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Metadichol® and CD33 Expression in Umbilical Cord Cells

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CD33 also known as Siglec-3 is endogenously expressed in stem cells and is a marker for the myeloid lineage of cells. Increased expression of CD33 thus allows it to bind to any Sialic Acids (SIAs). These acids are binding sites for pathogens and toxins. By binding to these acids, CD33 can prevent invasion of hosts by these pathogens. Down-regulation of CD33, increase the release of the pro-inflammatory cytokine TNF-α by monocytes that increases reactive oxygen species that are involved in diseases like diabetes mellitus, Alzheimer's, cardiovascular diseases asthma, and in various cancers. The up-regulation of CD33 using Metadichol ® was studied using Wharton's Jelly Mesenchymal Stem Cells (MSCs) isolated from human umbilical cord and were grown in p-35 dishes until confluent and treatment was carried out with different concentrations. One dish was untreated and considered as control. The treated and untreated cells were analyzed using Flow Cytometry. The cells treated at 100 pg of Metadichol ® has shown the highest increase (>400 fold) in CD33++ expression (48.77%) compared to untreated control (0.11%).
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Volume 9 • Issue 1 • 1000443
J Stem Cell Res Ther, an open access journal
ISSN: 2157-7633
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Research Article
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ISSN: 2157-7633
Raghavan, J Stem Cell Res Ther 2019, 9:1
DOI: 10.4172/2157-7633.1000443
Abstract
CD33 also known as Siglec-3 is endogenously expressed in stem cells and is a marker for the myeloid lineage
of cells. Increased expression of CD33 thus allows it to bind to Sialic Acids (SIAs). These acids are binding sites for
pathogens and toxins. By binding to these acids, CD33 can prevent invasion of hosts by these pathogens. Down-
regulation of CD33, increase the release of the pro-inammatory cytokine TNF-α by monocytes that increases reactive
oxygen species that are involved in diseases like diabetes mellitus, Alzheimer’s, cardiovascular diseases asthma, and
in various cancers.
The up-regulation of CD33 using Metadichol® was studied using Wharton’s Jelly Mesenchymal Stem Cells
(MSCs) isolated from human umbilical cord and were grown in p-35 dishes until conuent and treatment was carried
out with different concentrations. One dish was untreated and considered as control. The treated and untreated cells
were analyzed using Flow Cytometry. The cells treated at 100 pg of Metadichol® has shown the highest increase
(>400 fold) in CD33++ expression (48.77%) compared to untreated control (0.11%).
Metadichol® and CD33 Expression in Umbilical Cord Cells
Palayakotai R Raghavan*
Nanorx Inc, PO Box 131, Chappaqua, NY 10514, USA
*Corresponding author: Palayakotai R Raghavan, Nanorx Inc., PO Box 131,
Chappaqua, NY 10514, USA, Tel: 9146710224; E-mail: raghavan@nanorxinc.com
Received December 27, 2018; Accepted January 04, 2019; Published January
11, 2019
Citation: Raghavan PR (2019) Metadichol® and CD33 Expression in Umbilical
Cord Cells. Stem Cell Res Ther 9: 443. doi: 10.4172/2157-7633.1000443
Copyright: © 2019 Raghavan PR. This is an open-access article distributed under
the terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author and
source are credited.
Keywords: CD33; Cord blood; Stem cells; Multipotency; Umbilical
cord blood; Metadichol®; AHR; VDR; Inverse agonist; TNF-α; Cancer;
Diabetes
Abbreviations:MSCS: Mesenchymal Stem Cells; SIA: Sialic Acid;
HSCs: Hematopoietic Stem Cells; AML: Acute Myeloid Leukemia; GO:
Ozogamicin; VDR: Vitamin D Receptor; UCB: Umbilical Cord Blood
Introduction
CD33 is a transmembrane protein of the Siglec family [1]. Siglecs
bind to SIAs and are expressed by Hematopoietic Stem Cells (HSCs)
which are present in Umbilical Cord Blood (UCB) cells. Humans
express a larger family of CD33 related siglecs. Innate response is the
body’s rst line of defense, but it can also result in damage to host over
time. Siglecs act as a negative regulator in immune cells like monocytes
and macrophages to minimize damage [2]. is interaction is essential
in balancing the signals in a cell to bring about homeostasis. e best-
known Siglecs are CD22 and CD33. Over the last two decades, many
more Siglecs have been identied. Siglecs play a role in the regulation
of immune systems by binding to SIAs. Humans express a larger
family of CD33 related siglecs and can be present on the same cells,
e.g., monocytes express siglec-3, 5, 7, 9 and 10. Siglecs can carry out
immunological functions that could be positive or negative. For e.g.,
creating a barrier against pathogens thus reducing interactions and at
the same time weakening complement activation [3,4].
CD33 is a critical molecule in the inammatory response, depending
on the SIA microenvironment for its repressor activity. Reduced
CD33 leads to an increase in inammatory cytokines, such as IL-1b,
TNF-α, and IL-8. Hyperglycemia down-regulates CD33 expression and
triggers the spontaneous secretion of TNF-α by peripheral monocytes
and increased free radical generation. CD33 thus has a vital role in the
pathology of with type 2 diabetes [5,6]. SIA occupies the terminal end
in glycan molecules on the surfaces of cells. Pathogenic bacteria have
evolved to cover themselves in SIA that allows them to circumvent the
host’s innate immune response, or they can use it as a nutrient. Table 1
lists pathogens that bind to SIA and Table 2 lists pathogens that release
SIAs and diseases associated with it [7]. ese bacteria synthesize SIA
or scavenged or obtained from the host. Some but not all pathogens
have the ability to secrete a sialidase that releases SIA using host
sialoglycoconjugates. Free SIA is made available to pathogens by other,
sialidase-expressing bacteria living in the same niche [8] or by the host
in the course of inammation [9-12].
Treatment of human monocytes with anti-CD33 mAb induces the
production of the pro-inammatory cytokines IL-1b, TNF-α, and IL-
8. CD33 ligand removal from the monocyte surface by neuraminidase
Pathogens
Human Inuenza A
Avian Inuenza A
Human Inuenza C
Vibrio cholerae
Plasmodium falciparum
Helicobacter pylori
Table 1: Examples of pathogens that bind to sialic acids on human cell surfaces.
Sialic acid synthesized by pathogens
Pathogen Diseases
Neisseria meningitides B Meningitis
Escherichia coli K1 Neonatal Meningitis
Group B Streptococcus Neonate and infant infections
Campylobacter jujuni Enteritis, Guillian-Barre syndrome
Host silica acid taken up by pathogens
Hemophilus inuenzae Respiratory infections
Hemophilus ducreyi Chancroid
Sialic acid transferred by trans-sialidase
Trypanosoma Cruzi Chagas disease
Carynebacterium diptheraie Diphteria
Table 2: List of pathogens that release sialic acid and diseases associated with
them.
Citation: Raghavan PR (2019) Metadichol® and CD33 Expression in Umbilical Cord Cells. Stem Cell Res Ther 9: 443. doi: 10.4172/2157-7633.1000443
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Volume 9 • Issue 1 • 1000443
J Stem Cell Res Ther, an open access journal
ISSN: 2157-7633
resulted in IL-1b up-regulation, controlling monocyte activation. CD33
at the cell surface is crucial to maintaining monocytes in the resting
state. If there is decreased, levels of SIA in the microenvironment CD33
will induce IL-1b production by monocytes, thus participating in the
delivery of alarm signals [13].
CD33 is found to be expressed in 90% of Acute Myeloid
Leukemia (AML) blasts [14]. Clinical data have been shown with
immunoconjugates consisting of the humanized anti-CD33 antibody
(gemtuzumab) and the cytotoxic drug calicheamicin (ozogamicin) as an
eective anti-AML regimen. Ozogamicin (GO), the first drug conjugate
approved for clinical use for anti-leukemia therapy [15]. Aer binding
to CD33-antigens, gemtuzumab is taken into the cell via endocytosis.
A new expression of CD33-antigens becomes necessary on the cellular
surface of myeloid cells leads to endocytosis of gemtuzumab present,
leading to ecacy in killing cells [16].
e low expression of CD33 and the slow internalization of CD33/
antibody complexes leads to relatively limited CD33-mediated drug
uptake per unit of time; consequently, for an anti-CD33 antibody-
drug conjugate to be most successful, a highly potent toxin will be
required [17]. Several novel CD33-targeted therapeutics that may
overcome some of the limitations of earlier therapeutics are currently
in preclinical and early clinical development. e low expression of
CD33 and the slow internalization of CD33/antibody complexes leads
to relatively limited CD33-mediated drug uptake [18]. Targeting CD33
proved to be dicult and GO withdrawn from the U.S. and European
markets because of a lack of overall ecacy [19].
We recently showed that UCB cells on ex vivo treatment with
Metadichol® a Nanoemulsion of long-chain alcohols showed enriched
CD34+ cells [20]. Metadichol® is an inverse agonist [21] of Vitamin
D Receptor (VDR), a TNF-α inhibitor [22] and anti-diabetic agent as
well as anti-microbial agent [23,24]. is paper deals with Metadichol®
expression on UCB cells leading to increased CD33 expression similar
to what we saw in CD34 expression. e increased expression observed
with CD33 could be one possible mechanism that could explain its
diverse pharmacological actions of Metadochol® on multiple diseases
[25-38].
Experimental
Work was outsourced and carried out by Skandia Labs, Pvt Ltd,
Bangalore India Antibody: CD33-FITC Conjugate purchased from BD
Pharmingen.
Cell line: Umbilical Cord Blood (UCB) cells,
Procedure:
1. Culture 1 × 106 cells in a 6 well plate containing 2 ml of complete
media
2. Aer 24 hrs of incubation, cells are treated with 1 pg, 100 pg, 1
ng, 100 ng and 1 µg in serum-free DMEM media and incubated
for 72 hrs
3. Aer 72 hrs of treatment, cells were collected and, pelleted cells
at 4000 rpm for 5 minutes at room temperature and discard the
supernatant
Figure 1: Results of UCB cells treated with Metadichol®.
Citation: Raghavan PR (2019) Metadichol® and CD33 Expression in Umbilical Cord Cells. Stem Cell Res Ther 9: 443. doi: 10.4172/2157-7633.1000443
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Volume 9 • Issue 1 • 1000443
J Stem Cell Res Ther, an open access journal
ISSN: 2157-7633
4. Wash the cell pellet twice with 1X PBS
5. e cell pellet was re-suspended in 100 µL Sheath uid and
incubated with CD33-FITC antibody for 20 minutes in the dark
6. Post incubation, the cells were once washed with 1X PBS and
resuspended in Sheath uid
7. e treated and untreated cell populations were determined
using FACS Caliber (BD Biosciences, San Jose, CA)
Figure 1 shows the results of UCB cells treated with Metadichol®
1 pg, 100 pg, 1 ng, 100 ng and 1 µg of Metadichol® for 72 hrs. e cells
showed ten (CD33+) to hundred (CD33++) fold increased expression
of CD33. Cells treated at 1 ng Metadichol® showed a 15 fold increase in
expression of CD33+ cells (77.52%) compared to control cells (5%). e
cells treated at 100 pg showed highest increase (>400 fold) in CD33++
expression (48.77%) compared to untreated control (0.11%). e
reason we believe that there is less expression at higher concentration
may have to do with the pH which about 4.5 and this can aect some
but not all cell lines. In virus cell lines, we have noticed that it is toxic to
cancer cells at higher concentrations.
Discussion
We have shown previously that Metadichol® binds to VDR whose
natural ligand is Calcitriol. We have published Metadichol’s action
on biomarkers implicated in various diseases [25-28]. It exhibits
antimicrobial activity against parasites, viruses, and bacteria. e
shortest interaction path, between the two genes VDR and CD33
is shown in Figure 2. It was generated by a web-based program
ConsensusPathDB [39]. CD14 is an endogenous ligand for CD33 [40].
Calcitriol regulates CD14 in human cells. CD14 binding to CD33 leads
to TLR4-mediated signaling plays an essential role in initiating the
innate immune response [41].
Gonzales, et al., [5] have shown that diabetic patients have low levels
of CD33 when compared to healthy controls, whereas the TNF-α levels
are high. is work correlates with our studies that show Metadichol®
reduces sugar levels and also TNF-α level in diabetic rats. All these
downeld eects result from binding to nuclear receptor VDR (Figure 3).
Many pathogens incorporate SIAs into their surface glycoconjugates
through various mechanisms [42]. Research supports the notion that
SIA molecular mimicry can be exploited to subvert host immune
systems or to infect permissive target cells through an interaction with
various Siglecs. Bacterial, fungus and viruses produce SIAs. Pathogenic
microbes have evolved evolutionary mechanisms to interact with
Siglecs. ese pathogens displaying SIAs evade the immune system
and thus dampen host immune response. SIAs are recognized and
bind to CD33 related siglecs [43] and help maintain homeostasis of
host innate immune response, allowing an inammatory response that
is activated upon sensing of danger-associated molecular patterns or
pathogen-associated molecular patterns [44]. Enhanced expression of
CD33 thus allows it to bind to any SIAs present and those released by
pathogens and thus prevent infection of the host. Metadichol® is a food
derivative and free of toxic eects [45-47]. It can be safely used alone or
in combination with existing treatment protocols.
Conclusion
Metadichol increases expression of CD33 by four hundred and
yfold in Umbilical cord cells. is is important in innate immunity
as it binds to sialic acids it prevents the pathogens that makes use of
sialic acid to fool the host and gain entry into host cell to proliferate.
Diabetics have low levels of CD33 and raising these levels helps reduce
glucose levels CD 33expression has an important role in preventing
infectious diseases as well as in chronic disease like diabetes and for
maintaining innate immune function.
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... Metadichol at one picogram increases h-TERT (telomerase) expression by 16-fold 38 . Viral infection places a signi cant strain on the body. ...
Preprint
Full-text available
New pathogenic virus outbreaks, occurring with increasing regularity, are leading us to explore novel approaches, which will reduce the reliance on time-consuming vaccine modes to halt the outbreaks. The requirement is to find a universal approach to disarm any new and as yet unknown viruses as they appear. A promising approach could be targeting lipid membranes, which are common to all viruses and bacteria. The ongoing pandemic of severe acute respiratory syndrome-coronavirus 2 (SARS-COV-2) has reaffirmed the importance of interactions between components of the host cell plasma membrane and the virus envelope as a critical mechanism of infection. Metadichol®, a nano lipid emulsion, has been examined and shown to be a strong candidate to help stop the proliferation of SARS-COV-2. Naturally derived substances, such as long-chain saturated lipid alcohols, reduce the infectivity of various types of viruses, including coronaviruses such as SARS-COV-2, by modifying lipid-dependent attachment to human host cells. SARS-COV-2 uses the receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. Metadichol®, a nano lipid formulation of long-chain alcohols, has been shown to inhibit TMPRSS2 (EC50 96 ng/ml). Compared to the inhibitor camostat mesylate (EC50 26000 ng/ml), it is 270 times more potent. Additionally, Metadichol® is also a extremely weak inhibitor of ACE2 at 31 µg/ml. Further a live virus assay in Caco2 cells, Metadichol® inhibited SARS-CoV-2 replication with an EC90 of 0.16 µg/ml.
... Metadichol at one picogram increases h-TERT (telomerase) expression by 16-fold 38 . Viral infection places a signi cant strain on the body. ...
Preprint
Full-text available
New pathogenic virus outbreaks, occurring with increasing regularity, are leading us to explore novel approaches, which will reduce the reliance on time-consuming vaccine modes to halt the outbreaks. The requirement is to find a universal approach to disarm any new and as yet unknown viruses as they appear. A promising approach could be targeting lipid membranes, which are common to all viruses and bacteria. The ongoing pandemic of severe acute respiratory syndrome-coronavirus 2 (SARS-COV-2) has reaffirmed the importance of interactions between components of the host cell plasma membrane and the virus envelope as a critical mechanism of infection. Metadichol®, a nano lipid emulsion, has been examined and shown to be a strong candidate to help stop the proliferation of SARS-COV-2. Naturally derived substances, such as long-chain saturated lipid alcohols, reduce the infectivity of various types of viruses, including coronaviruses such as SARS-COV-2, by modifying lipid-dependent attachment to human host cells. SARS-COV-2 uses the receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. Metadichol®, a nano lipid formulation of long-chain alcohols, has been shown to inhibit TMPRSS2 (EC50 96 ng/ml). Compared to the inhibitor camostat mesylate (EC50 26000 ng/ml), it is 270 times more potent. Additionally, Metadichol® is also a extremely weak inhibitor of ACE2 at 31 µg/ml. Further a live virus assay in Caco2 cells, Metadichol® inhibited SARS-CoV-2 replication with an EC90 of 0.16 µg/ml.
... Metadichol at one picogram increases h-TERT (telomerase) expression by 16-fold [37]. Viral infection places a signi cant strain on the body. ...
Preprint
Full-text available
Background New pathogenic virus outbreaks, occurring with increasing regularity, are leading us to explore novel approaches, which will reduce the reliance on time-consuming vaccine modes to halt the outbreaks. The requirement is to find a universal approach to disarm any new and as yet unknown viruses as they appear. A promising approach could be targeting lipid membranes, which are common to all viruses and bacteria.The ongoing pandemic of severe acute respiratory syndrome-coronavirus 2 (SARS-COV-2) has reaffirmed the importance of interactions between components of the host cell plasma membrane and the virus envelope as a critical mechanism of infection. Metadichol®, a nano lipid emulsion, has been examined and shown to be a strong candidate to help stop the proliferation of SARS-COV-2.Naturally derived substances, such as long-chain saturated lipid alcohols, reduce the infectivity of various types of viruses, including coronaviruses such as SARS-COV-2, by modifying lipid-dependent attachment to human host cells. SARS-COV-2 uses the receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. Methods Metadichol was tested against TMPRSS2 ana ACE2 invitro using commercial available kits. Also it was tested against the live virus in Caco2 cells to test for inhibition of viral replication of SARS-COV-2.ResultsMetadichol®, a nano lipid formulation of long-chain alcohols, has been shown to inhibit TMPRSS2 (EC50 96 ng/ml). Compared to the inhibitor camostat mesylate (EC50 26000 ng/ml), it is 270 times more potent. Additionally, Metadichol® is also a weak inhibitor of ACE2 at 31 µg/ml. Further a live virus assay in Caco2 cells, Metadichol® inhibited SARS-CoV-2 replication with an EC90 of 0.16 µg/ml.Conclusions Metadichol inhibits SARS-COV-2 virus and since it a non toxic molecule can be easily tested in humans and as it has LD 50 of over 5000 mg/kilo and could help mitigate the crisis facing the world today.
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... Vitamin D3 is needed for definitive hematopoiesis and suggests potential therapeutic utility in HSPC expansion [41]. Metadichol ® has been shown earlierin ex vivo study to enriches CD34+ and also CD33+ cells using umbilical cord cells [42,43]. VD3 and analogs inhibit malignant cells growing in the blood [44], brain [45] and other cancers as well [46]. ...
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New pathogenic virus outbreaks, occurring with increasing regularity, are leading us to explore novel approaches, which will reduce the reliance on time-consuming vaccine modes to halt the outbreaks. The requirement is to find a universal approach to disarm any new and as yet unknown viruses as they appear. A promising approach could be targeting lipid membranes, which are common to all viruses and bacteria. The ongoing pandemic of severe acute respiratory syndrome-coronavirus 2 (SARS-COV-2) has reaffirmed the importance of interactions between components of the host cell plasma membrane and the virus envelope as a critical mechanism of infection. Metadichol®, a nano lipid emulsion, has been examined and shown to be a strong candidate to help stop the proliferation of SARS-COV-2. Naturally derived substances, such as long-chain saturated lipid alcohols, reduce the infectivity of various types of viruses, including coronaviruses such as SARS-COV-2, by modifying lipid-dependent attachment to human host cells. SARS-COV-2 uses the receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. Metadichol®, a nano lipid formulation of long-chain alcohols, has been shown to inhibit TMPRSS2 (EC50 96 ng/ml). Compared to the inhibitor camostat mesylate (EC50 26000 ng/ml), it is 270 times more potent. Additionally, Metadichol® is also a weak inhibitor of ACE2 at 31 µg/ml. Further a live virus assay in Caco2 cells, Metadichol® inhibited SARS-CoV-2 replication with an EC90 of 0.16 µg/ml.
Preprint
Full-text available
New pathogenic virus outbreaks, occurring with increasing regularity, are leading us to explore novel approaches, which will reduce the reliance on time-consuming vaccine modes to halt the outbreaks. The requirement is to find a universal approach to disarm any new and as yet unknown viruses as they appear. A promising approach could be targeting lipid membranes, which are common to all viruses and bacteria. The ongoing pandemic of severe acute respiratory syndrome-coronavirus 2 (SARS-COV-2) has reaffirmed the importance of interactions between components of the host cell plasma membrane and the virus envelope as a critical mechanism of infection. Metadichol®, a nano lipid emulsion, has been examined and shown to be a strong candidate to help stop the proliferation of SARS-COV-2. Naturally derived substances, such as long-chain saturated lipid alcohols, reduce the infectivity of various types of viruses, including coronaviruses such as SARS-COV-2, by modifying lipid-dependent attachment to human host cells. SARS-COV-2 uses the receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. Metadichol®, a nano lipid formulation of long-chain alcohols, has been shown to inhibit TMPRSS2 (EC50 96 ng/ml). Compared to the inhibitor camostat mesylate (EC50 26000 ng/ml), it is 270 times more potent. Additionally, Metadichol® is also a weak inhibitor of ACE2 at 31 µg/ml. Further a live virus assay in Caco2 cells, Metadichol® inhibited SARS-CoV-2 replication with an EC90 of 0.16 µg/ml.
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A b stract Metadichol® [1] is a Nanoemulsion of long-chain alcohols called as Policosanol and is present in foods such as rice, sugar cane, wheat, and peanuts. Metadichol® acts on Nuclear Vitamin D receptors (VDR) that have a ubiquitous presence in cells and tissues of the body to stimulate the immune system and inhibit a variety of disease processes, resulting from viral, bacterial and parasitic infections. Infectious agents can cause disease by avoiding normal host defense mechanisms or by subverting them to promote their replication. They do so by blocking VDR receptor that is responsible for innate immunity, and this suppression of the immune response leads to persistent infections. We present a case study of a patient who had acquired MRSA infections and how Metadichol® by its actions on the VDR has resolved the problem of this deadly disease without any side effects.
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Metadichol ® [1] is a Nanoemulsion of long-chain alcohols found in many foods. It is commonly called Policosanol and is present in foods such as rice, sugar cane, wheat, peanuts Metadichol acts as an inverse agonist on Nuclear Vitamin D receptors (VDR) that are present in cells throughout the body to stimulate the immune system and affects many biologIcal processes to modulate many diseases. Branched-chain amino acid transferase (BCAT1) catalyzes the reversible transamination of leucine, isoleucine, and valine branched-chain amino acids (BCAA) to their respective alpha-keto acids, liberating L-glutamate. When this gene is inhibited, the amino acid chains accumulated in the tissue triggering longevity in the nematodes. The health and longevity of the nematodes improved when BCAT1 was inhibited. Gabapentin has been shown to inhibit BCAT1, but IC50 is 10000 uM. Metadichol® inhibits BCAT1 with an IC50 of 3.3 um, 3000 times more potent than Gabapentin.
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Abstract Objective: To show the antiviral activity of Metadichol® against Zika virus by an in-vitro assay. Methods: The primary Anti-Zika virus assay was performed using real-time RT-qPCR (TaqMan) to measure extracellular Zika virus RNA copy number associated with virions released from vero cells. The ‘vero’ cell line (kidney epithelial cells extracted from an African green monkey) treated with antiviral test articles is infected with Zika virus followed by Zika virus associated RNA measurement in the cell culture supernatant. Antiviral compounds blocking any step of viral replication such as transcription, translation, encapsidation, the particle assembly and release were identified and characterized using this sensitive assay system. Findings: Metadichol® (1-2) in vitro assays,( inhibited the Zika Virus with a EC50 of 1.48 μg/ml. Conclusion: Metadichol is a safe and effective inhibitor for enveloped viruses in humans. Since it is known to bind to the vitamin D receptor (VDR), its action mechanism likely involves the competitive displacement of virus particles from VDR’s on host cell membranes. Metabolism studies of long chain alcohol in fibroblasts suggest that very long chain fatty alcohols, fatty aldehydes, and fatty acids are reversibly interconverted in a fatty alcohol cycle [3]. Metadichol consists of natural components of common foods (classified as GRAS), Metadichol has no known negative side effects. The inhibition of Zika virus by Metadichol is not surprising, given that we have recently published the results of Metadichol which showed broad-spectrum antiviral activity against Dengue, Ebola, H1N1, SARS, Chikungunya and other enveloped viruses.(4)
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Background Metadichol (1,2) is a Nano emulsion of long-chain alcohols called policosanols which are found in many foods like rice, wheat, grapes, sugar cane, apple and many others (3). It acts on membrane receptors in cells throughout the body to stimulate the immune system and inhibit a variety of disease processes, including those that result in metabolic diseases such as diabetes, obesity and hypertension. Methods A 38-year-old male of middle eastern origin was diagnosed as diabetic after complaining of tiredness and bouts of hunger. He was not on any medication and chose to be treated with Metadichol @ 10 mg per day. Findings Metadichol helped to lower his fasting blood sugar level from 300 mg/dl to normal in 6 weeks. His HBA1C was reduced from 9.8% to 6.2% in 12 weeks. After 32 more months, his diabetic indicators remain normal. Interpretation Metadichol is safe and effective in controlling blood sugar and HbA1C levels in humans. Metadichol has been shown to bind to the vitamin D receptor (2) as an inverse agonist. However, it acts more like a protean agonist ligand (4) to increase or decrease activity depending on the system. Since Metadichol has no known negative side effects and consists of natural components of common foods, Metadichol has the potential to serve as a novel treatment for type 2 diabetes.