Aetna Clinical Policy Bulletin, Antineoplaston Therapy and5. ^ Aetna Clinical Policy Bulletin, Antineoplaston Therapy andSodium PhenylbutyrateSodium Phenylbutyrate6.^ Blue Cross/Blue Shield Medical Policy, Antineoplaston Therapy6.^ Blue Cross/Blue Shield Medical Policy, Antineoplaston Therapy7.^ Burzynski SR (1999). "Efficacy of antineoplastons A10 and AS27.^ Burzynski SR (1999). "Efficacy of antineoplastons A10 and AS2--1". Mayo Clin. Proc. 74 (6): 6411". Mayo Clin. Proc. 74 (6): 6412. PMID 10377942.2. PMID 10377942.

8.^ Liau MC, Burzynski SR (1986). "Altered methylation complex8.^ Liau MC, Burzynski SR (1986). "Altered methylation complexisozymes as selective targets for cancer chemotherapy". Drugsisozymes as selective targets for cancer chemotherapy". Drugsunder experimental and clinical research 12 Suppl 1: 77under experimental and clinical research 12 Suppl 1: 7786. PMID86. PMID3743383.3743383.9.^ Jung M (2001). "Inhibitors of histone deacetylase as new9.^ Jung M (2001). "Inhibitors of histone deacetylase as newanticancer agents". Curr. Med. Chem. 8 (12): 1505anticancer agents". Curr. Med. Chem. 8 (12): 150511. PMID11. PMID11562279.11562279.


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National Cancer InstituteNational Cancer Instituteat the National Institutes of Healthat the National Institutes of Health

Studies of Specific MalignanciesStudies of Specific MalignanciesTreated with AntineoplastonsTreated with Antineoplastons

Last Modified:Last Modified: 09/17/201009/17/2010


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Prostate cancerProstate cancer

A phase II clinical trial using antineoplastonA phase II clinical trial using antineoplastonAS2AS2--1 in conjunction with low1 in conjunction with low--dosedose

diethylstilbestroldiethylstilbestrol(DES) was conducted by(DES) was conducted bythe developer and his associates in 14 patientsthe developer and his associates in 14 patientswith hormonallywith hormonally refractoryrefractory prostateprostatecancercancer.[.[1717]]

Thirteen patients were diagnosed withThirteen patients were diagnosed with stagestageIV prostate cancerIVprostate cancer, and one patient was, and one patient wasdiagnosed withdiagnosed with stage IIprostate cancerstage IIprostate cancer..

Ages ranged from 54 to 88 years.Ages ranged from 54 to 88 years.


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Previous therapy includedPrevious therapy included prostatectomyprostatectomy,,orchiectomyorchiectomy, radiation therapy, and treatment, radiation therapy, and treatmentwith DES,with DES, luteinizinghormoneluteinizinghormone--releasingreleasing

hormonehormone (LHRH) agonists,(LHRH) agonists, flutamideflutamide,,aminoglutethimideaminoglutethimide, and, and immunotherapyimmunotherapy..

Patients all showed disease progression after initialPatients all showed disease progression after initialresponse to treatment.response to treatment.

During the study, all 14 patients received oral AS2During the study, all 14 patients received oral AS2--1 in doses ranging from 97 to 130 mg/kg daily and1 in doses ranging from 97 to 130 mg/kg daily andDES in doses ranging from 0.01 to 0.02 mg/kgDES in doses ranging from 0.01 to 0.02 mg/kgdaily.daily.


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Patients exhibited few significant sidePatients exhibited few significant sideeffects.effects.

Overall, there were two completeOverall, there were two completeremissions, three partial remissions,remissions, three partial remissions,seven cases of stable disease, and twoseven cases of stable disease, and twocases of disease progression.cases of disease progression.

All patients were known to be alive 2All patients were known to be alive 2years after the beginning of the study.years after the beginning of the study.


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The two patients who showed diseaseThe two patients who showed diseaseprogression discontinued AS2progression discontinued AS2--11

treatment.[treatment.[1717]]

The use of DES in conjunction withThe use of DES in conjunction withAS2AS2--1 is a confounding factor in1 is a confounding factor in

interpreting any results of tumorinterpreting any results of tumorresponse.response.

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Dr Stanislaw BURZYNSKI