Our Targeted Peptide Technology, or TPT, targets the body’s immune cells and seems to explain the mechanism behind some autoimmune diseases while presenting a possible solution.

Our Targeted Peptide Technology, or TPT, targets the body’s immune cells and seems to explain the mechanism behind some autoimmune diseases while presenting a possible solution. Our current, second generation TPT compound is called VG1177.

Autoimmune diseases occur when the immune system attacks the body’s own cells, mistaking them for pathogens. In some cases, this confusion can arise from an initial infection, where the pathogen possesses antigens similar to tissue in the body. Additionally, the immune system can be activated non-specifically, that is, it mounts a chronic inflammatory response without a target. When non-infected, healthy self-cells are inappropriately targeted by the immune system, the resulting conditions, effects, and symptoms are termed chronic inflammatory and autoimmune diseases.

“We expect our TPT drug compounds to enable the body to destroy the cells that help trigger the symptoms of autoimmune diseases.”

Certain molecular patterns displayed on all cell surfaces allow the immune system to distinguish self from non-self cells as well as healthy cells from infected cells. When a given cell displays a non-self molecular pattern, that pattern alerts the immune system to the presence of pathogen(s) and provides an identity of the pathogen(s). This recognition of foreign markers initiates an immune response: acute inflammation followed by targeted destruction of invaders and of compromised self-cells.

Certain cells in the body ingest foreign, damaged or infected cells and then produce a receptor on the cells surface, called Major Histocompatibility Complex II, or MHC-II receptor. The MHC-II receptor allows other immune cells, called T-cells, to identify the foreign, damaged or infected cell and cause the cell’s death, eliminating the threat and stopping the immune response.

Our research indicates that the self-peptide called Class II-associated invariant chain peptide, or CLIP, can fit into MHC-II receptors, preventing T-cells from recognizing the MHC-II receptor and cause cell death. This prolongs a chronic, non-specific immune activation. Our research also indicates that these CLIP+ immune cells have increased pro-inflammatory characteristics.

We believe TPT can work by displacing the “armor” of CLIP from its place in an extracellular MHC-II receptor. We believe VG1177 will out-compete CLIP for the MHC-II groove because it is designed to have a higher binding coefficient than CLIP, effectively displacing CLIP and producing the desired anti-inflammatory therapeutic effect.

TPT, in a general sense, is related to discovering receptor-mediated pathways, pathways that can be found using receptors that other cells can bind to and designing peptides that can augment how those receptors function. These peptides, synthesized by our research team, have been engineered to work nearly universally in everyone’s MHC-II receptors. We expect our TPT drug compounds to enable the body to destroy the cells that help trigger the symptoms of autoimmune diseases.

We also believe that various other conditions, such as traumatic brain injury, hypertension, preeclampsia, glioblastoma, Type I and Type II diabetes, Lyme disease, Crohn’s disease, ulcerative colitis, lymphedema, staphylococcus, streptococcus, and sepsis infection, multiple sclerosis, transplant rejection, and Pediatric Autoimmune Neuropsychiatric Disorders (PANDAS) may be treatable using TPT.

Cancer tumors have a “greed” for glucose, and the selective use of amino acids, and/or fatty acids as sources of energy. MDT disrupts the pathways involved in the cancer cell’s ability to meet those survival requirements. Therefore, the cancer cells become more vulnerable to other cancer treatments.

Our Metabolic Disruption Technology, or MDT, program may be used in combination with a variety of existing drugs and compounds to treat drug resistant cancers. MDT compounds manipulate target cells’ methods for obtaining the energy they need to function, weakening the drug resistant cancer cells so that the cancer cells are more sensitive to the cancer treatment.

Cancer tumors have a “greed” for glucose, and the selective use of amino acids, and/or fatty acids as sources of energy. MDT disrupts the pathways involved in the cancer cell’s ability to meet those survival requirements. Therefore, the cancer cells become more vulnerable to other cancer treatments.

We believe a growing body of research indicates that interfering with cell metabolism could be the key to targeting cancer cells. Our research shows the way a cell metabolizes its sources of energy appears to determine whether it will survive the most common treatments for cancer chemotherapy and radiation. Cells that rely on glucose or sugar for fuel are easily damaged and killed. Cells that can change their metabolic strategy to use lipids can become deadly. They continue to survive and even thrive during cancer treatments, thereby assisting in the development of drug resistant tumors that can become lethal to their victims.

Every cell in the body produces, consumes, and stores energy using a distinct metabolic strategy to perform its normal functions. Each cell can use carbohydrate, protein, or fat in different proportions to insure that the cell has sufficient energy. The cell’s choice of fuel, i.e. the cell’s metabolic strategy, will change depending on its activation or differentiation state as well as its environment. For example, a cell that is dividing has different energy demands than one that is non-dividing and, thus, must employ an alternative metabolic strategy.

“…the consequences are two-fold: the cancer cells can no longer generate energy needed to survive and the disruption of the intracellular energy levels reduces their ability to repair damage from other cytotoxic agents, resulting in a much greater sensitivity to chemotherapy and radiation.”

Due to the fact that, in general, cancer cells grow very rapidly, cancer cells have very high energy demands. We have learned that some of the mechanisms the tumor cells use to meet their energy demands are unique to the tumor cell and are not used by normal cells, suggesting that those specific pathways could make clinically relevant therapeutic targets. As a result, our research now indicates that when the tumor cells’ specific energy strategies are interrupted with “metabolic disrupting” agents, the consequences are two-fold: the cancer cells can no longer generate energy needed to survive and the disruption of the intracellular energy levels reduces their ability to repair damage from other cytotoxic agents, resulting in a much greater sensitivity to chemotherapy and radiation.

Tumor cells exhibit at least two generalizable metabolic features that we have chosen as selective targets: high rate glycolysis, which is the process of breaking down glucose to smaller carbon-containing units in the intracellular fluid of the cell, and fatty acid oxidation, the process of breaking fats down to smaller carbon containing units in the cell’s powerhouse, the mitochondria. The preferential use of fatty acid oxidation in drug resistant cells is a particularly important focus of our therapeutic strategy because drug resistance, either acquired through drug treatment or inherent drug resistance, is the leading cause of death for cancer patients. For all of these reasons, our initial clinical compounds are comprised of pharmaceutical compositions that interfere with various aspects of high rate glycolysis and fatty acid oxidation.

Our research indicates that we are capable of interfering with the metabolic strategy of both drug sensitive and multi-drug resistant tumor cells. Our studies both in vitro and in tumor-bearing mice have demonstrated a lack of toxicity and impressive therapeutic activity of some compounds in multi-drug resistant cancer cells and an even more potent effect on both drug sensitive and drug resistant tumor cells when used in combinations. In addition, certain compounds have striking therapeutic activity in tumor-bearing mice when used together, or in conjunction with, standard chemotherapy.

Doctors at Scott & White Healthcare in Temple, Texas, and the Cancer Therapy and Research Center at the University of Texas at San Antonio, are conducting a Phase I Physician’s IND trial, for patients with solid tumors utilizing an MDT compound, called hydroxychloroquine, in combination with an existing cancer drug, called sorafenib, which is marketed as Nexavar®. Our MDT trials initially were only for ovarian cancer, but have since expanded to include other solid tumors, including those located in the breast, colon, liver, lung, and pancreas.

MDT Compound for Drug Resistant Cancer called Hydroxychloroquine
Hydroxychloroquine is a MDT compound that can be used, in combination with other cancer drugs, such as sorafenib, which is marketed as Nexavar ®, to treat drug resistant cancer. We hold a license to a pending patent application for the combination treatment. Our Physician-IND Phase I Study is testing the tolerability and toxicity of our patented technology in patients with advanced stage solid tumors. The study, which is ongoing in patients with solid tumors that do not respond to treatment or have returned after a period of improvement, examines the safety and efficacy of hydroxychloroquine, or HCQ, in combination with sorafenib, marketed as Nexavar®, which was co-developed by Bayer AG and Onyx Pharmaceuticals.

The study is designed with four cohorts, three cycles of administration in each cohort and four different patients in each cohort. Thus there are 16 total patients targeted to complete the trial. Sorafenib and HCQ are FDA approved and thus the study is testing the drugs in combination for safety and toxicity. The dosing for each cohort is as follows:

COHORT # SORAFENIB HCQ
1 400 mg 200 mg
2 600 mg 200 mg
3 800 mg 200 mg
4 800 mg 400 mg

As a Physician’s IND Phase I study, the investigators are primarily testing for safety, but are also testing for efficacy in reducing tumor mass or stunting tumor growth.

  • No patients have been dropped from the study for toxicity.
  • The primary investigator reported two clinical responses in cohort number 3 with four months of disease stabilization in a patient with metastatic ovarian cancer, which has spread throughout portions of the body, and five months of disease stabilization in a patient with triple-negative breast cancer, which is a type of cancer that does not express three genes that are key to traditional cancer treatment, making treatment more difficult.
  • The final patient in cohort number 3 has stage IV, or metastatic, adenocarcinoma of the lung, which is a common form of lung cancer, and has four separate lung lesions. During the course of the study, the four lesions have all regressed about 20% in size.

This study is being conducted at the Cancer Therapy and Research Center at the University of Texas Health Sciences Center at San Antonio. The primary investigator is medical oncologist Dr. Tyler Curiel, M.D., MPH and is based on the research of Dr. M. Karen Newell-Rogers, PhD, our Chief Scientific Advisor. In March 2014, the University of Texas Data Safety Monitoring Committee approved an expansion to cohort number 4. In the final cohort, the trial is at maximum sorafenib plus maximum HCQ. Cohort number 4 has enrolled the first 3 patients.

VG Life Sciences is in discussion with the University of Texas regarding the feasibility of expanding the study into a Phase II or an extended Phase I P-IND. This would involve using combination therapy dosing over a 1 year period to test for efficacy.

Make an Investment

Opportunities for purchasing stock in VG Life Sciences exist currently through traditional and discount brokerages, such as Charles Schwab, Scottrade, E*TRADE, TD Ameritrade, Fidelity, Merrill Edge, ShareBuilder, and more. Additional opportunities exist for institutional and accredited investors to support key phases of VG Life Sciences’ TPT and MDT pre-clinical and clinical trials.

Institutional and accredited investors interested in these opportunities should email investors@vglifesciences.com with a subject line of “Accredited Investor” for additional information.

For shareholder convenience, we have included a current quote, information regarding restricted stock, and links to SEC filings and discourses.


Quote

  • Stock VGLS $0.0959-0.0011 -1.13%
Chart of VGLS

Restricted Stock

Shareholders who hold physical certificates and want to have the restrictive legend removed and deposit their shares into a brokerage account can find information how to do so here. To deposit shares into a brokerage account, the shares must generally be free-trading and have no restrictions placed on them.

Please open and read the links below for additional step-by-step instructions. Once the restriction is removed, your broker will arrange for the shares to be deposited to your brokerage account.

“VGLS advancements are inspiring to the surrounding BioTech world, we look forward to supporting them in their future of discovery for an optimistic health outcome.”

Contact

VG LIFE SCIENCES CORPORATE COUNSEL
Robert A. Forrester, Esq.
1215 Executive Drive West, Suite 102
Richardson, TX 75081
Tel: 972-437-9898
Fax: 972-480-8406
Email: raforrester@sbcglobal.net

VG LIFE SCIENCES INC. STOCK TRANSFER AGENT
Registrar and Transfer Co.
10 Commerce Dr.
Cranford, NJ 07016-1010
Tel: 1-800-866-1340
Attention: Ana Gois, Account Manager
For more information, please email investor@vglifesciences.com


Shareholder Letters


SEC Filings & Disclosures

On June 20, 2014, the company filed a Form 10-12G with the Securities and Exchange Commission and, as of August 19, 2014, is required to make ongoing disclosures and reports under the SEC’s online EDGAR system including annual and quarterly reports on Form 10-QSB or Form 10-KSB, as well as Current Reports on Form 8-K. The company responded to SEC comments on September 10, 2014 and October 1, 2014. The company cleared SEC comments on October 14, 2014.

Previously, on March 25, 2009, the company filed a Form 15 with the Securities and Exchange Commission terminating its reporting obligations under Section 12(g) of the Securities Exchange Act of 1934. As a result, the company was no longer eligible or required to make ongoing disclosures and reports under the SEC’s online EDGAR system including annual and quarterly reports on Form 10-QSB or Form 10-KSB, as well as Current Reports on Form 8-K. The company addressed this gap in disclosure by making disclosures under the OTCIQ service.

SEC filings on EDGAR are available, however, investors should also consult the company’s disclosures made on the OTCIQ system (see below) and the company’s standard press releases.


Stock Information (As of September 26, 2014)

STOCK SHARES
Issued and Outstanding Common Shares 30,320,628
Authorized Common Shares 150,000,000
Issued and Outstanding Preferred Shares 9,715,443
Authorized Preferred Shares 20,000,000