GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Azapeptide analogues of the growth hormone releasing peptide 6 as cluster of differentiation 36 receptor ligands with reduced affinity for the growth hormone secretagogue receptor 1a.
Proulx. Caroline C; Picard. Émilie É; Boeglin. Damien D; Pohankova. Petra P; Chemtob. Sylvain S; Ong. Huy H; Lubell. William D WD
Key Findings
- Replacing certain amino acids in GHRP‑6 (e.g., D‑Trp2, Ala3, Trp4) cuts its ability to bind the GH secretagogue receptor by >100‑fold while keeping micromolar affinity for CD36.
- The D‑Trp2 residue is important for CD36 binding, but the first histidine can be swapped for alanine without losing CD36 affinity.
- Specific analogues ([azaTyr4]‑GHRP‑6, [Ala1, azaPhe2]‑GHRP‑6, [azaLeu3, Ala6]‑GHRP‑6) showed anti‑angiogenic activity in a choroid sprouting assay.
Practical Outcomes
- For DIY biohackers, these findings don’t change how you would currently use GHRP‑6, because the new analogues aren’t commercially available and haven’t been tested in people. The study does suggest that CD36‑related effects of GHRP‑6 could be separated from growth‑hormone release, but no actionable dosing or protocol advice emerges.
Summary
Scientists made new versions of the peptide GHRP‑6 that no longer trigger the growth‑hormone receptor (GHS‑R1a) but still stick to another protein called CD36. Some of these altered peptides also blocked tiny blood‑vessel growth in a lab test. The work is mostly about how the molecule can be tweaked, not about how to use GHRP‑6 for health or performance.
Abstract
The synthetic hexapeptide growth hormone releasing peptide-6 (GHRP-6) exhibits dual affinity for the growth hormone secretagogue receptor 1a (GHS-R1a) and the cluster of differentiation 36 (CD36) receptor. Azapeptide GHRP-6 analogues have been synthesized, exhibiting micromolar affinity to the CD36 receptor with reduced affinity toward the GHS-R1a. A combinatorial split-and-mix approach furnished aza-GHRP-6 leads, which were further examined by alanine scanning. Incorporation of an aza-amino acid residue respectively at the D-Trp(2), Ala(3), or Trp(4) position gave aza-GHRP-6 analogues with reduced affinity toward the GHS-R1a by at least a factor of 100 and in certain cases retained affinity for the CD36 receptor. In the latter cases, the D-Trp(2) residue proved important for CD36 receptor affinity; however, His(1) could be replaced by Ala(1) without considerable loss of binding. In a microvascular sprouting assay using a choroid explant, [azaTyr(4)]-GHRP-6 (15), [Ala(1), azaPhe(2)]-GHRP-6 (16), and [azaLeu(3), Ala(6)]-GHRP-6 (33) all exhibited antiangiogenic activity.
Study Information
pubmed
2012
2012-07-09T00:00:00.000Z
10.1021/jm300557t
35
47