Glow Blend 70 mg

Glow Blend is not a single compound. Each 70 mg vial holds three separately synthesised peptides co-lyophilised into one fill: the copper tripeptide GHK-Cu, the pentadecapeptide BPC-157, and TB-500, an N-acetylated fragment of thymosin beta-4. The three are physically mixed, not covalently joined. No single CAS number, molecular formula or molecular weight applies to the product, which is why those rows on this page are blank rather than filled with a value borrowed from one constituent. Blend ratios are also not standardised across suppliers, so a 70 mg blend from one source is not chemically interchangeable with a 70 mg blend from another.

GHK is glycyl-L-histidyl-L-lysine, a tripeptide first isolated from human plasma in 1973. The free peptide is C14H24N6O4, molecular weight 340.38 g/mol, and it carries CAS 49557-75-7. The copper complex is a separately registered substance: GHK-Cu carries CAS 89030-95-5 and the cosmetic INCI name copper tripeptide-1. Those two numbers are routinely conflated in supplier and database listings, which commonly print the free-peptide CAS above a page describing the copper complex, or the reverse. In GHK-Cu the tripeptide chelates a single copper(II) ion through the imidazole nitrogen of histidine, the alpha-amino nitrogen of glycine and the deprotonated amide nitrogen of the glycyl-histidyl peptide bond. Public databases also disagree on the complex formula. PubChem CID 378611 records Cu-GHK as C14H24CuN6O4, while the Wikipedia chembox and several supplier listings give C14H22CuN6O4 for the deprotonated complex. The two differ by two hydrogens, and therefore by roughly 2 g/mol, so no molecular weight for the complex is quoted here. The bound copper is the reason lyophilised GHK-Cu is blue rather than white.

BPC-157 is a 15-residue peptide, sequence GEPPPGKPADDAGLV, CAS 137525-51-0 for the free base, formula C62H98N16O22, molecular weight 1419.5 g/mol. That formula is exactly what the stated sequence computes to, residue by residue, which is the check worth doing before trusting any vendor's number. The primary literature describes the peptide as a partial sequence of a protein found in human gastric juice, from which the abbreviation body protection compound derives. TB-500 is the shortest of the three. It is a heptapeptide, Ac-LKKTETQ, corresponding to residues 17 to 23 of the 43-residue protein thymosin beta-4 with the N-terminus acetylated. TB-500 and thymosin beta-4 are routinely conflated in vendor material. They are different molecules of very different size, and the heptapeptide is what Esposito and colleagues actually recovered when they analysed material sold under the TB-500 name. All three constituents are produced by solid-phase peptide synthesis, with the GHK fraction subsequently complexed to a copper(II) salt.

No published study has examined this three-peptide combination as a unit. There is no peer-reviewed pharmacokinetic, stability, compatibility or interaction data for GHK-Cu, BPC-157 and Ac-LKKTETQ presented together, in any model, in vitro or in vivo. Every result below was measured on one constituent alone, usually in a rodent or a cell culture, and findings from separate compounds do not combine by addition. Read this section as three unrelated literatures that happen to share a vial.

For GHK-Cu, the most quantitative primary work is Simeon and colleagues, who used wound chambers implanted in rats with 2 mg GHK-Cu injections repeated twice weekly, and measured chamber dry weight, total protein, hydroxyproline content as a proxy for type I collagen, and uronic acid content as a proxy for glycosaminoglycans. They reported increases across those measures, together with enhanced accumulation of chondroitin sulfate and dermatan sulfate on electrophoresis. Northern blot in the same study showed decorin mRNA raised and biglycan mRNA lowered in wound tissue under GHK-Cu treatment; in cultured rat dermal fibroblasts the decorin effect reproduced, at an increase the authors put at 302 percent, while biglycan expression was not significantly affected (J Invest Dermatol, 2000). The 2018 review by Pickart and Margolina collects this work and the gene-expression literature that followed it. It is a review authored by the researcher who originally characterised the peptide, and carries the bias that implies.

The GHK-Cu animal record is not uniformly positive, and the negative result is worth stating plainly. Parker and colleagues applied a topical GHK-Cu gel twice daily for 10 days to irradiated dorsal flaps in rats, 13 treated against 10 controls. Mean ischaemic area was 5.0 cm2 (SD 0.9) in the treated group and 3.8 cm2 (SD 1.1) in controls, P = 0.011 against a pre-set significance threshold of P below 0.01 that the authors set to account for multiple comparisons. Caveolin-1 vessel counts were 209.0 (SD 111.1) treated versus 207.4 (SD 109.4) control, P = 0.973. Mean vessel luminal area was 525.7 um2 (SD 191.0) versus 422.8 um2 (SD 109.7), P = 0.118. VEGF staining intensity scored 0.34 (SD 0.19) versus 0.54 (SD 0.41), P = 0.169. The authors concluded that treated flaps showed no difference in flap ischaemia, blood vessel number or area, or VEGF expression (Otolaryngol Head Neck Surg, 2013).

The BPC-157 literature is large but almost entirely preclinical, and a substantial proportion of it originates from one research group in Zagreb. Chang and colleagues worked ex vivo and in vitro on rat Achilles tendon at 2 micrograms per millilitre. Fibroblast outgrowth was visible at day 2 in 5 of 10 tendon explants against 2 of 10 controls, and transwell migration of cultured tendon fibroblasts increased up to 2.3-fold. The same study recorded no direct effect on proliferation by MTT assay, with PCNA expression unaffected after 24 hours, but reported increased survival of treated cells under hydrogen peroxide stress. The authors attributed the outgrowth, survival and migration findings to dose-dependent increases in the phosphorylation of FAK and paxillin, with total protein levels unaltered (J Appl Physiol, 2011). On the human side, Sikiric and colleagues describe a BPC-157 formulation designated PL 14736 as having been tested in clinical phase 2 for inflammatory bowel disease and no further (Curr Med Chem, 2012). Primary results from that trial have not appeared in the peer-reviewed literature. BPC-157 has been listed by name in section S0 of the WADA Prohibited List since 2022, the first substance named as an example in that section.

For TB-500 the published record is thin and mostly indirect. Esposito and colleagues synthesised Ac-LKKTETQ and identified it by high-resolution mass spectrometry as the content of material marketed as TB-500, work performed to build an anti-doping detection method rather than to study the peptide's activity (Drug Test Anal, 2012). The functional work on this sequence is older and used the non-acetylated form. Philp and colleagues compared full-length thymosin beta-4 with its seven-residue actin-binding motif LKKTETQ and with peptides lacking part of that motif. In human umbilical vein endothelial cell migration assays and chick aortic arch sprouting assays, thymosin beta-4 and the isolated motif showed near-identical activity at approximately 50 nM, while peptides missing any portion of the motif were inactive (FASEB J, 2003). That result is for LKKTETQ, not for the N-acetylated peptide in this vial. The wider thymosin beta-4 literature, including the clinical programmes, used the full 43-residue protein rather than the heptapeptide, and results from one cannot be read onto the other. No controlled human trial of Ac-LKKTETQ itself has been published.