Anticort A Procaine Based Drug In The Treatment Of A Patient With Incurable Cancer
Anticort is a drug intended for the treatment of incurable cancers, where all the other therapeutic means had been exhausted and the patient gave up treatment, but not yet ready for hospice and "end of life" solution.
Las Vegas, Nevada (I-Newswire) August 20, 2011 - Anticort is an anti-cortisol/cortisol modulator drug able to counterreact Cortisol, the immune suppressor “hormone of stress”, the cause or main cause of cancers. Procaine, the active ingredient of Anticort is also an effective telomerase turn off/inhibitor, able to stop a telomerase gone berserk from manufacturing a continuous line of immortal cancerous cells, and subsequently destroy them, thus preventing these cells from building cancerous tumors.
Procaine is also a safe and effective anti-depressant drug after going successfully through a number of Phase II double blind studies and hundreds of patients treated under FDA regulations.
Anticort subject to adequate financing can be on the market within six months, no FDA approval needed, in full compliance with the marketing of off-label drugs, and based upon my (ATS) 40+ years experience with procaine,it will induce favorable and more than that, results.
CORTISOL AS THE CAUSE. OR MAIN CAUSE OF CANCERS.
MEDICAL HYPOTHESIS 13:31-44, 1984
CORTISOL AS THE CAUSE OF “STRESS” DISEASES
Alfred T. Sapse, 802 N. Venetian Drive, Miami, Fl 33139, U.S.A.
CORTISOL AND CANCER
1. Cortisol (Hydrocortisone, 17-hydroxy corticosteroid, (17-OHCS) is a hormone secreted by the adrenal cortex.
The raw material for cortisol is the exogenous cholesterol, which in normal conditions accounts for 80% of the total cortisol production, 20% being synthesized by the adrenal cortex.
1.Elevated levels of cortisol precede diseases and do not follow them.
Cancer. In vivo studies carried out by Walker, et al. show that in two groups of mice treated with low and high doses of cortisol, on a long tern basis, 56% of the mice died of sarcomas in the low cortisol group, whereas 76% died of sarcoma in the high cortisol regimen group.
In humans, in a paper titled “Does Endogenous Cortisol Play a Role in the Development of Cancer?” Klein from the National Cancer Institute (NCI) had shown that human lymphocytes are capable of metabolizing cortisol, an immune suppressor, into metabolites devoid of immunosuppressive capabilities.
This cortisol metabolizing action is enhanced b a lymphocytic - cortisol - metabolism - enhancing factor (LCMEF) that Klein had identified in the plasma. Through elegant experiments, Klein was able to show that cortisol induced lymphopenia, and disappearance of the LCMEF precedes appearance of cancers. He concludes that the destruction by cortisol of these two immunoresistance agents opens the way for malignant cells to proliferate and form tumors.
Elevated levels of cortisol have been found in all types of cancers (11-12).
2. Pergamon, Psychoneuroendocrinology, Oxford, U.K., Vol. 22 (supplement) pp S3-S10,1997 ©1997 Elsevier Science Ltd.
CORTISOL, HIGH CORTISOL DISEASES AND ANTI-CORTISOL THERAPY
Alfred T. Sapse
Steroidogenesis Inhibitors, Inc. 2001 East Flamingo Road, Suite 100-B Las Vegas, NV 89119 USA
In this communication, evidence will be presented to support the concept that ‘high cortisol’ is a cause or major cause of diseases; and conversely, that anti-cortisol drugs, when used in same, have induced beneficial results ranging from good to very impressive.
ANTICORT is a high dose form of stabilized procaine HC1. The rationale of using procaine is as follows:
(1) Procaine may act as a non-specific immune-regulator (Jurjus et al.), 1988 by inhibiting lymphocyte proliferation and phagocytosis of latex particles by monocytes.
(2) It may also serve as an anti-cortisol, steroidogenesis inhibiting agent, as shown by Noguchi et al., (1990) in an in vitro setting.
Anticort is now being used in a pilot clinical study in Brazil, for HIV+ and AIDS populations. The results obtained so far are very satisfactory and were reported in July, 1996 at the XIth International Congress on AIDS Vancouver, Canada (Sapse et al., 1996)
Sapse, AT, de Moraes, HB, Bensabat, S and Mosman T (1996) A pilot clinical study on 60 HIV+ and, AIDS patients, treated with ANTICORT XIth International Conference on AIDS, Vancouver Canada, abstract WeB3199.
PROCAINE TURNS-OFF TELOMERASE AND DESTROYS CANCEROUS CELLS -
A POTENTIAL NEW TREATMENT OF CANCER
In 1972, I (ATS) provided a grant to Earl Officer, Ph.D, Assistant Professor, Dept. of Pathology, University of Southern California (USC) to look into claims, that procaine has anti-aging capabilities. Earl Officer’s lab was performing pre-clinical research on promising drugs, among then anti-cancer drugs. I gave him a few samples of procaine for testing and two months later he invited me in his lab, where he submitted to me a full report and an Abstract titled:
THE EFFECT OF A PROCAINE COMPOUND ON THE GROWTH RATE OF AGED MOUSE EMBRYO FIBROBLASTS AND ON THE PATHOGENESIS INDUCED BY A RNA– C-TYPE VIRUS,
J.E. Officer, Dept. Pathology, USC Medical Sch., Los Angeles.
The growth rate of NIH Swiss mouse embryo fibroblast (MEF) when cultured in a low serum (2%) medium, remains constant for 6 passages, then declines and ceases after 9-10 generation. Infecting secondary MEF cultures with a wild mouse RNA C-Type virus immediately impaired the growth rate and by the 5th transfer a morphologically altered cell with an infinite growth capacity appeared. Procaine at a final concentration of 0.5% significantly stimulated cell growth when added to aged cells (late passage) and, in addition, increased the number of cell passages. Cell multiplication was slowed down when procaine was added to young cells (early passage). This effect was reversed by increasing the CA++ concentrations in the medium. When Procaine was continuously maintained in the growth medium of virus infected cultures, a delaying in the time of appearance of the viral-induced altered cell type was noted. The data indicates that Procaine can significantly affect the growth rate of both aging and young cells, and the pathogenesis induced by a murine C-type virus MEF cell cultures.
Earl then asked me to authorize him to send this Abstract to the 26th annual Meeting of the Gerontological Society, Miami Beach, November 5-9, 1973, that was subsequently published in the “Theoretical Aspects of Aging, Edited by Morris Rockstein, and published in the Academic Press, Inc., New York, San Francisco, London, 1974.
In plain English his report, centers on four experiments, where he cultured mouse embryo fibroblasts (MEF), the usual choice for this type of experiments.
In Experiment #1 he had grown a normal culture of MEF and shown that by adding procaine to the culture the MEF normal life span, grew from seven to nine generations. This experiment was used as a control for the next experiments.
Experiment #2 when a culture of MEF was treated with a cancer inducing RNA C virus, the MEF started developing normally until the fifth generation, when suddenly the cells started multiplying chaotically, out of control and soon forming a continuous line, showing that the MEF cells as expected, became cancerous cells.
Experiment #3 when the cancerous cells above were treated with a solution of procaine, the cells multiplication stopped after 2-4 hours, they became vacuolated and after 24-48 hours they were lysed (disintegrated). Today we are using another term for this cell destruction phenomenon, namely apoptosis or programmed cell death.
Experiment #4 Normal MEF cells were treated first with a procaine solution and next with a cancer inducing RNA type C virus and nothing happened, the MEF cell developed normally and died at the ninth generation, suggesting that procaine had prevented the MEF cells to become cancerous.
Earl and myself were practically shocked by these extraordinary results, Earl telling me, that in his 10 + years experimenting with potential anti-cancer, he had never seen similar results. Incidentally his research had shown that procaine has some anti-aging capabilities at the celular level.
THE 2009 NOBEL PRIZE IN MEDICINE FOR THE DISCOVERY OF TELOMERASE
On October 2009, the media all over the US had announced that three US scientists, Elisabeth Blackburn, Jack Szotak and Carol W. Greider, have received the Noble Prize in Medicine for the discovery of telomerase, an enzyme that controls two of the most vital functions of the human life namely senescence and cancer. Shortly after, I had in my hands an article by Blackburn, Szotak and Greider, titled “Telomeres and Telomerase, the path from maize, Tetrahymena and yeast to human cancer and aging” published in Nature Medicine, Vol. 12, Number 10, Oct. 2, 2006 pages 1133-1338, the most comprehensive and updated account of this extraordinary discovery. I read many articles on telomerase before, as a matter of fact, my first discovery of the connection between procaine and aging, that was published in the medical press in 2001, was based upon articles on telomerase published during 1999’s, but my attention was focused on telomerase and aging, as such I didn’t pay any attention to articles on telomerase and cancer.
This all changed when I read the 2006 article, when I came across page 1136 with the updated information about “Telomerase and Cancer”, where the three authors of the article, also quoting the names of some of their collaborators, kept using the words “Telomerase Inhibition” as it might limit growth of cancer cells “or” as being an effective way to kill cancer cells “or” as being an effective way to kill cancer cells “or as” being effective in fighting particular types of cancer” and to top it off, I read a comment made by Goran Hansson, Member of the Noble Prize Commission for Medicine, who stated very simply “Telomerase is active in many cancers and if you turn-off, or destroy the cells, you could be able to treat cancer”. The last words “if you turned-off or destroy the (cancerous) cells, you could be able to treat cancer sounded vaguely familiar, I knew I heard them before, but where?, and suddenly a few days later, a flash lit up, and then I remembered that it was Earl Officer who 40 years before, used the same words when he presented to me, in 1972, the results of his experiments where he had shown, that procaine was able to turn-off, through an unknown mechanism, normal cells into cancerous one, and then destroy them.
In the following weeks, I was looking for his presentation “The Effect of Procaine on the Growth Rate of Aged Mouse” at the Miami Beach 1974 Conference, also for the complete details of his experiments, and, I found them all, a little bit yellowish but still easily readable, all the details of his experiments, then I put them face to face, his 1972-74 research with the 2006 article regarding telomerase and cancer, and it became obvious to me that Earl Officer provided an answer in 1974, to a question that would be posed 40 years later, that “Yes it was procaine that stopped and then killed the cancerous cells, or to use the 2006 language “yes it was procaine that inhibited telomerase”.
So, where do we go from here?
1. I wanted to know if there are any other “telomerase turn-off” projects or drugs of this type. From my search it resulted that there are none, However I found in an interview granted by one of the Nobel Prize winners, where, when she was asked if she knew how to turn-off telomerase, she said no, she does not know how, but, that she applied for an $8. MM. grant from the government, and hoped that this money might help her find one.
2. I am looking to put together a team, to start the process that I hope, it would see the drug in the market shortly. Interested bona fide individuals or entities in US and abroad please contact
Alfred T. Sapse, MD (r), 1701 E. Katie Ave., #20, Las Vegas, NV 89119
Tel (702) 241-4050, Cell (702) 353-2466, Fax (702) 451-0097
About Endogenous Stem Cell Activators, Inc
Medical Research & DevelopmentLess..
Endogenous Stem Cell Activators, Inc
Dr. Alfred Sapse
1701 E. Katie Ave., #20
Phone : 702-241-4050
Published On:August 20, 2011
Print Release:Print Release
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