KLOW 80mg for Research in Canada

What is in KLOW, according to the batch report

KLOW is a four-peptide blend, and the only authoritative list of what a vial holds is its independent batch report. Janoshik test report #172068 (sample received 3 June, analysis 18 June 2026) for the current KLOW 80mg batch reports GHK-Cu 40.45 mg (35.88 mg of the tripeptide GHK plus 4.57 mg copper), BPC-157 10.73 mg, TB-500 10.49 mg — with the TB-500 line labelled “889 Da”, which is the acetylated seven-residue thymosin β4 fragment Ac-LKKTETQ rather than the whole 4963 Da protein^[16] — and KPV 11.08 mg. Added together those come to 72.75 mg against an 80 mg declaration (our sum; the report itself gives only the four component values). The report contains no purity percentage, so this site quotes none for KLOW. Each component has its own literature, nearly all of it in mice, rats and cell culture, and no published study has tested the four together. The vial is sold for laboratory research only.

Key facts

• KPV is Lys-Pro-Val, the last three residues (11–13) of α-melanocyte-stimulating hormone; it keeps the parent hormone’s anti-inflammatory activity in animal models without its pigmentary effect^[1]. It is the component that separates KLOW from GLOW.
• KPV’s best-studied model is mouse colitis: oral KPV reduced dextran-sulfate- and TNBS-induced colitis, and the peptide enters cells through the di/tripeptide transporter PepT1^{[3, 4]}.
• TB-500 here is the fragment (889 Da), whereas GLOW’s report reads “TB4” (full-length thymosin β4). Two different molecules under one trade name — see the TB-500 research guide.
• GHK-Cu and BPC-157 are covered in depth on the GLOW guide, the GHK-Cu guide and the BPC-157 guide; the anchor studies are summarised below.
• No blend data: the closest published comparison is a 2026 rat tendon study of BPC-157 plus TB-500, which found no additive effect^[18]. Nothing tests KPV or GHK-Cu alongside them.
• Regulatory status: none of the four has an approved drug product in Canada, the US or the EU.

Identity of the components

Identity values read from PubChem and ChEMBL on 30 September 2026; batch quantities from Janoshik #172068.

KPV: what has been studied

Where it comes from

α-Melanocyte-stimulating hormone (α-MSH) is a 13-residue peptide cut from pro-opiomelanocortin. Its anti-inflammatory effects — on NF-κB activation, adhesion molecules, cytokine production, IL-10 synthesis and T-cell activity — have been shown in animal models of fever, contact dermatitis, vasculitis, gut, brain, airway and eye inflammation, and arthritis; because α-MSH also darkens pigment, its C-terminal tripeptide KPV, which keeps the anti-inflammatory activity but not the pigmentary one, was singled out as an alternative^[1]. A 2000 study found that α-MSH and KPV inhibited Staphylococcus aureus colony formation and reduced viability and germ-tube formation of Candida albicans in vitro, over a range that included picomolar concentrations, and that the effect tracked a rise in cellular cAMP^[2].

Cell culture

In human intestinal epithelial lines (Caco2-BBE, HT29-Cl.19A) and Jurkat T cells stimulated with pro-inflammatory cytokines, nanomolar KPV inhibited NF-κB and MAP-kinase signalling and reduced cytokine secretion; competition and radiolabel experiments showed the peptide is carried into cells by the di/tripeptide transporter PepT1^[3].

Mouse

Dalmasso and colleagues added KPV to drinking water and reported a lower incidence of dextran-sulfate (DSS) and TNBS colitis with reduced pro-inflammatory cytokine expression^[3]. Kannengiesser and colleagues, in the same year, treated DSS colitis and CD45RB^hi transfer colitis: KPV-treated mice recovered earlier, regained more weight, had fewer inflammatory infiltrates and lower myeloperoxidase activity, and the effect persisted in mice lacking a functional melanocortin-1 receptor, so at least part of it is receptor-independent^[4]. In a 2016 azoxymethane/DSS model of colitis-associated cancer, KPV reduced tumour formation in wild-type mice but not in PepT1-knockout mice, again pointing to PepT1 as the route in^[5]. Later delivery work loaded KPV into hyaluronic-acid nanoparticles or a KPV-binding hydrogel to concentrate it in the inflamed colon of mice^{[6, 7]}.

Human

We found no clinical trial of KPV itself in PubMed. The 2008 review discusses it as a candidate for future development, which is where the published record stands^[1].

GHK-Cu, BPC-157 and TB-500 in brief

GHK-Cu: in fibroblast culture it raised collagen synthesis from picomolar concentrations without changing cell number^[8]; in rat wound chambers it increased dry weight, DNA, collagen and glycosaminoglycans in a concentration-dependent way^[9]; in rat ACL reconstruction its effect on knee laxity at 6 weeks had vanished by 12 weeks^[10]. BPC-157: a 15-residue gastric-juice peptide fragment characterised in 1993^[11], with rat data on Achilles tendon transection^[12] and on angiogenesis through VEGFR2^[13], and a 2025 systematic review reporting no clinical safety data^[14]. TB-500 (Ac-LKKTETQ): the seven-residue actin-binding motif of thymosin β4 reproduced the whole peptide’s endothelial migration and sprouting activity in vitro^[15]; the fragment was identified as the ingredient of TB-500 products in 2012 and is treated as a suspected doping agent, with a detection method in horses^{[16, 17]}. The single rat study combining BPC-157 with TB-500 found no additive benefit^[18].

KLOW vs GLOW: what the reports show

Study summary

What the evidence does not show

• There is no published study of KLOW or of any four-way GHK-Cu + BPC-157 + TB-500 + KPV mixture. Component results cannot be summed to predict a blend.
• KPV’s evidence is almost entirely mouse colitis and cell culture^{[3, 4, 5]}; no human trial of KPV was found. Its antimicrobial data are in-vitro^[2].
• The GHK-Cu animal effects are small studies from 1993–2015, one of which faded once treatment stopped^[10].
• Report #172068 gives no purity value, and the four component masses sum below the declared 80 mg; both facts are printed here as they stand.
• The TB-500 fragment is a suspected doping agent in the analytical literature^{[16, 17]}. Nothing on this page is a claim about skin, gut, recovery, inflammation or any effect in people.

Handling and storage for laboratory use

• Lyophilized powder in a sealed vial: cool, dry and dark for short periods; −20 °C for long-term storage per the site’s guidance; avoid repeated freeze–thaw.
• All four components are water-soluble; the mouse colitis studies delivered KPV in drinking water^[3] and the rat studies used saline^{[9, 18]}. A dissolved vial is a four-analyte sample; the blend COA guide covers reading one component at a time.
• Mass spectrometry separates the 889 Da fragment from 4963 Da thymosin β4 — the line on the report that tells KLOW’s TB-500 apart from GLOW’s.

References

1. Brzoska T, Luger TA, Maaser C et al. (2008). Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory and protective effects in vitro and in vivo, and future perspectives for the treatment of immune-mediated inflammatory diseases. Endocrine reviews 29(5):581-602. doi:10.1210/er.2007-0027. PMID 18612139
2. Cutuli M, Cristiani S, Lipton JM et al. (2000). Antimicrobial effects of alpha-MSH peptides. Journal of leukocyte biology 67(2):233-9. doi:10.1002/jlb.67.2.233. PMID 10670585
3. Dalmasso G, Charrier-Hisamuddin L, Nguyen HT et al. (2008). PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology 134(1):166-78. doi:10.1053/j.gastro.2007.10.026. PMID 18061177
4. Kannengiesser K, Maaser C, Heidemann J et al. (2008). Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflammatory bowel diseases 14(3):324-31. doi:10.1002/ibd.20334. PMID 18092346
5. Viennois E, Ingersoll SA, Ayyadurai S et al. (2016). Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of the anti-inflammatory PepT1-mediated tripeptide KPV in a murine model. Cellular and molecular gastroenterology and hepatology 2(3):340-357. doi:10.1016/j.jcmgh.2016.01.006. PMID 27458604
6. Xiao B, Xu Z, Viennois E et al. (2017). Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis. Molecular therapy : the journal of the American Society of Gene Therapy 25(7):1628-1640. doi:10.1016/j.ymthe.2016.11.020. PMID 28143741
7. Zhao Y, Xue P, Lin G et al. (2022). A KPV-binding double-network hydrogel restores gut mucosal barrier in an inflamed colon. Acta biomaterialia 143:233-252. doi:10.1016/j.actbio.2022.02.039. PMID 35245681
8. Maquart FX, Pickart L, Laurent M et al. (1988). Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+. FEBS letters 238(2):343-6. doi:10.1016/0014-5793(88)80509-x. PMID 3169264
9. Maquart FX, Bellon G, Chaqour B et al. (1993). In vivo stimulation of connective tissue accumulation by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+ in rat experimental wounds. The Journal of clinical investigation 92(5):2368-76. doi:10.1172/JCI116842. PMID 8227353
10. Fu SC, Cheuk YC, Chiu WY et al. (2015). Tripeptide-copper complex GHK-Cu (II) transiently improved healing outcome in a rat model of ACL reconstruction. Journal of orthopaedic research : official publication of the Orthopaedic Research Society 33(7):1024-33. doi:10.1002/jor.22831. PMID 25731775
11. Sikirić P, Petek M, Rucman R et al. (1993). A new gastric juice peptide, BPC. An overview of the stomach-stress-organoprotection hypothesis and beneficial effects of BPC. Journal of physiology, Paris 87(5):313-27. doi:10.1016/0928-4257(93)90038-u. PMID 8298609
12. Staresinic M, Sebecic B, Patrlj L et al. (2003). Gastric pentadecapeptide BPC 157 accelerates healing of transected rat Achilles tendon and in vitro stimulates tendocytes growth. Journal of orthopaedic research : official publication of the Orthopaedic Research Society 21(6):976-83. doi:10.1016/S0736-0266(03)00110-4. PMID 14554208
13. Hsieh MJ, Liu HT, Wang CN et al. (2017). Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation. Journal of molecular medicine (Berlin, Germany) 95(3):323-333. doi:10.1007/s00109-016-1488-y. PMID 27847966
14. Vasireddi N, Hahamyan H, Salata MJ et al. (2025). Emerging Use of BPC-157 in Orthopaedic Sports Medicine: A Systematic Review. HSS journal : the musculoskeletal journal of Hospital for Special Surgery 21(4):485-495. doi:10.1177/15563316251355551. PMID 40756949
15. Philp D, Huff T, Gho YS et al. (2003). The actin binding site on thymosin beta4 promotes angiogenesis. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 17(14):2103-5. doi:10.1096/fj.03-0121fje. PMID 14500546
16. Esposito S, Deventer K, Goeman J et al. (2012). Synthesis and characterization of the N-terminal acetylated 17-23 fragment of thymosin beta 4 identified in TB-500, a product suspected to possess doping potential. Drug testing and analysis 4(9):733-8. doi:10.1002/dta.1402. PMID 22962027
17. Ho EN, Kwok WH, Lau MY et al. (2012). Doping control analysis of TB-500, a synthetic version of an active region of thymosin β₄, in equine urine and plasma by liquid chromatography-mass spectrometry. Journal of chromatography. A 1265:57-69. doi:10.1016/j.chroma.2012.09.043. PMID 23084823
18. Biçer O, Adanir O, Güleryüz Y et al. (2026). Effects of BPC-157 and TB-500 on Achilles tendon healing in rats: A histopathological and biomechanical study. Joint diseases and related surgery 37(3):822-837. doi:10.52312/jdrs.2026.2951. PMID 42542926