Companion blog:
Urgent: (pregnant women/nursing mothers)
See Sotrovimab (second WHO drug) - monoclonal antibody treatment mutation targets cells central to fetal/newborn humoral immunity, mutation associated with leukemia - warning for pregnant/nursing mothers (scroll down to second half of article)
Important Companion Blog:
Covid-19 treatment protocols and vaccinations are inducing severe injury and death in recipients. The mechanisms/ingredients of Covid-19 vaccines and drug 'therapies' induce injury by design. (i.e, feature not a bug).
The latest WHO recommended drug therapies for treatment of Covid-19 ascribed illness may induce cancer, blood, clots, and death. The WHO is recommending the drugs be administered in combination with other drugs which increased lethal outcomes in clinical studies, and AGAINST package insert warnings for use.
First Drug:
Olumiant/Baricitinib
Drug. also paired with Remdesivir, now being recommended for use in severe Covid-19 attributed infection for treatment in combination with corticosteroids:
FDA warning for JAK inhibitor drugs includes latest WHO recommendation for Covid-19 attributed treatment: OLUMIANT (baricitinib) tablets, for oral use Initial U.S. Approval: 2018
"The World Health Organization has recommended two new drugs for COVID-19, providing yet more options for treating the disease. The extent to which these medicines will save lives depends on how widely available and affordable they will be.
The first drug, baricitinib, is strongly recommended for patients with severe or critical COVID-19. It is part of a class of drugs called Janus kinase (JAK) inhibitors that suppress the overstimulation of the immune system. WHO recommends that it be given with corticosteroids".
This recommendation goes against FDA warning: majority of patients who developed severe reactions leading to death were taking corticosteroids.
The warning label also states the drug should NOT be administered to patients with severe infections AT ALL:
AVOID USE OF OLUMIANT IN PATIENTS WITH ACTIVE SERIOUS INFECTION, it can INDUCE PNEUMONIA:
What is Barnicitinib?
"Baricitinib is an orally bioavailable inhibitor of Janus kinases 1 and 2 (JAK1/2), with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon administration, baricitinib binds to JAK1/2, which inhibits JAK1/2 activation and leads to the inhibition of the JAK-signal transducers and activators of transcription (STAT) signaling pathway".
In the pub med fact sheet it is an irritant, a health hazard, and environmental hazard:
Again, per the WHO article:
The first drug, baricitinib, is strongly recommended for patients with severe or critical COVID-19. It is part of a class of drugs called Janus kinase (JAK) inhibitors that suppress the overstimulation of the immune system
However, Janus Kinases are important for cell growth, survival and development and central to proper function of immune cells and hematopoietic cells (formation of blood cells)
"The Janus family kinases (Jaks), Jak1, Jak2, Jak3, and Tyk2, form one subgroup of the non-receptor protein tyrosine kinases. They are involved in cell growth, survival, development, and differentiation of a variety of cells but are critically important for immune cells and hematopoietic cells".
Janus Kinases play a central role in immune cell signaling and inhibition of cell function
Data from experimental mice and clinical observations have unraveled multiple signaling events mediated by Jak in innate and adaptive immunity. Deficiency of Jak3 or Tyk2 results in defined clinical disorders, which are also evident in mouse models.
"A striking phenotype associated with inactivating Jak3 mutations is severe combined immunodeficiency syndrome, whereas mutation of Tyk2 results in another primary immunodeficiency termed autosomal recessive hyperimmunoglobulin E syndrome. In contrast, complete deletion of Jak1 or Jak2 in the mouse are not compatible with life and, unsurprisingly, do not have counterparts in human disease".
i.e. suppression (inhibition) of JAK signaling results in immunodeficiency and hyperimmunoglobuilin E syndrome (associated with severe skin disorders/rashes/pustules and pneumonia)
The FDA side effect warning indicate the inhibition of JAK are inducing the expected immunodeficiency associated with this process with hyperimmunoglobulin E syndrome inducing pneumonia and skin lesions.
Severe skin rashes, pustules have been associated with Covid-19 attributed hospitalized infections.
"Urticarial eruptions associated with COVID-19 have been first reported by Recalcati [9] in his cohort of hospitalized patients, accounting for 16.7% of total skin manifestations. Urticaria-like eruptions have been subsequently described in other cohort studies".
Baricitinib was approved for Covid-19 attributed treatment in December of 2020 in conjunction with Remdesivir
Hyperimmunoglobulin E syndrome manifests in the same type of skin rashes and pustules being attributed to Covid-19:
Before reviewing the next WHO recommended drug treatment, it is important to consider the following: (regular readers may just scroll down)
Treatment protocols for Covid-19 attributed infection are inducing injury/death in recipients which are then being falsely attributed to Covid-19 through use of unsuitable testing methods/protocols and attribution standards.
Public health officials and states are implementing tests against FDA/CDC/WHO/test manufacturer use standards and 22 expert panel peer review warning documenting 10 severe errors with PCR (central test for detection of Sars CoV2, diagnostic method for Covid-19):
Additionally, Sars Cov2 has not been credibly scientifically documented as the causal agent for generic cluster symptoms attributed to Covid-19 (through testing 'useless' for purpose).
Sars CoV2 is a computer model of a 'virus' based on government owned genomic sequences predating 2020, with over 150 Freedom of Information Act requests seeking documentation and verification of scientifically valid isolation of Sars CoV2 from an infected human subject coming back 'evidence/documents do not exist':
See also:
The Emperor Has No Corona (video link)
Second WHO recommended drug:
"WHO has also conditionally recommended the use of a monoclonal antibody drug, sotrovimab, for treating mild or moderate COVID-19 in patients who are at high risk of hospitalization. This includes older patients, immuno-compromised, who have underlying conditions like diabetes, hypertension, and obesity, and those unvaccinated.
Sotrovimab is an alternative to casirivimab-imdevimab, a monoclonal antibody cocktail recommended by WHO in September 2021. Studies are ongoing on the effectiveness of monoclonal antibodies against Omicron but early laboratory studies show that sotrovimab retains its activity".
Sotrovimab is NOT FDA approved only Emergency Use Authorized:
Its Authorized Use is 'treatment of mild to moderate Covid-19 (non serious cold symptoms)
Here, the WHO is AGAIN recommending the use of a drug against its pharmaceutical manufacturer own warnings and use guidelines.
"WHO has also conditionally recommended the use of a monoclonal antibody drug, sotrovimab, for treating mild or moderate COVID-19 in patients who are at high risk of hospitalization".
Emergency Use Authorization states CLINICAL worsening of Covid-19 attributed symptoms with use of Sotrovimab requiring HOSPITALIZATION
Again, treatment with monoclonal antibodies may induce severe symptoms (including the very symptoms the drug is allegedly administered to suppress:
Serious side effects for monoclonal antibodies include SERIOUS INFECTION & CANCER:
Important 2 minute video explaining mechanism of monoclonal antibody 'therapy' and role in inducing cancer:
Bill Gates Endorses Monoclonal Antibodies/mechanism of cancer induction
(IMPORTANT)
FDA Definition Mechanism of Action:
"Sotrovimab is a recombinant human IgG1κ monoclonal antibody that acts by binding to a conserved epitope located on the spike protein receptor-binding domain of SARS-CoV-2, the virus causing COVID-19. The epitope is highly conserved, discouraging the development of viral resistance to the antibody.4 This prevents the spike protein mediated binding of SARS-CoV-2 and entry into human cells.2 Sotrovimab does not compete with human ACE2 receptor binding and inhibits an undefined step that occurs after viral attachment and before the fusion of the viral and cell membranes. The Fc component of sotrovimab includes M428L and N434S amino acid substitutions (LS modification) that result in a longer half-life.6
Here, the drug manufacturer is rationalizing utilizing cell binding/inhibition to cell receptors centrally important to humoral immunity and other central cell processes under the guise of inhibiting an 'undefined step' which supposedly stops Sars CoV2 from fusing to cells.
Medical gobbledygook
Sotrovimab:
Development and mechanism of action:
Sotrovimab has been engineered to possess an Fc LS mutation (M428L/N434S) that confers enhanced binding to the neonatal Fc receptor[11] resulting in an extended half-life and potentially enhanced drug distribution to the lungs.[12]
They are binding a FcLS mutation to neonatal Fc receptor:
Biding to neonatal FC receptor? What is that?
The neonatal Fc receptor (also FcRn, IgG receptor FcRn large subunit p51, or Brambell receptor) is a protein that in humans is encoded by the FCGRTgene
What does the FCGRT gene express?
Cell surface receptor that transfers passive humoral immunity from the mother to the newborn.. Binds to the Fc region of monomeric immunoglobulin gamma and mediates its selective uptake from milk (PubMed:7964511, PubMed:10933786). IgG in the milk is bound at the apical surface of the intestinal epithelium. The resultant FcRn-IgG complexes are transcytosed across the intestinal epithelium and IgG is released from FcRn into blood or tissue fluids. Throughout life, contributes to effective humoral immunity by recycling IgG and extending its half-life in the circulation. Mechanistically, monomeric IgG binding to FcRn in acidic endosomes of endothelial and hematopoietic cells recycles IgG to the cell surface where it is released into the circulation (PubMed:10998088). In addition of IgG, regulates homeostasis of the other most abundant circulating protein albumin/ALB (PubMed:24469444, PubMed:28330995).
FCGRN_HUMAN,P55899
So, Sotromivbab binds cell protein central for conferring humoral immunity in human being via breast milk.
Additionally, FcRN expression is important for passive IgG transfer:
FcRn expression is also temporally and developmentally modulated. During fetal life, FcRn expression in the syncytiotrophoblasts of the placenta is responsible for passive IgG transfer (Fig. 1A).
Why is this important?
"Placental transfer of maternal IgG antibodies to the fetus is an important mechanism that provides protection to the infant while his/her humoral response is inefficient. IgG is the only antibody class that significantly crosses the human placenta".
So, again,
" Sotrovimab has been engineered to possess an Fc LS mutation (M428L/N434S) that confers enhanced binding to the neonatal Fc receptor[11] resulting in an extended half-life and potentially enhanced drug distribution to the lungs.[12]"
They have engineered to attach a FcLS mutation onto Fc receptors central to humoral immunity of the fetus and newborn.
Mutations in FcLS are associated with development of Leukemia & Lymphoma:
Again, side effects for Sotrovimab (a drug approved to ostensibly treat non serious symptoms of a COLD are:
CANCER,
SEVERE INFECTION,
ANEMIA (reduction in red blood cells),
REDUCED WHITE BLOOD CELL COUNTS
There is ZERO medical/scientific rationale or justification for use of either Baricitinib or Sotrovimab. The drugs have SEVERE health risks and utilized against FDA own use warnings and COMBINED with other agents with equally safety/health risks.
Pregnant women and nursing mothers are being given a drug with an engineered mutation on cell receptors central to conferring humoral immunity to fetus/newborn. Mutations which are associated with development of leukemia and other severe health effects.
No clinical studies, potential for fetal transfer, no data on ANY short term/mid term/long term risk in pregnancy/lactating mothers: (receipt of monoclonal antibodies is defacto enrollment in medical experiment):
Military Deployed to Administer Monoclonal Antibodies in Nursing Homes:
Right now, the national guard is being deployed to administer monoclonal antibody therapy treatments in nursing homes:
Gov. Beshear: FEMA Strike Teams, Kentucky National Guard Assisting Hospitals as COVID-19 Cases Surge
The Governor will request additional long-term care nurses, assistance with monoclonal antibody injections
... help administer monoclonal antibodies to prevent serious illness from COVID-19 and keep Maine people out of critical care, preserving intensive care unit (ICU) capacity.....
Treatment protocols resulting in elderly death are again being attributed to Covid-19. Shortly after the deployment to administer 'treatment' with potentially lethal side effects, deaths rose again in Maine nursing homes.
For more documentation of Covid-19 protocol/treatment role in nursing home deaths and death clusters, please see this IMPORTANT article: