The Use of INFEPERIUM™ Against the Deadly Coronavirus
(ICPF is the research name of INFEPERIUM™ and is used in many studies and documents. INFEPERIUM™ is the registered trademark name and appears on all products.) INFEPERIUM™ has been cleared by the Medical and Ethical Investigational Review Board in Mexico for Clinical Trials to treat the SARS-CoV-2 that causes the COVID-19 (CoronaVirus) and is waiting on approval of the FDA Emergency Application for patient use.
The world is closely watching the spread of a deadly coronavirus outbreak. The Chinese city of Wuhan, the original epicenter, is in a state of quarantine, but this has not stopped its spread to other countries including Korea, Japan, Thailand and the United States. As we marshal forces to combat this we cannot deny that there will be vast international health and economic consequences.
Before curative remedies can be developed we must still moderate its spread and lethal effects by utilizing agents that can help NOW. It is here that we recommend the use of INFEPERIUM™, a Biological Response Modifier that promotes a cytokine response which will help one to prophylactically resist the virus from taking harbor as well as help eliminate any virus that has already made its presence felt.
Interferon gamma (IFN-γ) possesses well recognized antiviral activity. When INFEPERIUM™ was administered to mice the serum concentration of IFN-γ rose ~60 fold, reaching 597 pg/mL within 24 hours. INFEPERIUM™ was subsequently used in a double-blind study to see if puppies with canine parvovirus had a better survival rate; mortality went down from 45% (control) to 10% (treated).
These same percentages and up regulations of these Cytokines have been observed in human patients, tested by the Random Analyzer! Also, patients that were on the INFEPERIUM™ Therapy for whatever condition, were prophylactically protected from viral assaults of colds and Flu viruses. These patient observations established both the prophylactic and Therapeutic properties of INFEPERIUM™.
We encourage you to take advantage of this safe and effective treatment. If interested please contact ….
Figure 10. Mice were administered ICPF (trade name INFEPERIUM™) (5 mg) and at the indicated times thereafter, blood was taken and its serum analyzed for the release of cytokines: Representations of Inf-γ (Interferon-gamma), IL-6, IL-12, and GM-CSF: Granular Macrophage-Colony Stimulating factor are displayed. Cytokines profiles were assessed via Endogen™ Searchlight Array Technology.
Above Chart. Mice were administered ICPF (trade name INFEPERIUM™) (5 mg) and at the indicated times thereafter, blood was taken and its serum analyzed for the release of cytokines: Representations of Inf-γ (Interferon-gamma), IL-6, IL-12, and GM-CSF: Granular Macrophage-Colony Stimulating factor are displayed. Cytokines profiles were assessed via Endogen™ Searchlight Array Technology.
Please note the wavelike response – IL-peaks at ~3hours but returns to normal by 24 hours. IL-12, GM-CSF and Inf-gamma begin to rise at 3 hours but are significantly higher at 24 hours. This is typical of how cellular communication can take place with such “chemical messengers”
IL-12 is involved in the differentiation of naive T cells into Th0 cells, which will further develop into either Th1 cells or Th2 cells. It is known as a T cell-stimulating factor, which can stimulate the growth and function of T cells. It stimulates the production of interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) from T and natural killer (NK) cells, and reduces IL-4 mediated suppression of IFN-γ. T cells that produce IL-12 have a coreceptor, CD30, which is associated with IL-12 activity.
IL-12 plays an important role in the activities of natural killer cells and T lymphocytes. IL-12 mediates enhancement of the cytotoxic activity of NK cells and CD8+ cytotoxic T lymphocytes. There also seems to be a link between IL-2 and the signal transduction of IL-12 in NK cells. IL-2 stimulates the expression of two IL-12 receptors, IL-12R-β1 and IL-12R-β2, maintaining the expression of a critical protein involved in IL-12 signaling in NK cells. Enhanced functional response is demonstrated by IFN-γ production and killing of target cells.
IL-12 also has anti-angiogenic activity, which means it can block the formation of new blood vessels. It does this by increasing production of interferon gamma, which in turn increases the production of a chemokine called inducible protein-10 (IP-10 or CXCL10). IP-10 then mediates this anti-angiogenic effect. Because of its ability to induce immune responses and its anti-angiogenic activity, there has been an interest in testing IL-12 as a possible anti-cancer drug. However, it has not been shown to have substantial activity in the tumors tested to this date. There is a link that may be useful in treatment between IL-12 and the diseases psoriasis and inflammatory bowel disease.
IL-12p40: Exists as a monomer extracellularly and becomes bioactive when it forms a heterodimer with IL-12p35. This heterodimer (IL-12p70) is biologically active and is composed of independently regulated disulfide linked 40kDa and 35kDa subunits. Note: IL-12p70 was not seen in previous studies, IL-12p40 was chosen as a positive control for the cytokine assay, as its levels were expected to remain static at different timepoints in the serum. Whether or not a drop in IL-12p40 can be used as an indicator of IL-12p70 formation has not been validated in the literature at this time. IL-12p40 levels were consistent in the cytokine assay.
IL-6: A number of cytokines make up an IL-6 cytokine family. Membership in this family is based on a helical cytokine structure and receptor subunit makeup. IL-6 production is generally correlated with cell activation. Circulating IL-6 can be found in the blood of normal individuals in the 1 pg/mL range, with slight elevations during the menstrual cycle, modest elevations in certain cancers (melanoma) (10 pg/mL), and large elevations after surgery (30-430 pg/mL).
IL-6 has been described as both a pro-inflammatory and anti-inflammatory molecule, a modulator of bone resorption, a promoter of hematopoiesis, and an inducer of plasma cell development. IL-6 also has been shown to influence IL-4 production. It has been suggested that antigen-driven, APC-derived IL-6 may influence naive CD4+ T cells to produce IL-4 and express the IL-4 receptor. Thus, given the close approximation of APC and T cell, transient APC-derived IL-4 could initiate a T cell autocrine loop whereby naive T cells direct their own phenotype commitment. (A possible link from innate to adaptive immunity)
IFN-γ: Interferon gamma (IFN-γ) is produced by lymphocytes activated by specific antigens or mitogens. IFN-gamma shows antiviral activity and has important immunoregulatory functions. It is a potent activator of microphages and had antiproliferative effects on transformed cells. It can potentiate the antiviral and antitumor effects of the type I interferons.
IFN-γ is a potent activator of monocytic cell functions, including the stimulation of TNF-α and the control of IL-6 synthesis. These cytokines might act as autocrine or paracrine factors together with IFN- gamma in inducing biologic responses.
IL-6 & IFN-γ: Predominantly originates from macrophages, dendritic cells, and NK cells (NK cells are particularly important for IFN-γ release). When increased levels are paired, these cytokines play a role in the early phase of host defense mechanisms; especially important for bacterial infections.
KC also observed
Blinded Study (as shown in slide below):
Control: n=25 ICPF: n=25
Unblinded study, 56 dogs were treated (40% reduction in mortality)
Puppies were presented to a veterinary clinic and if diagnosed with parvovirus were randomly placed into two treatment groups (one group received a placebo and the other received ICPF (5mg).
Interferon gamma (an anti-viral cytokine) has been shown to be up-regulated