Peerless Peptides

BPC-157 + GHK-Cu + KPV + TB-500 Blend

Four-peptide research preparation

A fixed-composition research preparation containing BPC-157 (synthetic 15-amino-acid pentadecapeptide), GHK-Cu (copper(II) coordination complex of the glycyl-L-histidyl-L-lysine tripeptide), KPV (α-melanocyte-stimulating hormone C-terminal tripeptide Lys-Pro-Val), and TB-500 (synthetic heptapeptide Ac-LKKTETQ corresponding to residues 17-23 of thymosin beta-4) in a single lyophilized vial. Combined administration of these four compounds has not been characterized in the peer-reviewed literature. No peer-reviewed study of any 2-, 3-, or 4-component combination of BPC-157, GHK-Cu, KPV, and TB-500 has been published as of May 2026.

Available for laboratory research use only.

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Biochemical Profile

CAS Number
137525-51-0 (BPC-157), 89030-95-5 (GHK-Cu), 67727-97-3 (KPV), 885340-08-9 (TB-500)
Molecular Formula
C62H98N16O22 (BPC-157), C14H22CuN6O4 (GHK-Cu), C16H30N4O4 (KPV), C38H68N10O14 (TB-500)
Molecular Weight
1419.54 g/mol (BPC-157), 402.9 g/mol (GHK-Cu), 342.44 g/mol (KPV), 889.02 g/mol (TB-500)
Purity
≥98% (GHK-Cu); ≥99% (BPC-157, KPV, TB-500) (HPLC-UV per component (RP-HPLC plus ICP-MS Cu content for GHK-Cu))
PubChem CID
9941957 (BPC-157), 378611 (GHK-Cu), 125672 (KPV), 62707662 (TB-500)
Amino Acid Sequence
Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val (BPC-157) | Gly-His-Lys (1:1 Cu(II) complex, GHK-Cu) | H-Lys-Pro-Val-OH (KPV) | Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln (TB-500)

Per-Component Mechanism Summary and the Combined-Administration Evidence Gap

This preparation contains four research peptides with distinct, well-separated mechanism literatures. Each component has been investigated in isolation; no peer-reviewed study has characterized the combined molecular pharmacology of these four compounds administered together.

BPC-157 has been investigated as a modulator of nitric oxide signaling and as an upstream effector in the VEGFR2-Akt-eNOS angiogenesis pathway in rodent preparations[1]. The receptor-binding profile has not been established; no specific high-affinity receptor has been identified in the indexed peer-reviewed literature. Approximately 87% of the ~200 PubMed-indexed BPC-157 papers are authored by the Sikirić research group at the University of Zagreb. The only independent pharmacokinetic study (Xu 2022) reported plasma half-lives of approximately 15 minutes intravenous in rat, 5 minutes intravenous in beagle dog, and 20-30 minutes intramuscular[2].

GHK-Cu presents an ATCUN-style amino-terminal Cu(II)/Ni(II) binding site with reported log K of approximately 16.44 at physiological pH, sufficient to extract Cu(II) from serum albumin in vitro[3]. The Reims group at Faculté de Médecine (Maquart, Borel, Hornebeck) reported observations on collagen synthesis in dermal fibroblast culture at picomolar to nanomolar concentrations, and identified the GHK triplet within the alpha-2(I) chain of collagen[4]. The receptor-binding profile has not been characterized; no specific high-affinity receptor has been identified. The 1994 Phase III Iamin gel trial in diabetic neuropathic ulcers failed to beat control as a drug, but the 1996 FDA Class I medical-device clearance for topical use persists.

KPV has been investigated as the C-terminal anti-inflammatory fragment of α-MSH. Multiple primary studies reported KPV anti-inflammatory activity independent of melanocortin-receptor signaling. Land (2012) reported that KPV translocated into the nucleus and competed for importin-α3 binding with the NF-κB p65/RelA subunit, blocking p65 nuclear import without affecting upstream IκBα phosphorylation[5]. Dalmasso (2008) at Emory reported PepT1-mediated intestinal uptake with Km of approximately 160 micromolar[6].

TB-500 (Ac-LKKTETQ) corresponds to the actin-binding region (residues 17-23) of the parent protein thymosin beta-4 (Tβ4, 43-amino-acid, MW ~4921 Da). Tβ4 is the principal G-actin-sequestering protein in most metazoan cells; the 7-mer reproduces the actin-binding contact[7]. The two molecules differ by approximately 5x in mass and should not be conflated; every RegeneRx-sponsored clinical trial used the full 43-mer parent.

Combined-mechanism investigation across these four molecules has not been published. The four published mechanism literatures are mechanistically distinct (gastric mucosal NO modulation, copper coordination chemistry, NF-κB nuclear-import competition, and actin sequestration). No peer-reviewed pharmacokinetic, pharmacodynamic, or receptor-occupancy study has investigated the combined administration profile.

Research Applications

Component Composition

This preparation supplies four distinct synthetic research peptides as a single lyophilized vial. BPC-157 is a synthetic 15-amino-acid pentadecapeptide (Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val), CAS 137525-51-0, molecular formula C62H98N16O22, molecular weight 1419.54 g/mol, PubChem CID 9941957. GHK-Cu is the 1:1 coordination complex of the tripeptide Gly-His-Lys with copper(II), CAS 89030-95-5, molecular formula C14H22CuN6O4, molecular weight 402.9 g/mol, PubChem CID 378611; the complex must be disambiguated from GHK free peptide (CAS 49557-75-7, no Cu) and prezatide copper acetate (CAS 130120-57-9, the bis-acetate drug form), and per-batch ICP-MS confirms Cu stoichiometry. KPV is H-Lys-Pro-Val-OH (the free-acid form), CAS 67727-97-3, molecular formula C16H30N4O4, molecular weight 342.44 g/mol, PubChem CID 125672; it must be distinguished from the N-acetylated, C-amidated form Ac-Lys-Pro-Val-NH2 (CAS 112965-21-6, MW ~384.48), and HPLC purity is read at 210-220 nm because KPV contains no aromatic residues. TB-500 is the synthetic acetylated heptapeptide Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln, CAS 885340-08-9, molecular formula C38H68N10O14, molecular weight 889.02 g/mol, PubChem CID 62707662; it must be distinguished from the full 43-residue parent protein thymosin beta-4 (MW ~4921 Da, CAS 77591-33-4), which differs by approximately 5x in mass.

BPC-157 Research Summary

BPC-157 was first described by the Sikirić research group at the University of Zagreb in 1991-1993 as a fragment of a putative ~40 kDa 'body protection compound' protein. The parent protein has never been formally sequenced or assigned a UniProt entry. The published literature is dominated by preclinical rat-model work in gastric mucosal injury, tendon repair, and wound preparations, with approximately 87% of the ~200 indexed papers originating from the Zagreb laboratory[1][8]. Mechanism work has examined nitric oxide signaling and the VEGFR2-Akt-eNOS angiogenesis pathway in rodent preparations; the Chang research group at Chang Gung University, Taiwan, is the only non-Zagreb laboratory to have published substantive original mechanism research, with observations on cell-survival and Vinculin/F-actin distribution in cultured tendon explants[9]. The Xu 2022 independent pharmacokinetic study reported plasma half-lives of approximately 15 minutes intravenous in rat, 5 minutes intravenous in beagle dog, and 20-30 minutes intramuscular, with bioavailability ranging 14-19% in rats and 45-51% in dogs[2]. No randomized, placebo-controlled, peer-reviewed efficacy study in any indication has been published. NCT07437547 (Phase 2 acute hamstring strain, Hudson Biotech) is the first BPC-157 trial registered outside the Sikirić research orbit in 33 years and is recruiting as of February 2026[10].

GHK-Cu Research Summary

GHK-Cu was first isolated from human plasma by Loren Pickart at the University of California, San Francisco in 1973. The Gly-His-Lys triplet appears as an internal motif in albumin (UniProt P02768), collagen alpha-2(I) (P08123), SPARC/osteonectin (P09486), and thrombospondin-1 (P07996), and is liberated proteolytically at sites of tissue injury. The reported log K of approximately 16.44 at physiological pH places GHK among the strongest Cu(II) chelators of any short peptide[3]. The strongest non-Pickart mechanism corpus is the Reims group at Faculté de Médecine (Maquart, Pickart, Laurent, Gillery, Monboisse, Borel), with the 1988 FEBS Letters paper reporting observations on collagen synthesis in dermal fibroblast culture at picomolar to nanomolar concentrations[4]. The topical-route human evidence consists of the Mulder 1994 multicenter RCT in diabetic neuropathic ulcers (industry-sponsored, evaluator-blinded)[11], the Leyden 2002 AAD conference abstract (never published in a peer-reviewed journal), and the Miller 2006 split-face CO2-laser study, which reported no statistically significant benefit in blinded objective measures of erythema or wrinkle measurement[12]. NCT07437586 (CuHeal, Hudson Biotech, Phase 2 topical gel) is the first credible drug-development pathway entry GHK-Cu has seen since the 1994 Phase III Iamin failure[13]. No randomized controlled trial of injectable GHK-Cu in any human indication has been published in the indexed literature.

KPV Research Summary

KPV was characterized by Marlene Hiltz and James Lipton at UT Southwestern in a 1989 FASEB Journal paper as the minimal C-terminal anti-inflammatory fragment of α-MSH that retained activity in a murine picryl-chloride contact-dermatitis ear-swelling model despite lacking the central HFRW melanocortin-receptor pharmacophore[14]. Getting (2003) reported a direct head-to-head comparison of core α-MSH peptides (containing HFRW) against the KPV C-terminal fragment in mouse peritonitis: core peptides activated macrophages through melanocortin receptors and elevated cAMP, while KPV failed to elevate cAMP yet reduced immune-cell accumulation comparably[15]. Land (2012) reported that KPV translocated into the nucleus of human bronchial epithelial (BEAS-2B) cells and competed for importin-α3 binding with NF-κB p65/RelA, blocking p65 nuclear import[5]. Dalmasso (2008) at Emory reported PepT1-mediated intestinal epithelial transport with Km of approximately 160 micromolar; oral KPV administration in drinking water was associated with reduced disease activity score in murine DSS- and TNBS-colitis preparations[6]. As of May 2026, no peer-reviewed Phase 1, Phase 2, or Phase 3 RCT of KPV peptide for any indication has been published; ClinicalTrials.gov returns no registered trial with KPV as the investigational product.

TB-500 Research Summary

TB-500 is the synthetic acetylated heptapeptide Ac-LKKTETQ corresponding to residues 17-23 of the parent protein thymosin beta-4 (Tβ4). The 7-mer (MW 889 Da) is the form sold in laboratory research commerce; full-length Tβ4 (MW ~4921 Da) is the form used in every RegeneRx-sponsored clinical trial[7]. The actin-binding motif maps to residues 17-22 of the parent protein (LKKTET); X-ray crystallography demonstrated that essentially the entire 43-residue Tβ4 chain wraps the actin monomer in solution, with LKKTET as the high-affinity contact region[16]. Philp (2003) reported that the LKKTETQ 7-mer and full Tβ4 displayed comparable activity at sub-micromolar concentrations in endothelial cell-migration and aortic-ring sprouting assays[17], and the same group's 2003 db/db diabetic and aged-mouse dermal wound study is the foundation of the commercial premise that the 7-mer recapitulates full-Tβ4 dermal activity. The four completed Phase 3 trials in the RegeneRx ophthalmic program (ARISE-1, ARISE-2, ARISE-3 dry-eye; SEER-3 European neurotrophic keratopathy) all missed pre-specified primary endpoints. RegeneRx filed SEC Form 15 in August 2023, terminating its public-company reporting obligations. NCT07487363 (Hudson Biotech, Phase 1/2 cardiovascular biomarkers) is the first publicly registered US trial using the LKKTETQ 7-mer by name[18].

Combined Administration & Status

No peer-reviewed study of any 2-, 3-, or 4-component combination of BPC-157, GHK-Cu, KPV, and TB-500 administered together has been published in the indexed literature as of May 2026. The four mechanism literatures (gastric mucosal NO modulation, copper coordination chemistry, NF-κB nuclear-import competition, and actin sequestration) are mechanistically distinct, and combined pharmacokinetic, pharmacodynamic, and receptor-occupancy data are absent from the published record. This product is supplied as a fixed-composition single-vial research preparation; the underlying biology is independent and the combined-administration evidence base is empty. The current regulatory status of each component is structurally distinct. BPC-157, KPV, and TB-500 were each removed from FDA 503A Category 2 (Do-Not-Compound) effective April 22, 2026, as part of the 12-peptide Kennedy reclassification cohort, and all three are on the Pharmacy Compounding Advisory Committee Day 1 docket scheduled for July 23, 2026, with a proposed indication framed as wound healing and inflammatory conditions[19]. Removal from Category 2 does not confer Category 1 status or compoundability. GHK-Cu was also removed from 503A Category 1 and Category 2 effective April 22, 2026, by procedural nominator withdrawal, but is NOT on the July 23-24, 2026 PCAC docket; GHK-Cu has been grouped for a separate February 2027 PCAC review alongside LL-37, Dihexa Acetate, PEG-MGF, and Melanotan II. Per-component WADA status: BPC-157 is explicitly listed under S0 (Non-Approved Substances), banned at all times with no Therapeutic Use Exemption pathway; KPV, TB-500, and GHK-Cu are not explicitly named on the 2026 Prohibited List, though the S0 catch-all may apply at competition control[20]. Australia's TGA has scheduled BPC-157 as Schedule 9 (Prohibited Substance) effective July 1, 2026; TGA scheduling decisions on the other three components are pending.

Reconstitution & Storage

Recommended Diluent
Bacteriostatic water (0.9% benzyl alcohol). Reducing-agent buffers (ascorbate, thiols) and phosphate buffers are unsuitable for the copper complex.
Storage (lyophilized)
-20°C, dry, dark, sealed amber vial with desiccant
Storage (reconstituted)
2-8°C, single-use aliquots only; use within 14 days (limited by GHK-Cu stability)
Shelf Life
18-24 months lyophilized at -20°C (limited by GHK-Cu component)

Research References

  1. [1] Sikirić P, Seiwerth S, Rucman R, et al. Stable gastric pentadecapeptide BPC 157-NO-system relation. Curr Pharm Des. 2014;20(7):1126-1135. PMID:23755725
  2. [2] Xu T, Zhang Z, et al. Pharmacokinetics, bioavailability, and tissue distribution of body protection compound 157 (BPC 157) in rats and beagle dogs. Front Pharmacol. 2022;13:1052033. PMID:36588717
  3. [3] Sigel H, Martin RB. Coordinating properties of the amide bond. Stability and structure of metal ion complexes of peptides and related ligands. Chem Rev. 1982;82(4):385-426. doi:10.1021/cr00050a003
  4. [4] Maquart FX, Pickart L, Laurent M, Gillery P, Monboisse JC, Borel JP. Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+. FEBS Lett. 1988;238(2):343-346. PMID:3169264
  5. [5] Land SC. Inhibition of cellular and systemic inflammation cues in human bronchial epithelial cells by melanocortin-related peptides: mechanism of KPV action and a role for MC3R agonists. Int J Physiol Pathophysiol Pharmacol. 2012;4(2):59-73. PMID:22837805
  6. [6] Dalmasso G, Charrier-Hisamuddin L, Nguyen HTT, Yan Y, Sitaraman S, Merlin D. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134(1):166-178. PMID:18061177
  7. [7] Safer D, Elzinga M, Nachmias VT. Thymosin β4 and Fx, an actin-sequestering peptide, are indistinguishable. J Biol Chem. 1991;266(7):4029-4032. PMID:1996337
  8. [8] Sikirić P, Petek M, Rucman R, et al. A new gastric juice peptide, BPC. An overview of the stomach-stress-organoprotection hypothesis and beneficial effects of BPC. J Physiol Paris. 1993;87(5):313-327. doi:10.1016/0928-4257(93)90038-uPMID:8298609
  9. [9] Chang CH, Tsai WC, Lin MS, Hsu YH, Pang JHS. The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration. J Appl Physiol. 2011;110(3):774-780. doi:10.1152/japplphysiol.00945.2010PMID:21030672
  10. [10] Hudson Biotech. BPC 157 for Acute Hamstring Muscle Strain Repair. ClinicalTrials.gov Identifier: NCT07437547. Phase 2, n=120 estimated, status: recruiting since February 2026 (verified 2026-05-19). Primary endpoints: time to return to sport, MRI hamstring injury volume.
  11. [11] Mulder GD, Patt LM, Sanders L, Rosenstock J, Altman MI, Hanley ME, Duncan GW. Enhanced healing of ulcers in patients with diabetes by topical treatment with glycyl-l-histidyl-l-lysine copper. Wound Repair Regen. 1994;2(4):259-269. PMID:17147644
  12. [12] Miller TR, Wagner JD, Baack BR, Eisbach KJ. Effects of topical copper tripeptide complex on CO2 laser-resurfaced skin. Arch Facial Plast Surg. 2006;8(4):252-259. PMID:16847171
  13. [13] Hudson Biotech. Topical GHK-Cu (Copper(II)-Peptide Complex) Gel to Accelerate Re-Epithelialization of Standardized Acute Skin Wounds (CuHeal). ClinicalTrials.gov Identifier: NCT07437586. Phase 2, n=60 estimated, status: recruiting (verified 2026-05-19). Primary endpoint: time to complete re-epithelialization.
  14. [14] Hiltz ME, Lipton JM. Antiinflammatory activity of a COOH-terminal fragment of the neuropeptide alpha-MSH. FASEB J. 1989;3(11):2282-2284. PMID:2550304
  15. [15] Getting SJ, Schiöth HB, Perretti M. Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptides. J Pharmacol Exp Ther. 2003;306(2):631-637. PMID:12750433
  16. [16] Irobi E, Aguda AH, Larsson M, et al. Structural basis of actin sequestration by thymosin-β4: implications for WH2 proteins. EMBO J. 2004;23(18):3599-3608. PMID:15329672
  17. [17] Philp D, Huff T, Gho YS, Hannappel E, Kleinman HK. The actin binding site on thymosin β4 promotes angiogenesis. FASEB J. 2003;17(14):2103-2105. PMID:14500546
  18. [18] Hudson Biotech. TB-500 (17-23 fragment) for cardiovascular biomarkers in stable atherosclerotic cardiovascular disease. ClinicalTrials.gov Identifier: NCT07487363 (Phase 1/2, recruiting; 80 estimated participants; verified 2026-05-19).
  19. [19] Frier Levitt analysis. FDA Removes 12 Peptides from 503A Category 2 (Do-Not-Compound List), Schedules July 23, 2026 PCAC Review. April 2026. BPC-157, KPV, TB-500, and MOTS-c on the July 23, 2026 PCAC Day 1 docket with proposed indication framed as wound healing and inflammatory conditions. GHK-Cu removed from 503A Category 1 and Category 2 effective April 22, 2026 by procedural nominator withdrawal and grouped for a separate February 2027 PCAC review.
  20. [20] World Anti-Doping Agency. 2026 Prohibited List. International Standard, effective January 1, 2026. BPC-157 is listed under S0 (Non-Approved Substances), banned at all times with no Therapeutic Use Exemption pathway. KPV, TB-500, and GHK-Cu are not explicitly named on the 2026 list; the S0 catch-all may apply at competition control.

Scientific Journal Author

Predrag Sikirić, MD, PhD

Department of Pharmacology, University of Zagreb School of Medicine

Landmark Publications

  • Sikirić P, Petek M, Rucman R, et al. A new gastric juice peptide, BPC. J Physiol Paris. 1993;87(5):313-327. (PMID 8298609) — foundational characterization of the parent BPC concept from which BPC-157 was derived.
  • Sikirić P, Seiwerth S, Rucman R, et al. Stable gastric pentadecapeptide BPC 157-NO-system relation. Curr Pharm Des. 2014;20(7):1126-1135. (PMID 23755725) — consolidates the nitric oxide signaling mechanism literature.
  • Sikirić P, Seiwerth S, Brcic L, et al. Stable gastric pentadecapeptide BPC 157 as a novel cytoprotective mediator. Curr Pharm Des. 2018;24(18):1990-2001. (PMID 29879879) — secondary-literature synthesis review.

Dr. Sikirić is independently cited here as the originating researcher of BPC-157 at the University of Zagreb. This blend preparation contains three additional research peptides whose originating researchers are independently recognized in the per-component PDP entries: Loren Pickart, PhD (GHK-Cu, isolated from human plasma at the University of California, San Francisco in 1973; deceased December 10, 2023); James M. Lipton, MD with co-discoverer Marlene E. Hiltz (KPV, characterized at UT Southwestern in 1989); and Allan L. Goldstein, PhD (thymosin family of peptides at The George Washington University). There is no affiliation, financial relationship, or endorsement between any of these originating researchers, the University of Zagreb, the University of California San Francisco, UT Southwestern Medical Center, The George Washington University, or any associated entity, and Peerless Peptides.

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