Overview

Our Studies Show the Potential for Cancer Inhibition Without Toxicity

SanRx's founder, Dr. Phillip Moheno, began studying active pterins several years ago. Pterin occurs naturally in humans and in animals and is an integral and necessary part of their biological function. Pterin is present in human cells, amniotic fluid, urine and other body fluids. Pterins give butterfly wings their color. Pterin, technically, is considered a vitamin though not one of the better known common 13 vitamins.

Dr. Moheno's studies led to the successful testing of pterin plus calcium in mice for inhibiting mouse mammary gland cancers. It was observed that pterin plus calcium favorably altered levels of certain immune system substances connected to human-like tumor growth in mice. No toxicity was observed in these mice at three times the therapeutic dose. Lowered IDO (indoleamine 2,3-dioxygenase) levels were also observed. High levels of IDO have been linked to tumor growth.

A Promising New Cancer Drug – DCP – Emerges

Subsequently, our very promising drug, DCP (dipterinyl calcium pentahydrate), was developed by Dr. Moheno and his team with the expectation that it would even improve on the results with pterin plus calcium. In mouse studies (mice with human like breast cancer tumors) with DCP performed by a reputable third-party laboratory, the results were dramatic. More favorable levels of IDO and cytokines connected with enhancing cancer immunity were observed. No toxicity was detected at three times the therapeutic dose of DCP. The study involved 12 mice. The mice administered DCP experienced highly significant (p < .0001) halting of tumor growth with DCP. Every one of the control mice receiving no DCP experienced significant tumor growth.

We believe that these mouse studies are unusually predictive of effectiveness in humans. Historically, mouse studies, where even a small statistically significant positive response was found, have led to useful and profitable drugs for human cancer therapies. In this case, there was a highly significant response, with the DCP-treated mice experiencing a strong halting of tumor growth. In addition, the immune mechanism tied to IDO, as it relates to tumor growth, appeared to be the same in humans and mice.

Increasing IDO Enhances the Immune System's Effectiveness Against Cancer

SanRx's data indicate that the likely mechanism of action of DCP is to inhibit action of the key immune system enzyme, IDO, which has been linked to immune response of T cells, B cells, Natural Killer cells and dendritic cells. Increased IDO levels allow cancer cells to escape destruction by the immune system. In a healthy immune system with normal levels of IDO, cancer cells are identified and destroyed by an immune system response. By therapeutically decreasing IDO levels in an abnormal immune system that has elevated IDO levels with DCP, the immune system's ability to destroy cancer cells is restored and enhanced. Increased IDO levels have been associated with the incidence of breast cancer, squamous cell carcinoma, lung cancer, uterine cancer, colorectal cancer, and melanoma.

Patents

Below is a list of the patents our Founder and Chief Scientist, Dr. Phillip Moheno, has submitted. To date three have been awarded.

  • Moheno, P. 2011. Novel pterin antineoplastic agents. Japanese Patent Registration
    No. 4780834.

  • Moheno P., Pfleiderer, W. 2010. Dipterinyl calcium pentahydrate (DCP) and therapeutic methods based thereon. United States Patent 7,662,820.

  • Moheno, P. 2002. Pterin antineoplastic agents. United States Patent 6,358,953.

  • Moheno, P. 1996. Anti-neoplastic compositions and methods for application thereof. United States Patent 5,534,514.

Publications

The following publications by SanRx have appeared in medical journals.

  • Nikoulina SE, Fuchs D and Moheno P. Effect of Orally Administered Dipterinyl Calcium Pentahydrate (DCP) on Oral Glucose Tolerance in DIO Mice. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy. 2012; in press.

    http://www.sanrx.com/documents/SanRxDCPDiabetesPaperRev2-020812.pdf

  • Moheno P, Morrey J, Fuchs D. Effect of dipterinyl calcium pentahydrate on hepatitis B virus replication in transgenic mice. J Transl Med. 2010 Mar 31;8(1):32. [Epub ahead of print] PubMed PMID: 20356392.

    http://www.translational-medicine.com/content/8/1/32

  • Moheno P, Pfleiderer W, Fuchs D. Plasma Cytokine Concentration Changes Induced by the Antitumor Agents Dipterinyl Calcium Pentahydrate (DCP) and Related Calcium Pterins. Immunobiology 2009;214:135-141.

    http://www.ncbi.nlm.nih.gov/pubmed/19167992

  • Moheno P, Pfleiderer W, Fuchs D. Plasma Cytokine Changes Induced by the Antitumor Agents Dipterinyl Calcium Pentahydrate (DCP) and Related Calcium Pterins. Pteridines 2008;19:49.

  • Moheno, P., Pfleiderer, W., Dipasquale, A. G., Rheingold, A. L., and Fuchs, D. Cytokine and IDO metabolite changes effected by calcium pterin during inhibition of MDA-MB-231 xenograph tumors in nude mice. International Journal of Pharmaceutics 2008;355:238-248.

    http://www.ncbi.nlm.nih.gov/pubmed/18272305

  • Moheno P, Winkler C, Pfleiderer W, Barral AM, Scuderi, R, Carlson J, Fuchs D. Mechanism of Action Studies with the Antitumor Agent Calcium-pterin. Pteridines 2007;18:50.

  • Winkler C, Schroecksnadel K, Moheno P, Meerbergen E, Schennach H, Fuchs D. Calcium-pterin suppresses mitogen-induced tryptophan degradation and neopterin production in peripheral blood mononuclear cells. Immunobiology 2006;211:779-784.

    http://www.ncbi.nlm.nih.gov/pubmed/17113915

  • Moheno PBB, Winkler C, Fuchs D, Ryan JC, Meerbergen EJ. Role of calcium pterin in natural killer (NK) cell activation and indoleamine 2,3-dioxygenase (IDO) modulation for antitumor activity. Pteridines 2005;16:140.

  • Moheno PBB. Calcium pterin as an antitumor agent. International Journal of Pharmaceutics 2004;271:293-300.

    http://www.ncbi.nlm.nih.gov/pubmed/15129997

  • Stea B, Backlund Jr. PS, Berkey (Moheno) PB, Cho AK, Halpern BC, Halpern RM and Smith RA. Folate and pterin metabolism by cancer cells in culture. Cancer Research 1978;38:2378-2384.

    http://cancerres.aacrjournals.org/content/38/8/2378.long