It is almost 3 years since the PBT2 patent deal between Queensland and ATH was done. One of the important issues was the COVID epidemic with antibiotic-resistant bacteria that PBT2 could kill.
Now it looks like also ATH434 could be important to keep COVID patients alive by reducing iron, at least in theory if you read this paper below.
IMO, there is a big need for both PBT2 and ATH434. We need to get them to the market. There are no tissues that could stand iron overload. It is not only brain problems as we think as ATH investors, but lung, heart, liver, etc, and even joints, and intervertebral discs which will become degenerated if there is iron overload harming the cells.
There is a lot to be investigated with ATH434 when it comes to the pharmacy.
I am posting here the COVID-related paper:Liver Iron Overload Drives COVID-19 Mortality: a Two-Sample Mendelian Randomization Study
Huimin Tian 1, Xiangjie Kong 2, Fulei Han 2, Fangjie Xing 2, Shuai Zhu 2, Tao Xu 3, Weijing Wang 2, Ning Song 4, Yili Wu 2AffiliationsDOI: 10.1007/s12011-023-03878-8
- PMID: 37814169
Abstract
Iron overload has been associated with an increased risk of COVID-19 severity and mortality in observational studies, but it remains unclear whether these associations represent causal effects. We performed a two-sample Mendelian randomization (MR) to determine associations between genetic liability to iron overload and the risk of COVID-19 severity and mortality. From genome-wide association studies of European ancestry, single-nucleotide polymorphisms associated with liver iron (n = 32,858) and ferritin (n = 23,986) were selected as exposure instruments, and summary statistics of the hospitalization (n = 16,551) and mortality (n = 15,815) of COVID-19 were utilized as the outcome. We used the inverse-variance weighted (IVW) method as the primary analysis to estimate causal effects, and other alternative approaches as well as comprehensive sensitivity analysis were conducted for estimating the robustness of identified associations. Genetically predicted high liver iron levels were associated with an increased risk of COVID-19 mortality based on the results of IVW analysis (OR = 1.38, 95% CI: 1.05-1.82, P = 0.02). Likewise, sensitivity analyses showed consistent and robust results in general (all P > 0.05). A higher risk of COVID-19 hospitalization trend was also observed in patients with high liver iron levels without statistical significance. This study suggests that COVID-19 mortality might be partially driven by the iron accumulation in the liver, supporting the classification of iron overload as one of the independent death risk factors. Therefore, avoiding iron overload and maintaining normal iron levels may be a powerful measure to reduce COVID-19 mortality.
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