@windyshores this is not a quote, rather, its a observation or preliminary conclusion that I made after reading various clinical trials. Forteo marketed dose is 20mcg, deemed as minimum safe and effective dose to general population. There are higher doses tested according to Lilly, but 20mcg achieve the primary goal, that is, reduction of fracture risk, with secondary goal being increase in bmd, with statistical significance.

Forteo's molecule is a 34 amino acid peptide, an exact sequence (1-34) to that of natural parathyroid hormone, which contains 84 amino acid. By comparison, tymlos contains 34 amino acids also, but it's a synthetic analog of natural human parathyroid hormone, i.e., its component of amino acids differ from that of forteo. So maybe we are comparing dark green apples to light green apples here. Because the difference in amino acid composition, we could get the molecular weight of each drug for a comparison. To be more precise, we could use mmol for comparison. My guesstimate is that since both have 34 amino acids, weight wise will be approximately same. Using mmol, we are looking at a lot more abaloparatide (80mcg converted to mmol) molecules vs teriparatide (20mcg converted to mmol) to achieve approximate similar results, with abaloparatide in a slight advantage. That's my deduction. Research paper often cites that the reason for tymlos's advantage is due to its altered configuration of binding at receptor site. This puzzles me because why it takes 4x as many molecules of abaloparatide/tymlos to achieve approximate same clinical results when compared to teriparatide/forteo? If tymlos’ slight better clinical results can be explained by altered receptor binding configuration hence earlier uncoupling, the required 4x more molecules/peptides for tymlos makes me wonder why.