This is an antibiotic that has figured prominently in recent news items about cases of Duchenne due to premature "stop codons." In these cases the complete gene for dystrophin is never "decoded" or translated so that this critical muscle protein is not made, or at least not made in full form. Research on mdx mice that simulate human Duchenne has shown that when gentamycin is administered, the premature stop codon is somehow ignored so that the entire gene transcript can be "read" and dystrophin can be produced. A preliminary trial on Duchenne young men is underway, and hopes are high that this will work in humans as well as it did in the model mice. Unfortunately, this treatment would only work for those instances (about 10% of all Duchenne cases) in which the gene defect is a premature stop codon.
"Also, bear in mind that clen isn’t great for your heart, and can cause some issues there (enlargement of ventricles, etc…) but most studies showing clen to cause heart problems are with animals, and even though the dosing is almost similar to what humans take (in some studies it’s within the range of what would be double of a large human dose...) it’s important to remember that animals have more beta-2 receptors and they cause certain event chains that humans’ beta-2 receptors may not. Clen causes cardiac hypertrophy and cardiac necrosis (cell death)to some degree, in some cases."
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