http://news.excite.com/news/pr/011108/ca-heph-presents-eff.

Thu, Nov 08 8:07 AM EST

SAN DIEGO, Nov. 8 /PRNewswire/ -- Hollis-Eden Pharmaceuticals, Inc. (NASDAQ:HEPH) today announced data from three separate presentations at the Cytokine Odyssey 2001 meeting held this week in Maui, Hawaii. The presentations include clinical results with the Company's lead immune regulating hormone, HE2000, indicating that treatment with the compound in HIV patients significantly reduced elevated levels of a number of well-known inflammatory mediators throughout the five-month treatment period. Chronic high levels of inflammation have been shown in numerous studies to be correlated with progression to many AIDS-related conditions in HIV patients. The presentations also include data from two preclinical studies with another immune regulating hormone, HE2200, which showed positive findings in a model of inflammatory bowel disease as well as in a model of bone loss. While pharmaceuticals such as corticosteroids act to reduce inflammation, chronic use of these compounds has been shown to lead to immune suppression and bone loss. The studies presented at this meeting, however, build on a rapidly emerging body of scientific data indicating that Hollis-Eden's immune regulating hormones have the potential to reduce inflammation while at the same time boosting immune responses and preserving bone.

The new clinical findings support and expand upon data previously reported on the ability of HE2000 to reduce transcript numbers for key inflammatory mediators such as TNF-alpha, COX-2, IL-1-beta and IL-6. These new results are from a preliminary analysis through three treatment cycles with HE2000 administered subcutaneously as a monotherapy to HIV patients in South Africa. The placebo-controlled study, conducted in 24 patients, compares two different doses of HE2000 administered once daily for five days every 6 weeks. Prior to dosing with HE2000, HIV patients had dramatically elevated transcript levels of inflammatory mediators including TNF-alpha (11 fold increase), COX-2 (8 fold increase), IL-1-beta (10 fold increase) and IL-6 (43 fold increase) relative to healthy South African volunteers. This indicates that these HIV infected patients were experiencing broad-based systemic inflammatory immune dysregulation before treatment with HE2000. After dosing with HE2000, these same patients experienced significant declines in transcripts for TNF-alpha, COX-2, IL-1-beta and IL-6 as well as other inflammatory mediators. Levels of all of these inflammatory mediators were significantly reduced in both dose groups, and these decreases were sustained throughout the five-month treatment period despite the fact that patients received only intermittent treatment with HE2000. No drug-related serious adverse events were reported during the course of this study.

In addition to the effects of reducing inflammatory mediators, the presentation also included data on the ability of HE2000 to increase mRNA transcripts associated with cell-mediated immunity in these same patients. Cell-mediated immunity is a critically important component of immunity that is designed to combat intracellular pathogens such as viruses and certain parasites. Further evidence for improvements in cell-mediated immunity was also presented in a preliminary analysis of an HIV substudy designed to look at additional immune responses. After treatment with HE2000, the analysis demonstrated that immune responses to phytohemagglutitin (PHA), commonly lost in the later stages of AIDS, candida, a common AIDS opportunistic infection, and p24 antigen (an HIV protein) had been restored in these patients. These results support previous clinical and preclinical findings with HE2000 indicating improvements in both innate and cell-mediated immunity.

A number of studies in the medical literature have shown that increases in inflammatory cytokines such as TNF-alpha, IL-1-beta, IL-6 and the enzyme COX-2 can lead to an increase in HIV viral replication and decreases in dendritic cells and hematopoiesis, which, in turn, lead to a progressive loss of innate and cell-mediated (Th1) immunity. It is this chronic inflammatory dysregulation and progressive loss of innate and cell-mediated immunity that is believed to ultimately lead to AIDS and the life threatening opportunistic infections, cancers, wasting and dementia that compromise the patient. By quieting down this rampant systemic inflammation, Hollis-Eden believes that immune regulating hormones have the potential to induce the immune system to mount appropriate innate and cell-mediated immune responses that will keep the virus in check and slow or prevent the progression to AIDS-related conditions.

The clinical data presented at this meeting also have potential implications for a wide variety of other indications associated with chronic inflammatory dysregulation. Drugs designed to inhibit a single inflammatory mediator have been shown in clinical trials to be effective agents in treating a number of autoimmune conditions, including arthritis, inflammatory bowel disease and psoriasis. Monoclonal antibody drugs designed to inhibit only TNF-alpha are projected to generate sales in excess of $1 billion in 2001, and sales of drugs designed to inhibit only COX-2 are projected to approach $5 billion annually this year. As described above, immune regulating hormones appear to affect multiple mediators (including TNF-alpha and COX-2) involved in the inflammatory cascade in patients with systemic inflammation, and appear to do so without causing immunosuppression, a problem experienced with many current anti-inflammatory drugs. Hollis-Eden's immune regulating hormones have shown impressive preclinical activity in models of a number of autoimmune conditions including arthritis, psoriasis and multiple sclerosis.

The preclinical data presented at this meeting reinforced these opportunities. One of these presentations focused on the effects of HE2200 in a preclinical model of inflammatory bowel disease. In this experiment HE2200 was compared to sulfasalazine (SZ), a standard of care for ulcerative colitis. The results of a histological analysis demonstrated HE2200 was superior to SZ in controlling inflammation in the colon and in reducing the incidence of ulcerations, resulting in a more normal mucosal histology. In addition, as seen in previous studies, HE2200 was more effective than SZ in reducing the incidence of diarrhea.

In the third presentation, HE2200 was studied for effects on bone loss in a well-accepted bone loss model. This study reported HE2200 demonstrated significant bone-sparing effects including statistically significant increases in bone mineral content, bone formation and endochondral growth rate in the HE2200 treated animals. The endochondral growth rate is of particular interest due to the fact that the chronic use of corticosteroids in childhood diseases and immune disorders can damage the endochondral growth rate inhibiting normal bone development.

"This data has the potential to help drive a paradigm shift in immune- based therapy because chronic administration of traditional anti-inflammatory drugs has resulted in immune suppression (e.g., glucocorticoids and TNF-alpha inhibitors)," said Dr. Christopher Reading, Vice President of Scientific Development, Hollis-Eden Pharmaceuticals. "This new class of immune regulating hormones appears to produce durable decreases in elevated transcripts of inflammatory mediator genes without causing immune suppression. In fact, the compounds appear to improve both innate and cell-mediated immunity. The results presented today in HIV and inflammatory bowel disease presages opportunities in autoimmunity, cancer and aging where inflammatory mediators inhibit immunity and cause deterioration of health."

"We believe no drug is as effective at controlling disease as a well functioning immune system" stated Richard B. Hollis, Chairman and CEO of Hollis-Eden. "Unfortunately there are many conditions in which the immune system becomes dysregulated and stops functioning as it is supposed to. These conditions include chronic infectious diseases like HIV, autoimmune conditions such as inflammatory bowel disease, as well as cancer and the aging process itself. At Hollis-Eden our core focus is on understanding the common causes of this dysregulation and developing safe, cost-effective therapies that can correct immune system defects. Because we are focused on addressing dysfunction in pathways that are common to many diseases, we believe that if we are able to successfully develop such agents, they may have utility in a number of conditions."

"We have identified a class of immune regulating hormones and hormone analogs that appear to regulate gene transcription in the body to control immune function. These hormones are known to be depleted in a number of diseases and immune system disorders. It is thus very exciting to see in these studies that, by giving immune regulating hormones to reverse these hormonal deficits, we are altering gene transcription in humans to reduce the levels of a number of important inflammatory mediators associated with pathology in multiple disease states, while at the same time allowing restoration of important immune responses. The clinical results are further complemented by these new preclinical studies indicating that administering these immune regulating hormones can provide important functional benefits. This exciting new data will help our scientific team prioritize the most promising indications for accelerated clinical development and commercialization."

Hollis-Eden Pharmaceuticals, Inc. is a development-stage pharmaceutical company based in San Diego, California, engaged in the development of products for the treatment of infectious diseases and immune systems disorders. The Company's vision is to become the world leader in immune regulating hormones and their application to numerous diseases. Hollis-Eden is conducting a series of clinical trials with HE2000 in South Africa and the United States in HIV infected patients and has recently commenced clinical trials with HE2000 in Singapore for the treatment of hepatitis B and in Thailand for malaria- infected patients. Studies with the Company's immune regulating hormones are also planed in hepatitis C infected patients. The Company is also conducting a Phase I clinical trial in the United States with another of its immune regulating hormones, HE2200. In addition, through its relationship with Aeson Therapeutics, the Company also has access to HE2500, which is in clinical trials in the United States in cardiovascular disease and actinic keratosis. For more information on Hollis-Eden, contact the Company's website at http://www.holliseden.com .

Statements made in this press release may constitute forward-looking statements and are subject to numerous risks and uncertainties, including the failure to successfully complete clinical trials, the Company's future capital needs, the Company's ability to obtain additional funding and required regulatory approvals, the development of competitive products by other companies, and other risks detailed from time to time in the Company's filings with the Securities and Exchange Commission. The actual results may differ materially from those contained in this press release.

For further information please contact: Dan Burgess of Hollis-Eden Pharmaceuticals, +1-858-587-9333, ext. 218.
 

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