Procaine Turns-Off Telomerase And Destroys Cancerous Cells - A Potential New Treatment Of Cancer
Procaine is a drug that turns off telomerase, stops production of cancer cells & destroys the same. Procaine is a candidate for potential treatment of cancer.
Online, August 8, 2011 (Newswire.com)
In 1971 I started a company Rom-Amer Pharmaceuticals Ltd. in Los Angeles, intended to introduce on the American market Gerovital H3 (GH3) a buffered procaine drug developed by Ana Aslan, a Romanian Gerontologist, and intended to treat depression in an aged population. A few months before, as Assistant Research IV at the Dept. of Bacteriology UCLA, I discovered with the help of Medlar, UCLA's computer that procaine was a mono-amine oxidiaze inhibitor (MAOI), the mono-amine oxidiaze being the enzyme of depression.
Next I resigned my positions at UCLA and Cedars-Sinai Medical Center Los Angeles, and as "NIH Special Research Fellow", signed an exclusive contract with an appropriate Romanian authority to introduce GH3 in the US, raised $500,000 through a Reg A offering, thus Rom-Amer becoming a publicly traded company, and started preparing an Investigational New Drug Application (IND), the first step before going to the FDA, claiming GH3 to be a safe and effective drug in the treatment of depression in an 60+ population.
I then selected a team of researchers, to carry-on the pre clinical studies required in an IND. Among them was Earl J. Officer Ph D., Assistant Professor, Dept. of Pathology, University of Southern California (USC) whose lab was performing pre clinical studies on promising drugs, among them anti-cancer drugs, and gave him some samples of GH3. Two months later I was invited to his lab at USC where he showed me the results re: GH3. All his experiments were carried out in tissue culture settings, and using a mouse embryo fibroblast (MEF) the usual choice for carrying out pre clinical studies.
In his Experiment #1 he had grown a normal culture of MEF and shown that by adding GH3 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 type 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 multiplications 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 than told me that he never encountered this type of results before. Needless to say, I was very impressed, and more than that, and then the harsh reality took over and I told Earl that all my funds were tied up with the GH3/depression project. We were both very sad. Few days later Earl prepared an Abstract of his work titled: The Effects of Gerovital H3 on the growth rate of aged mouse embryo fibroblast on the pathogenesis induced by the RNA C-type virus (enclosed) and provided me with a full report of his experiments.
Earl sent 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. A few months later Earl Office had been killed in an accident when his bike was hit by a car. He was a talented researcher and a good friend.
INTERVIEW WITH CAROL W. GREIDER Ph.D. 2009 NOBEL PRIZE LAUREATE IN MEDECINE.
This interview took place on September 14, 2009 at Greider's office at the John Hopkins University, Department of Molecular Biology, Baltimore, MD. I came across this interview under very special circumstances when trying to find out if there are any other entities in the field of telomerase turn-off drugs. During this interview she was asked if she knew how to turn-off telomerase, and she said she does not know how but she said that she had submitted a grant application for $8mm, that she hoped, might help her find an answer. In reply to another question she said that Geron her former employer "Believes it has a experimental article called GRN 134, which inhibits telomerase expression in same pre clinical studies". Next, when she started making some remarks about her previous relations with Geron, I decided to send the whole interview to the Geron management. I realized that this interview took place 1 1/2 years ago, and many things have changed since, or she probably submitted a copy of this interview to Geron, but nevertheless I believe that it was my duty to inform Geron.
In sum, it seems to me that as on September, 2009, there was no drug experimental or on the market capable to turn telomerase off, and that in the present there is a race among some major companies looking to find this type of drug.
THE EFFECT OF GEROVITAL H3 ON THE GROWTH RATE OF AGED MOUSE EMBRYO FIBROBLASTS AND ON THE PATHOGENESIS INDUCED BY A RNA C-TYPE VIRUS.
J.E. Officer, Dept. of 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 generations. Infecting secondary MEF cultures with a wild mouse RNA C-type virus immediately impaired the growth rate and by the 5th transfer a morphologiclly altered cell with an infinite growth capacity appeared. Gerovital H3 (GH3) 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 GH3 was added to young cells (early passage). This effect was reveresed by increasing the CA++ concentration in the medium. When GH3 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 GH3 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.
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 on 2001 and 2002, 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.
That 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, plus also quoting the names of some of their collaborators, they 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 came back to my memory, it was Earl Officer who 40 years before, said the same thing after he presented to me, in 1972, the results of his experiments where he had shown, that procaine was able to turn-off, the unknown mechanism, that transformed normal cells into cancerous one, and then destroy them off.
I remember his face when I told him that I cannot finance his research on cancer because I committed all of them in the procaine US aging project. His final remark was "it is a pity, it could have been a new approach to treat cancer", and then a few months late he died in a tragic accident...
In the following weeks, I was frantically looking for his presentation "The Effect of Gerovital H3 on the growth rate of aged mouse "at" the Miami Beach 1974 Conference, also for the complete details of his experiments, and then deep in one box marked "1974" year, I found them all, a little bit yellowish but easily readable, all the details of his experiments then I put them face to face his 1972-74 document with the 2006 article regarding to telomerase and cancer. It looked 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".
The present situation and where do we go from here?
1. I have a drug that can stop the production of cancerous cells (including cancerous stem cells?) and destroy the existing one, leading to a potential treatment of cancer.
This is a tall statement, at a time when billions of dollars are being spent, to find an effective treatment of this disease. This is bound to elicit doubts, hostility and even the commiting of illegal acts, in order to get access to my technology.
Regarding the doubts and hostility matters, they can be dealt with by my providing both the protocal and vials of procaine to bonafide scientists working in the field of telomerase, as I am sure that the results obtained by them would confirm our results. Regarding the illegal activities, there are many already and range from being threatened with arrest, my wife being forcefully placed in a nursing home if I do not disclose certain results of my research on telomerase, also a break in at a storage place, where I keep some of my belongings, a vitriolic campaign against me carried out in Google and other media, framing me with some phony accusations, all intended to prevent me into releasing my research to the medical research media regarding the "taming" of telomerase. The man behind all these is an FDA agent, Douglas M. Loveland and I am not sure that his activities are approved by the FDA, or that they are for the FDA'S benefits. As such I sent a letter o Margaret A. Hamburg, M.D., Commisioner of the Food and Drug Administration (FDA), Rockville, MD, a paragraph which I am enclosing here within.
Margaret A. Hamburg, M.D.
Commissioner Food and Drug Administration (FDA)
Rockville, MD 20852-1448
The enclosed material would provide evidence that one of the FDA employees, a Mr. Douglas M. Loveland had used severe coersion on my wife Renee Sapse in order to have her pressure me into disclosing to Mr. Loveland certain information regarding my research.
Shortly after this happening my wife's mental and physical functions deteriorated rapidly, that led to a long and painful suffering and death March 30, 2010.
In reply to this letter I have received a positive reply from Dara A. Corrigan, FDA Associate Commissioner for Regulatory Affairs, and I am waiting to see the results. In the meantime where do we go from here? -
I know what I have, also I know that I cannot carry all this by myself. As such I am looking into forming a "think tank", with retired and semi-retired executives from a pharmaceutical and other companies, top business men, corporate lawyers familar with the U.S. and international law, top corporate CPA and the other necessary secretarial, communications and others.
Interested parties should submit a CV and other pertinent data via e-mail or fax, and I would reply ASAP.
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Alfred T. Sapse, M.D. (r)
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