Research

Tesamorelin: Research Overview of a GHRH Analog
A research overview of Tesamorelin, a stabilized GHRH analog. Covers its mechanism of action at the pituitary, preclinical and clinical research on visceral adiposity, cognitive function, and body composition. For research use only. Read more...
GHK-Cu (Copper Peptide): Research Overview
A research overview of GHK-Cu (copper peptide), covering its mechanism of action, preclinical findings in skin biology, antioxidant activity, and hair follicle research. For research use only. Read more...
“GLP-3” Isn’t What Most People Think It Is (and That’s Why the Research Gets Messy)
I’m going to be annoyingly precise up front, because sloppy labels create sloppy conclusions. “GLP-3” gets thrown around online  like it’s a normal human gut hormone sitting next to GLP-1 and GLP-2.  Read more...
Tadalafil: the “36-hour” PDE5 inhibitor that refuses to stay in the ED box
Tadalafil has a funny public reputation: the “weekend pill.” That stereotype isn’t totally wrong—but it’s also the least interesting way to think about the molecule. Pharmacologically, tadalafil is a phosphodiesterase-5 (PDE5) inhibitor. Translation: it blocks the enzyme that degrades cyclic GMP in smooth muscle, so nitric-oxide signaling “sticks” longer and blood vessels relax more readily. The reason tadalafil became tadalafil (and not just “another sildenafil”) is kinetics: it clears slowly enough that meaningful levels can hang around beyond a day. That’s the scaffolding underneath the “up to 36 hours” clinical... Read more...
BPC-157 Research Uses: A Mechanism-First, Skeptical Review From the Independent Track
Executive summary I left a master’s program because I got tired of writing elegant narratives around fragile datasets. BPC-157 is exactly the kind of topic that rewards that kind of cynicism: the preclinical literature reports broad, often dramatic healing effects across tissues (gut, tendon/ligament, muscle, nerve, bone, vascular/organ injury models), frequently at very low doses, with comparatively little independent replication and minimal human evidence. [1] Mechanistically, there is credible cell- and pathway-level work supporting pro-repair signaling—especially vascular/endothelial biology (VEGFR2 internalization and downstream Akt–eNOS signaling; NO-dependent vasomotor effects; endothelial migration and... Read more...