VBLOCK™ v2 – Antiviral Anti-COV Formula

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VBLOCK™v2 (formerly COVHIB) formula has been designed to block the functional entry point of CoV and it’s replication by the use of herbal furin inhibitors combined with other anti-virals and immune system modulators such as; Luteolin, Niclosamide, Scutellaria Baicelancis(oroxylin), Andrographis, Vitamin C, Liquorice, Silimarin, Luteolin, Isatis, Citrulline, Ivermectin & R-ALA.

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The new coronavirus (2019-nCoV / SARS-CoV-2) infecting Humans has been sequenced and the genomic information has been released, despite a high similarity with the genome sequence of SARS-CoV, they have identified a novel furin-like cleavage site in the Spike protein of the new coronavirus (see below). This has presented a possible functional consequence of this cleavage site in the viral cycle, pathogenicity and thus a potential achilles heel in the use of antiviral agents to reduce the infection and replication within the body.

The acquisition of the furin cleavage site might be viewed as a ‘gain of function’ that enabled a bat coronavirus to jump into humans and begin its current epidemic spread. 2019-nCOV has some similarities to the SARS-CoV from 2003 outbreak which was known to actively replicate in the intestinal tract (source), this is important in knowing if oral-based treatment can offer protection.

VBLOCK™v2 (formerly known as COVHIB) formula has been designed to block this functional entry point of CoV and it’s replication by the use of herbal furin inhibitors combined with other anti-virals and immune system modulators such as; Luteolin, Niclosamide (NES), Andrographis, Scutellaria Baicelancis(oroxylin),  Liquorice, Silimarin, Isatis, Zinc L-Citrulline, & now 3mg Ivermectin (18 Jan 2021).
(Note: VBLOCK™v2 has not been tested on 2019-nCoV in a clinical setting ).


Targets: Furin, NLRP3, TGF-β, importin alpha/beta-1,  Notch, ERK,
CDK’s, WNT, TMPRSS2, ACE2, PLPro, EIF2, PKC/PI3k/Macrop’, IL-10.

Key Studies: Very recent studies have been published on 2019-nCoV in 2021, [scroll to end].

The understanding of how a virus infects and replicates is an intensely complicated mechanism and so to keep things brief and fairly clear, we will paraphrase the key aspects of what the scientific community has revealed as a possible strategy to reduce the ability of this virus to hijack the replication machinery within human cells.

Although viruses have evolved sophisticated strategies to exploit the metabolism, protein synthesis and trafficking pathways of an infected cell, the host (human) is not defenceless. Besides innate and adaptive immune responses that directly target components of the virus, infected cells may also restrict viral spread by limiting the availability of cellular factors that are critical for viral replication, so called ‘virus dependency factors’. The entry of CoV and influenza into host cells relies on the binding of viral particles to cell-surface receptors and the endocytosis of virus–receptor complexes. The endosomal pathway initiates the fusion of the viral envelope with the host cell membrane to deliver viral nucleocapsid into the cell. CoV also enters cells via a nonendosomal pathway.

In February 2020, the team at Unité des Virus Émergents, Marseille, France have furin-like peculiar furin-like cleavage site in the S-protein of 2019-nCoV which is lacking in other CoV’s which may have implications for the viral life cycle. They identified a peculiar furin-like cleavage site in the Spike protein of the 2019-nCoV (SARS-CoV-2), lacking in the other SARS-like CoVs. They suggested anti-2019-nCoV therapeutics should include furin and serine protease inhibitors (eg: Quercetin & Luteolin).

Also in February 2020, research teams from Chinese Medical Universities upon studying the 2019-nCov (SARS-CoV-2) and considered the time required to develop specific therapeutic drugs to tackle the epidemic, drug repositioning may be the only solution to the epidemic of sudden infectious diseases. They used bioinformatics analysis on the proteins encoded by the novel coronavirus genes was systematically conducted, and the proteins of SARS-CoV-2 were compared with other coronaviruses, such as SARS-CoV and MERS-CoV. Theyused these proteins and human relative proteins [human ACE2 and type-II transmembrane serine protease (TMPRSS2) enzymes] as targets to screen ZINC U. S Food and Drug Administration approved drug database (ZINC drug database, ZDD), their own database of traditional Chinese medicine and natural products (including reported common anti-viral components from traditional Chinese medicine), and the database of commonly used anti-viral drugs (78 compounds) by virtual ligand screening method.

From this they identified targets, 3CLpro, PLpro, RdRp and helicase as the most important targets for the development of small-molecule inhibitors due to their clear biological functions and vital enzyme active site.

PLpro / 3CLPro : Herbs; Isatis, EGCG, Scutellaria Baicalencis, Citrus Aurantium(hesperidin ) & Andrographis.
Drugs: Ribavirin, valganciclovir and thymidine, anti-bacterial drugs (chloramphenicol, cefamandole and tigecycline), muscle relaxant drug (chlorphenesin carbamate), anti-tussive drug (levodropropizine). For Spike protein, they found only one compound, natural hesperidin was targeting the binding between Spike RBD and human ACE2. They cautioned against ACE2 direct inhibitors because a poor prognosis could be induced by the inhibition of ACE2 enzyme activities, for ACE2 was considered as a protective factor of lung injury.


The entry of CoV and IFV into host cells relies on the binding of viral particles to cell-surface receptors and the endocytosis of virus–receptor complexes (fig. left). The endosomal pathway initiates the fusion of the viral envelope with the host cell membrane to deliver viral nucleocapsid into the cell. CoV also enters cells via a nonendosomal pathway. CoV and IFV enter host cells via pH- and receptor-mediated endocytosis, involving clathrin-dependent or independent endocytic pathways. Influenza also utilizes macropinocytosis as an alternative entry pathway to the acidic late-endosomal compartment. Much research has been done since the SARS-CoV pandemic of 2003.

Recently, niclosamide, a U.S. Food and Drug Administration (FDA)-approved antiparasitic drug used in humans33,34,35, has been identified as an effective antiviral agent against a number of pH-dependent viruses, such as human rhinoviruses and influenza virus36, severe acute respiratory syndrome-coronavirus37, Chikungunya virus38, and flaviviruses39,40,41. These studies suggested that the broad antiviral activity of niclosamide is associated with neutralization of endo-lysosomal pH that interferes with pH-dependent membrane fusion which is a critical step for virus entry36.

In 2004 it was found that Niclosamide, an existing antihelminthic drug, was able to inhibit replication of a newly discovered coronavirus, SARS-CoV where viral antigen synthesis was totally abolished at a niclosamide concentration of 1.56 μM, as revealed by immunoblot analysis. Thus, niclosamide represents a promising drug candidate for treatment of SARS-CoV infection. The mechanism which Niclosamide (NICL) exploits is also applicable to the 2019-nCoV outbreak because it uses both endocytosis and a ph-dependant furin cleavage mechanism. The broad antiviral activity of niclosamide is associated with neutralisation of endo-lysosomal pH that interferes with pH-dependent membrane fusion which is a critical step for virus entry. https://www.nature.com/articles/s41598-019-45095-1

(The above diagram has not been fully updated yet for VBLOCK v2)
The entry of CoV and Influenza Virus into host cells relies on the binding of viral particles to cell-surface receptors and the endocytosis of virus–receptor complexes. The endosomal pathway initiates the fusion of the viral envelope with the host cell membrane to deliver viral nucleocapsid into the cell. CoV also enters cells via a nonendosomal pathway. Activation of the host protein kinases PKR, PERK, HRI and GCN2 can phosphorylate the eIF2α to attenuate translation. Assembly of viral particles requires the host TMPRSS2 for cleavage of CoV spike and IFV HA in the Golgi apparatus to produce viral progeny to be released by budding. In addition, the NF-κB pathway is activated through inactivation of IκBa to induce proinflammatory cytokines, such as IFNs, for innate immune response to viral infection. These host-based pathways are targetable by repurposed agents to control viral infection. Representative herbal agents have a pink background. Green thick arrows indicate induction. Green thick stop signs indicate inhibition. Scissor signs indicate proteolytic cleavage.


Furin cleaves and activates a variety of mammalian, viral and bacterial substrates. The serine protease furin is essential for proper activation of a variety of cellular precursor proteins. Numerous viruses exploit furin for the activation of their glycoproteins and several bacterial exotoxins are activated by furin mediated cleavage. Notably, positive feedback loops can further enhance the oncogenic potential of furin. For example, the furin substrate TGF-β not only increases furin micro RNA expression, but also enhances its proteolytic activity by an unknown mechanism. Furin and TGFb can be modulated/inhibited by Liquorice, Skullcap, Andrographis, Luteolin & Astragalus.

To date, furin-mediated cleavage has been described for envelope glycoproteins encoded by numerous evolutionarily diverse virus families, including Herpes, Corona, Flavi (Dengue), Toga, Borna, Bunya, Filo, Orthomyxo, Paramyxo, Pneumo and Retroviridae, therefore furin represents a potential target for us to aim to inhibit. Because of the key role of furin in the pathogenesis of cancer and infectious diseases, its suitability as a therapeutic target has raised significant interest for several years. Many laboratories have explored the possibility to limit tumor growth, viral replication or bacterial intoxication by reducing the amount or proteolytic activity of furin.

Spike Glycopprotein

The spike glycoprotein of the newly emerged SARS-CoV-2 contains a potential cleavage site for furin proteases. This observation has implications for the zoonotic origin of the virus and its epidemic spread in China.

The membrane of coronaviruses harbors a trimeric transmembrane spike (S) glycoprotein (pictured) which is essential for entry of virus particles into the cell. The S protein contains two functional domains: a receptor binding domain, and a second domain which contains sequences that mediate fusion of the viral and cell membranes. The S glycoprotein must be cleaved by cell proteases to enable exposure of the fusion sequences and hence is needed for cell entry.

The nature of the cell protease that cleaves the S glycoprotein varies according to the coronavirus. The MERS-CoV S glycoprotein contains a furin cleavage site and is probably processed by these intracellular proteases during exit from the cell. The virus particles are therefore ready for entry into the next cell. In contrast, the SARS-CoV S glycoprotein is uncleaved upon virus release from cells; it is likely cleaved during virus entry into a cell.


What is Furin?

Furin, a member of the proprotein convertase family, is a multi-domain proteinase, the catalytic domain of which is similar in structure to bacterial subtilisin. Furin functions in the Golgi apparatus, in the secretory vesicles and, potentially, also on cell surfaces. This unique specificity proteinase cleaves after basic residues many functionally important cellular proteins, including soluble and membrane-tethered metalloproteinases, integrins, signaling receptors, growth factors, hormones and neuropeptides, and transforms them into their respective mature forms [source]. In addition to processing cellular precursor proteins, furin is also exploited by numerous bacterial and viral pathogens. Pathogenic viruses and bacterial toxins employ host furin to become fully functional and to allow entry into host cells and to cause disease onset.


Ivermectin is an FDA-approved broad spectrum anti-parasitic agent (Gonzalez Canga et al., 2008) that in recent years has been shown to have anti-viral activity against a broad range of viruses (Gotz et al., 2016; Lundberg et al., 2013; Tay et al., 2013; Wagstaff et al., 2012) in vitro.  Ivermectin acts by inhibiting the host importin alpha/beta-1 nuclear transport proteins, which are part of a key intracellular transport process that viruses hijack to enhance infection by suppressing the host antiviral response. Ivermectin is therefore a host-directed agent, which is likely the basis for its broad-spectrum activity in vitro against the viruses that cause dengue, Zika, HIV, and yellow fever.


Schematic of ivermectin’s proposed antiviral action on coronavirus. IMPa/ß1 binds to the coronavirus cargo protein in the cytoplasm (top) and translocates it through the nuclear pore complex (NPC) into the nucleus where the complex falls apart and the viral cargo can reduce the host cell’s antiviral response, leading to enhanced infection. Ivermectin binds to and destabilises the Impa/ß1 heterodimer thereby preventing Impa/ß1 from binding to the viral protein (bottom) and preventing it from entering the nucleus. This likely results in reduced inhibition of the antiviral responses, leading to a normal, more efficient antiviral response.

Targeting viral entry

The entry of CoV and IFV into host cells relies on the binding of viral particles to cell-surface receptors and the endocytosis of virus–receptor complexes. The endosomal pathway initiates the fusion of the viral envelope with the host cell membrane to deliver viral nucleocapsid into the cell. CoV also enters cells via a nonendosomal pathway. Thus, endosomal and nonendosomal pathways should be considered as targets to block viral entry into host cells, as depicted in above diagram.


VBLOCK2™ Ingredients per 2 x Vegan Capsules
Andrographis 5:1 Extract (†) (furin inhibitor) 500mg *
Niclosamide NES (99%) 100mg *
Scutellaria Baicalencis 5:1 Extract (†) (furin inhibitor) 300mg *
Isatis 5:1 Extract (†) 300mg *
Liquorice 5:1 Extract (†) 200mg *
Vitamin C (Ascorbic Acid) 100mg *
R-Alpha Lipoic Acid (†) 60mg *
Silimarin Extract (†) 60mg *
Luteolin Extract (from Pagoda flower)(†) (furin inhibitor) 80mg *
L-Citrulline(†) 100mg *
Organic Black Pepper 5mg *
Zinc Picolinate 5mg *
Ivermectin 6mg *
Other ingredients: HPMC Hypromellose (vegetable capsule), zero fillers, (†) tested, * Daily value not established

Suggested Usage

VBLOCK™v2 is a broad-based nutraceutical formula containing herbal extracts and other nutrients which have been shown to provide antiviral support. VBLOCK™v2 aims to block the pathways which are used for infection and replication. VBLOCK™v2 is best supported with Vitamin D3, Zinc,  Vitamin C (1g, 2x a day, take every 30mins if infected), Magnesium – Calcium Channel Blocker (epsom salt baths), Omega 3 DHA, & Glutathione.
Dietary: Eat Celery and Spinach if you can get it.  It is also recommended that in infected areas municipal water is filtered before use, or distilled. Take 2 capsules with water/alcohol 2 times per day after food, increase this if risk of infection is higher or if already infected. Niclosamide is better absorbed with Biofuze.  Adverse events following Ivermectin is more common in people with very high burdens of larval Loa loa worms in their blood.

Caution: VBLOCK™v2 should not be used at the same time as chloroquine or Fenbendazole.

Safety of Niclosamide

Niclosamide is a well established molecule which has been used in several countries since 1960. The drug has been used extensively since then and is listed on the WHO Model List
of Essential Medicines 2003 and the WHO Model Formulary 2004. Potential adverse events are extremely rare considering it’s widespread use in fish farming, but can include: nausea, retching, abdominal pain, light-headedness & pruritus. No paediatric specific problems have been documented and niclosamide is not contraindicated in small children. Geriatrics: No human studies and animal data to suggest carcinogenicity but plenty showing potential anti-tumor effects. The below review supports the continuous use of Niclosamide as no major safety concerns have been raised. Niclosamide should not be used at the same time as chloroquine, HCQ or Fenbendazolehttps://archives.who.int/eml/expcom/expcom14/niclosamide/safety_review_08feb05.pdf

Clinical Studies

Genes Affected Used by COVID-19


The spike glycoprotein of the new coronavirus 2019-nCoV contains a furin-like cleavage site absent in CoV of the same clade (April 2020)

SARS-CoV-2 therapeutic targets (2020)

A review on flavones targeting serine/threonine protein kinases for potential anticancer drugs

Inhibition of Severe Acute Respiratory Syndrome Coronavirus Replication by Niclosamide

The mechanisms of action of Ivermectin against SARS-CoV-2: An evidence-based clinical review article

Ivermectin inhibits the replication of SARS-CoV-2 in vitro

A structural mechanism of flavonoids in inhibiting serine proteases

Luteolin restricts dengue virus replication through inhibition of the proprotein convertase furin

Neutralisation of Acidic Intracellular Vesicles by Niclosamide Inhibits Multiple Steps of the Dengue Virus Life Cycle In Vitro

LUTEOLIN inhibits V-ATPase
Luteolin inhibition of V-ATPase A3-D2 interaction decreases osteoclast resorption activity

Inhibitors of V-ATPases: old and new players

Since SARS-CoV is known to actively replicate in the intestinal tract. Diarrhea was more frequently observed during the first week of illness. Intestinal biopsy specimens obtained by colonoscopy or autopsy showed minimal architectural disruption but the presence of active viral replication within both the small and large intestine. Coronavirus was also isolated by culture from these specimens, and SARS-CoV RNA can be detected in the stool of patients for more than 10 weeks after symptom onset.

Following endocytosis, endosomal acidification leads to the fusion of the viral envelope protein with the host membrane, facilitating the release of the viral genome. Vacuolar-type ATPase (V-ATPase), the proton-pumping enzyme that generates the low intra-vacuolar pH, is required for viral endocytosis and infection in vitro. Niclosamide acts as a proton carrier which blocks endosomal acidification to inhibit human rhinovirus and influenza virus infection.

Niclosamide Is a Proton Carrier and Targets Acidic Endosomes with Broad Antiviral Effects

Antiviral activities of niclosamide and nitazoxanide against chikungunya virus entry and transmission. (2016)

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4 reviews for VBLOCK™ v2 – Antiviral Anti-COV Formula

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  1. Mr MacNeil (verified owner)

    Verified reviewVerified review - view originalExternal link | usUnited States

    VBLOCK v2 knocked out the corona virus in days. My wife was extremely ill until she started taking this supplement . I ordered more of it to have on hand for future viruses. Great product, excellent service and fast delivery to the USA. (April 20 2020)

  2. Sohial (verified owner)

    Verified reviewVerified review - view originalExternal link | auAustralia

    Great product and always good to have on hand. Thanks

  3. Anonymous (verified owner)

    Verified reviewVerified review - view originalExternal link | gbEngland, United Kingdom

    Great ingredients. Easy to swallow

  4. Diane R. (verified owner)

    Verified reviewVerified review - view originalExternal link | usNew York, United States

    So glad I found this on your site, many doctors will not prescribe and this is important for those of us that can not get the jab

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