CDC document titled: “COVID-19 Vaccines: Update on Allergic Reactions, Contraindications, and Precautions.”
Page 20: “Ingredients Included in mRNA COVID vaccines.”
“SM-102: heptadecan-9-yl 8-((2-hydroxyethyl) (6-oxo-6-(undecyloxy) hexyl) amino) octanoate.”
Document published by the Cayman Chemical Company of Ann Arbor, Michigan: “Safety Data Sheet acc. to OSHA HCS.” (04/11/2021)
This data sheet lists the effects of SM-102.
“For research use only, not for human or veterinary use.”
Adverse effects/warnings re SM-102: “Suspected of causing cancer. Suspected of damaging fertility or the unborn child. Causes damage to the central nervous system, the kidneys, the liver and the respiratory system through prolonged or repeated exposure. Very toxic to aquatic life with long lasting effects.”
"Application of the substance / the mixtureFor research use only, not for human or veterinary use."
This is probably just conspiracy theory nonsense. Roll up the sleeve!
SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2
Also, this study back in March reports troubling findings regarding the S protein in the mRNA vaccines.finds the spike protein used in covid-19 "vaccines" causes strokes, heart attacks, and blood clots.
"SARS-CoV-2 infection induces EC inflammation, leading to endotheliitis.1,5 Because S protein decreased ACE2 level and impaired NO bioavailability, we examined whether S protein entry is indispensable for dysfunctional endothelium. As shown in Figure [F], i, the endothelium-dependent vasodilation induced by acetylcholine was impaired in pulmonary arteries isolated from Pseu-Spike-administered hamsters, whereas the endothelium-independent vasodilation induced by sodium nitroprusside was not affected. We also compared the acetylcholine- and sodium nitroprusside–induced vasodilation of pulmonary vessels from ACE2-D or ACE2-L mice. As anticipated, acetylcholine-induced vasodilation was hindered in pulmonary arteries isolated from ACE2-L mice in comparison to ACE2-D mice (Figure [F], ii). There was, however, little difference in sodium nitroprusside–induced vasodilation between ACE2-D and ACE-L animals.
Although the use of a noninfectious pseudovirus is a limitation to this study, our data reveals that S protein alone can damage endothelium, manifested by impaired mitochondrial function and eNOS activity but increased glycolysis. It appears that S protein in ECs increases redox stress which may lead to AMPK deactivation, MDM2 upregulation, and ultimately ACE2 destabilization.4 Although these findings need to be confirmed with the SARS-CoV-2 virus in the future study, it seems paradoxical that ACE2 reduction by S protein would decrease the virus infectivity, thereby protecting endothelium. However, a dysregulated renin-angiotensin system due to ACE2 reduction may exacerbate endothelial dysfunction, leading to endotheliitis. Collectively, our results suggest that the S protein-exerted EC damage overrides the decreased virus infectivity. This conclusion suggests that vaccination-generated antibody and/or exogenous antibody against S protein not only protects the host from SARS-CoV-2 infectivity but also inhibits S protein-imposed endothelial injury."